hepatobiliary surgery blumgart

V m

Ronald S. ChamberlainLeslie H. Blumgart

a d e m e c uV a d e m e c u m

Table of contents1. Essential Hepatic and Biliary

Anatomy for the Surgeon

2. Imaging of the Liver, BileDucts and Pancreas

3. Endoscopic and PercutaneousManagement of Gallstones

4. Interventional Radiologyin Hepatobiliary Surgery

5. Perioperative Care andAnesthesia Techniques

6. Benign Tumors of the Liver:A Surgical Perspective

7. Hepatocellular Carcinoma

8. Periampullary Cancer andDistal Pancreatic Cancer

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HepatobiliarySurgery

9. Hepatic Resection for ColorectalLiver Metastases: SurgicalIndications and Outcomes

10. The Surgical Approach to Non-Colorectal Liver Metastases:Patient Evaluation, Selectionand Results

11. Surgical Techniques of OpenCholecystectomy

12. Laparoscopic Cholecystectomyand the LaparoscopicManagement of Common BileDuct Stones

13. Surgical Techniques forCompletion of a BilioentericBypass

(excerpt)

Ronald S. Chamberlain, MD, MPA, FACSBeth Israel Medical Center

Albert Einstein College of MedicineNew York, New York

Leslie H. Blumgart, MD, FACS, FRCS (Eng, Edin),FRCPS (Glas)

Memorial-Sloan-Kettering Cancer CenterNew York, New York

Hepatobiliary Surgery

GEORGETOWN, TEXAS

U.S.A.

v a d e m e c u m

L A N D E SB I O S C I E N C E

VADEMECUMHepatobiliary Surgery

LANDES BIOSCIENCEGeorgetown, Texas U.S.A.

Copyright ©2003 Landes BioscienceAll rights reserved.No part of this book may be reproduced or transmitted in any form or by anymeans, electronic or mechanical, including photocopy, recording, or anyinformation storage and retrieval system, without permission in writing from thepublisher.Printed in the U.S.A.

Please address all inquiries to the Publisher:Landes Bioscience, 810 S. Church Street, Georgetown, Texas, U.S.A. 78626Phone: 512/ 863 7762; FAX: 512/ 863 0081

ISBN: 1-57059-630-1

Library of Congress Cataloging-in-Publication DataHepatobiliary surgery / [edited by] Ronald S. Chamberlain, Leslie H.Blumgart.

p.; cm. -- (Vademecum)Includes bibliographical references and index.Ronald S. Chamberlain ISBN 1-57059-630-11. 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 2001617.5´56059 -- dc21

00-064876

While the authors, editors, sponsor and publisher believe that drug selection and dosage andthe specifications and usage of equipment and devices, as set forth in this book, are in accordwith current recommendations and practice at the time of publication, they make nowarranty, expressed or implied, with respect to material described in this book. In view of theongoing research, equipment development, changes in governmental regulations and therapid accumulation of information relating to the biomedical sciences, the reader is urged tocarefully review and evaluate the information provided herein.

The surgical care of patients is a full commitment. As most ofyou will realize, accepting any additional commitments beyondclinical medicine is a burden that is borne by the family of thepracticing surgeon. This past year has been a tremendous bur-den on my family as several works came to fruition. To Kim,the light and joy in my life — thank you, I love you. To Courtneyand Taylor, Daddy is so proud of both you. You are all the sourcesof my inspiration and contentment.

Ronald S. Chamberlain

Dedication

Contents

Preface ............................................................................ xiii

1. Essential Hepatic and Biliary Anatomyfor the Surgeon ................................................................. 1

Ronald S. Chamberlain and Leslie H. BlumgartIntroduction ............................................................................................... 1The Liver .................................................................................................... 1Parenchyma (The Liver Substance) ............................................................. 2Hepatic Veins (OUTFLOW) ...................................................................... 4Hepatic Venous Anomalies ......................................................................... 6Hepatic Arteries (INFLOW) ....................................................................... 6The Biliary Tract ....................................................................................... 10The Common Bile Duct ........................................................................... 11Gallbladder and Cystic Duct ..................................................................... 12Anomalous Biliary Drainage ..................................................................... 16Summary .................................................................................................. 17

2. Imaging of the Liver, Bile Ducts and Pancreas ................ 20Douglas R. DeCorato, Lawrence H. Schwartz

Test Selection ............................................................................................ 21Hepatic Lesions ........................................................................................ 23

3. Endoscopic and Percutaneous Managementof Gallstones ................................................................... 34

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

4. Interventional Radiology in Hepatobiliary Surgery ........ 42Lynn A. Brody and Karen T. Brown

Introduction ............................................................................................. 42Diagnostic Procedures ............................................................................... 42Therapeutic and Palliative Procedures ....................................................... 49

5. Perioperative Care and Anesthesia Techniques ................ 73Mary Fischer, Enrico Ferri, Jose A. Melendez

Introduction ............................................................................................. 73Preoperative Evaluation ............................................................................. 73Hepatic Evaluation ................................................................................... 74Intraoperative Management ...................................................................... 74Postoperative Care .................................................................................... 76

6. Benign Tumors of the Liver: A Surgical Perspective ........ 81Ronald S. Chamberlain

Introduction ............................................................................................. 81Evaluation ................................................................................................. 81Benign Liver Tumors ................................................................................. 85Additional Liver Tumors ........................................................................... 97Conclusions .............................................................................................. 99

7. Hepatocellular Carcinoma ............................................ 101Bryan Clary

Introduction ........................................................................................... 101Etiology .................................................................................................. 101Diagnosis and Pretreatment Planning ..................................................... 102Treatment ............................................................................................... 104Conclusion ............................................................................................. 110

8. Periampullary Cancerand Distal Pancreatic Cancer ........................................ 111

Richard D. SchulickIntroduction ........................................................................................... 111Pancreaticoduodenectomy for Periampullary Cancer .............................. 112Distal Pancreatectomy for Distal Pancreatic Cancer ................................ 115

9. Hepatic Resection for Colorectal Liver Metastases:Surgical Indications and Outcomes .............................. 121

Ronald P. DeMatteo, Yuman FongIntroduction ........................................................................................... 121Epidemiology .......................................................................................... 121Preoperative Evaluation ........................................................................... 121Physical Examination .............................................................................. 122Laboratory Tests ...................................................................................... 122Imaging .................................................................................................. 122Surgical Indications ................................................................................. 123Surgical Results ....................................................................................... 124Survival ................................................................................................... 125Prognostic Variables ................................................................................ 126Recurrent Hepatic Metastases ................................................................. 127Conclusion ............................................................................................. 127

10. The Surgical Approachto Non-Colorectal Liver Metastases: Patient Evaluation,Selection and Results .................................................... 129

Jonathan B. KoeaIntroduction ........................................................................................... 129Patient Selection ..................................................................................... 129Preoperative Staging ................................................................................ 132Techniques of Resection .......................................................................... 136

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

11. Surgical Techniques of Open Cholecystectomy ............. 146Ronald S. Chamberlain

Introduction ........................................................................................... 146Clinical Presentation ............................................................................... 146Preoperative Studies ................................................................................ 147Perioperative Management ...................................................................... 149Operative Technique for Cholycystectomy .............................................. 149Surgical Technique .................................................................................. 152

12. Laparoscopic Cholecystectomy and the LaparoscopicManagement of Common Bile Duct Stones .................. 156

Fredrick BrodyIntroduction ........................................................................................... 156Indications .............................................................................................. 156Laparoscopic Cholecystectomy ............................................................... 156Laparoscopic Common Bile Duct Exploration ........................................ 162

13. Surgical Techniques for Completionof a Bilioenteric Bypass ................................................. 165

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

14. Hilar Cholangiocarcinoma:Surgical Approach and Outcome .................................. 183

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

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

15. Surgical Management of Gallbladder Cancer ................ 201Ronald P. DeMatteo, Yuman Fong

Introduction ........................................................................................... 201Anatomical Considerations ..................................................................... 201Preoperative Evaluation ........................................................................... 202Clinical Presentations .............................................................................. 202Surgical Approach ................................................................................... 205Summary ................................................................................................ 207

16. Techniques of Hepatic Resection .................................. 208Sharon Weber, William R. Jarnagin, Leslie H. Blumgart

Introduction ........................................................................................... 208Operative Technique ............................................................................... 208Right Hepatectomy ................................................................................. 209Extended Right Hepatectomy (Right Hepatic Lobectomy

or Right Trisegmentectomy) ................................................................. 214Left Hepatectomy ................................................................................... 215Left Lateral Segmentectomy (Left Lobectomy) ........................................ 218Extended Left Hepatectomy (Left Trisegmentectomy) ............................ 218Caudate Lobe Resection (Segment I Resection) ...................................... 222Segmental Resection ............................................................................... 224Wedge Resections ................................................................................... 225Postoperative Care .................................................................................. 226

17. Technique for Placementof the Hepatic Arterial Infusion Pump ......................... 227

N. Joseph EspatIntroduction ........................................................................................... 227When Should HAIP Therapy Be Considered? ........................................ 228Preoperative Patient Evaluation ............................................................... 228Surgical Technique for the HAIP Placement ........................................... 229Considerations for Patients with Variant Anatomy .................................. 231Replaced Right Hepatic Artery (RRHA) ................................................. 231Replaced Left Hepatic Artery (RLHA) .................................................... 232Trifurcation of the Common Hepatic Artery (CHA)

into RHA, LHA and GDA .................................................................. 232Creation of the Subcutaneous Pump Pocket ............................................ 232Assessment of Hepatic Perfusion ............................................................. 235Brief Comments on Technical Complications ......................................... 235Summary ................................................................................................ 237

18. Non-Resectional Hepatic Ablative Techniques:Cryotherapy and Radiofrequency Ablation ................... 238

Ronald S. Chamberlain and Ronald KaleyaIntroduction ........................................................................................... 238Indications for Non-Resectional Ablative Therapies ................................ 238Additional Indications and Contraindications ......................................... 239Cryotherapy ............................................................................................ 239Radiofrequency Ablation ........................................................................ 244Results .................................................................................................... 249Summary ................................................................................................ 253

19. Surgical Techniques in the Managementof Hepatic Trauma or Emergencies ............................... 257

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

20. Liver Transplantation .................................................... 270Patricia A. Sheiner, Rosemarie Gagliardi, D. Sukru Emre

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

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

Editors

Contributors

Ronald S. Chamberlain, MD, MPA, FACSChief, Hepatobiliary Surgery and Pancreatic Surgery

Program Director, General SurgeryBeth Israel Medical Center

Albert Einstein College of MedicineNew York, New York

Chapters 1, 6, 11, 14, 18

Leslie H. Blumgart, MD, FACS, FRCS (Eng, Edin),FRCPS (Glas)

Chief, Hepatobiliary ServiceEnid A. Haupt Chair in Surgery

Memorial Sloan-Kettering Cancer Center, New YorkChapters 1, 13, 14, 16

Fredrick BrodyDepartment of SurgeryCleveland Clinic FoundationCleveland, OhioChapter 12

Lynn A. BrodyDivision of Interventional RadiologyMemorial Sloan-Kettering Cancer CenterNew York, New YorkChapter 4

Karen T. BrownDivision of Interventional RadiologyMemorial Sloan-Kettering Cancer CenterNew York, New YorkChapter 4

Bryan ClaryDepartment of SurgeryDuke University Medical CenterDurham, North CarolinaChapter 7

Douglas R. DeCoratoDepartment of RadiologyMemorial Sloan-Kettering Cancer CenterNew York, New YorkChapter 2

Ronald P. DeMatteoDepartment of SurgeryMemorial Sloan-Kettering Cancer CenterNew York, New YorkChapters 9, 15

Sukru EmreMiller Transplantation InstituteMount Sinai Medical CenterNew York, New YorkChapter 20

N. Joseph EspatDepartment of SurgeryUniversity of Illinois at ChicagoChicago, IllinoisChapter 17

Enrico FerriDepartment of AnesthesiologyMemorial Sloan-Kettering Cancer CenterNew York, New YorkChapter 5

Mary FischerDepartment of AnesthesiologyMemorial Sloan-Kettering Cancer CenterNew York, New YorkChapter 5

Yuman FongDepartment of SurgeryMemorial Sloan-Kettering Cancer CenterNew York, New YorkChapters 9, 15

Amber A. GuthNew York University School of MedicineSurgical ICUBellevue Hospital CenterNew York, New YorkChapter 19

Rosemarie GagliardiMiller Transplantation InstituteMount Sinai Medical CenterNew York, New YorkChapter 20

William R. JarnaginDepartment of SurgeryMemorial Sloan-Kettering Cancer CenterNew York, New YorkChapter 16

Ronald N. KaleyaDepartment of SurgeryMontefiore Medical CenterBronx, New YorkChapter 18

Jonathan B. KoeaHepatobiliary ServiceDepartment of SurgeryMemorial Sloan-Kettering Cancer CenterNew York, New YorkChapter 10

Robert C. KurtzGastroenterologyMemorial Sloan-Kettering Cancer CenterNew York, New YorkChapter 3

Jose A. MelendezDepartment of AnesthesiologyMemorial Sloan-Kettering Cancer CenterNew York, New YorkChapter 5

H. Leon PachterDepartment of SurgeryNew York University School of MedicineDirector, Division of Shock and TraumaBellevue Hospital CenterNew York, New YorkChapter 19

Seth RichterDepartment of GastroenterologyMemorial Sloan-Kettering Cancer CenterNew York, New YorkChapter 3

Pierre F. SaldingerDanbury HospitalDanbury, ConnecticutChapter 13

Patricia A. SheinerMiller Transplantation InstituteMount Sinai Medical CenterNew York, New YorkChapter 20

Richard D. SchulickDepartment of Surgery and OncologyThe Johns Hopkins HospitalBaltimore, MarylandChapter 8

Lawrence H. SchwartzDepartment of RadiologyMemorial Sloan-Kettering Cancer CenterNew York, New YorkChapter 2

Sharon WeberHepatobiliary ServiceDepartment of SurgeryMemorial Sloan-Kettering Cancer CenterNew York, New YorkChapter 16

PrefaceHepatobiliary Surgery is a technical manual and not a textbook. Although

some chapters are robust in their discussion of anatomic and physiologicdetail, others are written in a purely “how to” style. At its core, the book iswritten as a reference and guidebook for practicing surgeons, gastroenter-ologists, and interventional radiologists with an interest in hepatobiliary dis-eases. However, we believe it will also be of great value to medical studentson surgery clerkships, general surgery residents, and surgical oncology fel-lows as they pursue excellence in their education and training.

Mastery of hepatobiliary surgery requires one to not only be an accom-plished surgical craftsman, but also a competent internist, knowledgeablegastroenterology collaborator, and skilled interpreter of radiologic images.No one medical discipline has a patent on knowledge and opinion, andmost complex hepatobiliary problems are best managed by securing the opin-ion of experts in all disciplines before embarking on a treatment plan. Thisbook attempts to parallel that dialogue by collating the expertise, experienceand opinion of all of these disciplines and distilling it down into one vol-ume. Please note, this book is not gospel about how unique patients shouldbe managed, nor does it claim to present the only way in which variousoperative procedures and interventions can be performed. Rather, this bookpresents a strategy that works for us and can hopefully be utilized to enhanceyour practice and the care of your patients.


Acknowledgments

This book represents a group project. There are many people whose effortswe acknowledge here and many others whose names we may fail to mentionbut to whom we remain grateful. We acknowledge …

Our contributing authors, whose generosity in compiling, collating andwriting up their experience has made this effort possible.

The committed editorial, organizational, and proofreading expertise pro-vided by Judy Lampron. Judy’s tremendous energy and tireless efforts incommunicating and cajoling contributors, devoting hours to late night andweekend manuscript review sessions, and providing constant support madeit all possible.

Maria Reyes whose professionalism and expertise in the editorial processhave contributed greatly to the successful and timely completion of this work.

Tireless efforts from Kim Mitchell, Cynthia Dworaczyk, and Ron Landesfrom Landes Bioscience have made this all possible.


CHAPTER 1CHAPTER 1

Hepatobiliary Surgery, edited by Ronald S. Chamberlain and Leslie H. Blumgart.©2003 Landes Bioscience.

Essential Hepatic and Biliary Anatomyfor the Surgeon

Ronald S. Chamberlain and Leslie H. Blumgart

IntroductionThat every surgeon will experience complications is a certainty. Yet, major surgi-

cal complications are often avoidable and frequently the result of three tragic surgi-cal errors. These errors are: 1) a failure to possess sufficient knowledge of normalanatomy 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 theseerrors are remediable with study and effort. In regard to the last error, most surgeonslearn humility through their failures and at the expense of their patients, while somenever learn.

The importance of a precise knowledge of parenchymal structure, blood supply,lymphatic drainage, and variant anatomy on outcome is perhaps nowhere moreapparent then in hepatobiliary surgery. Though the liver was historically an areawhere few brave men dared to tread, and even fewer returned a second time, recentadvances in anesthetic technique and perioperative care now permit hepatic surgeryto be performed with low morbidity and mortality in both academic and commu-nity hospitals. That said, surgeons are duly cautioned to inventory their own skillsand knowledge before venturing forward into the right upper quadrant. This chap-ter will review functional biliary and hepatic anatomy necessary for the conduct ofsafe and successful hepatic operations.

The Liver

Surface AnatomyThe 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 onthe right side, although it is not uncommon for the left lateral segment to arch overthe spleen. The superior surface of the liver is molded to and abuts the undersurfaceof the diaphragm on both the right and left sides. During normal inspiration, theliver 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 poste-rior surface where it reflects onto the undersurface of the diaphragm to form theright and left triangular ligaments. The liver is attached to the diaphragm and ante-rior abdominal wall by three separate ligamentous attachments, namely the falci-form, round, and right and left triangular ligaments. (Figure 1.1) The falciformligament, which is situated on the anterior surface of the liver, arises from the ante-

2 Heptobiliary Surgery

1

rior leaflets of the right and left triangular ligaments and terminates inferiorly wherethe ligamentum teres enters the umbilical fissure. The gallbladder is normally at-tached to the undersurface of the right lobe and directed towards the umbilicalfissure. At the base of the gallbladder fossa, is the hilar transverse fissure throughwhich the main portal structures to the right lobe course. Additional importantlandmarks on the posterior liver surface include a deep vertical groove in which theinferior vena cava is situated and a large bare area (i.e. no peritoneal coating) that isnormally in contact with the right hemidiaphragm and right adrenal gland. The leftlateral segment of the liver arches over the caudate lobe that is situated to the left ofthe vena cava. The caudate lobe is demarcated on the left by a fissure containing theligamentum venosum (a remnant of the umbilical vein). Additional left-sided im-portant surface features include the gastrohepatic omentum located between the leftlateral segment and the stomach. The gastrohepatic omentum may contain replacedor accessory hepatic arteries. Finally, there is usually a thick fibrous band that envel-ops the vena cava high on the right side and runs posteriorly towards the lumbarvertebrae. This band, which is sometimes referred to as the vena caval ligament,must be divided to allow proper visualization of the suprahepatic cava and righthepatic 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

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

3Essential Hepatic and Biliary Anatomy for the Surgeon

1

right and left lobe, the true “anatomic” or “surgical” right and left lobes of the liverare defined by the course of the middle hepatic vein that runs through the mainscissura of the liver. Although various descriptions of the internal anatomy of theliver have been proffered over the last century, Couinaud’s (1957) segmental anatomyof the liver is the most useful for the surgeon.

Couinaud’s classification system divides the liver into four unique sectors basedupon the course of the three major hepatic veins. Each sector receives its bloodsupply from a separate portal pedicle. Within the main scissura lies the middle he-patic vein that courses from the left side of the suprahepatic vena cava to the middleof the gallbladder fossa. Functionally, the main scissura divides the liver into sepa-rate right and left lobes which have independent portal inflow, and biliary architec-ture. (Figs. 1.2 and 1.3) An artificial line that divides the liver into right and lefthemilivers is known as Cantlie’s line. The right hepatic vein runs within the rightsegmental scissura and divides the right lobe into a right posterior and anteriorsector, while the left hepatic vein follows the path of the falciform ligament anddivides the left lobe into a medial and lateral segment.

The right and left lobes of the liver are further divided into eight segments basedupon the distribution of the portal scissurae. At the hilus, the right portal vein pur-sues a very short course (1-1.5 cm) before entering the liver. Once entering thehepatic parenchyma, the portal vein divides into a right anterior sectoral branchthat arches vertically in the frontal plane of the liver and a posterior sectoral branchthat follows a more posteriorlateral course. The right portal vein supplies the anterior(or anteriormedial) and posterior (or posteriorlateral) sectors of the right lobe. Thebranching pattern of these sectoral portal veins subdivides the right liver into foursegments—Segments V (anterior and inferior) and VIII (anterior and superior) formthe anterior sector, and Segments VI (posterior and inferior) and VII (posterior andsuperior) form the posterior sector.

In contrast to the right portal vein, the left portal vein has a long extrahepaticlength (3-4 cm) coursing beneath the inferior portion of the quadrate lobe (Seg-ment VIB) enveloped in a peritoneal sheath (the hilar plate.) Upon reaching theumbilical fissure, the left portal vein runs anteriorly and superiorly within the liversubstances, and gives off horizontal branches to the quadrate lobe medially (Seg-ments 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 itlies mostly on the left side (Fig. 1.4). More precisely, it is the most dorsal portion ofthe liver situated behind the left lobe and embracing the retrohepatic vena cava fromthe hilum to the diaphragm. The portion of the caudate lobe that is within the rightliver is usually quite small and lies posterior to Segment IVB. Figure 1.3 illustratesthe location of the caudate lobe which lies between the left portal vein and vena cavaon the far left, and the middle hepatic vein and vena cava within the right liver. Thecaudate lobe receives blood vessels and biliary tributaries from both the right andleft hemilivers. The right side of the caudate lobe, and the caudate process, receivesits blood supply from branches of the right or main portal vein, while the left side ofthe caudate receives a separate vessel from the left portal vein.


1

Aberrant segmental anatomy of the liver is uncommon. The presence of a di-minutive left lobe is the most common anomaly reported and is important onlybecause it may serve as a limitation to the performance of extended right hepatecto-mies. Although reports of “accessory” hepatic lobes are not uncommon, these donot represent separate segments with independent intrahepatic vascular supply, butrather elongated tongues of normal liver tissue. Riedel’s lobe is the most common ofthese “accessory” lobes and is reality an extended piece of liver tissue hanging inferi-orly 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 alwayspresent as direct communications between the vena cava and the posterior surface of

Fig. 1.2. Segmental and sectoral anatomy of the liver. The liver is divided into threemain scissurae by the right, middle, and left hepatic vein branches. The middlehepatic courses through the main scissura (or Cantlie’s line) and divides the liverinto 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 lefthepatic vein divides the left lobe into medial (Segments IV A and B) and lateralsegments (Segments II and III). The intrahepatic branching of the right and lefthepatic ducts, arteries and portal veins (shown) in the horizontal plane of the liverdivides the liver into eight separate segments. The caudate lobe (Segment I) is nei-ther part of the right or left lobe. Rather the caudate lobe receives venous and arterialbranches from both the right and left side of the liver, and drains directly into theinferior vena cava. Reprinted with permission from: Surgery of the Liver and BiliaryTract (3rd Edition), Blumgart LH, Fong Y (Eds.) W.B. Saunders, London, UK (2000).


1

the right lobe. Uniquely, the caudate lobe (Segment I) drains principally throughdirect communication with the retrohepatic cava.

The hepatic veins lie within the three major scissurae of the liver dividing theparenchyma into the right anterior and posterior sectors, and the right and leftlobes. (Figs. 1.2 and 1.3) The right hepatic vein lies within the right scissura (orsegmental 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

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


1

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

Hepatic Venous AnomaliesAlthough the outline above should suffice as cursory knowledge of hepatic venous

anatomy, it is far from exhaustive. For example, large accessory right hepatic veinsare commonly found, and an appreciation of these structures on axial imaging canbe 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 anextended left hepatectomy. Most importantly, the surgeon embarking on hepaticresection should have a thorough knowledge of the internal course of the hepaticveins, 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 ce-

liac arterial anatomy as described in most major anatomic treatise is found in only60% of cases. An accessory hepatic artery refers to a vessel that supplies a segment ofliver that also receives blood supply from a normal hepatic artery. An aberrant he-patic artery is called a replaced hepatic artery as it represents the only blood supplyto a specific hepatic segment. Precise knowledge of normal hepatic arterial anatomyis 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 dia-phragmatic hiatus. The celiac trunk itself is typically very short and divides into theleft gastric, splenic, and common hepatic arteries shortly after its origin. (Figure1.5). The common hepatic artery typically passes forward for a short distance in theretroperitoneum where it then emerges at the superior border of the pancreas andleft side of the common hepatic duct. The common hepatic artery supplies 25% ofthe liver’s blood supply, with the portal vein supplying the remaining 75%.

After arising from the celiac axis, the common hepatic artery turns upward andruns lateral and adjacent to the common bile duct. The gastroduodenal artery thatsupplies the proximal duodenum and pancreas is typically the first branch of thecommon hepatic artery. The right gastric artery takes off shortly thereafter and con-tinues within the lesser omentum along the lesser curve of the stomach. At thispoint the common hepatic artery is referred to as the proper hepatic artery. Theproper hepatic artery courses towards the hilum and soon divides into the right andleft hepatic arteries. Prior to the bifurcation, a small cystic artery branches off toprovide blood supply to the gallbladder. While coursing through the hepatoduodenalligament the hepatic artery proper, common bile duct, and portal vein are enveloped


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in a peritoneal sheath within the hepatoduodenal ligament. The proper hepatic ar-tery bifurcates earlier than the common bile duct and portal vein. In 80% of casesthe right hepatic artery courses posterior to the common hepatic duct before enter-ing the hepatic parenchyma. In 20% of cases, the right hepatic artery may lie ante-rior to the common hepatic duct. Upon reaching the hepatic parenchyma, the righthepatic artery branches into right anterior (Segments V and VIII), and right poste-rior sectoral branches (Segments VI and VII). The posterior sectoral branch initiallyruns horizontally through the hilar transverse fissure (of Gunz) normally present atthe base of Segment V and adjacent to the caudate process. The left hepatic arteryruns vertically towards the umbilical fissure where it gives off a small branch (oftencalled the middle hepatic artery) to Segment IV, before continuing on to supplySegments II and III. Additional small branches of the left hepatic artery supply the

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


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caudate lobe (Segment I), although caudate arterial branches may also arise from theright hepatic artery. The sectoral and segmental bile ducts and portal veins followthe course of the hepatic artery branches. Intrahepatic branching of these structureswill be discussed in more detail below.

The blood supply to the common bile duct is varied and multiple. Branches ofthe common hepatic, gastroduodenal, and pancreaticoduodenal arteries have all beenshown to provide arterial supply at various levels.

Hepatic Arterial AnomaliesVariations in the arterial blood supply to the liver are common. Although the

hepatic artery typically arises from the celiac axis, complete replacement of the mainhepatic artery or its branches occur with variable frequency. Similarly, duplicationor accessory hepatic arterial branches, particularly an accessory left hepatic artery,may be more the norm than an anomaly. The most common hepatic arterial anomalyinvolving a replaced vessel is a replaced right hepatic artery (25%). In this situation,the replaced right hepatic artery usually arises from the superior mesenteric arteryand runs lateral and posterior to the portal vein within the hepatoduodenal liga-ment. (Fig. 1.6). In rare instances, the entire common hepatic artery, or its indi-vidual branches may arise directly off the celiac trunk or aorta.

Portal Venous AnatomyThe 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

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


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

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


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and inferior pancreatic vessels. In addition, the left gastric vein and inferior mesen-teric vein typically drain into the splenic vein, but in rare instances these vessels mayenter the portal vein directly. Surgical dogma states that there are no venous brancheson the anterior surface of the portal vein and, for the most part this is true–mostveins enter the portal vein tangentially from the side. However, having paid homageto surgical dogma, the reality is that small anterior venous branches may exist, andany manipulation posterior to the pancreatic neck and anterior to the portal veinshould be performed with maximum operative exposure and care.

Access to the portal vein is typically obtained by identifying the superior mesen-teric vein on the inferior surface of the pancreas. In some circumstances it is neces-sary to first locate the middle colic vein within the transverse mesocolon and followit inferiorly to the SMV. The length of the SMV is highly variable, and may rangefrom only a few millimeters up to 4 cm. In many circumstances the SMV is madeup of two to four venous branches that coalesce shortly before joining the portalvein rather than a single dominant vein. The inferior pancreaticoduodenal vein,which can be quite prominent, is the only vein that normally enters the SMV di-rectly. Proper identification of this vein is necessary to avoid injury (and often sub-stantial blood loss). All other pancreatic venous tributaries enter the portal veinrather than the SMV.

In the performance of a pancreaticoduodenal resection, early division of the com-mon bile duct (CBD) provides great exposure to the right lateral side of the portalvein and facilitates the creation of a “tunnel” above the portal vein and beneath thepancreas. Once a determination has been made regarding the resectability of thepancreatic lesion, we favor early transection of the common bile duct. If the tumorlater 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 andduodenum, and direct entry of the portal vein into the inferior vena cava—a con-genital “portocaval” shunt. The importance of careful dissection around the portalvein cannot be overemphasized. Inadvertent injury or transection of the portal veinor a main tributary is difficult to correct and remains among the most lethal ofsurgical errors.

Intrahepatic Arterial and Portal Venous AnatomyThroughout the course of the liver, the sectoral and segmental bile ducts, hepatic

arteries and portal venous branches run together. (Fig. 1.8) Whereas knowledge ofprecise 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 AnatomyThe 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 theposterior head of the pancreas to enter the medial wall of the second portion of theduodenum. The gallbladder and cystic duct form an additional portion of this ex-trahepatic 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 ofthe right and left bile ducts lies to the right of the umbilical fissure and anterior tothe 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 rightanterior sectoral duct (Segments V/VIII) shortly after entering the hepatic paren-chyma. 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 hepaticparenchyma at the umbilical fissure. Lowering the hilar plate (i.e., connective tissueenclosing the left hepatic elements and Glisson’s capsule) at the base of the quadratelobe provides great exposure to both the biliary hilum and the extrahepatic portionof the left hepatic duct. (Figure 1.7)

The Common Bile DuctBy 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 por-tal vein and lateral to the common hepatic artery. If the hepatic artery bifurcatesearly, 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 lefthepatic duct runs at the base of the quadrate lobe (Segment 4) and is covered bythe hilar plate (a layer of connective tissue running between the hepatoduodenalligament and the Glissonian capsule of the liver). Dividing this layer demonstratesthe extrahepatic portion of the left hepatic duct arising from the umbilical fissure.(Numbers 2,3,4 and refer to segmental liver anatomy). Reprinted with permissionfrom: Surgery of the Liver and Biliary Tract (3rd Edition), Blumgart LH, Fong Y (Eds.)W.B. Saunders, London, UK (2000).


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

Gallbladder and Cystic DuctThe 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 isseparated from the liver parenchyma by the cystic plate, a layer of connective tissuearising from Glisson’s capsule and in continuity with the hilar plate at the base ofSegment IV. In rare instances, the gallbladder is only loosely attached to theundersurface 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 ordouble gallbladders, (b) septated gallbladders, or (c) gallbladder diverticula.(Fig. 1.9A).

The cystic duct arises from the infundibulum of the gallbladder and runs me-dial and inferior to join the common hepatic duct. The cystic duct is typically 1-3mm in diameter and can range from 1 mm to 6 cm in length depending upon itsunion with the common hepatic duct. Spiral mucosal folds, referred to as valves ofHeister, are present in the mucosa of the cystic duct. Cystic duct abnormalities areuncommon and include (a) double cystic ducts (very rare), (b) aberrant cystic ductentry sites, and (c) aberrant cystic duct union with the common hepatic duct. (Fig-ure 1.9 A and B) Aberrant entry points for the cystic duct include a low entry into

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


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1.9A (A) Main variations of the gallbladder and cystic duct, (B) septums of the gallblad-der, (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 entryinto the main right hepatic duct or sectoral duct. Aberrant union of the cystic ductand common hepatic duct can take multiple forms including (a) absence of a cysticduct (< 1%) , (b) parallel course of the cystic duct and common hepatic artery witha shared septum (20%), and (c) an anomalous passage of the cystic duct posterior tothe 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 tothe 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 orlobar hepatic artery, aberrant course of the cystic artery over the cystic duct, andvarious other anomalies have been reported. A careful intraoperative determinationof cystic artery anatomy is important to prevent unnecessary hemorrhage duringcholycystectomy.

Intrahepatic Bile Duct AnatomyAn understanding of intrahepatic ductal anatomy is obviously important and

vital to the performance of high biliary anastomoses for cholangiocarcinoma (Klatskintumors), an intrahepatic bilioenteric bypass, and complex hepatic resections such ascaudate lobectomy, and left and right trisegmentectomy. The right and left lobes ofthe liver are drained separately by the right and left hepatic ducts. In contrast, 1–4smaller ducts from either the right or left hepatic ducts drain the caudate lobe.Within the liver parenchyma, the intrahepatic biliary radicals parallel the majorportal triad tributaries directed toward each hepatic segment of the liver. More spe-cifically, bile ducts are usually situated superior to its complementary portal veinbranch, 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-dividedinto sub-segments (IVa, superior, and IVb, inferior) so conceptually both the rightand left hepatic ducts each drain four segments. Although the left hepatic ductoriginates within the liver and terminates in the common hepatic duct, it is easier todescribe its’ path in reverse since the extrahepatic areas are readily visible to theoperating surgeon. After the bifurcation into the right and left hepatic ducts, the leftduct courses towards the umbilical fissure along the undersurface of Segment IVbabove and behind the left branch of the portal vein. Access to this area can be gainedby lowering the hilar plate (described above). Several small branches from the quad-rate lobe (Segment IV) and the caudate lobe (Segment I) may enter the left duct atthis location. The left hepatic duct is formed within the umbilical fissure by theSegment III (lateral) and Segment IVb (medial) ducts. Following the course of theumbilical fissure vertically towards the falciform ligament, the Segment II (lateral),and Segment IVa (medial) branches are formed. Although a careful and tediousdissection is required to access the segmental biliary ducts for anastomoses, (e.g., aSegment III bypass), control of the segmental portal triads to all areas of left lobe isreadily achievable within the umbilical fissure. (see Fig. 1.11)

The right hepatic duct emerges from the liver at the base of Segment V just toright of the caudate process. This duct drains Segments V, VI, VII, and VIII andoriginates 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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almost horizontal course at the base of Segments V and VI that can often been seenlying within a transverse fissure on the superficial surface of the liver. Segmentalbiliary branches from Segments VI (inferior) and VII (superior) converge to formthe main right posterior sectoral duct. Segmental branches from Segments V andVIII form the right anterior sectoral duct. While the right posterior sectoral duct fol-lows a horizontal course, the right anterior sectoral duct runs almost vertical withinSegment V, and receives branches from both Segment V (inferior) and VIII (superior).

Fig. 1.10. Cystic artery anomalies. (A) Typical course, (B) double cystic artery, (C) cysticartery crossing anterior to the main bile duct, (D) cystic artery originating from the rightbranch of the hepatic artery and crossing the common hepatic duct anteriorly, (E) cys-tic artery originating from the left branch of the hepatic artery, (F) cystic artery originat-ing 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 permis-sion 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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Biliary drainage of the caudate lobe is less predictable. Conceptually, thecaudate lobe has three distinct areas—a right part, a left part, and the caudateprocess. In some instances three separate bile ducts may be present. The cau-date process represents a narrow bridge of tissue that connects the caudate tothe right lobe (Segment V). In more than 75% of cases the caudate drains intoboth the right and left hepatic ductal system, but isolated drainage into theright (< 10%), or left hepatic duct (~15%) can occur.

Anomalous Biliary DrainageNormal intra- and extrahepatic biliary anatomy is present in approximately 75

percent of cases. (Fig. 1.12) Every effort should be made to define existing intrahe-patic anatomy based on preoperative imaging since failure to do so may result indevastating complications. Anomalies in both sectoral and segmental anatomy may

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


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

Anomalous Sectoral Biliary AnatomyAlthough 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 theleft hepatic duct may exist in up to ~15% of cases. (Fig. 1.12) In 20% of cases one ofthe right sectoral ducts, more commonly the anterior sectoral duct, may enter thecommon hepatic duct distal to the confluence. If this situation is not recognized itcan be very dangerous, and represents a common cause of injury during laparoscopiccholecystectomy. Less commonly (~5%) the right posterior sectoral duct (and rarelythe right anterior sectoral duct) may cross to enter the intrahepatic portion of theleft hepatic duct. Failure to appreciate this anomaly prior to right or left hepatec-tomy can lead to significant postoperative problems. Note some authorities believethat this anomaly represents the most common intrahepatic biliary variation.

Anomalous Segmental Biliary AnatomyA large number of segmental biliary anomalies have been reported. Most are

unimportant to the surgeon and of anatomical interest only. Figure 1.13 illustratesthe more common anomalies that have been reported within the right lobe and themedial segment of the left lobe.

SummaryA comprehensive understanding of normal and aberrant anatomy is the corner-

stone of surgery. The truth of this statement is nowhere more apparent than in theperformance of complex hepatobiliary surgery. Mastery of the segmental anatomyof the liver, as well as a comprehensive understanding of both normal and anoma-lous arterial, venous and biliary anatomy are the sine qua non for performing safehepatic resections. Recent advances in perioperative management of patients withhepatobiliary diseases (detailed elsewhere) permit the surgeon to perform increas-ingly radical hepatic procedures (upon sicker patients.) Although the expertise of-fered by our radiology and anesthesiology colleagues is important, it is incumbentupon every surgeon who performs liver resection to be well prepared. An age-oldsurgical axiom states “98% of the surgical outcome is determined in the operatingroom.” A good outcome in the performance of hepatic resections requires one tobecome a student of the game.

Selected Readings1. 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 1980191:584-592

2. Couninaud C. 1957 Le Foi. Etudes anatomogiques et chirurgicales. Masson, Paris.3. 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 commonhepatic duct (C1), right anterior duct draining into the common hepatic duct; (C2),right posterior duct draining into the common hepatic duct, (D) ectopic drainageof a right sectoral duct into the left hepatic ductal system (D1, right posterior sectoralduct draining into the left hepatic ductal system; D2, right anterior sectoral ductdraining into the left hepatic ductal system, (E) absence of the hepatic ductconfluence, (F) absence of right hepatic duct and ectopic drainage of the rightposterior duct into the cystic duct. Reprinted with permission from: Surgery of theLiver 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 SegmentV, (B) variations of Segment VI, (C) variations of Segment VIII, (D) variations of SegmentIV. Note there is no variation of drainage of Segments II, III, and VII. Reprinted withpermission 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 Ductsand Pancreas

Douglas R. DeCorato, Lawrence H. SchwartzImaging of the upper abdomen including the liver, biliary tree and pancreas has

evolved rapidly over the past ten years. Fast imaging techniques using both com-puted tomography (CT) and magnetic resonance imaging (MRI) permit dynamiccontrast-enhanced imaging in seconds. Similarly, ultrasonography (US), an integralpart of hepatobiliary imaging for both benign and malignant disease, has seen markedadvances due to improved technology. Modalities such as nuclear medicine andangiography play a more specialized role in the identification and characterizationof pathology. For example, although nuclear medicine is limited in its evaluation ofhepatic lesions, it is a physiologic examination that can aid in detecting disease ofthe gallbladder, biliary tree, and postoperative complications such as bile leaks.

These three imaging modalities, which are utilized most commonly, have certaincharacteristics that are unique to each. A detailed discussion of the physical proper-ties and principles underlying each imaging technique is beyond the scope of thischapter, and interested readers are referred to the additional reading section at theend of the chapter. Basic principles will be outlined below.

US is based on the transmission or reflection of sound waves (echoes) as theypass through tissue. Structures are described with regard to their relative echogenicitycompared with surrounding structures. A hyperechoic lesion has more echoes thanits surroundings and thus appears slightly brighter than the adjacent tissue. Ahypoechoic mass has fewer echoes and thus appears darker.

CT is based on the absorption of x-ray by structures. This absorption undergoesa mathematical calculation to generate specific attenuation values in Hounsfieldunits (HU). Structures are referred to as high or low attenuation or hyper- orhypodense lesions. A hyperdense or high attenuation lesion appears brighter thanbackground structures or has been enhanced; a low attenuation or hypodense lesionis darker than background structures. It cannot be assumed that a low attenuationlesion has not been enhanced, or a high attenuation lesion has been enhanced. Spe-cific criteria exist for enhancement by CT based on an increase of 10 HU from anoncontrast study to a contrast study.

MRI uses a strong magnetic field to image innate protons within organs. Signalintensity is based on sequence parameters and the relative abundance of protons.Commonly used terms for MR sequences include T1, T2, and gradient echo. Similarto US and CT, structures are described as hypointense and hyperintense. T1-weightedimages will display fluid as dark (hypointense), and are classically thought of as

21Imaging of the Liver, Bile Ducts and Pancreas

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displaying anatomic information. Certain MR contrast agents, such as gadoliniumchelates, are administered with T1-weighted images (mostly gradient echo images, asequence that can be adjusted to generate rapid T1-weighted images). T2-weightedimages generate bright (hyperintense) fluid and are generally used to identify patho-logic processes.

Imaging of the hepatobiliary system is dependent on the suspected underlyingdisease, pretest likelihood of a positive study, and clinical suspicion of concurrentunderlying disease process (for example, cirrhosis). The initial study, if chosen prop-erly, may be able to both identify the underlying disease process and provide staginginformation 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 availabilityand relatively low cost. A patient with a negative ultrasound, and low pretest likeli-hood of disease, may need no further workup. However, patients with a high pretestlikelihood of disease may require a different initial examination. Once a lesion orunsuspected underlying parenchymal disease is identified on US, a second imagingtest may be necessary. A comparison between the three main imaging modalities issummarized in Table 2.1.

Test SelectionThe 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, USis an excellent screening test for many patients; however, body habitus, underlyinghepatic disease, and overlying bowel gas can limit an otherwise diagnostic examina-tion. 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 contraindi-cated or not administered for other reasons. A noncontrast CT scan markedly limitsidentification of small lesions and hinders characterization. MRI routinely acquiresmultiple sequences that aid in lesion identification and characterization. MRI has aset of absolute contraindications for scanning (Table 2.2). Additionally, since noradiation is administered, precontrast images are routinely obtained. MRI scannersare variable in both speed and quality. Low field strength systems and “open” mag-nets may not afford the resolution necessary for preoperative planning.

Contrast administration is an important aspect of both CT and MRI. CT scansprincipally use iodinated contrast material, while MRI has a variety of contrast agentsavailable of which gadolinium is the most common. Patients allergic to iodine willusually not cross-react with gadolinium-based agents and, thus, may be safely referredfor 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 andpancreatic abnormality is beyond the scope of this Chapter, but general guidelinesare discussed below and summarized in Table 2.3.

Evaluation of the liver is best done with MRI, as it provides improved lesiondetection and characterization. In addition, MRI can precisely define underlyingliver processes, such as fatty infiltration, which can sometimes be confused with otherdiagnoses 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

MRI CT UltrasoundResolution Superior contrast Superior spatial Spatial resolution

resolution resolution dependent ontransducer selected

Contrast material Superior safety High safety profile No contrastprofile than CT of nonionic administeredand lower volumes contrast. Requiresare administered relatively high

doses of iodinatedcontrast for study

Radiation None Ionizing radiation Noneused

Speed Rapid imaging Rapid imaging Imaging timetime available time. Entire exam operator dependent

may be performedin under a minute

Technique Variable depending More uniform than Standard imageson hardware and MR, while still with additionalsoftware somewhat variable images acquired

depending on theclinical situation

Cost Relatively high High Moderate

Availability Less than CT Readily available, Generally available,usually 24 hrs/day but may be limited

at certain periodsdue to staffing

Table 2.2. Contraindications for MR imaging*

Absolute contraindications Relative contraindications

Pacemaker PregnancyNeurostimulator Recent intravascular stentCerebral aneurysm clip of unknown composition. ClaustrophobiaPossible metallic foreign body in the globe. Critically ill patients

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

new contrast agents, such as ferumoxides (Feridex), which have been shown to im-prove lesion detection in certain cases.

The selection of an ideal imaging technique for abnormalities of the biliary treeis 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 evalua-tion is performed for suspected malignant disease, MRI is superior to both CT and


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US since bowel gas will not interfere with evaluation of the distal common bile ductor the identification of periportal and retroperitoneal adenopathy (Fig. 2.5). Pancre-atic imaging is best obtained with CT if contrast administration is not contraindi-cated. If iodinated contrast cannot be administered, or the CT is equivocal, MRI isthe next test of choice. MRI and CT are equivalent with regard to vascular encase-ment and adenopathy in the setting of pancreatic adenocarcinoma. Microcysticadenomas may be better delineated with MRI, as the small cysts are more easilydepicted (Fig. 2.6). Pancreatitis is best evaluated with CT especially if the patient isunstable or in critical condition.

The next section will review the more commonly encountered lesions of theliver, biliary tree and pancreas and their associated imaging features.

Hepatic LesionsHepatic 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, acyst 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 onheavily T2-weighted images (TE> 180). The lesion is typically hypointense onT1-weighted images and, as with CT, does not enhance with contrast administration.

Hemangiomas are the most common benign hepatic tumors. These lesions aretypically hyperechoic on US and are either well defined or have lobulated borders(Fig. 2.2A). Hemangiomas typically reveal low attenuation on the noncontrast CTstudy and peripheral nodular enhancement following contrast administration(Fig. 2.2B). On MRI, hemangiomas display similar signal intensity to cysts and arehyperintense on T2 and heavily T2-weighted images (Fig. 2.2C). Initial peripheralnodular enhancement is seen after contrast administration, and the lesion may ormay not completely fill on delayed contrast imaging.

The enhancement patterns of particular lesions are often critical to their charac-terization. Specific lesion types enhance during the arterial dominant phase(hypervascular) while others do not (Fig. 2.3A). The most common lesions demon-strating arterial dominant phase enhancement include hepatocellular carcinoma,hepatic adenomas, focal nodular hyperplasia, and metastatic disease. Other condi-tions include coexistent hepatic disease. For example, patients with underlyingcirrhosis and a hypervascular lesion are considered to have hepatocellular carcinoma(HCC) until proven otherwise (Fig. 2.3B). In addition to arterial dominant

Table 2.3. Test selection based on body part

CT MR Imaging Ultrasound

Liver 2 1 3Biliary Tree 3 1 1Pancreas 1 2 3

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


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

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


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

Fig. 2.2B. A CT examination of the same patient demonstrates a lesion (arrow) withperipheral 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) whichis hyperintense on T2 weighted images. The fluid is bright (please note CSF arrow).Gadolinium enhanced MRI (not shown) will also demonstrate the classic periph-eral nodular enhancement pattern when present.

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


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

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


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enhancement, HCC typically demonstrate a pseudocapsule of compressed paren-chyma. Adenomas may demonstrate heterogeneous appearances from prior hemor-rhage, while focal nodular hyperplasia (FNH) may have a characteristic central scar.The scar in FNH enhances late after contrast, and on MRI is hyperintense onT2-weighted images.

Diseases metastatic to the liver display a variable appearance depending on theprimary underlying malignancy. Sonographic evaluation may demonstrate multiplehypoechoic lesions, or lesions with a hypoechoic rim or halo pattern (Fig. 2.4A).Metastases on CT scanning usually demonstrate a thick, irregular rim with enhance-ment (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 moreheavily T2-weighted images (blend in with hepatic parenchyma) (Fig. 2.4B). En-hancement patterns are somewhat variable but similar to CT findings; metastaticlesions tend to have irregular or rim enhancement.

Biliary calculi are usually hyperechoic on US and generally demonstrate posterioracoustic shadowing (Fig. 2.4C). These stones are most commonly seen on US in thebiliary tree and gallbladder. On CT scanning, stones appear hyperdense and are easyto delineate. MRI of the biliary tree can be accomplished using magnetic resonancecholangiopancreatography (MRCP) which is a new, exciting technique combining rapidT2-weighted sequences with ultrafast images in multiple planes. Calculi are hypointensecompared 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 priorsurgical interventions, can present with scarring and stricture formation which canbe difficult to differentiate from a primary malignancy. The presence of a stent orpneumobilia can add to the imaging difficulty.

Pancreatic imaging is most accurately performed with CT, or MRI if the CT isequivocal. US can obtain diagnostic images of the pancreas. However, body habitusand bowel gas may obscure imaging of part or the entire pancreas (Fig. 2.6). Adeno-carcinoma of the pancreas generally appears as a hypovascular mass best seen in thelate arterial phase of injection on both CT and MRI. Vascular invasion or encase-ment is easily depicted as well as associated lymphadenopathy. Both CT and MRImay be acquired to generate angiographic images of the surrounding vessels. Neu-roendocrine tumors of the pancreas are usually hypervascular in nature on contrastenhanced images and are typically hyperintense on T2 weighted MR images. Cysticneoplasms of the pancreas may also demonstrate characteristic appearances (Figs.2.7A, 2.7B). Calcifications, while seen on MRI are better appreciated on CT im-ages. 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 ahypervascular lesion (arrows) biopsy proven to be HCC.

Fig. 2.4B. An axial T2-weighted image with fat suppression from an MRI examperformed 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 examinationdemonstrates a small soft tissue tumor (arrowheads) surrounding an endoscopicallyplaced 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 isnot appreciated as it is on the ultrasound.

Fig. 2.6. Pancreatic mass: Ultrasound examination demonstrates a normal appearingpancreatic 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 thebody of the pancreas with cystic components (arrow).

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


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Selected Reading1. In: Rumack CM, Wilson SR, Charboneau JW, eds. Diagnostic Ultrasound: Mosby

Year Book; 1991.2. In: Edelman RR, Hesselink JR, Zlatkin MB, eds. Clinical Magnetic resonance

imaging. 2nd ed: W.B. Saunders; 1996.3. In: Lee JKT, Sagel SS, Stanely RJ, P. HJ, eds. Computed Body Tomography with

MRI Correlation. 3rd ed: Lippincott Williams and Wilkins; 1998.

CHAPTER 3


Endoscopic and Percutaneous Managementof Gallstones

Seth Richter and Robert C. Kurtz

IntroductionManagement of gallstone disease has changed dramatically in the last two decades.

Before the use of laparoscopic techniques, conventional surgical methods of openlaparotomy were used to remove the diseased gallbladder. If common bile duct gall-stones 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 de-scribed. With this endoscopic procedure, gastroenterologists could identify the am-pulla of Vater and insert a thin plastic cannula through it and into the common bileduct and pancreatic duct. An iodinated contrast agent was injected into the biliarysystem, and tumors or gallstones could be seen on fluoroscopy. The continued im-provement in instrument development and the expansion of endoscopic trainingprograms has made ERCP universally available. The skilled endoscopist workingwith a cooperative patient can often perform a diagnostic ERCP in 15 to 20 min-utes. Success rates for cannulating the common bile duct and pancreatic duct arewell over 90%. Now, side-viewing electronic duodenoscopes are used to afford ex-cellent visualization of the ampulla. As an adjunct to ERCP, the development ofendoscopic sphincterotomy (ERS) in 1973 enabled therapeutic maneuvers in thebiliary system to be routinely performed. Endoscopic sphincterotomy gave the gas-troenterologist the ability to place stents in the bile duct to palliate malignant ob-struction and to fragment and remove retained common bile duct stones. Theseimportant clinical situations previously either required surgical correction or a per-cutaneous, transhepatic catheter. ERCP has allowed for less invasive diagnostic andtherapeutic maneuvers to be performed.

Today, laparoscopic cholecystectomy is the procedure of choice for removing adiseased gallbladder. If there is concern that there may also be concomitant choledoch-olithiasis, the gastroenterologist will perform an ERCP, endoscopic retrograde sphinc-terotomy, and remove the bile duct stones without the need for open laparotomy.

Endoscopic Retrograde SphincterotomyEndoscopic retrograde sphincterotomy (ERS) refers to the division of the circu-

lar muscles of the biliary sphincter using diathermy current delivered through anendoscopically positioned sphincterotome. The initial step in sphincterotomy is se-

35Endoscopic Management of Hepatobiliary and Pancreatic Disorders

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lective cannulation of the common bile duct. This is achieved by cannulating theduodenal papilla and under fluoroscopic guidance maneuvering the sphincterotomeinto the common bile duct. It is imperative that selective cannulation of the bileduct is confirmed fluoroscopically to avoid pancreatic trauma due to the electrocau-tery, and subsequent acute pancreatitis. The electrical incision is made by controlledapplication of a blended cutting/coagulating current through the exposedsphincterotome wire. Complete control of wire tension and electrosurgical currentis maintained at all times. On occasion, deep cannulation of the common bile ductby 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 passspontaneously. However active stone extraction is favored to avoid stone impaction,biliary obstruction, and cholangitis.

Several authors have recently advocated the use of endoscopic papillary dilata-tion instead of ERS to allow the endoscopic removal of small common bile ductstones. They cite a lower complication rate, with fewer episodes of post-ERS bleed-ing. In young patients, papillary dilatation may avoid some of the long-term prob-lems that have been associated with ERS. Most endoscopists, however, still favorendoscopic sphincterotomy.

Bile Duct Stone RetrievalCommon duct stones less than 15 mm can usually be removed by standard

extraction methods using either balloon catheters or wire baskets. Stones that arelarger in size usually need to be broken up prior to removal. Under fluoroscopicguidance, a balloon catheter is inserted into the common bile duct, above the levelof the stone. It is then inflated and withdrawn, pulling the stone out of the bile ductahead of the balloon. If there are multiple bile duct stones, the lowest stone shouldbe removed first. The balloon catheters used for stone extractions do not carry therisk of stone impaction that a Dormia basket does. The balloon will burst or slide bya stone that is difficult to extract.

The Dormia basket offers an advantage over balloon catheters in that it is ofteneasier to entrap the stone in the basket, and it will also allow more traction force tobe used when extracting the stone. The technique used with the basket is similar tothat used with the balloon catheters. The basket is advanced beyond the stone to beremoved. This is done with the basket in the closed position. As with the ballooncatheters care must be taken not to push the stone more proximal into the intrahe-patic ducts as this makes extraction much more difficult. Once past the stone, thebasket is opened and maneuvered to entrap the stone. After the stone is entrapped itis removed by withdrawing the basket while applying traction to the basket catheter.After completion of stone extraction by either balloon catheter or basket method, acholangiogram is performed to confirm that no stones remain in the biliary ductsystem. With these techniques, about 85% to 90% of bile duct stones can be re-moved successfully. Failure to remove bile duct stones can be due to several reasonswhich include the inability to get to the ampulla because of anatomic problems, theinability to cannulate the bile duct, and large bile duct stones.


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Large Bile Duct StonesStones 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 thatcan be safely produced. As mentioned previously, stones less than 15 mm can beremoved by standard methods, using balloon catheters or retrieval baskets. Largerstones, in general, require fragmentation prior to removal. The common endoscopicmethods for stone fragmentation are mechanical lithotripsy and intracorporeal lithot-ripsy using either laser or electrohydraulic probes to cause stone fragmentation.

Mechanical LithotripsyMechanical lithotripsy is often the best initial option for fragmentation and re-

moval of large stones that cannot be removed by the standard techniques. This pro-cedure can be utilized safely and effectively during the initial endoscopic procedure.The Sohendra lithotripter is one type of mechanical lithotripter and is an indispens-able tool for the gastroenterologist who deals with gallstone disease. It is especiallyuseful when the retrieval basket containing the large gallstone can not be withdrawnfrom the bile duct through the sphincterotomy site. When impaction of the stone inthe basket occurs, the handle of the basket is cut off, the endoscope is removed overthe basket sheath, and then the outer Teflon sheath covering the wires of the basketis also removed. A flexible metal tube is then threaded over the basket wires, underfluoroscopic guidance, into the bile duct, to the level of the basket and stone. It actsas a solid surface onto which the basket and stone are pulled tightly using thelithotripter crank handle. Generally, the stone fragments as a result of the force oftightening the basket wires. If the stone does not fragment, the basket itself, willbreak, enabling its withdrawal from the bile duct. Other methods will then be neededto deal with the stone. This technique has made it possible for patients to avoidsurgery because of a stone that has become impacted in a retrieval basket.

Mechanical lithotripters that can pass through the endoscope have also facili-tated stone fragmentation. These consist of a wire basket within a Teflon sheathattached to a handle that passes through the endoscope instrument channel. Endo-scopic sphincterotomy is also necessary before inserting the lithotripter into the bileduct. The basket within the teflon sheath is inserted above the stone. The basket isthen opened and the stone is trapped in the basket. After the entrapment of thestone, it can be crushed on a metal sheath, which is extended over the inner Tefloncatheter which in turn is attached to a winding mechanism used to increase pressureon the stone in the basket. When cranked, the system retracts the basket and stoneagainst the metal sheath, causing the stone to fragment. The stone fragments canthen be removed with a basket or balloon catheter. Overall, mechanical lithotripsyhas a success rate of approximately 85%-90% for crushing and removing bile ductgallstones that are refractory to standard extraction techniques.

Laser LithotripsyLaser lithotripsy devices rely on the conversion of the laser energy to thermal and

mechanical energy in order to produce gallstone fragmentation. Concerns of bileduct 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 andDrug Administration has approved only the 504 nm Coumarin Flashlamp PulsedDye laser for use in the biliary system. This system produces a unique laser pulsethat is absorbed on the stone surface and creates a plasma cloud that rapidly expandsand contracts, resulting in a shock wave causing stone fragmentation. Recently laserlithotripsy has been possible under fluoroscopic guidance. This so called “smartlaser” resulted from the development of a device that can identify duct stones byanalyzing back scattered light and interrupting the laser pulse in case of bile ducttissue contact.

Electrohydraulic LithotripsySimilar to laser lithotripsy, electrohydraulic lithotripsy (EHL) relies on the appli-

cation of a shock wave created at the surface of the stone. The EHL probe consists oftwo coaxial isolated electrodes at the tip of a flexible catheter. The catheter is capableof delivering electric sparks in short rapid pulses. This leads to a hydraulic shockwave 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 thepotential risk for bile duct injury appears to be greater with EHL.

Complete duct clearance rates with laser lithotripsy and EHL is approximately85%. Both of these procedures are also limited by the fact that they are both highlyspecialized procedures that are not available in all centers. In addition they require avery high level of expertise to be used safely and successfully.

Biliary EndoprosthesisIn the small number (about 5%) of cases where either gallstone extraction is

incomplete or not possible, the endoscopic insertion of a biliary endoprosthesis isrecommended. This maneuver will buy time and allow for improvement in thepatient’s condition until complete stone extraction is achieved either by using addi-tional endoscopic techniques or by subsequent surgical intervention. Endobiliarystents come in a variety of sizes and shapes. Nasobiliary drainage catheters are in-serted into the bile duct, make a large loop in the duodenum, and come out throughthe 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 endmay prevent the bile duct stone from impacting in the ampulla. Metal endobiliarystents are a more permanent solution and should not be used if surgery or additionalstone removal techniques are to be employed. Endobiliary stents are used to providebiliary decompression, treat or prevent cholangitis and sepsis, and to prevent stoneimpaction in the distal common bile duct and ampulla. The insertion of anendobiliary stent can help change an emergent surgical situation into a more elec-tive one. In patients who are poor surgical candidates because of significant co-morbid medical problems, the use of an endobiliary stent can represent an acceptablelong-term solution, when attempts at endoscopic stone removal are unsuccessful.

Rendezvous TechniqueIf the ampulla and common bile duct can not be cannulated, a combined radio-

logical and endoscopic technique can be performed called the “rendezvous” tech-nique. 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 thebile duct opening in the ampulla. Endoscopy is performed at the same time. Theguide wire is identified, grasped, and pulled through the endoscope. A wire-guidedsphincterotome is inserted over the percutaneously placed guide wire, and ERS isperformed in the usual fashion.

Complications of Endoscopic TherapyComplications of endoscopic therapy include bleeding, perforation, pancreati-

tis, and cholangitis. The overall complication rate is about 8%-10%, with a mortal-ity rate of 0.8%-1.5%. Bleeding occurs in approximately 2.5%-5% of cases and isalmost always as a result of the endoscopic sphincterotomy. Unfortunately, bleedingcan be massive and life threatening. It is important to recognize that significantbleeding can present several days after endoscopic sphincterotomy. Treatment rangesfrom electrocautery or sclerotherapy if the bleeding occurs during the endoscopicprocedure, to angiography and embolization, or surgical intervention in patientswho fail endoscopic therapy.

Retroperitoneal perforation occurs in less than 1% of cases. It is more likely tooccur when either the endoscopic sphincterotomy is too large or when the electricalcut deviates from the recommended orientation in the ampulla. The diagnosis canbe made at the time of procedure on fluoroscopy and x-ray, if air or contrast is seenoutside the bile duct or duodenum. Most cases of retroperitoneal perforation can bemanaged conservatively if the diagnosis is made promptly.

Pancreatitis is the most common complication of ERS and occurs in approxi-mately 3%-6% of cases. It is more likely if there has been injection of contrast intothe pancreatic duct, especially if the pancreatic duct is filled under pressure and so-called pancreatic acinarization occurs. ERCP-related pancreatitis is usually mild andmanifested by abdominal pain, nausea, and vomiting that occurs within several hoursof the procedure. Most cases are self-limited, but on occasion, severe pancreatitiscan occur with all of its inherent complications. Serum amylase levels are not rou-tinely checked after uncomplicated ERCPs, as they are almost always elevated.

Cholangitis is an uncommon complication if the ERCP, ERS and stone extrac-tion is done properly. It has a frequency of about 0.1%-0.5%. This complicationoccurs when an obstructed biliary system is not adequately drained at the end of theendoscopic procedure. Cholangitis and sepsis can be minimized by assuring adequatebiliary drainage if there is a question of incomplete stone clearance and by using pre-and post-procedure antibiotics for patients with evidence of biliary obstruction.

Percutaneous Stone ExtractionThere 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 subtotalgastrectomy with gastrojejunostomy for gastric cancer. The afferent loop is oftenlong, and the ampulla cannot be approached by endoscopy. Other common indica-tions include large periampullary diverticula, duodenal stenosis, and multiple intra-hepatic stones. In these situations, percutaneous cholangiography, biliary drainage,and stone extraction are appropriate. Utilizing an imaging technique such as trans-abdominal ultrasound or CT scan, a needle can be used to puncture the liver andaccess 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 ductstones are fragmented first, either with a mechanical lithotripter in a fashion similarto 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 canbe pushed by catheters through the ampulla and into the duodenum. If multipleintrahepatic stones are present, the percutaneous tract can be dilated, and the stonesmay be removed by the use of Dormia baskets through the dilated tract. This proce-dure can be tedious and frequently must be done in several stages. Percutaneous bileduct stone removal has also been successful in the high-risk patient who has a percu-taneous cholecystostomy tube. A skilled radiologist can use the cholecystostomy as ameans to enter the biliary tree and deal with bile duct stones. The complication rateof percutaneous stone extraction is somewhat higher that endoscopic stone removaland approaches 10%. As with endoscopic methods, bleeding, pancreatitis, and cholan-gitis are the most common problems encountered. The success rate of the percutane-ous techniques should be better than 90%, limited primarily by anatomic abnormalities.

Specific Clinical Problems

Cholangitis and SepsisCholangitis 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 butmay rarely be secondary to either benign or malignant bile duct strictures, especiallyif the biliary system has been previously instrumented. The majority of patients willpresent with a clinical picture of right upper quadrant abdominal pain, fever, andjaundice: the so-called “Charcot’s triad”. However patients can also present withfulminant, life-threatening sepsis.

Patients without complete biliary obstruction may respond to conservativemeasures, intravenous hydration, and antibiotics. If patients do not show a rapidclinical response, and for those that develop generalized sepsis, urgent drainage ofthe obstructed biliary tree is required. Biliary drainage can be performed by severaltechniques which in part depend on the experience of the medical staff and theseverity of the patient’s illness. In patients with multiple stones in the biliary systemextending well up into the liver, an open surgical procedure, stone extraction, and T-tube placement may be the best approach. If there is a high-grade stricture at thehilus of the liver, percutaneous biliary drainage would be most appropriate. Endo-scopic biliary decompression is most beneficial for distal biliary obstruction. Unfor-tunately, an open operation in these severely ill patients carries a high mortality rateof up to 40%. Endoscopic drainage has become the favored modality if the expertiseis available and the biliary abnormality is appropriate.

Endoscopic biliary decompression may be achieved by endoscopic sphinctero-tomy and stone extraction, nasobiliary drainage, or by placement of a biliary stentdepending on the nature and cause of the obstruction. For obstruction secondary tostone disease, sphincterotomy with stone extraction is the procedure of choice, as itresolves the problem in one endoscopic session. However the insertion of anendobiliary stent may be the best option for the seriously ill patient or for the pa-tient with a large common bile duct gall stone. In addition, ERCP can delineate the


3

cause of the obstruction and can provide a sample of bile for bacterial culture orcytology if a malignant stricture is suspected.

The effect of biliary decompression is often dramatic with a rapid resolution ofpain, fever, and other signs of sepsis. Once the infection is controlled, repeat ERCPcan be performed, and if any stones were left during the initial procedure, they canthen be removed.

Acute Gallstone PancreatitisGallstone disease is a leading cause of acute pancreatitis in Western countries

accounting for 34%-54% of cases. Initially endoscopists were reluctant to performERCP 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 withsevere acute gallstone pancreatitis. Endoscopic sphincterotomy with stone extrac-tion has been compared with conventional treatment in patients with suspectedgallstone pancreatitis. Common bile duct stones were found on ERCP in 63% ofpatients with severe attacks compared with 26% of patients with mild attacks. Com-plications of pancreatitis were significantly less frequent in the group who had earlyERCP, ERS, and stone extraction, and the benefit was more marked in those pa-tients with severe pancreatitis. This demonstrated that ERCP can be performed inacute pancreatitis and that there was significant benefit from early stone extraction,especially in patients with severe pancreatitis.

The Era of Laparoscopic CholecystectomyLaparoscopic cholecystectomy has revolutionized the management of gallblad-

der disease. Laparoscopic cholecystectomy has replaced open cholecystectomy asthe modality of choice for patients with gallbladder stones. This has led to signifi-cant changes in the algorithm used in patients with both gallbladder disease andpresumed common bile duct stones. However, the laparoscopic management of com-mon duct stones is more complicated then laparoscopic cholecystectomy alone. Thisprocedure requires advanced surgical expertise and instrumentation. Thuslaparoscopic cholecystectomy is still frequently coupled with ERCP, ERS, and stoneextraction when common bile duct stones are suspected.

Generally, in the patient with gallbladder disease, if there is a low suspicion ofcommon duct stones, there appears to be little if any value in performing routineERCP prior to laparoscopic cholecystectomy. Studies have shown that there is a lowyield of detecting unsuspected common duct stones and clinically important biliaryduct anatomic variants compared with the known complication rate of ERCP. Pa-tients in whom there is a high suspicion of common duct stones, than is those thathave a history of jaundice or abnormal liver function studies, are more likely tobenefit from preoperative ERCP, ERS, and stone extraction. Patients identified ashaving a medium risk of a common bile duct stone create a clinical dilemma. Somehave suggested routine intravenous cholangiography and selective ERCP in thesepatients. These issues may also be resolved based on the skills of the endoscopistsand surgeons at each institution. A patient with a history of mild pancreatitis, nor-mal liver function studies, and no evidence of common bile duct stones on non-invasive imaging should not routinely have a preoperative ERCP.


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Selected Reading1. Park AE, Mastrangelo MJ Jr. Endoscopic retrograde cholangiopancreatography in

the management of choledocholithiasis. Surg Endosc. 2000 Mar;14(3):219-26.2. Erickson RA, Carlson B. The role of endoscopic retrograde cholangiopancreatography

in patients with laparoscopic cholecystectomies. Gastroenterology. 1995Jul;109(1):252-63.

3. Cotton PB. Endoscopic retrograde cholangiopancreatography and laparoscopiccholecystectomy. Am J Surg. 1993 Apr;165(4):474-8.

4. Johnson AS, Ferrara JJ, Steinberg SM, Gassen GM, Hollier LH, Flint LM. Therole of endoscopic retrograde cholangiopancreatography: sphincterotomy versuscommon bile duct exploration as a primary technique in the management of cho-ledocholithiasis. Am Surg. 1993 Feb;59(2):78-84.

5. Duensing RA, Williams RA, Collins JC, Wilson SE. Managing choledocholithi-asis in the laparoscopic era. Am J Surg. 1995 Dec;170(6):619-23.

6. Tham TC, Lichtenstein DR, Vandervoort J, Wong RC, Brooks D, Van Dam J,Ruymann F, Farraye F, Carr-Locke DL. Role of endoscopic retrogradecholangiopancreatography for suspected choledocholithiasis in patients undergo-ing laparoscopic cholecystectomy. Gastrointest Endosc. 1998 Jan;47(1):50-6.

7. Chang L, Lo SK, Stabile BE, Lewis RJ, de Virgilio C. Gallstone pancreatitis: aprospective study on the incidence of cholangitis and clinical predictors of re-tained common bile duct stones. Am J Gastroenterol. 1998 Apr;93(4):527-31.

8. van Der Velden JJ, Berger MY, Bonjer HJ, Brakel K, Lameris JS. Percutaneoustreatment of bile duct stones in patients treated unsuccessfully with endoscopicretrograde procedures. Gastrointest Endosc. 2000 Apr;51(4 Pt 1):418-22.

9. Welbourn CR, Mehta D, Armstrong CP, Gear MW, Eyre-Brook IA. Selective pre-operative endoscopic retrograde cholangiography with sphincterotomy avoids bileduct exploration during laparoscopic cholecystectomy. Gut. 1995 Oct;37(4):576-9.

10. Tham TC, Lichtenstein DR, Vandervoort J, Wong RC, Brooks D, Van Dam J,Role of endoscopic cholangiopancreatography for suspected choledocholithiasis inpatients undergoing laparoscopic cholecystectomy. Gastrointest Endosc. 1998Jan;47(1):50-6.

11. Freeman ML, Nelson DB, Sherman S, Haber GB, Herman ME, Dorsher PJ, MooreJP, Fennerty MB, Ryan ME, Shaw MJ, Lande JD, Pheley AM. Complications ofendoscopic biliary sphincterotomy. N Engl J Med. 1996 Sep 26;335(13):909-18.

12. Mehta SN, Pavone E, Barkun JS, Bouchard S, Barkun AN. Predictors of post-ERCP complications in patients with suspected choledocholithiasis. Endoscopy.1998 Jun;30(5):457-63.

13. Nelson DB, Freeman ML. Major hemorrhage from endoscopic sphincterotomy:risk factor analysis J Clin Gastroenterol. 1994 Dec;19(4):283-7.

14. Sharma VK, Howden CW. Meta-analysis of randomized controlled trials of endo-scopic retrograde cholangiography and endoscopic sphincterotomy for the treat-ment of acute biliary pancreatitis. Am J Gastroenterol. 1999 Nov;94(11):3211-4.

CHAPTER 4

Interventional Radiology in HepatobiliarySurgery

Lynn A. Brody and Karen T. Brown

IntroductionThe 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 relation-ship between the hepatobiliary surgeon and the interventional radiologist benefitsboth doctors and patients, and is best accomplished in the background of a teamcomprised of surgeons, gastroenterologists, radiologists and appropriate medical spe-cialists such as oncologists and hepatologists.

This chapter will provide a guide to the procedures performed by interventionalradiologists that may be useful when caring for the hepatobiliary surgery patient.

Diagnostic Procedures

Needle Biopsy

General ConsiderationsPercutaneous needle biopsy may be performed to diagnose primary or secondary

neoplasms, or in cases of diffuse hepatic disease and/or hepatic dysfunction. Fineneedle aspiration (FNA), biopsy, and core biopsy, can be performed depending onthe indication. Fine needle aspiration is typically performed using a 20-25 gaugeneedle and provides material for cytological analysis and/or culture. A wide varietyof 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 thepresence of a cytotechnologist who determines whether adequate material has beenobtained in order to maximize the likelihood that the procedure is not terminatedprematurely. FNA is typically adequate for diagnosing metastatic disease, particu-larly when the original material is available for comparison. Further examinationusing immunohistochemical analysis and other special studies may permit determi-nation of a primary site in the case of metastatic disease with no known primary, or incases when tissue from the primary tumor is unavailable for comparison. Fineneedle biopsy of primary neoplasms may also be diagnostic dependent on localcytopathologic expertise.

Core specimens provide tissue for surgical pathology and allow for architecturalevaluation of the specimen. In the liver, this is utilized most often to distinguish well-differentiated hepatocellular carcinoma (HCC) from normal liver. Core specimens are


43Interventional Radiology in Hepatobiliary Surgery

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

IndicationsMany primary hepatic neoplasms, both benign and malignant, can be confi-

dently diagnosed by cross sectional imaging. Hemangiomas in the liver often have acharacteristic appearance with both ultrasound and magnetic resonance imaging(MRI), with MRI being most likely to afford a confident diagnosis. MRI can alsoaccurately identify focal nodular hyperplasia (FNH) and may be helpful in supporting

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

44 Hepatobiliary Surgery

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a diagnosis of a hepatic adenoma. Needle biopsy is rarely requested to diagnosethese entities and is best avoided in suspected hemangioma as bleeding complica-tions may occur. In addition, in those select cases, needle biopsy rarely adds muchinformation beyond that observed from imaging studies and an excisional biopsy isoften indicated if uncertainty remains.

HCC can be confidently diagnosed based on an appropriate constellation ofclinical, laboratory and radiographic criteria. Patients with hepatic neoplasm(s) inthe setting of cirrhosis and/or hepatitis B or C, with an elevated alpha-fetoproteinlevel, 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 dis-ease is usually performed by the gastroenterologist based on anatomic landmarks.Occasionally, landmarks may be unreliable, as in patients who have undergone priorhepatic resections, in which case the biopsy can be performed with imaging guid-ance. The presence of ascites may also make unguided biopsy difficult.

Transjugular liver biopsy allows for acquisition of a core specimen in patientsbeing evaluated for diffuse hepatic disease whose thrombocytopenia or coagulopathyrenders standard percutaneous techniques more dangerous. The liver is accessedfrom a hepatic vein, using an automated device advanced from a jugular approach.The needle is advanced from an intravascular approach within the liver taking carenot to puncture the hepatic capsule.

TechniqueNeedle biopsy is performed under imaging guidance, using either ultrasound or

computed tomography (CT) (Figs. 4.1B, 4.1C). MRI may be utilized more frequentlyin the future. Operator preference and equipment availability generally determinethe modality for guidance which is used. Procedures are generally performed on anout-patient basis using local anesthesia with or without conscious sedation.

ComplicationsComplications of needle biopsy are rare. Bleeding is quite uncommon in our

experience and is typically self-limited when it does occur. Small subcapsularhematomas are most common. Pneumothorax may occur during biopsy of highhepatic lesions. Fortunately, the majority of these pneumothoraces are small and donot require placement of a chest tube. Tumor seeding has been reported but isextremely uncommon. Percutaneous pancreatic biopsy may incite pancreatitis.

Diagnostic AngiographyWith the enormous recent advances in cross sectional imaging techniques, diag-

nostic angiography is rarely performed today. Tumor characterization and vascularinvolvement are better demonstrated by many other modalities. At our institution,diagnostic angiography is performed most commonly in conjunction with CT angio-portography or to evaluate arterial anatomy prior to placement of hepatic arterialinfusion pumps. Studies are under way to determine whether equivalent informa-tion may be obtained using triple phase CT or contrast enhanced MRI. Early datasuggest 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 themass. The notch is directed anteriorly at the edge of the lesion.


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CT Arterial PortographyThere are some surgeons who still feel that CT arterial portography (CTAP)

represents the “gold standard” for evaluating the liver for tumor(s). As mentionedpreviously, studies are being conducted to determine the value of CTAP relative toother less invasive imaging modalities.

TechniqueA selective catheter is typically placed from a right femoral artery approach using

the Seldinger technique. The type of selective catheter utilized is based on operatorpreference. Catheters as small as 4F may be used. At our institution, a 5F catheter isgenerally used. Contrast is injected into the celiac and superior mesenteric arteriesto 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 mesen-teric artery (SMA). In the case of replaced or accessory hepatic vessels arising fromthe SMA (most commonly an accessory or replaced right hepatic artery), the cath-eter is positioned in the splenic artery or very distally in the SMA in order to avoidreflux to the hepatic arterial branch during scanning. Once the catheter is posi-tioned, the patient is transferred to the CT scanner for the CTAP. The study shouldbe performed on a spiral CT scanner (Figs. 2.2A-H). Contrast is injected into thearterial catheter at a rate of approximately 3 cc per second. After an appropriatedelay to allow filling of the portal vein (typically 40-60 seconds for catheters in theSMA, slightly shorter for catheters in the splenic artery), spiral scanning is per-formed from the dome to the tip of the liver. After a second delay (20-30 seconds) toallow for some filling in of perfusion artifacts, spiral scanning is then performed inthe reverse direction. The catheter is then removed and the patient returns 3-4 hourslater for delayed imaging.

InterpretationCTAP 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 themost sensitive for demonstrating areas of decreased portal perfusion. The later im-ages, in particular the delayed, or hepatic excretion phase images, are then used todifferentiate tumor from perfusion artifact. In general, tumors are visible on each ofthe three sets of images while perfusion artifacts will disappear over time. It is im-portant to understand that there are locations in which perfusion artifacts typicallyoccur, which may be unrelated to tumor. These areas occur most commonly at theback of Segment IV and along the umbilical fissure.

Percutaneous Transhepatic CholangiographyLike diagnostic angiography, percutaneous transhepatic cholangiography (PTC)

has largely been replaced by improved noninvasive imaging. High quality ultra-sound, CT, MRI or, most recently, magnetic resonance cholangiopancreatogram(MRCP) can accurately demonstrate the level of biliary obstruction, ductal abnor-malities, and the presence of vascular or parenchymal involvement. Multiplanarreconstruction with CT or MRCP allows images to be presented in a familiar for-mat. PTC may be associated with bleeding, bile peritonitis and sepsis and should bereserved for those cases in which noninvasive imaging is inconclusive or where


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functional information is needed. At our institution, this is done most commonly toevaluate the status of bilioenteric anastamoses in cases of suspected partial orintermittent occlusion.

TechniqueThe procedure is generally performed using conscious sedation and local anes-

thesia. Prophylactic antibiotics are administered. A right or left-sided approach ischosen based on anatomic considerations and operator preference. Punctures maybe performed using fluoroscopic or sonographic guidance. Sonographic guidanceaffords the advantage of allowing a duct to be targeted directly, thus minimizing thenumber of needle passes; however, it requires the availability of a good quality ultra-sound machine and a high degree of operator skill. Left-sided punctures are easier toperform under ultrasound guidance since intercostal imaging is avoided.

PTC techniques will be described further in the section on percutaneous biliarydrainage.

Fig 4.2A. Early phase image through the upper liver shows two lesions in the lateralsegment and one in Segment VIII.Figs. 4.2A-J. CT portogram in a patient with metastatic colorectal carcinoma. Theangiographic catheter is in the superior mesenteric artery. The study consists ofthree phases. The early images are acquired in a cephalad to caudad direction,immediately following the injection of iohexol 140 radiographic contrast into thesuperior 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. Themiddle phase images are obtained after approximately 20 to 30 seconds and areacquired in the reverse direction. The final phase is obtained approximately 4 hourslater, without additional contrast.


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

Fig. 4.2C. Late phase images. The three lesions are seen on these two images. Thelesion in Segment VIII and the lesion in the lateral aspect of Segment II/III are verylow attenuation and likely to represent cysts. The small mass medially in the leftliver (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 lowattenuation anteriorly in Segment IV, abutting the umbilical fissure.

Therapeutic and Palliative Procedures

Percutaneous Cholecystostomy

General ConsiderationsPercutaneous cholecystostomy (PC) is generally performed in patients with acute

cholecystitis who are too ill to undergo cholecystectomy. The procedure is most oftenperformed in acute acalculous cholecystitis. Acalculous cholecystitis typically occurs inelderly and/or extremely ill patients, frequently in the intensive care unit. Definitivediagnosis may be difficult, but should be suspected in this patients in whom there is noother explanation for fever and leukocytosis, or when the gallbladder is distended andtender. PC may represent definitive treatment in these patients. Given the relative easeand safety, of performing PTC, most interventional radiologists have a low thresholdfor performing this procedure in the appropriate clinic situation.

PC may also be performed in cases of calculous cholecystitis in patients consid-ered poor operative candidates. When gallstones are present, the ultimate treatmentdepends on the clinical situation. The procedure may be temporizing in patientswhose condition improves enough to allow for definitive cholecystectomy. In pa-tients who remain poor surgical candidates, stones may be removed percutaneouslyfrom the gallbladder or common bile duct, and balloon sphincterotomy may beperformed. Rarely, PC may be performed to provide biliary drainage in cases ofdistal obstruction.


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

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


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

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


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TechniquePC 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 ofacalculous cholecystitis, thick dark bile is aspirated at the time of drainage. As in-flammation 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 becapped until the tract has matured (we generally wait at least 3 weeks), at whichpoint the tube can be removed.

Percutaneous Biliary Drainage

IndicationsPercutaneous biliary drainage is indicated in cases of obstructive jaundice caus-

ing cholangitis or intractable pruritus, or where an elevated bilirubin precludes othertreatment. This latter situation occurs most commonly in patients requiring chemo-therapy, but may also apply in patients being considered for hepatic embolization.Asymptomatic jaundice does not require treatment. In particular, intervention solelyto reduce a high bile duct obstruction (at or above the confluence) may cause manymore problems than it solves. We usually try to avoid treating patients when crosssectional imaging suggests subsegmental isolation, as the goals of drainage can rarelybe accomplished. Preoperative biliary drainage remains controversial except for thetreatment of biliary sepsis.

The hepatobiliary disease management team should evaluate each patient todetermine the need for drainage. Once the need for drainage is determined, con-sideration should be given as to whether an endoscopic or percutaneous drainageapproach is more appropriate. In general, patients with low bile duct obstructionare managed endoscopically by the gastroenterologists. Percutaneous drainage isreserved for cases of high bile duct obstruction or for patients whose biliary treecannot be accessed endoscopically (e.g., previous bypass procedure or gastric orduodenal tumors).

TechniqueAs 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 percu-taneous biliary drainage. It is important to identify the level of obstruction, thestatus of the portal vein, the presence of hepatic atrophy or ascites, and the extent ofparenchymal disease. Operator preference, while important, is secondary to the needto maximize the safety and efficacy of the procedure.

Punctures are generally performed using 21 or 22 gauge needles. Right-sideddrainage 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. Afterthe needle is inserted into the liver, contrast is injected until the biliary tree is opaci-fied. Multiple passes may be necessary until a duct is visualized. If the initial ductpunctured is not optimal for placement of a drainage catheter, a second needle isused to puncture a suitable duct once the ducts have been filled with contrast. Theoptimal 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 anadequate 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 innerintroducer sheath, and a 7F outer introducer sheath. The inner two pieces are re-moved leaving the outer portion of the introducer, through which catheters andwires of appropriate size to perform the drainage can be placed. Generally, everyattempt is made to cross through the obstruction in order to allow placement of aninternal-external drainage catheter that has a loop in the duodenum and sideholes above and below the level of obstruction. The interventionalist has alarge armamentarium of catheters and guidewires to facilitate passage through varioustypes of obstructions. At times, an obstruction cannot be negotiated nor is it preferableto minimize manipulation in the setting of sepsis; in these cases an external catheteris placed initially. Attempts are generally made at a later time to convert the initialcatheter to an internal-external catheter. At the time of initial drainage, bile specimensare 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 accom-plished with one catheter. The higher the obstruction, the less likely it is that onedrainage will suffice. It is unnecessary to drain every hepatic segment in order tonormalize bilirubin and relieve pruritus. Unfortunately, the need to drain multiplesegments seems more common in the setting of cholangitis, where isolated systemsare contaminated and continue to cause symptoms in the absence of drainage. Asmentioned previously, we ardently avoid treating patients where cross sectional im-aging suggests subsegmental isolation, but will at times place as many as three drain-age catheters (generally one left-sided catheter, one catheter in the right anteriorsector and one in the right posterior sector). Whereas each catheter is difficult forthe patient to tolerate, every effort is made to use as few catheters as possible.

ComplicationsWith the advent of micropuncture technology, targeted punctures, and improved

antibiotics, biliary drainage is much safer now than when first developed. Majorcomplications include bleeding and sepsis. Coagulopathy must be addressed priorto drainage and all patients should receive prophylactic antibiotics. Complicationssuch as pneumothorax and biliary-pleural fistula are very uncommon.

Internal Stent Placement

General ConsiderationsInternal stents may provide drainage with improved quality of life compared to

percutaneous drainage catheters. Most interventionalists place self-expanding, flexiblemetallic stents. Metal stents cannot be changed, and because of limited duration ofpatency (generally 5-7 months) they are rarely employed in benign disease (Figs.4A-D). Plastic stents can be placed percutaneously and may be appropriate incertain situations.

While most patients and referring physicians are anxious to have percutaneousdrainage catheters converted to internal stents as quickly as possible, it is important


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to consider each case carefully to determine the appropriate timing for internaliza-tion. In general, when one is confident that no future drainage procedures will benecessary or possible, it is appropriate to place an internal stent. In cases of low bileduct obstruction, stent placement may be primarily performed. In cases where astent would extend above the confluence, the stent may interfere with future inter-ventions and placement should be delayed until all necessary drainage procedureshave been performed. Multiple stents may be placed at the same time. Nearly allmetallic 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 immedi-ately (as is often the case), a small angiographic catheter (usually 5F) may be leftthrough or above the stent to maintain access to the biliary tree. The patient isbrought back to the interventional suite the following day to assess stent expansionand 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 InterventionsPercutaneous, transhepatic biliary access may also be used to allow balloon dila-

tion of strictures, removal of intrahepatic stones, and delivery of brachytherapy orother intraductal therapies.

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


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Most interventional radiologists and surgeons agree that the best long-term out-come for treatment of bile duct strictures can be expected from primary repair by anexperienced hepatobiliary surgeon. Surgical success may be more limited in patientswho are poor surgical candidates, have portal hypertension, or who have had previ-ous attempts at surgical repair. These patients may best be treated with percutane-ous drainage and balloon dilatation. The best results of percutaneous treatment canbe expected in cases of short segment, late presentation, low bile duct strictures.

Balloon dilatation is generally performed as a staged procedure after placementof a percutaneous drainage catheter. Strictures well below the confluence can gener-ally be treated with one balloon. Strictures at or near the hilus may require two ormore catheters that permit sequential or simultaneous dilation (using “kissing bal-loons”) at more than one site. After initial dilatation, a 10-12 F drainage catheter isleft across the treated stricture(s) for approximately 4 weeks, at which time the pa-tient returns for cholangiographic evaluation. If narrowing persists, repeat dilationmay be performed with a larger balloon, followed by another 4-week period withthe drainage catheter across the treated segment. Once the stricture is shown to bewell treated, a catheter is left above rather than across the treated area. This catheteris then capped, allowing a physiologic trial of the adequacy of dilation to be per-formed. If this is well tolerated by the patient, the catheter can be removed. Patientswho fail repeated dilation may require long-term catheter drainage or an attempt atsurgical repair or bypass. As mentioned earlier, due to limited long-term patency, weare hesitant to place metallic stents to treat benign disease. Stents may be placed inpatients with limited life expectancy due to comorbid conditions or in other rarecases. A proposed etiology for restenosis after metal stent placement is that the metal

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


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wire in biliary stents may cause chronic irritation and mucosal hypertrophy. For thisreason, we prefer to use a stent with the least amount of metal in contact with theduct wall to treat benign disease.

Brachytherapy involves the local delivery of radiation and may be used to treatintraductal tumor. The radiation source is generally delivered via catheters placedthrough recently inserted metal stents. In addition to providing local treatment oftumor, brachytherapy may prolong the patency of metallic stents by decreasing therate of tumor ingrowth.

Percutaneous Abscess DrainagePercutaneous drainage techniques may be useful in treating patients with abdomi-

nal abscesses, including hepatic abscess. Percutaneous drainage may be necessary to

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


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

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 lateralsegment to the distal duodenum. The stent has not yet been opened or shortened toits stated dimensions and is seen extending from the distal 3rd duodenum to theleft hepatic duct.


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

Fig. 4.3E. One day after placement of the stent. The stent has opened and short-ened. Scout image prior to injection of contrast. An angiographic catheter is stillpresent through the stent to allow injection of contrast to assess for stent patencyand location within the biliary tree.


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Abscesses which develop spread from the portal venous system may be associatedwith septic pyelophlebitis. Imaging findings of a hepatic mass with portal vein occlu-sion may mimic those of primary hepatocellular carcinoma. Absence of clinical orimaging findings of cirrhosis, clinical signs and symptoms of infection, and appro-priate antecedent history suggest the correct diagnosis. Percutaneous needle aspira-tion may be performed for confirmation and be followed by percutaneous drainage.Hepatic abscesses are frequently multi-septated, and it is often impossible to com-pletely evacuate them at the time of initial catheter placement. However, with im-age-guided catheter manipulation and appropriate antibiotics, most abscesses canbe effectively managed with a single catheter. There are those who advocate treat-ment with aspiration alone or with aspiration combined with intracavitary antibiot-ics. While this obviates the need for patients to deal with a catheter, more than oneaspiration is generally required for complete treatment.

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


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Percutaneous Hepatic Cyst DrainageSimilar 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 becomesymptomatic due to their large size which can cause pain or compression of adjacentstructures. Historically, therapy for large hepatic cysts has been surgical, now oftenperformed laparoscopically. However, percutaneous drainage is a viable alternativewhich may obviate the need for surgery in a variety of situations. Catheter place-ment may be combined with sclerotherapy using absolute alcohol, betadine solu-tion, or an antibiotic solution.

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


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

Percutaneous Methods for Ablation of Hepatic Neoplasms

General ConsiderationsWhile surgery remains the best hope for curative treatment in patients with most

primary and secondary malignancies of the liver, many patients are not candidatesfor resection at the time of their presentation. This may be due to the extent ordistribution of disease, underlying liver function or general medical condition of thepatient. For these patients, minimally invasive, percutaneous ablative techniquesrepresent attractive therapeutic alternatives. Ablative therapies performed byinterventional radiologists include arterial embolization or chemoembolization, andchemical or thermal ablation.

Embolotherapy

General ConsiderationsTransarterial embolization of hepatic tumors is made possible by the dual blood

supply of the liver. While the preponderant blood flow to normal hepatic paren-chyma comes from the portal vein, the major blood supply to many liver tumors isderived from the hepatic arterial system. This treatment has been used primarily to

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


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treat hypervascular tumors such as hepatocellular carcinoma, neuroendocrine me-tastases, certain sarcomas, and metastases from ocular melanoma.

Some authors believe that embolic therapy should include the local administra-tion of chemotherapy, referred to as chemoembolization. They theorize that pro-longed retention of chemotherapeutic agents can be accomplished by concomitantintra-arterial administration of chemotherapy and embolic material, including io-dized oil and particulate matter such as Gelfoam or polyvinyl alcohol particles. Atour institution, bland embolization (without chemotherapy) is performed. We be-lieve that tumor necrosis results from ischemic cell death, and our technique at-tempts to maximize tumor ischemia while limiting side effects and complicationsassociated with chemotherapeutic agents.

IndicationsEmbolization is performed in an attempt to prolong survival in patients with

hepatocellular carcinoma and non-neuroendocrine, hypervascular liver metastases

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


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who are not surgical candidates. Since neuroendocrine tumors tend to be quite in-dolent, embolization of neuroendocrine metastases is generally indicated for reliefof symptoms due to hormonal production or tumor bulk. Embolization is occasion-ally performed to control rapidly enlarging masses.

ContraindicationsEmbolization 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 dependingon the distribution of disease, presence of reconstitution, and direction of flow. Therisk of hepatic failure must be considered carefully in this situation. Embolizing verylarge tumors carries an increased risk of abscess formation, and size greater than 12cm is a relative contraindication to embolization.

TechniquePatients are premedicated with prophylactic antibiotics and antiemetics. Patients

with neuroendocrine tumors are given prophylactic octreotide as well. Even nonfunc-tional neuroendocrine tumors may produce a low level of hormone(s). During or im-

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


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mediately after embolization, massive cell death may result in the release of vasoactivesubstances that can cause hemodynamic instability in the absence of premedication.

A right femoral arterial approach is preferred. Arterial anatomy and portal veinpatency is assessed (Fig. 4.5A). The arterial vascular supply to the tumor(s) is thendetermined. The embolization technique varies slightly based on the distributionand type of tumor. Focal cancers are treated as sub-selectively as possible, with thesmallest particles available (currently 50 micron PVA). Sub-selective treatment in-volves injecting the embolic material suspended in radiographic contrast directlyinto the arterial branches supplying the mass via catheters, or microcatheters posi-tioned under fluoroscopic/angiographic guidance. Patients with multifocal diseaseare also treated as selectively as possible, but this frequently necessitates emboliza-tion of an entire hemiliver. Even if disease is widespread and bilateral, only onehemiliver is treated at a time to minimize the risk of hepatic failure. Embolization iscomplete when antegrade flow in the vessel(s) supplying the tumor(s) is no longerpresent (Fig. 4.5B). At times it is necessary to use larger particles (100 or 200micron) as the embolization progresses in order to limit the length of the pro-cedure and amount of contrast used. It is also occasionally necessary to searchfor other nonhepatic arterial branches supplying the tumors, most commonlythose 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. Allpatients are maintained on antibiotics and antiemetics for 24 hours. Many patientswill require patient-controlled analgesia (PCA) pumps. PES is generally self-limited,and typically lasts from 24-72 hours.

Percutaneous Ethanol Injection Therapy (PEIT)

General ConsiderationsAbsolute ethanol causes cell dehydration and denaturation as well as small ves-

sel occlusion, presumably due to endothelial cell damage. PEIT has been used totreat focal HCC. In general, up to three tumors smaller than 5 cm in diameter canbe treated. It is thought that HCC masses are relatively “soft” in the background ofa “hard” cirrhotic liver, promoting distribution of alcohol in the tumors. The conversesituation occurs with most secondary liver tumors, and PEIT is not indicated formetastases.

TechniquePEIT is most commonly performed using ultrasound guidance but CT guidance

may also be used. Procedures are performed using local anesthesia with conscious seda-tion. We use a 22 G Westcott type needle to deliver the ethanol, but almost any needlecan 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. Evenwhen the lesion can be well covered in a single treatment, most patients are broughtback the following day for at least a “touch-up”. The platelet count should be checkeddaily until treatment is complete as thrombocytopenia may occur after each treatment.

Ideally, we perform PEIT the day after arterial embolization in an attempt tomaximize cytotoxic insult to the tumor, although PEIT certainly may be performedas 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 dayafter 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 de-ployed from within the shaft of the probe and opened to various diameters. Groundingpads are placed on the patient to form an electrical circuit. Current is then appliedto the tip(s) of the probe. Ionic agitation causes frictional heating and results incoagulation necrosis. Current flow decreases as impedance from tissue desiccationincreases. Currently, the largest diameter necrotic lesion that can be created with asingle probe is approximately 5 cm. Larger areas of necrosis can be created by heat-ing overlapping spheres of tissue.

Probes are currently 15-19 G, and are most commonly positioned using ultra-sound guidance. The effectiveness of RFA may be limited by surrounding struc-tures. Large vessels, such as the inferior vena cava or major hepatic or portal veinbranches, may act as “heat sinks.” Flowing blood through these vessels allows ap-plied energy to be dissipated and cools the edge of the adjacent tumor making itimpossible to achieve a “treatment margin.” One must also consider potential riskto adjacent structures such as bowel, gallbladder and diaphragm.

As with PEIT, this ablative treatment is usually performed using local anesthesiaand 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 branchesof both the anterior and posterior divisions of the right hepatic artery.


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Other Percutaneous Ablative TherapiesCryoablation probes are not yet small enough to be placed percutaneously, and

percutaneous thermal ablative treatments are currently limited to those that causenecrosis through heating. In addition to RFA, other less popular modalities thatcause coagulative thermal necrosis include interstitial laser photocoagulation, per-cutaneous microwave coagulation therapy and high-intensity focused ultrasound.These techniques are investigational and not widely used at this time; and discus-sion of each technique is beyond the scope of this chapter.

Portal Vein EmbolizationSince most of the trophic blood flow to the liver is via the portal vein, emboliza-

tion of a portion of the portal vein will cause atrophy of the embolized segments orhemiliver with hypertrophy of the untreated portion. This procedure may be usefulfor patients who will undergo resection of a large amount of functional hepaticparenchyma in order to resect a small volume of disease and/or those who will be leftwith a very small amount of residual liver after resection. At our institution, we havebegun to perform embolization of the right portal vein prior to right trisegmentectomyin patients with small left lateral segments and a large volume of uninvolved right-sidedparenchyma.

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


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TechniqueA 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 toavoid inadvertent injury to the liver that will remain postoperatively. Various embo-lic materials have been employed. We use medium size polyvinyl alcohol (PVA)particles (200µ-300µ) but have also used absolute ethanol. Ethanol requires the useof occlusion balloons and is not visible radiographically making it somewhat morecumbersome.

Patients generally wait approximately 2-4 weeks after portal vein embolizationbefore they undergo resection.

Transjugular Intrahepatic Portosystemic Shunts (TIPS)

IndicationsTIPS is indicated for the treatment of recurrent variceal bleeding which

has not responded to medical and/or endoscopic therapy, or for the control ofrefractory ascites.

ContraindicationsAbsolute contraindications include severe hepatic failure and severe right heart

failure, both of which would be exacerbated by shunt creation. Relativecontraindications include portal vein thrombosis, HCC, hepatic metastases, andpolycystic disease involving the liver.

TechniqueThe procedure can usually be performed using conscious sedation. Ideally, the

right internal jugular is used, although TIPS can be done using the left internaljugular vein or the external jugular veins. A catheter is placed through a long sheathinto 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 wireis then advanced to the superior mesenteric or splenic vein and pressures are re-corded. The shunt tract is then predilated with a balloon, after which a flexiblemetal stent, usually 10 or 12 mm, is deployed and dilated. Increasingly, coveredstents are being utilized to prevent thrombosis thought to result from communica-tion with the biliary tree. Pressure gradients between the portal and systemic sys-tems are obtained. Ideally, a successful TIPS will produce a gradient between theportal 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 meta-static to liver. The patient had one mass in the lateral segment and another in thecentral aspect of Segment VIII, adjacent to the right hepatic vein and the inferiorvena cava, and approaching the middle hepatic vein. The patient underwent em-bolization of the right portal vein in anticipation of right trisegmentectomy andwedge resection of the lateral segment mass.Fig. 4.6A. Contrast enhanced CT image demonstrating the mass in Segment VIIIbefore embolization.


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

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


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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 branchesremain patent. Opacified vessels overlying the right hemiliver are patent SegmentIV branches.

Fig. 4.6E. Contrast enhanced CT image at the level of the Segment VIII lesion, approxi-mately 2 weeks after embolization of the right portal vein. Note the left liver hypertro-phy 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 thestriking perfusion defect in the right hemi-liver.

Fig. 4.6G. Contrast enhanced CT image at the level of the Segment III lesion, approxi-mately 2 weeks after embolization of the right portal vein. Note the enlargement of thelateral 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 defectin the right hemi-liver.

CHAPTER 5


Perioperative Care and AnesthesiaTechniques

Mary Fischer, Enrico Ferri, Jose A. Melendez

IntroductionThe evolution of surgical techniques and anesthetic care is such that the most

challenging procedures have become available for sicker patients. This Chapterexamines the preoperative, intraoperative and postoperative considerations that guidethe anesthetic management of liver surgery.

Preoperative EvaluationThe preoperative status of the patient is currently the main factor in the determi-

nation of the anesthetic risk for any surgical procedure.

Cardiac EvaluationPerioperative cardiac morbidity is one of the leading causes of perioperative death.

The incidence of myocardial ischemia occurring in patients with coronary arterydisease (CAD) can reach 74%. Myocardial infarction occurs in 2% of the patients.The incidence of perioperative ischemic complications is significantly reduced byβ-blocker therapy. Table 5.1 shows other factors associated with increased cardiacmorbidity. A complete history and physical examination, followed by a 12-lead EKG,are the basic components of the preoperative evaluation. Radio-nucleotide stresstest 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 than10 years, cirrhotic cardiomyopathy must be expected. Cardiac dysfunction can fol-low 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 EvaluationPostoperative pneumonia is a major risk for patients with poorly compensated

respiratory disease. Anesthesia reduces the functional residual capacity leading toalveolar collapse. Emphysema, bronchitis and asthma predispose to airway closureand respiratory failure can follow. Asthma and bronchospasm must be treated priorto an anesthetic. To establish the extent of disease, and to optimize therapy, patientsmay require pulmonary function tests and blood gas analysis. Severe chronic bron-chitis may require corticosteroids and antibiotics.


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Hepatic EvaluationThe operative outcome after liver surgery strictly depends on the preoperative

metabolic liver function and the extent of the parenchymal resection. Mild or well-compensated chronic hepatic disease does not increase risk of death compared tothe general population. Liver function must be estimated from the Child’s classifica-tion, as aminopyrine breath test and indocyanine green clearance are not readilyavailable for clinical use. Routine evaluation should include CBC, clotting factors,serum electrolytes, serum albumin, bilirubin and liver enzymes.

Intraoperative ManagementSurgical stimulation and manipulation of the liver dramatically increases the

hepatic oxygen extraction ratio. At the same time, there is a 16% drop in hepaticblood flow associated with anesthesia and mechanical ventilation and a 40% decreasewith splanchnic surgery. This may be due to a direct effect on the hepatic venousbed mediated through the hepatic sympathetic innervation. Further impairment onhepatic blood flow results from decreases in cardiac output from intraperitonealinsufflation and a head-up tilt. The anesthesiologist should optimize the oxygendelivery-oxygen extraction ratio, and avoid inducing hypotension, hypovolemia andanesthetic overdoses which cause reductions of cardiac output and systemic pressureresulting in decreases in hepatic blood flow.

Low Central Venous Pressure AnesthesiaFluid load is commonly practiced prior to the resection in order to prevent

hypotension during episodes of uncontrolled bleeding. This procedure results invena caval distension which may interfere with surgical dissection. Low central venouspressure anesthesia (LCVP), below 5 mm Hg, eliminates vena caval distension andeases mobilization of the liver to permit dissection of the retrohepatic vena cava, and

Table 5.1. Preoperative factors associated with postoperative life-threateningcomplications or fatal cardiac complications

History: Age > 70 yrsMyocardial infarction in previous 6 months

Physical Examination: S3 gallop or jugular venous distentionImportant aortic stenosis

Electrocardiogram: Rhythm other than sinus or premature atrial contractions> 5 Premature ventricular contractions/min at any time

General Status: Po2 < 60 or Pco2 > 50 mm Hg,K < 3.0 or HCO3 < 20 meq/lBUN > 50 or creatinine > 3.0 mg/dlAbnormal SGOT,Signs of chronic liver disease or patient bedridden

Operation: Intraperitoneal, intrathoracic or aortic operationEmergency operation

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

75Perioperative Care and Anesthesia Techniques

5

major hepatic veins. LCVP is usually performed in combination with inflow andoutflow control.

Investigators have demonstrated a relationship between extent of intraoperativeblood loss and morbidity and mortality. The blood loss resulting from a vascularinjury is directly proportional to both the pressure gradient across the vessel wall andthe fourth power of the radius of the injury. Lowering CVP lessens the pressure com-ponent of the equation and minimizes the radial component of flow by reducing vesseldistension, thereby reducing hepatic venous bleeding during parenchymal transection.

Strict fluid restriction is practiced until the liver resection is completed, althoughsmall fluid boluses may be given to maintain hemodynamic stability. Intravascularhypovolemia is counteracted with 15˚ head-down tilt. This improves venous returnand preserves renal function. The technique requires appropriate cannulation andtransfusion equipment to face emergency fluid resuscitation. A high level of vigi-lance is obligatory.

Anesthesia is maintained with a combination of isoflurane in O2 and fentanylwhich provides minimal hemodynamic changes. The combination of fluid restrictionand minimal vasodilation from narcotics is usually sufficient to achieve the desiredconditions. In some cases, further peripheral dilation may be achieved by first usingmorphine. Only a very small number of patients require intravenous nitroglycerin.

LCVP-anesthesia increases the risk of intraoperative air emboli. Restriction ofnitrous oxide in the gas mixture helps by preventing the enlargement of circulating airpockets. It is crucial to have rapid occlusion of open venous channels; this results in avery low incidence (0.4%) of clinically significant air emboli. Monitoring is performedwith end-tidal CO2. Transesophageal echocardiography has proven to be sensitive.

Anesthesia for Vascular IsolationHepatic vascular isolation is an alternative surgical approach for liver resection.

It induces a decrease in venous return with a resulting decrease in cardiac index andincrease in systemic vascular resistance. Anesthetic management requires the increasein CVP to improve cardiac filling and maintain cardiac output. Vasopressors may berequired during the vascular isolation phase. Metabolic acidosis and hyperkalemiamay occur after prolonged vascular isolation. Appropriate therapy is mandatory. Insome cases, the procedure needs to be abandoned due to persistent hypotensionand/or low cardiac index. This technique is more complex, conveys higher bloodloss and transfusion rates, and does not show better results than portal triad clamp-ing with extrahepatic control of the hepatic veins (Table 5.2).

Obstructive JaundiceAcute biliary obstruction is associated with an increase in liver blood flow, which

is decreased with chronic obstruction, possibly secondary to increased portal resis-tance. Decompression of chronic biliary obstruction may result in hemodynamicimpairment and shock. Biliary sepsis may exacerbate this state. Aggressive hemody-namic monitoring is required to reduce mortality.


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Postoperative Care

Immediate Postoperative ConcernsImmediate postoperative concerns common to all major intra-abdominal proce-

dures are bleeding, intravascular volume, renal function, and oxygenation. Thereare also some unique issues in patients undergoing hepatobiliary surgery. Liverregeneration following partial hepatectomy involves rapid cell division (as early as24-72 hours) and may be critically dependent on cellular ATP stores. Supplementa-tion of intravenous fluids with KPO4 (30-40 mmol/day) should be part of the stan-dard postresectional therapy. In these patients, the hepatic resection overlaps withaltered drug pharmacodynamics and pharmacokinetics and attention must be paidto anesthetic elimination and postoperative pain management. Routine parenteraladministration of vitamin K commonly corrects the coagulation abnormalities within48 hours. More rapid correction may be accomplished by fresh frozen plasma.

Nonimmediate Complications

JaundiceA bile duct injury at the time of surgery should be suspected when postoperative

extrahepatic obstructive jaundice occurs. Other more common causes of elevatedunconjugated hyperbilirubinemia include hematoma reabsorption and hemolysisof transfused blood (Table 5.3). Hepatocellular injury is another possibility in thedifferential diagnosis of postoperative jaundice. Common etiologies are sepsis, lowtotal hepatic blood flow, and infectious hepatitis. When all other factors are

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

Author Technique Total Major Blood TransfusionsCases Resections* loss (cc) (units

or cc)**Mean** Median

Delva et al, HVI 35 35 – – 8.0 ± 8.31989†

Emre et al, HVI 16 13 1866 ± 1683 1325 –1993Hannoun et al, HVI 15 15 – – 5.8 ± 4.71993Habib et al, HVI 56 33 1651 ± 1748 1200 930 ± 7501994Emond et al, HVI 48 44 1255 ± 1291 – 1.9 ± 2.61995Belghiti et al, HVI 24 24 1195 ± 1105 – 2.5 ± 3.41996Melendez et al† 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.


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Table 5.3. Differential diagnosis of postoperative jaundice*

Increased Bilirubin Load Biliary Obstruction Hepatocellular InjuryBlood transfusion Intrahepatic cholestasis Hepatic hypoxemiaHematoma Drug induced Exacerbated chronicHemolytic anemia Infection induced hepatitisExtracorporeal circulation Extrahepatic cholestasis Acute hepatitis: viral,Hemolysis Bile duct injury alcoholic

Pancreatitis Gilbert’s diseaseRetained gallstones Sepsis

TraumaToxins, 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 enlarge-ment in diameter of injury and increase in the bleeding driving pressure.

eliminated, the diagnosis of anesthetic related hepatotoxicity might be entertainedif halothane was used. With newer, less controversial volatile anesthetics, it is rarelyseen today.


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AscitesAscites 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 effecteven in the presence of severe hypoalbuminemia. The treatment of ascitesunderscores bed rest and sodium restriction, to be followed by spirono-lactone if a spontaneous diuresis is not restored. If life threatening com-plications such as cardiac or respiratory compromise occur, these patientsrequire hemodynamic monitoring. Paracentesis should be attempted incase ascites persists.

Renal FailureFollowing hepatobiliary surgery, rapidly progressive renal failure may occur. The

differential diagnosis includes acute tubular necrosis, prerenal azotemia andhepatorenal syndrome. Hepatorenal syndrome is the development of otherwiseunexplained renal failure with urine sodium < 10 meq/l, hyperosmolar urine, olig-uria (< 400 ml/24hrs), fractional excretion of sodium (FeNa+) < 1, and urine creati-nine to plasma creatinine ratio > 30:1 in patients with advanced liver disease. Thepathophysiology of hepatorenal syndrome is based on the pooling of blood in thesplanchnic bed and the resultant decrease in plasma volume. The kidney perceives adecreased glomerular filtration rate and causes a vasoconstriction that shunts bloodaway 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 sponta-neous recovery has been reported, mortality is very high. These patients, generallycirrhotic, may benefit from liver transplant.

Pulmonary CareHepatopulmonary syndrome is defined by liver disease, increased alveolar arte-

rial gradients, and evidence of reduced intrapulmonary vascular resistance. In cir-rhotic patients, an increased synthesis of nitric oxide has been demonstrated thatmay lead to arteriovenous shunts in the lungs. The resulting hypoxemia requiresoxygen supplementation and may progress to respiratory failure.

Glucose MetabolismWe might expect the postoperative patient to be prone to hypoglycemia second-

ary to diminished glycogen reserves, increased insulin levels, and impaired gluco-neogenesis. Yet, dangerous hypoglycemia is rare. Routine (5%) dextrose solutionsshould be infused while monitoring glucose serum levels.


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CoagulationHypocoagulability derives from thrombocytopenia or reduced synthesis of vita-

min K dependent factors; cholestasis also decreases vitamin K absorption and hepaticstores. Improvements in coagulation may be achieved with vitamin K 10 mg/day.Another cause of bleeding is fibrinogen deficiency; this situation may benefit fromfresh frozen plasma transfusion. Decreased serum concentration of protein S, proteinC and antithrombin III result in hypercoagulable states that can lead to disseminatedintravascular coagulation (DIC).

SepsisAbdominal sepsis is the most common cause of mortality after hepatic resection.

Preoperative biliary manipulation, infected bile, biliary stones, ascites, and bloodloss may all predispose to abdominal sepsis. Other sources of sepsis include therespiratory and urinary systems. Wound infection and a central line catheter shouldalso be considered as possible sources of infection.

Gastrointestinal BleedingThe incidence of GI bleeding is 5%, with a mortality reaching 50%. The bleed-

ing site can usually be identified by endoscopy. Treatment includes transfusions,antacids and H2 blockers. All postoperative hepatobiliary patients should be treatedprophylactically. About 30% of cirrhotic patients have esophageal varices. The emer-gent treatment should combine blood product transfusion to correct the coagulopathy,gastric endoscopy with variceal banding or sclerotherapy, and possibly, octreotide25-100 mcg/min to control bleeding. Life saving procedures may include compres-sion of the varices via a Sengstaken-Blakemore tube. As rebleeding occurs in 50% ofpatients, a definitive surgical treatment should be pursued.

EncephalopathyHepatic encephalopathy may be precipitated by GI bleeding, infection, drugs,

diet or dehydration. It manifests as a sudden change in a patient’s mental status orthe onset of asterixis. The precise pathogenesis remains unknown. The historicalpostulate has been the accumulation of endogenous ammonia. Other etiologies havebeen suggested, including changes in the blood-brain barrier permeability, abnor-mal neurotransmitter balance, altered cerebral metabolism, impairment of neuronalNa+-K+ ATPase activity, and increased endogenous benzodiazepines. Standard therapyis devised to reduce levels of ammonia and other potentially toxic metabolites.Flumazenil has been administered with some improvement; however, proteinrestriction and lactulose administration are still practiced.

Suggested Reading1. Belghiti J, Noun R, Zante E et al. Portal triad clamping or hepatic vascular exclu-

sion for major liver resection—A controlled study. Ann Surg 1996; 224:155-61.2. Brown BR. Postoperative jaundice. In: Brown BR, ed. Anesthesia in Hepatic and

Biliary Tract Disease. Philadelphia: F.A. Davies 1988:265-273.3. 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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4. Emre S, Schwartz ME, Katz E et al. Liver resection under total vascular isolation-variations on the theme. Ann Surg 1993; 217:15-9.

5. Emond J, Wachs ME, Renz JF et al. Total vascular occlusion for major hepatec-tomy in patients with abnormal liver parenchyma. Arch Surg 1995; 130:824-31.

6. 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.

7. Gitlin N. Hepatic encephalopathy. In: Zakim D, Boyer TD, eds. Hepatology ATextbook of Liver Disease. 3rd.edition. Philadelphia: WB Saunders 1998; 605-17.

8. Goldman L, Caldera DL, Nussbaum SR et al. Multifactorial index of cardiac riskin noncardiac surgical procedures. New Engl J Med 1997; 297:845-50.

9. Habib N, Zografos G, Dalla Serra G et al. Liver resection with total vascular exclu-sion for malignant tumors. Br J Surg 1994; 81:1181-4.

10. Hannoun L, Borie D, Delva E et al. Liver resection with normothermic ischemiaexceeding 1 h. Br J Surg 1993; 80:1161-5.

11. Krowka MJ, Cortese DA. Hepatopulmonary syndrome. Current concepts in diag-nostic and therapeutic considerations. Chest 1994; 105:1528-1537.

12. Melendez JA, Arslan V, Fischer M et al. Peri-operative outcome of major hepaticresections under low central venous pressure anesthesia—blood loss, blood trans-fusion and the risk of postoperative renal dysfunction. J Am Coll Surg 1998;178:620-25.

CHAPTER 1CHAPTER 6

Benign Tumors of the Liver:A Surgical Perspective


IntroductionBenign liver tumors are common and account for 83% of all hepatic tumors

identified on diagnostic imaging or at the time of laparoscopy. Benign liver tumorsmay arise from either epithelial or mesenchymal cells. In rare instances, a variety ofmiscellaneous disorders may masquerade as liver tumors (Table 6.1). The frequencyof different types of liver tumors is not well understood, but suffice it to say, farmore than 50% of all hepatic lesions are either hemangiomas or benign cysts(Table 6.2). Focal nodular hyperplasia (FNH), metastatic tumors from an undiag-nosed primary cancer site, hepatic adenomas, focal fatty infiltration, and hepatocel-lular carcinomas are the next most common diagnoses in descending order offrequency. Additional benign tumors have also been described; however, most if notall, are sufficiently rare as to be labeled medical “fascinomas.”

The infrequency of symptoms associated with most benign and many malignantliver tumors complicates the process of establishing a firm diagnosis when hepatictumors are identified incidentally. Despite significant advances in a variety of diag-nostic imaging modalities, the appearance of these lesions is often not clear-cut andbiopsy or resection is indicated as diagnosis is mandatory. Indeed, the most com-mon indication for surgical management of “benign” liver tumors is the inability toexclude a possible malignancy. Table 6.3 reviews an MSKCC experience in treating152 patients with “presumably” benign liver tumors between 1995 and 1998. Fifty-four percent of patients underwent operation, in part or solely to exclude a potentialmalignant diagnosis. Less common indications for surgical management included:

1. Relief of debilitating symptoms2. To reduce the risk of rupture (a rare event), or potential for malignant

transformation.3. To treat life-threatening complications of rupture or hemorrhage.

EvaluationThe most “appropriate” work-up for an asymptomatic patient with a newly iden-

tified solid liver tumor is unclear and it is difficult to recommend precise algo-rithms. In general, the workup should be individualized based upon patient age,sex, personal medical and social history, as well as the stage and suspected histologyof the tumor in question. Physical examination is typically unrevealing unless thetumor is expansive, and in this setting, pain or abdominal discomfort is normally



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Table 6.1. Benign solid tumors of liver

Cell of origin Tumor

EpithelialHepatocellular Focal nodular hyperplasia (FNH)

Hepatocellular adenoma (HA)Regenerative nodule

Cholangiocellular Biliary adenomaBiliary cystadenoma

Other Epitheliod leiomyoma

MesenchymalEndothelial Hemangioma

HemangioendotheliomaAdultInfantile

Mesothelial Solitary fibrous tumorOther names: benign mesothelioma or fibroma

Adipocyte LipomaMyelolipomaAngiomyelipoma

MiscellaneousTumors Biliary hamartoma

Pseudotumors Focal fatty infiltrationAdrenal neoplasmInflammatory pseudotumorChronic abscess

Table 6.2. Incidental solid liver tumors: Diagnostic frequency for varioushistologies3

Tumor Relative frequencyHemangioma 52%Focal nodular hyperplasia 11%Metastatic tumor (TxNxM1) 11%Hepatocellular adenoma 8%Focal fatty infiltration 8%Hepatocellular carcinoma 6%Extrahepatic process 3%

(e.g., abscess, adrenal tumor)Other benign hepatic process 1%

83Benign Tumors of the Liver

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

Diagnosis Total Age Resected Operated on Symptoms(Mean) (%) to exclude a (%)

malignancy (%)

Hemangioma 75 55 35 14 23(47) (40) (66)

FNH 33 42 16 9 8(48) (56) (50)

Adenoma 10 39 8 6 6(80) (75) (75)

Cyst 26 56 15 5 8(58) (33) (53)

Polycystic liver 4 46 4 0 4(100) (100)

Hydatid cyst 4 48 4 0 4(100) (100)

Total 152 49 82 34 53(54) (41) (65)

present. Hepatomegaly may develop in the setting of a large hepatic cyst, cavernoushemangioma, parenchymal bleed into a hepatocellular adenoma, or polycystic liverdisease, but is not diagnostic. Laboratory tests, including liver function tests, areinvariably normal in asymptomatic patients with liver tumors and are, therefore,not helpful. In rare instances, serum transaminase levels may be elevated in patientsexperiencing an acute hemorrhage, thrombosis, or necrosis of tumor, but it is notpathognomonic for a particular liver pathology. Elevated serum tumor markers, suchas alpha fetoprotein (AFP), carcinoembryonic antigen (CEA), and CA-19-9, arerarely elevated in benign liver tumors and should suggest the likelihood of an under-lying malignancy.

In most instances, radiologic studies can provide a precise diagnosis based on thecharacteristic appearance of the tumor; however multiple studies yielding comple-mentary data are required (Table 6.4). In Chapter 4, Decorato and Schwartz pro-vide a detailed discussion of the advantages and disadvantages of various hepatobiliaryimaging techniques.

In brief, ultrasonography is the most common initial study since it can effec-tively differentiate between cystic and solid neoplasms. Contrast-enhanced com-puted 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 mostuseful imaging modality with regard to differentiating between “indeterminate” and

84H

eptobiliary Surgery

6

Table 6.4. The radiographic appearance of common benign liver tumors

Tumor Ultrasound CT MRI Tc 99 RBC scan Tc 99 SC scan

Hemangioma Hyperechoic Very sensitive Very sensitive Highly specific Not indicatedWell-demarcated Isodense on noncontrast scan Isodense on T1 Very sensitiveIncreased vascular flow Contrast: Irregular peripheral Hyperdense on T2 Blood pooling ofCentral venous pooling enhancement Gadolinium enhanced radionucleotideDelayed central filling scan shows similar

findings to contrast CT

Focal Nodular Nonspecific Isodense on noncontrast CT Isodense of T1 & T2 Not indicated Takes up Tc 99 SCHyperplasia ?Hyperechoic may be well-demarcated on Early hyperdense Contains bile(FNH) contrast CT with central scar appearance after ducts and

— often isodense gadolinium Kupffer cellsNonspecific

Hepatic Nonspecific Nonspecific Nonspecific Nonspecific Generally doesAdenoma ?Hyperechoic Hyperechoic Hyperechoic Not indicated not take up Tc 99

Increased blood flow SC because of theon duplex scanning lack of bile ducts

and Kupffer cellsNonspecific

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


6

malignant tumors. Although many liver tumors have a characteristic angiographicappearance, the information it provides can currently be obtained by noninvasiveimaging modalities in most situations. Laparoscopy can be used as a diagnostic toolin some patients by allowing the surgeon to obtain a reliable tissue biopsy usingminimally invasive techniques. In rare cases, the surgical management may be car-ried out laparoscopically as well.

Benign Liver Tumors

HemangiomaHemangiomas are the most common benign solid tumors of the liver and occur

in two variants, capillary hemangiomas and cavernous hemangiomas. Capillary he-mangiomas are the most common, but are clinically insignificant. They are typicallysmall, hypervascular lesions (< 2 cm) encountered at the time of laparotomy andmay be the source of considerable diagnostic uncertainty. Establishing the diagnosisand excluding a malignancy is all that is required.

Cavernous hemangiomas are clinically more relevant because of the potential forcomplications and associated symptoms. Cavernous hemangiomas have been reportedin up to 7% of patients at autopsy and occur more commonly in adults than inchildren. The etiology of cavernous hemangiomas remains uncertain; however, theymost likely represent benign congenital hamartomas. Although the incidence ofcavernous hemangioma has been reported as 1.3-6 times higher in women than inmen, the higher incidence of hemangioma in females is likely a reflection of referralbias rather than a true difference in incidence. Sex hormones have not been linkedetiologically to the development of hemangiomas. Cavernous hemangiomas mayvary in size from less than 1 cm, to “giant hemangiomas” which may be greater than30-40 cm. The size of a hemangioma correlates with symptoms, as it is usually largepedunculated tumors that are encountered at surgery. These tumors are often sharplydemarcated from surrounding liver tissue, have a spongy appearance, and may bepartly necrotic or fibrotic. Occasionally, infarct of the hemangioma may cause it tobe completely fibrosed and, in rare cases, calcified. When this occurs, these tumorscan be extremely difficult to distinguish from other benign and malignant tumors.The acute nature of some symptoms related to hemangioma may, in fact, not berelated to increase in size, but rather thrombosis and infarct that lead to focal fibrosisand obliteration of vascular channels in part or whole.

Clinical PresentationSymptoms 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 stretch-ing or inflammation of Glisson’s capsule. Occasionally, a large hemangioma maypresent as a nontender mass in the right upper quadrant, but more often the physi-cal examination reveals only vague upper abdominal tenderness with no mass. Itmay be possible to auscultate a bruit over a large hemangioma, but this is not pathog-nomonic. Rarely, a hemangioma may rupture resulting in a hemoperitoneum andshock requiring emergency surgical care.

Severe thrombocytopenia and the development of a consumptive coagulopathyhave been associated with cavernous hemangiomas of the liver. Although the


6

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

PathologyHistorically, hemangiomas are typically well demarcated and distinct from the

surrounding hepatic parenchyma. The sharp interface between hemangioma andnormal liver parenchyma permits surgical enucleation in most cases. However, notall hemangiomas are enucleable, and the histologic features of the tumor-liver inter-face 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 beendescribed. A “fibrolamellar interface”, characterized by a capsule-like fibrous ring ofvariable thickness, is most common. The normal hepatic parenchyma is often atro-phic, and a plane between the hemangioma and the normal liver tissue can be welldefined. A second variant, the “interdigiting” pattern, is marked by the lack of afibrous lamella surrounding the hemangioma which is replaced by an ill-definedplane between normal liver tissue and the vascular channels of the hemangioma.These tumors can be quite hazardous to remove without a formal resection. Twoadditional histologic variants have been identified, including a “compression” inter-face, in which the periphery of the tumor is well demarcated in the absence of afibrous lamella and an “irregular or spongy” variant which appears to intercalateinto the surrounding liver parenchyma making complete excision hazardous andunnecessary. 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 macro-scopic and microscopic examination. In rare instances, an atypical hemangiomamay be confused for other liver conditions including peliosis hepatis, hemorrhagictelangiectasia (Osler–Rendu–Weber), hemangioendothelioma and other malignantvascular tumors. As a rule, percutaneous biopsy of a suspected hemangioma shouldbe avoided as this may result in unnecessary and uncontrollable hemorrhage. Symp-tomatic lesions, large lesions, or indeterminate lesions should be managed surgically.

Radiologic EvaluationThe initial radiologic evaluation of a suspected hemangioma is often dictated by

the clinical presentation. In most instances, hemangiomas are discovered inciden-tally on a study performed for other reasons and the degree of diagnostic certaintyprovided by this study may obviate the need for additional imaging. If a patientpresents with dull, nonspecific right upper quadrant complaints, ultrasonography istypically the first study performed. On ultrasound (US), a hemangioma appears as ahyperechoic mass well demarcated from the surrounding liver. The number andlocation of the lesion(s) can be precisely defined on B-mode ultrasound, and theaddition of duplex ultrasonography can provide information with regard to peripheralblood flow and central pooling of venous blood. On a noncontrast CT scan,hemangiomas appear as a hypodense mass which exhibits a characteristic pattern ofirregular peripheral nodular enhancement after initial injection of contrast material.Delayed CT scanning, several minutes after contrast injection, demonstrates central


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

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

TreatmentObservation is the most appropriate treatment for nearly all asymptomatic

hemangiomas. To date, there are no documented instances in which a hemangiomahas spontaneously ruptured while being observed. Trastek et al followed 36 patientswith a cavernous hemangioma for up to 15 years (mean 5.5). Among this groupwere two infants who were treated with steroids; one child responded. One adultpatient was also treated with external beam radiation and showed marked reductionin the size of the lesion. The other 33 patients were observed with no other treat-ment. There were no spontaneous ruptures and, most importantly, no changes in

88H

eptobiliary Surgery

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


6

symptoms over the course of follow up. In four patients the size of the hemangiomaincreased and in three patients the size decreased. Foster followed 44 patients withhemangiomas for a period ranging from 2 months to 12 years. There were no reportsof rupture, death, or change in clinical symptoms in their series. In the absence ofclinical symptoms, the careful observation of all asymptomatic hemangiomas is therecommendation of most experienced liver surgeons.

Hepatic resection for a hepatic hemangioma should be approached no differentlythan surgery for other tumors of the liver. The surgeon should have extensive knowl-edge of the anatomy and vascular supply of the liver. The extent of the liver resectionrequired for removal is directly related to the anatomic location of the lesion and itsproximity to major blood vessels. In patients with symptomatic hemangiomas, someform of treatment is often necessary. Patients with disabling pain, pressure symptoms,or acute symptoms related to the hemangioma should undergo surgical resection. Thelocation of the hemangioma is critical to planning surgical resection. Large centrallesions that abut the portal vein, hepatic outflow tract, or inferior vena cava over a longdistance may pose a prohibitive surgical risk even in experienced hands. In these situa-tions, alternative therapeutic modalities should be considered. Unlike malignant le-sions, the resection of a hemangioma does not require the surgeon to remove a marginof normal tissue with the tumor. As such, the most appropriate treatment for mosthemangiomas is enucleation. In some cases, however, it may be safer and more rationalto perform formal lobectomy or extended resection.

The effectiveness of hepatic artery ligation as a treatment for hemangioma hasbeen described anecdotally; however, its benefit is likely transient. Hepatic arterial

Fig. 6.3. Sagittal view of a large cavernous hemangioma as visualized on T1 andT2 weighted images.


6

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

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 liverretains some contrast but is significantly less intense than the spleen and heart. Acavernous hemangioma is seen arising from the left lobe of the liver.


6

fying the use of radiotherapy in hemangiomas is scant. However, if surgical therapyis not possible, radiotherapy seems a reasonable alternative approach to the treat-ment of symptomatic hemangiomas.

Special Issues: Hemangiomas in ChildrenHepatic hemangiomas of infancy and childhood are different lesions from those

seen in adults. These lesions are typically large, and if so, their symptoms are rarelysubtle. The vast venous lakes within these lesions can function as tremendous siphonsfor a large amount of the total cardiac output leading to severe congestive heartfailure and death. In children who develop high output cardiac failure, the initialtreatment usually consists of digitalis, diuretics, oxygen, corticosteroids and hepaticartery ligation. Radiation treatment is often employed and may result in improvedcardiac performance. In contrast to adults, the risk of spontaneous rupture of hepatichemangiomas that occur in infancy is great. Similarly, Kasabach-Merritt syndromein association with life-threatening thrombocytopenia and afibrinogenemia, occursmore frequently and may result in death in a high proportion of affected infants. Asopposed to the conservative approach to treatment of hemangiomas recommendedfor adults, hemangiomas of infancy and early childhood frequently require life-sav-ing surgical treatment and should be referred immediately to an experienced pediat-ric tertiary center.

Focal Nodular HyperplasiaFocal 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 men-strual age. FNH tumors are almost always asymptomatic lesions discoveredincidentally during a radiological work-up for other reasons. In rare instances, theymay present as a palpable abdominal mass on physical examination. Although a raretumor prior to the 1960s, the incidence of FNH has increased markedly in the lastthree decades. Notably, the increased incidence in FNH has occurred concurrentwith the introduction and widespread use of ultrasound and CT scanning in clinicalpractice, as well as the development and acceptance of the oral estrogen contraceptivepill (OCP). Whether the increased reporting of FNH tumors represents a true changein incidence or merely reflects the proficiency of scanning in identifying these lesionsis unclear, but the latter is probably the case. Klatskin and Vana et al reported sepa-rate series of patients with FNH tumors in which they suggested an etiologic rela-tionship between OCP usage and the development of both FNH and hepaticadenoma. However, numerous reports of FNH prior to the 1960s, and its frequentoccurrence in individuals who have never used OCP, cast significant doubt on theexistence of any etiologic association between OCP use and FNH. The potentialeffect of pregnancy on FNH (as well as hepatic adenomas) remains poorly under-stood. Scott et al have reported a single case of a female who had used OCPs for 11years prior to developing an FNH. After stopping the OCP, the tumor regressed; itsubsequently increased in size during a later pregnancy. Although their report isprovocative, data linking pregnancy and changes in the size or symptoms of anFNH tumor are scant. As opposed to hepatic adenoma, there are no reports ofspontaneous rupture of FNH during pregnancy. Importantly, although it may beimpossible (without surgical resection) to distinguish an FNH from a well differen-


6

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

PathologyMacroscopically, FNH appear as pale firm lesions distinct from the surrounding

liver (Fig. 6.5). Histologically, FNH tumors are sharply demarcated from the nor-mal liver but lack a true capsule. The architecture of these lesions suggests a regen-erative rather than a neoplastic process, and as such, they can be difficult to distinguishfrom regenerating nodules associated with cirrhosis. Bile duct hyperplasia, and Kupffercells are generally prominent in FNH, and often allow differentiation from otherlesions by radionucleotide scanning. Radiographically, FNH are described as havinga “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 andprominent thick-walled blood vessels divided by fibrous septae.

Clinical PresentationMost FNH tumors are solitary, although 20% may be multiple when identified.

FNH often occurs in association with other benign hepatic tumors such as heman-giomas. These lesions are small (< 3 m), and intraoperatively they appear as pale redto brown, firm nodules with prominent blood vessels on the surface. Larger lesionscan be particularly difficult to distinguish from well-differentiated hepatocellularcarcinoma (HCC). Nearly all FNH tumors are asymptomatic, and unlike otherbenign liver tumors, spontaneous rupture is extremely rare. In our experience inmanaging 33 patients with FNH tumors, there were no spontaneous ruptures, andthe most common indication for surgical resection was the inability to exclude apotential hepatic malignancy.

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


6

EvaluationAs 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 thesuspicion of a malignancy rather than an FNH. Most radiologic studies of FNH arenonspecific. FNH are visible by ultrasound but exhibit no characteristic features.Technicium-99 labeled sulfur colloid scintigraphy may be helpful in demonstratingthe presence of Kupffer cells within a hepatic tumor, but a positive result is notspecific since both hepatic adenoma and HCC can contain Kupffer cells (Fig. 6.6).Helical contrast CT scanning may demonstrate a well-demarcated lesion with theappearance of a central scar during the portal venous phase, but these lesions areoften isodense and undetectable. MRI may demonstrate a hypodense lesion with acentral scar, but these findings are not pathognomonic for FNH (Fig. 6.7). The useof reticuloendothelial agents such as Ferridex, which are taken up selectively byKupffer cells, can increase the specificity of both CT and MRI; however, the resultsare not specific to FNH. Angiography typically demonstrates a hypervascular masswith enlarged peripheral vessels and a single central feeding artery.

TreatmentIn 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, enucleationof the tumor is sufficient treatment. More often, a firm histologic diagnosis isunavailable on frozen section, and a formal resection (with a rim of normal tissue) isrequired in the unfortunate event that the final pathology demonstrates a malignantlesion. In situations in which the tumor is truly felt to be an FNH based on radio-logic features, particularly if it is small and centrally located, a trial of close observa-tion with repeat imaging every 3-4 months is rational. Any change in size, numberor symptoms of the lesion(s) should prompt reconsideration of surgical resection.Even in the absence of strong evidentiary data, discontinuation of OCP use in allpatients with resected or unresected FNH seems prudent.

Hepatic AdenomaHepatic 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 adenomashas increased alarmingly since the late 1960s. Unlike FNH however, a persuasivebody of literature has emerged demonstrating an etiologic link between OCP usageand the development of a hepatic adenoma. The risk of developing a hepatic adenomais commensurate with length of OCP usage and age over 30. Ninety percent ofpatients who develop a hepatic adenoma have used OCPs and the incidence amongthose who have used the OCP for more than 2 years is 3-4 per 100,000. Interest-ingly, the risk of developing a hepatic adenoma while taking OCP may be related tothe amount of estrogen in OCP preparation, and if so, current low estrogen OCPpreparations should decrease the incidence of hepatic adenomas in the future. Re-gression of hepatic adenoma upon cessation of OCP use has been well documented;however, progression can occur. There is no convincing evidence linking pregnancyto the development of hepatic adenoma, but it may increase the incidence of com-plications associated with hepatic adenomas. In addition to estrogens, several otherhormone therapies, including androgens, clomiphene, danazol and human growth


6

hormone have been linked to the development of hepatic adenomas and other be-nign liver tumors. Individuals affected with type I glycogen storage disease, galac-tosemia, Klinefelter’s syndrome, and Turner’s syndrome may also have an increasedincidence of hepatic adenomas.

PathologyGrossly 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 con-taining considerable glycogen. Unlike FNH, portal triads and bile ducts are absentand the existing blood vessels are thin-walled. In contrast to FNH, hepatic adenomasappear expansive and neoplastic. Bile ducts are distinctly absent from hepatic ad-enomas. Whether hepatic adenomas undergo malignant transformation remainsunresolved. Several authors have reported instances in which hepatocellular carci-noma was found adjacent to or within a hepatic adenoma. Further complicatingthis for the surgeon is the fact that histologic differentiation between a hepaticadenoma and a well-differentiated HCC can be very difficult. Differentiation is madeeven harder in patients with fibrolamellar HCC since this tumor, like hepaticadenoma, occurs most commonly in menstrual-aged females.

Clinical PresentationUp to one third of all cases of hepatic adenoma initially present with an acute

rupture and intraperitoneal bleeding. Additional complaints can include abdomi-nal pain, pressure, and nonspecific gastrointestinal symptoms. Unless clinical evi-dence of acute hemorrhage is evident, serological tests (including liver functiontests) are invariably normal. Tumor markers, such as CEA, α-fetoprotein and CA-19-9), are not elevated.

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


6

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Radiographic EvaluationFindings on radiographic evaluation are typically nonspecific. Ultrasound dem-

onstrates a tumor with mixed echogenicity and an overall heterogeneous appear-ance. CT scan can yield a wide spectrum of disparate findings, but typicallydemonstrates a hypodense lesion on noncontrast imaging with a variegated appear-ance following contrast administration. MRI findings are similar to those on CTand are nonspecific (Fig. 6.9). A Tc99 sulfur colloid scan may be useful in differen-tiating between a hepatic adenoma and an FNH, as hepatic adenomas usually lackbile ducts and appear as a “cold nodule.” Angiographically, hepatic adenomas arehypervascular lesions with areas of necrosis and hemorrhage.

TreatmentAll hepatic adenomas should be resected and considered to harbor dysplastic

changes or frank cancer until pathologic review of the entire tumor (and not a lim-ited biopsy) proves otherwise. Similarly, control of bleeding from ruptured hepaticadenomas in unstable patients is best done surgically. However, if surgical explorationis not feasible, angiographic embolization can be a life saving, temporary maneuveruntil transfer to a center with surgical capability is possible. Intraoperatively, hepaticartery ligation of the right, left, or main vessel can similarly be a life-saving proce-dure if hepatic resection is contraindicated. All women diagnosed with a hepaticadenoma should be advised to stop OCP use for life. Yearly follow-up with imagingis advised for all patients and is mandatory in those patients whose hepatic adenomais not causally linked to OCP use. There is little information available relating to thesafety of pregnancy in the setting of a hepatic adenoma. Although it appears thatpregnancy is safe after resection of a hepatic adenoma, women with a hepatic adenomathat has not been treated should be advised to avoid becoming pregnant.

Fig. 6.8. Hepatic adenoma. A, On gross appearance hepatic adenomas appear assoft, tan lesions. B, Microscopically, hepatic adenomas are composed of monoto-nous sheets of hepatocytes containing considerable glycogen. Portal triads andbile ducts are absent and the existing blood vessels are thin-walled. Venous lakesand zones of necrotic ghost are characteristic.


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

Additional Liver Tumors

Epithelial Tumor

Biliary HamartomasBile duct adenomas, or hamartomas, are common tumors. They are noteworthy

as they are often mistakenly interpreted as metastatic tumor by the operating sur-geon. (Note: Biopsy and confirmation of a malignancy for all hepatic lesions ismandatory. This is most important in situations in which the presence of a meta-static liver tumor will alter the proceedings of the operation.) Biliary hamartomasappear as small gray-white nodules that lie beneath the capsule of the liver and are


6

frequently multiple. Microscopically, they are composed of mature bile ducts sur-rounded by fibrous tissue.

Mesenchymal Tumors

Solitary Fibrous TumorOther 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 intraoperativeappearance (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 andare firm, white-to-gray, lesions that may be well or ill-defined. Histologically, mosthave a bland appearance with a classic short storiform (so-called patternless) patternand absence of cellular atypia, mitoses and/or necrosis; however, in malignant can-cer there may be marked cellular atypia and a high mitotic rate. Immuno-histochemically, all the SFTs show a strong positive reaction against antibodies forCD-34 and vimentin. The diagnosis of either a benign or malignant solitary fibroustumors is impossible without definitive histologic review, and surgical resection isindicated in all circumstances.

Lipoma, Myelolipoma, or AngiomyelipomaFatty tumors of the liver are extraordinarily rare. Although several reports of

primary lipomas have appeared, there are no reports of a primary hepatic liposar-coma. Most benign fatty hepatic tumors have been encountered at the time of autopsy,with rare reports of operative resection of these tumors. Multiple variants includingmyelolipoma, angiolipoma, and angiomyolipoma have been described. The term“pseudolipoma” has been given to an extracapsular fatty tumor with involutionalchanges. This lesion probably results when a free-floating piece of fat, e.g., an appendixepiploica, becomes trapped between diaphragm and liver surface. Definitive diag-nosis requires surgical resection to exclude malignancy.

Mesenchymal HamartomasMesenchymal hamartomas represent extremely rare congenital liver tumors that

occur most commonly in infants less than 1 year of age. Unlike biliary hamartomasthat are clinically insignificant, mesenchymal hamartomas can reach enormous sizeresulting in significant impairment of hepatic function. Microscopically, hamarto-mas display a myxoid background of highly cellular embryonal mesenchyme withrandom groupings of hepatic cells, bile ducts and cysts. The cystic component isgenerally the most prominent feature resulting in a “honeycomb” appearance.Although benign tumors, mesenchymal hamartomas can result in death due to masseffect and/or hepatic insufficiency. All mesenchymal hamartomas should be com-pletely excised if feasible. If complete surgical excision is not possible or prohibitivefor other reasons, surgical debulking may be sufficient since there have been noreports of recurrence after an incomplete surgical resection.


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MyxomaTo 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 inva-sive. Both children remained disease-free at time of report. Only a single adult caseof hepatic myxoma has appeared. This involved a 58-year-old male with a left lobemyxoma that ruptured. Definitive diagnosis was not made until four months laterat autopsy. Similar to other rare hepatic tumors, surgical resection is generally indi-cated to exclude malignancy.

TeratomaAt least seven benign teratomas have been reported. Most occur in children.

They may be cystic and usually are encapsulated and easily resected. Surgical resec-tion is indicated to exclude malignancy.

ConclusionsAn accurate histologic diagnosis and knowledge of their natural history is key to

the management of patients with benign liver tumors. While radiology has madegreat strides in identifying and characterizing the features of both benign and malig-nant liver tumors, the final burden of responsibility for diagnosis and therapy remainson the surgeon’s shoulders. Increasing experience, improved surgical techniques,and better perioperative care, currently permits hepatic resection to be performedwith a high level of safety. However, as we learn more about the prognosis andnatural history of most benign tumors, a conservative approach consisting of obser-vations and serial imaging seems appropriate for most asymptomatic patients inwhich a malignancy is not suspected.

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


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

Selected Readings1. Ishak KG, Rabin L. Benign tumors of the liver. Med Clin North Am 1975;

59:995-1013.2. Ishak KG. Mesenchymal tumors of the liver. In: Okuda K, Peters RL eds. Hepato-

cellular Carcinoma. Wiley, New York, 1976 pp. 247-307.3. 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.

4. Clatworthy HW, Boles ET, Newton WA. Primary tumors of the liver in infantsand children. Arch Dis Child 1960; 35:22–28.

5. Edmundson HA. Tumors of the liver and intrahepatic bile ducts. Atlas of tumorpathology. Section VII Fasicle 25. Armed Forces Institute of Pathology. 1958.

6. Vana J, Murphy GP, Aronoff BL, Baker HW. Survey of primary liver tumors andoral contraceptive use. J Tox Environ Health 1979; 5:255–273.

7. Klatskin G. Hepatic tumors: possible relationship to use of oral contraceptives.Gastroenterology 1977; 73:386–394.

8. Scott LD, Katz AR, Duke JH, Cowan DF, Maklad NF. Oral contraceptives, preg-nancy, and focal nodular hyperplasia of the liver. JAMA 1984; 251:1461–3.

9. Whelan Jr, Baugh JH, Chandon S. Focal nodular hyperplasia of the liver. Ann Sur-gery 1973; 177:150–8.

10. Foster JH, Berman M. Solid Liver Tumors. W B Saunders, Philadelphia. 1977.11. Leese T, Farges O, Bismuth H. Liver cell adenomas: a 12-year surgical experience

from a specialist hepatobiliary unit. Ann Surg 1988; 208(5):558–64.12. Craig J R, Peters R L, Edmondson H A. Tumors of the liver and intrahepatic bile

ducts. AFIP Atlas of Tumor Pathology. Fascicle 26. 1989.13. Goodman ZD. Benign tumors of the liver. In: Okuda K, Ishak K G (eds.) Neo-

plasms of the liver. Springer-Verlag, Tokyo 1987.14. 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 1CHAPTER 7

Hepatocellular Carcinoma

Bryan Clary

IntroductionAlthough uncommon in the United States, primary cancer of the liver (hepato-

cellular carcinoma) is the fourth leading cause of cancer death worldwide, accountingfor approximately 427,000 deaths in 1998. There is a striking geographical varia-tion in the incidence of this malignancy. Eighty percent of cases occur in developingcountries. The areas of highest incidence are Western and Central Africa, Easternand Southeast Asia, and Melanesia. The incidence in these locations ranges from 30to nearly 100 cases per 100,000 individuals per year. In contrast, the incidence inWestern countries including the United States, Great Britain, and South America, islow (2-3 per 100,000). This variation is mostly due to a higher incidence of chronicviral hepatitis and liver injury. As the proportion of noncirrhotics is greater in theWest and the underlying causes of liver injury differ, the treatment options are some-what different from those of Eastern patients as well. This Chapter will summarizethe basic characteristics of this disease and discuss the alternative treatments.

EtiologyUnderlying chronic liver disease is present in the majority of patients presenting

with hepatocellular carcinoma (HCC). In general, any chronic injury to the livercan result in HCC, although the most established and important association hasbeen with viral hepatitis. In the Far East, approximately 85% of patients with HCChave underlying cirrhosis, most commonly resulting from hepatitis B infection.Individuals who are seropositive for Hepatitis B surface antigen have at least a 100-foldincreased 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 whereHepatitis B infection is not endemic, there remains a strong association betweenHCC and Hepatitis B infection. For example in the United States, 25% of patientswith HCC test seropositive for Hepatitis B, a figure which is approximately 6 timesthat of the general population. When HCC develops in association with cirrhosis inWestern patients, it is more commonly a result of Hepatitis C. Approximately 70%of cirrhotic patients with HCC in Japan and Southern Europe are seropositive forHepatitis C, whereas in the United States, this figure is approximately 40-50%. It isthought that cirrhosis arising in the setting of Hepatitis C carries a greater risk ofdeveloping HCC. For patients with cirrhosis from Hepatitis B, the estimated risk is0.5% per year. In contrast, the risk of developing HCC over a 10-year period inpatients with Hepatitis C has been reported to be nearly 50%. In Western series,



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

Diagnosis and Pretreatment Planning

PresentationPatients with HCC commonly present with advanced lesions given the silent

nature of this disease. The most common symptoms among patients with advanceddisease include abdominal pain, weight loss, fatigue, early satiety, and abdominaldistention. It is possible, although infrequent, for HCC to spontaneously ruptureand bleed. A dramatic increase in pain and tenderness in a patient with a knownHCC should lead the physician to suspect this potentially catastrophic event. Tumorrupture is much frequent in the Far East series and has been reported to be the modeof presentation in up to 10-15% of patients. Jaundice, if present, may be secondaryto hepatocellular dysfunction, portal vein obstruction, or ductal obstruction in thepresence of locally advanced lesions. Small lesions are usually asymptomatic andfound either during an evaluation prompted by abnormal liver function tests, inci-dentally on abdominal imaging performed for other reasons. Although screeningpatients with hepatitis and cirrhosis for HCC has been shown to result in detectionat earlier stages, the survival benefit of such programs is not clear.

Laboratory EvaluationLaboratory evaluation is performed to both confirm the diagnosis and estimate

the degree of underlying liver impairment. The laboratory evaluation of a patientsuspected of having HCC should include liver function tests, complete blood counts,serum electrolytes and creatinine, coagulation parameters, serological tests for hepa-titis, and α-fetoprotein (AFP). Although a number of sophisticated tests have beendescribed to predict liver failure and mortality following hepatectomy, it is our prac-tice to utilize the Child-Pugh classification (Table 7.1). In our experience, the typeof laboratory and clinical studies influence the treatment strategy. Hypercalcemiaand erythrocytosis are potential paraneoplastic manifestations of HCC and a biopsyis not necessary. AFP levels are elevated in 75-90% of patients. A level higher than500 ng/dl in a patient with a liver mass is diagnostic of HCC. An AFP level greaterthan 2,000 ng/dl is often indicative of disseminated disease.

103Hepatocellular Carcinoma

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ImagingThe 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, and5. to aid in the planning of nonsurgical approaches in the patients who are

candidates for surgical resection. Ultrasound (US), which is readily avail-able and inexpensive, is commonly employed in the screening of high riskpatients.

On ultrasound, HCC is commonly isoechoic, with normal liver limiting theassessment of the extent and number of lesions. In cirrhotic patients, regenerativenodules are difficult to distinguish from HCC. Despite its limitations, US can bevery useful in delineating the presence and extent of portal venous and biliary ductalinvolvement and remains an important component in the preoperative evaluation.Computerized tomography (CT), which is widely available, is technology ratherthan operator dependent (as opposed to US) and remains the most widely utilizedimaging test in these patients. On CT, HCC is isodense with the surrounding liverparenchyma following contrast injection and, thus, it is important to review bothnoncontrast and contrast-enhanced images. Assessment of the portal and hepaticveins is dependent upon the timing of contrast injection, and as such, if performedincorrectly, is often inadequate to fully assess these structures. Doppler ultrasoundor magnetic resonance imaging (MRI) should be routinely done to complement CTevaluation of HCC. At our institution (Memorial Sloan-Kettering Cancer Center),MRI is felt to be the single best imaging test for treatment planning. MRI withgadolinium enhancement allows for the identification, quantification and charac-terization 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 Dopplerultrasound or MRI readily demonstrates these vascular structures. Preoperative an-giography with embolization has been recommended by some authors, although wedo not routinely recommend this, except in those patients awaiting total hepatec-tomy/transplantation since the wait for an available cadaveric donor may be months.

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

Points1 2 3

Serum Bilirubin (mg/dl) <2.0 2.0-3.0 >3.0Serum Albumin (g/dl) >3.5 2.8-3.5 <2.8Protime Elevation (sec) 1-3 4-6 >6Ascites None Slight ModerateEncephalopathy (grade) None 1-2 3-4

Grade A 5-6 pointsB 7-9 pointsC 10-15 points


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BiopsyThe role of percutaneous biopsy in the assessment of patients with suspected

HCC is controversial. Risks include bleeding, pneumothorax, injury to adjacentorgans, and tumor dissemination. Imaging studies in combination with the labora-tory evaluation and clinical scenario generally provide sufficient information to makean accurate preoperative diagnosis. A resectable lesion suspicious for HCC, in apatient 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 andan AFP level greater than 500 ng/dl. Percutaneous needle biopsy is useful if diagnos-tic doubt exists in a patient with an unresectable lesion or in patients with anindeterminant lesion outside the field of the intended resection that would renderthem unresectable.

TreatmentThe rationale for treatment of HCC is predicated upon an incomplete under-

standing of the natural history of this disease. As a malignancy, HCC has the capac-ity to metastasize. However, patients more often succumb to the local effects ofadvanced liver lesions (biliary tract infection, liver failure) than from the less directeffects of metastatic disease. The variability of outcomes in patients with what appearto be similar stages of disease makes it difficult to draw firm conclusions about manyof the proposed modes of therapy. Randomized trials comparing no treatment tosurgery, or ablative therapies, have not been conducted and will likely never beperformed. Likewise, randomized trials comparing surgery to ablative forms of therapyhave also not been performed. Patients with small HCC (< 3 cm) who are nottreated have been shown to have survival rates of up to 88% at one year and 55% attwo years. The natural history of patients with HCC is affected not only by the stageof the malignancy (Tables 7.2, 7.3) but also the degree of underlying liver dysfunc-tion. In patients not undergoing ablation or resection, the median survival for earlystage disease (Okuda stage I) appears to be 9-12 months. In advanced disease, this issignificantly shortened. In most series addressing patients who are deemedunresectable either because of advanced tumor characteristics or because of advancedliver dysfunction from underlying cirrhosis, a significant proportion die from liverfailure and/or the consequences of portal hypertension (hemorrhage). Surgicalresection remains the only potentially curative option in the treatment of HCC. Inaddition to being technically feasible, resectability is also determined by

1. the general medical condition of the patient,2. the absence of extrahepatic disease, and3. the ability to leave adequate residual liver parenchyma.

The latter may be achieved through orthotopic liver transplantation followingcomplete or total hepatectomy. An algorithm followed by the author’s institutionfor 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 processoccurs resulting in the growth of all cellular elements within the remnant. Within2-3 weeks, the remnant has assumed a size close to that of the original liver and


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

Table 7.2. TNM staging of hepatocellular carcinoma

T-StagingT1- No poor prognostic features (multiplicity, size >2 cm, vascular invasion)T2- One poor prognostic featureT3- Two or three of the poor prognostic featuresT4- Bilobar disease, tumor involving major portal or hepatic venous branches

N-StagingN0- No nodal involvementN1- Regional nodal involvement

M-StagingM0- No distant metastatic diseaseM1- Distant metastatic disease present

T-Stage N-Stage M-StageStage 1 T1 N0 M0Stage 2 T2 N0 M0Stage 3 T3 N0 M0

T1-3 N1 M0Stage 4A T4 N0-1 M0Stage 4B T-Any N-Any M1

Table 7.3. Okuda staging of hepatocellular cancer

Adverse Factor

Tumor Size >50% hepatic involvementAscites PresentSerum Albumin <3gm/dlSerum Bilirubin >3mg/dl

Stage I No adverse factorsStage II 1-2 adverse factorsStage III 3-4 adverse factors


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demonstrated in a large series recently published by the Memorial Sloan-Ketteringgroup, curative resection often involves major hepatectomy. In this contemporaryWestern series (1992-1998), 75% of resected patients had a primary tumor size ofgreater than 5 cm and required a formal lobectomy or greater 66% of the time.Prognostic factors of outcome following resection included margin status, the pre-operative AFP level, tumor size, and the presence of vascular invasion. Neither thepresence of cirrhosis nor the etiology of the underlying cirrhosis (present in 65%)were significant predictors of a poor outcome. Although the mortality followingresection 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 tumorexcision and replacement of dysfunctional liver parenchyma. The outcome follow-ing OLT for HCC is clearly dependent upon the extent of liver involvement at thetime of treatment. The best results are recorded in patients who had HCC discov-ered incidentally during transplantation performed for liver insufficiency. Patientswith tumors smaller than 5 cm have a median survival that exceeds 5 years, whereasin patients with a tumor size greater than 5 cm, it is approximately 2 years. Althoughcontroversy exists over the role of total hepatectomy with OLT in the treatment ofHCC, the lack of donor livers continues to limit the possible implications of thisdebate. According to UNOS (United Network for Organ Sharing) figures, 4,413cadaveric liver transplants were performed in 1998. Of these, only 87 (2.1%) weregiven to recipients with malignant neoplasms. UNOS survival data on transplantsperformed from 1989 through 1998 demonstrate a 5-year survival of 41% for patientswith a primary malignant neoplasm of the liver compared to an overall survival of74% for all patients undergoing cadaveric liver transplant. The median waiting timefor a cadaveric liver was 1.4 years in 1998. As total hepatectomy with OLT represents

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


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the only potentially curative option in patients with Childs B or C categories, andthe wait time for a patient with Childs A would be excessively long, many centershave begun to explore the use of living-related donors as a source of grafts. Theauthor is, in general, opposed to the use of living donors given the significant mor-bidity (30-40%) and mortality (2-5%) risks to the donor and the high rate of tumorrecurrence in the recipients. Tumor recurs in the majority of patients following OLTand is the main reason for the significantly reduced post-OLT survival compared topatients transplanted for benign diagnoses.

For these considerations, the author’s recommendation is that partial hepatec-tomy with curative intent should be performed whenever possible in patients with-out cirrhosis or with Childs A classification cirrhosis. Patients with advanced cirrhosis,and small T1 or T2 lesions, should be referred for total hepatectomy with cadavericOLT as should patients with well compensated cirrhosis and a small lesion that issituated such that a large amount of functional hepatic tissue would be sacrificed inthe resection. Consideration of a living-related liver donor should be limited to veryextraordinary situations.

ChemotherapyChemotherapy, whether given systemically or via intra-arterial means, appears

to have a minimal impact on the clinical course of patients with HCC. Agents thathave been utilized include doxorubicin, 5-fluorouracil (5-FU), and cisplatin. Althougha response rate of up to 20% has been reported, there are no long-term survivorsamong this group of patients. Intra-arterial chemotherapy delivered through animplantable pump has also been tried. Despite an apparent increase in the responserate, the morbidity and potential mortality associated with general anesthesia, andthe laparotomy required for implantation, limit this approach in patients withadvanced liver dysfunction.

Cryoablation and Radiofrequency AblationCryoablation has been demonstrated to be a safe palliative mode of therapy. In

order to safely perform this procedure, laparotomy is generally performed, althougha laparoscopic approach may be reasonable in certain instances. This is performedby inserting an insulated cryoprobe through the liver substance into the center ofthe mass. Multiple freeze-thaw cycles are performed using super-cooled liquid nitro-gen. Intraoperative monitoring with ultrasound delineates the growing iceballensuring a margin of normal parenchyma. Experience with cryoablation in the treat-ment of HCC has been limited mainly to the Far East, the largest series of whichwas reported by Zhou and colleagues from China. In this series, patients with lesionssmaller than 5 cm (unresectable secondary to concurrent cirrhosis), had a 5-yearsurvival of 49% versus a 5-year survival of 22% for the entire group. The authorutilizes cryoablation in patients who are unresectable at the time of laparotomywhere the morbidity of a general anesthetic and laparotomy has already been incurred.Larger tumors and those near major vascular structures are relative contraindicationsas the efficacy is diminished in these situations. More recently, interest has beenshifted to thermal ablation by radiofrequency (RFA). Although this may be usedintraoperatively at the time of laparotomy, it can also be administered via a percuta-neous 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 intraabdominalorgans require an open approach (or possibly laparoscopic). Curley and colleaguesat MD Anderson Cancer Center have presently presented a large series of RFA (donevia laparotomy) in the treatment of various hepatic neoplasms. This treatment appearssafe, yet the long term results are not known at this time. Thermal ablation withmicrowave and laser technology have also been described with similar safety profilesin comparison to RFA. Although the three methods of thermal ablation appeareffective in patients with small tumors, they are generally not appropriate for largertumors or those adjacent to the major vessels and bile ducts. We currently utilizethis form of therapy (percutaneous) in Childs B and C patients with small lesionssituated in anatomically accessible sites. We are beginning to explore the use of thismodality intraoperatively as an alternative to cryotherapy.

Arterial InterruptionHCC 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 whenlesions were found to be unresectable at the time of laparotomy. In patients withportal hypertension, nonselective ligation of the main hepatic arteries carries a sig-nificant risk of hepatic ischemia and liver failure. Mortality following these nonse-lective ligations was as high as 13% in some series. With current angiographictechniques, selective blockade of the hepatic artery branches supplying the tumorscan be performed through embolization. Selective embolization is safe and widelyreported in the literature. In many centers, embolization is conducted with the con-comitant intra-arterial infusion of chemotherapeutic agents (chemoembolization).Complications following embolization or chemoembolization can occur and thereported mortality is as high as 5-10%. Postembolization syndrome (fever, leukocy-tosis, pain) occurs in up to 90% of patients and is usually self-limiting. Liver ab-scess, gallbladder necrosis, gastroduodenal ulceration, and splenic infarction are muchless common. Acute hepatic failure following hepatic artery embolization is an omi-nous complication and appears to be predicted by the presence of large tumors(exceeding 50% parenchymal replacement) and hyperbilirubinemia. The procedure-related mortality ranges from 2.8% for Childs A cirrhotics, to 8% for Childs Bcirrhotics, and to an unacceptable 37% for patients with Childs C cirrhosis. En-cephalopathy, biliary obstruction and jaundice are contraindications to emboliza-tion. Tumors greater than 12 cm in size present a relative contraindication. Portalvenous occlusion in the absence of adequate portal venous collaterals also representsa contraindication. The results of embolization with or without intra-arterial che-motherapy have been described in numerous retrospective studies and a small num-ber of randomized trials. In comparison to historical controls, this form of therapyappears to offer benefit when compared to best supportive care. Long-term survivalis achieved in a minority of patients although no randomized trial has demonstrateda benefit when compared to observation. The addition of chemotherapy to embo-lization (chemoembolization) although theoretically attractive, does not appear tooffer any benefit, and the complication rate appears to be higher. Until further con-firmatory 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 resec-tion.

Preoperative embolization may be appropriate in patients with only mild liverdysfunction who are awaiting total hepatectomy for HCC given the relatively longwaiting times for cadaveric grafts. Embolization should not be utilized in patientsawaiting partial hepatectomy since it is unlikely to improve the resectability andmay be associated with complications.

Ethanol InjectionPercutaneous ethanol injection (PEI), under either ultrasonographic or CT guid-

ance, is utilized as an ablative form of therapy in many centers for patients withsmall tumors. As practiced, this form of therapy is limited to patients whose tumorsare smaller than 4 cm in size. PEI can be performed intraoperatively upon the find-ing of unresectability, yet its main advantages is that it can be done in a nonoperativesetting. Long-term follow-up by a number of groups has demonstrated long termsurvival in a significant minority of patients. Livraghi and colleagues from Italy havepublished one of the largest studies documenting the outcome of patients followingPEI. In their series (1995), the five year survival rates for solitary/< 3 cm, solitary/3-5 cm, solitary > 5 cm, and multiple tumors were 50%, 37%, 30%, and 26%, respec-tively. 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%. Al-though these outcomes appear quite good, they are in part a reflection of the naturalhistory of small HCC. Still, this represents a relatively safe mode of therapy in pa-tients with more moderate to advanced liver dysfunction. In patients with mild liverdysfunction who are unresectable, PEI has been combined with embolization as ameans of treating moderately sized (3-8 cm) and often multiple lesions (< 5). Arandomized trial by Bartolozzi and colleagues demonstrated a better than 3-yearsurvival in patients undergoing this combined treatment approach (52%) comparedto embolization alone (30%). It is the author’s practice to combine PEI with embo-lization in patients with small lesions (< 4-5 cm) even when multiple (less than 5).

RadiationExternal 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. Whole-liver radiation with doses of more than 4000 cGy are associated with a greater than50% risk of radiation hepatitis and liver failure. Recent advances in the technique ofconformal radiation, with three dimensional treatment planning, have increased theapplicability of external beam radiotherapy. The use of radiation sensitizing agentsincluding 5-FU, the fluoropyrimidines, and gemcitabine has also led to an increasedinterest in radiation therapy. In general, external beam radiation therapy is utilizedin patients with large, unilateral, symptomatic tumors that are unresectable.

Radioembolization of liver tumors with Yttrium-90 microspheres has recentlybeen described as a means of delivering a therapeutic radiopharmaceutical. Thesespheres have a mean tissue penetrance of 2.5 mm, with a maximum of 10 mm. Onlya few preliminary reports exist detailing the experience with this technique andsuggest that this modality is quite safe. Clinical trials examining efficacy are in progress.


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ConclusionThe treatment of hepatocellular carcinoma should be directed at complete tumor

extirpation whenever possible. The treatment approach is individualized accordingto resectability and the presence of underlying liver dysfunction. In patients withoutcirrhosis, or only mild liver dysfunction, partial hepatectomy is the best therapeuticoption. For patients with severe liver dysfunction, total hepatectomy with orthoto-pic liver transplantation should be considered for T1 and T2 lesions. If, during thecourse of an operative exploration a tumor is found to be unresectable, we recom-mend ablation (cryoablation or RFA) as a palliative measure when possible. Patientswith Childs A or Childs B liver dysfunction who are clearly unresectable on thebasis of preoperative imaging can be approached with transcutaneous embolizationwith or without concomitant PEI depending on the size, number, and expertise atone’s respective institution. Ablation should be considered in patients on the wait-ing list for orthotopic liver transplantation (percutaneous RFA, embolization, PEI)as a temporary treatment. Patients with Childs C cirrhosis may be candidates forPEI and potentially percutaneous RFA although these should be performed only inpatients who are still reasonably functional. Patients with symptomatic large lesionsnot amenable to ablation may be candidates for external beam radiotherapy as apalliative treatment.

The algorithm presented by the author is based upon the available data withinthe existing literature. Much of this data is flawed and primarily retrospective. Varia-tions to this algorithm in protocol settings, and preferably in the context of random-ized trials are encouraged, as there remains much to be learned about the propertreatment of this malignancy.

Selected Reading1. 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.

2. Fong Y, Sun RL, Jarnagin W et al. An analysis of 412 cases of hepatocelullar carci-noma at a Western center. Ann Surg 1999; 229:790-800.

3. Livraghi t, Giorgio A, Marin G et al. Hepatocellular carcinoma and cirrhosis in746 patients: long-term results of percutaneous ethanol injection. Radiology 1995;197:101-8.

4. Brown KT, Nevins AB, Getrajdman GI et al. Particle embolization for hepatocel-lular carcinoma. J Vasc Interven Rad 1998; 9:822-828.

5. Clavien PA, ed. Malignant liver tumors. Malden: Blackwell Science, 1999.

CHAPTER 1CHAPTER 8

Periampullary Cancerand Distal Pancreatic Cancer

Richard D. Schulick

IntroductionThe first successful treatment of a periampullary carcinoma occurred over a cen-

tury ago. In 1899, William S. Halsted of The Johns Hopkins Hospital described atransduodenal local ampullary resection with reanastomosis of the pancreatic andbile ducts to the duodenum in a patient presenting with obstructive jaundice. Thepatient subsequently developed obstructive jaundice three months after the initialoperation and required a second operation in which a cholecystoduodenostomy wasperformed to decompress the biliary tree. The patient died six months later and anautopsy revealed recurrent ampullary carcinoma invading into the head of the pan-creas and duodenum.

The first en bloc resection of the head of the pancreas and duodenum forperiampullary carcinoma is credited to Codivilla, who performed the procedure atthe beginning of the 20th century; unfortunately the patient did not survive thepostoperative period. In 1912, Kausch, a German surgeon, performed the first suc-cessful partial pancreaticoduodenectomy in two stages.

In 1935, Allen Oldfather Whipple (Fig. 8.1) reported his experience in treatingthree patients with ampullary cancer using a two-stage formal pancreaticoduodenectomyat the annual American Surgical Association meeting. He subsequently reported ona total of 37 pancreaticoduodenectomies during his career, with the operation evolvingfrom a two-stage to a one-stage procedure by the early 1940s. His one-stage opera-tion involved reconstruction with an end-to-end choledochojejunostomy, an end-to-side pancreaticojejunostomy and an end-to side gastrojejunostomy. Theseanastomoses were performed to the proximal jejunum, which was constructed in aretrocolic fashion.

In 1937, Brunschwig, from the University of Chicago and later from MemorialSloan-Kettering Cancer Center, extended the indication for pancreaticoduodenectomyto 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% insome series, leading some authorities to abandon the procedure. In the last severaldecades, improved hospital morbidity, mortality, and survival afterpancreaticoduodenectomy have been reported. Many centers now report operativemortalities of less than 4%.



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Distal pancreatectomy for a lesion in the body or tail of the pancreas was out-lined by Mayo in 1913. The last section of this Chapter deals with the technicaldetails of this operation.

Pancreaticoduodenectomy for Periampullary CancerExposure for the Whipple procedure can be performed through a vertical mid-

line incision from the xiphoid process to several centimeters below the umbilicus.Alternatively, a bilateral subcostal incision can be used. Exposure is greatly enhancedwith the use of a mechanical retracting device.

Fig. 8.1. Allen O. Whipple.

113Periampullary Cancer and Distal Pancreatic Cancer

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The first portion of the Whipple procedure is devoted to assessing the extent ofdisease and resectability. There is debate as to the benefits of a staging laparoscopyversus open staging in anticipation of surgical resection or palliation. Proponents oflaparoscopy employ minimally invasive techniques to evaluate for the presence ofmetastatic disease in the peritoneal cavity or liver, and some advocate the use oflaparoscopic ultrasonography to assess for local disease involvement. If metastatic orlocally unresectable disease is discovered, the procedure is terminated, and patientswith obstructive jaundice are referred for placement of a percutaneous transhepaticexpandable metallic bile duct stent. Laparotomy is performed only if they developgastric outlet obstruction. Opponents of laparoscopy prefer to perform palliativebiliary and gastric bypasses, as well as chemical splanchnicectomy, in patients whoare found to be unresectable. The incidence of gastric outlet obstruction due to amass in the head of the pancreas approaches 20% in some series.

At open exploration, the entire liver is assessed for the presence of metastases notseen by preoperative imaging studies. The celiac axis is inspected for lymph nodeinvolvement. Tumor-bearing nodes within the resection zone do not contraindicateresection because long-term survival is sometimes achieved with peripancreatic nodalinvolvement. The parietal and visceral peritoneal surfaces, the omentum, the liga-ment of Treitz, and the entire small and intra-abdominal large intestine are carefullyexamined for the presence of metastatic disease. An extensive Kocher maneuver isperformed by elevating the duodenum and head of the pancreas out of theretroperitoneum and into the midline, allowing visualization of the superior mesen-teric artery at its origin with the aorta. The porta hepatis is assessed by mobilizingthe gallbladder out of the gallbladder fossa, and dissecting the cystic duct down tothe junction of the common hepatic and common bile duct. The common hepaticartery and proper hepatic artery should also be assessed to determine that they arefree of tumor involvement.

If the intraoperative assessment reveals localized disease without tumor encroach-ment upon resection margins, the resection is performed in relatively standard fash-ion. If assessment reveals evidence of local tumor extension implying potentialunresectability, the normal sequence for performing the pancreaticoduodenectomyshould be modified. The easiest and safest portions of the resection should be per-formed first. Many tumors that initially appear unresectable can be successfullyresected by patiently beginning the operation where it is easiest and finishing harderportions later.

The distal common hepatic duct is divided close to the level of the cystic duct entrysite early during the operation. This allows caudal retraction of the common bile ductand nicely opens the dissection plane on the anterior surface of the portal vein. Duringthese maneuvers, the portal structures should be assessed for a replaced right hepaticartery originating from the superior mesenteric artery. If found, this vessel should bedissected and protected from damage. The gastroduodenal artery is next identified andclamped atraumatically. This maneuver confirms its identity as well as confirming thatthe hepatic artery is not being supplied solely by retrograde flow through superiormesenteric artery collaterals (in the setting of celiac axis occlusion).

For a classic Whipple procedure, a 30-40% distal gastrectomy is performed bydividing the right gastric and right gastroepiploic arteries. The antrectomy is thencompleted 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 thepylorus with a linear stapling device. The right gastric artery can often be spared butmay be taken if it allows better mobilization of the duodenum. The gastrointestinaltract is divided distally at a point of mobile jejunum, typically 10-20 cm distal to theligament of Treitz. The mesenteric vessels to this initial portion of the jejunum arecarefully divided over clamps and tied to avoid bleeding. Once the proximal jejunumis separated from its mesentery, it can be delivered dorsal to the superior mesentericvessels from the left to the right side.

Performing a more extensive Kocher maneuver can identify the superior mesen-teric vein caudal to the neck of the pancreas. The superior mesenteric vein is identi-fied running anterior to the third portion of the duodenum and is frequentlysurrounded by adipose tissue as it receives tributaries from the uncinate process andneck of the pancreas, the greater curve of the stomach, and from the transversemesocolon. In this location, the superior mesenteric vein is identified by dissectingthe fatty tissue of the transverse mesocolon away from the uncinate process of thepancreas. Division of the branches emptying into the anterior surface of the supe-rior mesenteric vein allows continued cephalad dissection. The plane anterior to thesuperior mesenteric vein is developed under direct vision, avoiding branches andtumor involvement. Care is taken to protect the splenic vein as it joins the superiormesenteric vein posterior to the neck of the pancreas. After the plane anterior to theportal vein and superior mesenteric vein is complete, a Penrose drain is looped underthe neck of the pancreas.

Stay sutures are placed superiorly and inferiorly on the pancreatic remnant toreduce bleeding from the longitudinal segmental pancreatic arteries. The pancreaticneck is then divided using the electrocautery after confirming a free plane anteriorto the portal and superior mesenteric veins. The Penrose drain, previously placedbehind the neck of the pancreas, is used to elevate the pancreatic tissue to be dividedand protect the underlying major veins. The site of the main pancreatic duct shouldbe noted so it can be incorporated into the subsequent reconstruction.

The specimen now remains connected by the head and uncinate process of thepancreas. These structures are separated from the portal vein, superior mesentericvein and superior mesenteric artery. This is performed by serially clamping, dividingand tying the smaller branches off the portal and superior mesenteric vessels. Dis-section should be performed flush to these structures to remove all pancreatic andnodal tissue in these areas. Great care is taken not only to avoid injury to the supe-rior mesenteric artery and vein at this level, but also to ensure complete removal ofall pancreatic tissue and lymph nodes near these vascular structures. With theseareas dissected, the specimen is removed and the pancreatic neck margin, uncinatemargin and common hepatic duct margins are marked for the pathologists. To speedup analysis of these frozen section margins, the common hepatic duct margin andthe pancreatic neck margin may be sampled earlier and sent to pathology while themain specimen is still being removed.

There are multiple options for reconstruction after pancreaticoduodenectomy.Most commonly, the reconstruction first involves the pancreas, followed by the bileduct, and then the duodenum. The issues and controversies surrounding the pan-creatic and biliary reconstruction are outlined by multiple papers specificallyaddressing 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 groupsfavor a separate Roux-en-Y reconstruction for the pancreas or even a double Roux-en-Y reconstruction for the pancreas and the bile duct. Controversy continuesregarding the best type of pancreaticojejunostomy, the importance of duct-to-mucosasutures, and the use of pancreatic duct stents. At the Johns Hopkins Hospital, thepancreatic reconstruction is typically performed with an end-to-end or end-to-sidepancreaticojejunostomy to the proximal jejunum brought through a defect in themesocolon to the right of the middle colic artery. The pancreatic remnant should becircumferentially cleared and mobilized for 2-3 cm to allow for an optimal anasto-mosis. The pancreaticojejunostomy is typically performed in two layers (Fig. 8.2).The outer layer consists of interrupted silk sutures that incorporate the capsule ofthe pancreas and the seromuscular layers of the jejunum. The inner layer consists ofa running absorbable suture (or interrupted absorbable sutures) that incorporatesthe capsule and a portion of the cut edge of the pancreas and the full thickness of thejejunum. If possible, the inner layer incorporates the pancreatic duct to splay itopen. When completed, this anastomosis nicely invaginates the cut surface of thepancreatic neck into the jejunal lumen.

The biliary anastomosis is typically performed with an end-to-sidehepaticojejunostomy approximately 10-15 cm down the jejunal limb from thepancreaticojejunostomy (Fig. 8.3). This anastomosis is typically performed with asingle layer of interrupted absorbable sutures. In general, T-tubes are not used forthis anastomosis. If the patient has a percutaneous biliary stent then this is left inplace, traversing the anastomosis.

The third anastomosis performed is the duodenojejunostomy in cases of pyloruspreservation or the gastrojejunostomy in patients who have undergone classicpancreaticoduodenectomy with distal gastrectomy. This anastomosis is typically per-formed 10-15 cm downstream from the hepaticojejunostomy, proximal to the jejunumtraversing the defect in the mesocolon (Fig. 8.4). Alternatively, if a Roux-en-Y limb isutilized, a fourth anastomosis between the jejunum and the jejunum is necessary.

After the reconstruction is completed, closed suction drains are left in place todrain the biliary and pancreatic anastomoses. Some groups prefer not to place closedsuction drains, accepting that if a fluid collection becomes clinically evident postop-eratively, percutaneous drainage by interventional radiology may be required.

Distal Pancreatectomy for Distal Pancreatic CancerStaging with laparoscopy is often of benefit in patients with distal pancreatic

cancers. If metastatic disease is found, distal pancreatectomy and splenectomy areunlikely to help in the palliation of the patient. Exposure for a distal pancreatec-tomy and splenectomy can be obtained through a vertical midline incision from thexiphoid process to several cm below the umbilicus. Alternatively, a bilateral subcos-tal incision can be used. Exposure is greatly enhanced with the use of a mechanicalretracting device. Folded sheets placed behind the patient underlying the spleen canalso enhance exposure, especially in patients with a deep body habitus.

The lesser sac should be entered by elevating the greater omentum off the trans-verse colon. The splenic flexure of the colon should also be mobilized caudally andaway from the spleen by dividing the lienocolic ligament. The spleen can technicallybe preserved for benign disease; however, for cancer, most groups prefer to remove


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

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


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“U” stitches of absorbable suture should then be placed. The electrocautery device isthen 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 ofthe lesion. The pancreatic remnant is then overseen to complete the resection. Thepancreatic remnant is then oversewn to complete the resection.

Fig. 8.3. Choledochojejunostomy.


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


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Suggested Reading1. Halsted WS. Contributions to the surgery of the bile passages, especially of the

common bile duct. Boston Med Surg J 1899; 141:645-654.2. Sauve L. Des pancreatectomies et specialement de la pancreatectomie cephalique.

Rev Chir (Chir) 1908; 37:335-385.3. Kausch W. Das carcinom der papilla duodeni und seine radikale Entfeinung. Beitr

Z Clin Chir 1912; 78:439-486.4. Whipple AO, Parson WB, Mullins CR. Treatment of carcinoma of the ampulla of

Vater. Ann Surg 1935; 102:763-779.5. Whipple AO. A reminiscence: Pancreaticoduodenectomy. Rev Surg 1963;

20:221-225.6. Whipple AO. Observations on radical surgery for lesions of the pancreas. Surg

Gynecol Obstet 1946; 82:623-631.7. Crist DW, Sitzmann JV, Cameron JL. Improved hospital morbidity, mortality and

survival after the Whipple procedure. Ann Surg 1987; 206:358-365.8. Fernandez-del Castillo C, Rattner DW, Warshaw AL. Standards for pancreatic

resection in the 1990’s. Arch Surg 1995; 130:295-300.9. 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.

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


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

10. Trede M, Schwall G, Saeger H-D. Survival after pancreaticoduodenectomy: 118consecutive resections without an operative morality. Ann Surg 1990; 221:447-458.

11. Yeo CJ, Cameron JL, Sohn TA et al. Six hundred fifty consecutive pan-creaticoduodenectomies in the 1990s: Pathology, complications, outcomes, AnnSurg 1997; 226:248-260.

12. Yeo CJ, Cameron JL, Maher MM et al. A prospective randomized trial ofpancreaticogastrostomy versus pancreaticojejunostomy after pancreatico-duodenectomy. Ann Surg 1995; 222:580-592.

13. Cameron J. Atlas of Surgery, volume I. Philadelphia: B.C. Decker Inc., 1990.

CHAPTER 1CHAPTER 9

Hepatic Resection for Colorectal LiverMetastases: Surgical Indicationsand Outcomes

Ronald P. DeMatteo, Yuman Fong

IntroductionThe liver is a common site of metastasis for colorectal adenocarcinoma. Radical

surgical extirpation is the most effective therapy for colorectal hepatic metastasesand offers the only chance of cure. Recent improvements in radiologic imaging,understanding of hepatic anatomy, surgical techniques, and perioperative care havemade liver resection safe. Consequently, the indications for hepatectomy have broad-ened. Up to 85% of the liver may be resected because hepatic regeneration quicklyensues and the liver regains its functional capacity. However, it is becoming increas-ingly obvious that multimodality therapy must be utilized to improve upon thecurrent surgical results. Effective chemotherapy, either systemic or hepatic arterial,and biologic or molecular therapy are needed to treat occult microscopic diseasethat remains following complete gross tumor removal. This review encompasses theepidemiology, preoperative evaluation, surgical indications, and surgical results forpatients with hepatic colorectal metastases.

EpidemiologyThere are approximately 150,000 cases of primary colorectal cancer in the United

States each year. Hepatic metastases from colorectal cancer are common. About25% of patients with colorectal carcinoma have liver metastases at the time of initialpresentation and an additional 25% will develop liver metastases, usually within thefirst three years. Unlike liver metastases from other gastrointestinal neoplasms, thosefrom colorectal cancer may occur as a single metastasis or as a few tumors located ina limited distribution. In the absence of systemic disease, these patients are ame-nable to resection. Unfortunately, despite those favorable peculiarities, only about5-10% of patients with liver metastases are resectable for cure.

Preoperative Evaluation

HistoryThe 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, andpostoperative complications. It is customary to review the original pathology slides.The type and duration of chemotherapy should be ascertained if it was administered.



9

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

Physical ExaminationThe examination of a patient with colorectal liver metastasis focuses primarily

on the general health of the patient. The cardiovascular status is of particular impor-tance. Typically, only large or inferior masses are palpable on abdominal examina-tion. Previous incisions should be noted, especially if laparoscopy or the placementof a hepatic artery pump is intended. Rectal examination with stool guaiac shouldalways be performed.

Laboratory TestsStandard liver function tests are often normal despite the presence of multiple

hepatic metastases. The serum carcinoembryonic antigen (CEA) level is a valuablemarker in those with recurrent colorectal cancer. However, there has been consider-able debate as to whether vigilant surveillance of patients with resected primarycolorectal cancer impacts upon their survival. In fact, most studies have not showna survival advantage. However, relatively few patients have been studied and thebenefit in individual cases cannot be excluded. Therefore, the patient’s past CEAlevels, if any, should be determined and a new level drawn. Once patients develophepatic metastases, the CEA level is a useful marker of therapeutic response and is aharbinger of further recurrence. It must be remembered that about 25% of tumorsdo not secrete CEA.

ImagingRadiologic imaging is a critical component of the preoperative investigation of a

patient with colorectal liver metastasis. In fact, it is often used to determine whetherthe patient should be considered further for resection. There are now numeroustests in the armamentarium of the radiologist for the characterization of hepaticmetastases (see Chapter 2). Helical computed tomography (CT) is currently the testof choice. It is widely available and can rapidly acquire information regarding thenumber, size, and location of intrahepatic tumors. The relationship to vascular andbiliary structures is depicted. Newer CT techniques utilize reconstructions to pro-vide detailed information regarding hepatic artery and portal vein anatomy. CT alsosurveys the presence of extrahepatic disease.

A variety of other radiologic tests have also proven useful in the assessment ofpatients with colorectal metastasis to the liver. In the hands of a skilledultrasonographer, duplex ultrasound can detect small lesions, distinguish cysts fromsolid lesions, and demonstrate the involvement or proximity to vascular and biliarystructures. Intraoperative ultrasound is routinely used to search for occult intrahe-patic disease although it usually just confirms the findings gleaned from preopera-tive imaging. Magnetic resonance (MR) is useful to detect small metastases or to

123Hepatic Resection for Colorectal Liver Metastases

9

differentiate benign tumors (especially hemangiomas) from malignant lesions. His-torically, CT portography has been the gold standard for detecting colorectalmetastases. However, it is invasive and expensive and probably does not offer muchadvantage over other imaging techniques. Arteriography is still used to define hepaticarterial anatomy in preparation for hepatic artery pump placement but is likely tobe 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 patientswith recurrent colorectal cancer. It probably has limited value for detecting occultintrahepatic metastases but may prove useful in identifying extrahepatic diseaseincluding nodal metastasis and pelvic recurrence. Exploratory laparoscopy is usefulto detect occult intrahepatic lesions, extrahepatic disease such as peritoneal dissemi-nation, and unsuspected liver cirrhosis. It identifies unresectable disease in aboutthree-quarters of patients who cannot undergo liver resection. However, with theincreased use of intrahepatic pump chemotherapy and ablative techniques forunresectable disease, it spares laparotomy in only about 10% of patients.

Preoperative biopsy of liver tumors in patients with a history of colorectal canceris 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 isgenerally reserved for those patients with unresectable disease in order to confirmthe diagnosis.

Surgical IndicationsA few factors govern whether a patient with hepatic colorectal metastasis is oper-

able. First, the patient must be in acceptable health to tolerate the physiologic con-sequences of hepatectomy and liver regeneration. In particular, the cardiovascularstatus of the patient should be investigated preoperatively, particularly in elderlypatients. However, age alone is not a contraindication for resection as it has beenshown that hepatectomy may be accomplished with similar morbidity, perioperativemortality, and survival in patients greater than 70 years old.

Next, the primary colorectal cancer must be resected (or resectable) and the pres-ence of other extrahepatic disease must be excluded. Extrahepatic disease signifiesunfavorable tumor biology and is associated with a poor outcome. The one excep-tion is that selected patients with lung metastases from colorectal cancer may benefitfrom both lung and liver resection. Preoperative workup should include a recentcolonoscopy, chest x-ray and chest CT. Bone scan and head CT are reserved forpatients with symptoms that suggest involvement of these sites. PET is an investiga-tional test although many patients that are now referred to tertiary centers havealready undergone PET scanning.

Lastly, the intrahepatic disease and its relation to the major biliary and vascularstructures must allow for complete tumor clearance and preservation of an adequateliver remnant. What exactly constitutes an adequate margin of resection has beendebated and there are conflicting data. Certainly, negative microscopic margins shouldbe emphasized. Whether a minimum margin of normal tissue is necessary is notclear and it may not be attainable in many large and ill-placed tumors. Considerableeffort is now being focused on increasing resectability in patients with multiple,diffuse tumors or an inadequate amount of uninvolved liver. Preoperative portal


9

vein embolization has been used recently to induce hypertrophy of the uninvolvedparenchyma in order to reduce the likelihood of postoperative liver failure in patientswho require sacrifice of a large proportion of functional liver. For instance, in patientswho require an extended right hepatectomy for a small tumor that is situated betweenthe middle and right hepatic veins, a percutaneous embolization of the right portalvein (and possibly also the Segment IV branches) will induce hypertrophy of the leftlateral segment within a few weeks time. This may make the resection safer. Alterna-tively, staged hepatectomies are also being performed in patients with multifocaldisease to provide tumor clearance in patients who do not have an adequate amountof normal liver to undergo a single procedure. As more effective systemic chemo-therapeutic agents become available for colorectal metastases, preoperative chemo-therapy may render additional patients resectable.

The optimal timing of hepatic resection in patients with colorectal liver me-tastases is not well defined. For example, the ideal timing for hepatectomy in pa-tients with synchronous colorectal metastasis is unclear. Patients with small tumorsmay benefit from a period of observation after the primary tumor is controlled toallow for the development of additional liver metastases or to reveal unfavorablebiology that would render liver resection less effective. Patients with larger tumorsmay be treated with simultaneous resection. However, patients requiring an extendedresection (especially an extended left hepatectomy) that entails removal of a largeproportion of functional liver parenchyma are generally treated with staged colorectaland liver resections. Furthermore, when a low anterior resection or an abdomino-perineal resection is required, hepatectomy is usually performed as a separate proce-dure unless it is a minor resection. Patients discovered to have a small volume of liverdisease at the time of laparotomy for the primary colorectal tumors are probablybest served by avoiding wedge resections. Biopsy of the lesion is also usually unnec-essary when the diagnosis is obvious. Patients should be staged postoperatively andthen undergo anatomic based-resection at a later date. Anatomic resection providesbetter tumor clearance since the rate of positive margins is 2% versus up to 30% forwedge resection. It also minimizes blood loss, reduces operative time, and preservesnormal tissue. In patients with metachronous liver colorectal metastases, similardebate exists regarding the timing of operative intervention. Generally, patients withsmall tumors, multifocal small tumors, and short disease-free intervals are observedfor a few months to better select those who will benefit from hepatectomy.

Surgical Results

ComplicationsSuccessful outcome in hepatic surgery depends largely upon minimizing intra-

operative blood loss. In a series of 496 consecutive liver resections (including 46%extended resections and excluding wedge excisions) performed at Memorial Sloan-Kettering Cancer Center (MSKCC) from December 1991 to April 1997, the medianblood loss was 645 ml. Only 25% of patients required allogeneic transfusion ofpacked red blood cells within the first day. Excessive blood loss is not only associatedwith increased perioperative morbidity but also with a shorter time to recurrenceand decreased survival after resection of colorectal liver metastases.


9

Specialized teams can perform liver surgery safely. The metabolic and physi-ologic derangements that result from partial hepatectomy are reflected by a morbid-ity rate of up to 40%. Extended resections can be accomplished with similar overallmorbidity and mortality to that of lesser resections. Hemorrhage and liver failureare the most serious complications after partial hepatectomy. Hemorrhage may occurduring the operation due to technical reasons or in the early postoperative course asa result of coagulopathy or bleeding from the raw surface of the liver. Late postop-erative bleeding may originate from the gastrointestinal tract in the setting of hepaticdysfunction. Hepatic failure is often a sequela of bleeding or infection and may belife-threatening. It occurs in just a few percent of patients. Cardiovascular events,including myocardial infarction and pulmonary embolism, may be minimizedthrough careful preoperative evaluation, intraoperative deep venous thrombosis pro-phylaxis, and early postoperative ambulation. The reported incidence of renal fail-ure after hepatectomy is about 1% and that of pneumonia is about 2%. Ascites isalso a concern, especially in patients who undergo resection of a large proportion oftheir functioning parenchyma. Significant intra-abdominal fluid collections developpostoperatively in about 15% of patients and manifest as a fever or leukocytosis.Most collections contain serosanguinous fluid (or some bile) and usually can be de-tected and treated prior to the development of a frank abscess. Intraabdominal collec-tions can almost always be managed with percutaneous drainage. True biliary fistulasare uncommon, especially with the advent of pedicle ligation techniques, which obvi-ate extrahepatic portal dissection and thus minimize the chance of biliary injury.

Most large centers have now reported an operative mortality below 5% for resec-tion of colorectal liver metastases. This is in sharp contrast to the operative mortalityrates of up to 20% for hepatectomy just a few decades ago. The overall operativemortality for the last 1,001 patients who underwent resection of colorectal metastasesat MSKCC was 2.8%. The decline in perioperative mortality is due to several fac-tors. First, the surgical anatomy of the liver is now more precisely defined. Next, vastimprovements have been made in surgical techniques such as extrahepatic control ofthe hepatic veins and segmental resections. Anesthetic techniques have also contrib-uted greatly to reduce intraoperative blood loss through the use of low central venouspressure during hepatectomy. Consequently, the retrohepatic inferior venal cavaldissection and parenchymal transection are accompanied by less blood loss. Impor-tantly, low central venous pressure is not significantly associated with the develop-ment of renal failure.

SurvivalThe results of surgical resection must be interpreted in the context of the natural

history of untreated colorectal metastases to the liver. Scheele reported a mediansurvival of 30 months in resected patients compared to 14.2 months in resectablepatients who did undergo hepatectomy and 6.9 months in unresectable patients. Ofthe 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 ofsurgical resection. In contrast, surgical resection of hepatic colorectal metastases hasbeen 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 widelyreproduced and are consistent. Some cures are achieved as 10-year survival is about


9

20% and 20-year survival is 15%. In an analysis of 96 actual 5-year survivors atMSKCC, the actuarial 10-year survival rate was 78%. No other treatment modalityhas been shown to provide comparable results.

Nevertheless, despite convincing retrospective evidence, the value of hepatec-tomy in prolonging survival and curing some patients has not been universallyaccepted. Certainly, the patients who undergo resection have been selected becauseof their favorable tumor biology, but resection appears to be of benefit even underthose circumstances. A prospective randomized trial has not been performed andwill likely never be done given the overwhelming evidence that has accumulated infavor of hepatectomy.

Prognostic VariablesSeveral prognostic factors have been reported to predict survival after hepatic

resection of colorectal metastases. A multivariate analysis of the MSKCC data iden-tified seven variables as negative predictors of outcome. Five of these are preopera-tive characteristics and have been included in a proposed clinical scoring system.The variables are: positive nodal status of the primary colorectal tumor, disease-freeinterval from the primary to the first liver metastasis of less than 1 year, preoperativeCEA greater than 200 ng/ml, more than one liver tumor, and size of the largesttumor greater than 5 cm. Patients with 0, 3, or 5 of these factors had 5-year survivalrates of 60, 20, and 14%, respectively.

The other two variables are the presence of extrahepatic disease or a positivemicroscopic margin. The rate of positive hepatoduodenal lymph nodes has beenreported to be as high as 28% and is associated with poor survival. Although radicalportal lymphadenectomy is not routinely performed during liver resection forcolorectal metastasis, its addition must be considered. As noted previously, theexception to extrahepatic disease is the presence of resectable lung metastases. Agroup of 81 selected patients at our institution who had both liver and lung resection

Table 9.1. Results of resection for colorectal liver metastases

Operative SurvivalAuthor N Mortality 1 yr 3 yr 5 yr

(%)

Foster JH1978* 168 5 – – 20Hughes KS1986* 607 – – – 33Rosen CB1992 280 4 84 47 25Gayowski TJ1994 204 0 91 43 32Scheele J1995 434 4 85 45 33Fong Y1999 1,001 3 89 57 37

*multi-institutional series


9

(most had a single lung metastasis) for colorectal metastases actually had similarsurvival as those who just had liver metastases alone.

The utility of these prognostic factors in the clinical management of an indi-vidual patient is somewhat limited, however, although they may be used to avoidsurgery in a patient with compromised general medical health. Otherwise, only thepresence of extrahepatic disease and the inability to achieve complete tumor clear-ance are absolute contraindications to resection. Patients who undergo palliativeresection or who have positive resection margins have been shown to have similarsurvival as unresectable patients. Several authors have also stressed the need to obtaina 1 cm margin noting a 45% 5-year survival with a 1 cm margin versus a 23% 5-yearsurvival with less than 1 cm. However, we have found that the presence of a negativemargin is most important and have found no difference between margins of lessthan or greater than 1 cm.

Recurrent Hepatic MetastasesPartial hepatectomy for colorectal liver metastases only occasionally results in

cure since 80-90% of patients recur and most eventually die from their cancer. Inabout a third of the patients who recur, the disease is isolated to the liver. Scheelereported that on multivariate analysis, recurrence was predicted by satellite metastases,size greater than 5 cm, nonanatomic liver resections, positive nodes in the primarytumor, and synchronous colorectal and liver disease. In a recent MSKCC study, areduction in intrahepatic recurrence following partial hepatectomy for colorectalmetastasis from 40% to 10% at 2 years has been demonstrated with the addition ofadjuvant hepatic arterial FUDR chemotherapy to systemic 5-FU. A survival advan-tage at 2 years was also detected with 86% survival in the patients who receivedpump and systemic therapy versus 72% for patients given intravenous chemotherapyalone.

Subsets of the patients with isolated recurrence in the liver are candidates forrepeat hepatectomy that offers the only meaningful chance of prolonged survival.The experience with repeat partial hepatectomy is scant because such resectionscomprise less than 5% of all hepatectomies for colorectal metastasis (Table 9.2).However, with the increasing safety of hepatic surgery, more reoperations for intra-hepatic recurrence are now being performed. Although repeat hepatectomy is tech-nically more challenging due to the presence of adhesions, the change in morphologyof the liver, and the altered position of the vasculature, the perioperative morbidityand mortality are comparable to that of initial resections. Repeat hepatectomy resultsin a 5-year survival as high as 42% in selected patients. Subsequent recurrence iscommon and in our own experience, 20 of 25 patients recurred with a mediandisease free interval of 9 months although median survival was 30 months. How-ever, in the absence of any other effective therapy, patients with isolated liver recur-rence should be considered for repeat hepatectomy.

ConclusionPartial hepatectomy for hepatic colorectal metastases has become a safe and

effective therapy over the last two decades. Approximately one-third of patients willachieve long-term survival, although only a small fraction will actually be cured.Consequently, all patients should be evaluated for resection in the absence of


9nonpulmonary extrahepatic disease. Patients who are borderline candidates for re-section due to their distribution of disease, or limited amount of uninvolved paren-chyma, may benefit from preoperative chemotherapy or portal vein embolization.For recurrence after resection, repeat hepatectomy provides a survival benefit forsome patients. It is clear that further improvements in survival following hepatec-tomy for colorectal metastases will depend on the development of more effectiveadjuvant therapies. Adjuvant hepatic arterial chemotherapy appears to be one suchemerging approach.

Suggested Reading1. 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. AnnSurg 1999; 230:309-318.

2. Kemeny N, Huang Y, Cohen AM et al. Hepatic arterial infusion of chemotherapyafter resection of hepatic metastases from colorectal cancer. N Engl J Med 1999;341:2039-2048.

3. Scheele J, Stangl R, Altendorf-Hofmann A. Hepatic metastases from colorectalcarcinoma: impact of surgical resection on the natural history. Br J Surg 1990;77:1241-1246.

4. Scheele J, Stang R, Altendorf-Hofmann A et al. Resection of colorectal liver me-tastases. World J Surg 1995; 19:59-71.

5. Fernandez-Trigo V, Shamsa F, Sugarbaker PH. Repeat liver resections from colorectalmetastasis. Repeat Hepatic Metastases Registry. Surgery 1995; 117:296-304.

Table 9.2. Results of repeat resection for recurrent colorectal liver metastases

Operative SurvivalAuthor N Mortality Morbidity 1 yr 3 yr 5 yr

(%)

Elias D1993 28 4 32 85 35 –Nordlinger B1994* 116 1 25 78 33 –Fong Y1994 25 0 28 90 30 30

Fernandez-Trigo V1994* 170 – 19 86 45 32Adam R1997 64 0 20 87 60 42Yamamoto J1999 90 48 31

*multi-institutional series

CHAPTER 1CHAPTER 10

The Surgical Approach to Non-ColorectalLiver Metastases: Patient Evaluation,Selection and Results

Jonathan B. Koea

IntroductionLiver resection for metastatic cancer has been reported for over a century. How-

ever, it was not until 1977 when Foster and Berman published a report of liverresection for a variety of several metastatic cancers that the concept gained generalacceptance. Subsequent investigators have demonstrated that hepatic resection formetastatic colorectal cancer can be routinely undertaken with a perioperative mor-tality of less than 5%, and a 5 year disease free survival of at least 30%. This issignificantly better than nonsurgical treatment with either chemotherapy or radia-tion in terms of patient survival, treatment related complications, and mortality.

The role of hepatic resection and cytoablative techniques in the management ofnon-colorectal metastases is less well defined, although for metastatic neuroendo-crine tumors, hepatic resection appears to offer long-term palliation and a chance ofcure. Medical management with chemotherapeutic approaches and radiation con-tinues 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 interestin the resection of liver metastases from a variety of non-colorectal cancers. While inmany centers these patients are still considered to be incurable and are managedsolely based upon symptoms, there is a growing body of literature suggesting thataggressive treatment of selected patients results in an improved quality of life, pro-longed survival and possible cure (Fig. 10.1).

This Chapter reviews the methods of investigation, patient selection, and resultsfor resection and cytoreductive techniques in the management of non-colorectalliver metastases. It must be emphasized that little is currently known of the naturalhistory of resected metastases in many conditions, and as such, only carefully se-lected patients should be considered for aggressive management as part of prospec-tive clinical series and trials.

Patient Selection

Tumor BiologyHepatic 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 vari-ables have been put forth to aid in the selection of patients for hepatic resection.



10

Disease Free IntervalFong et al showed that in patients with metastatic colorectal carcinoma, a dis-

ease-free interval of < 12 months after resection of the colorectal primary was asso-ciated with adverse outcome. Disease-free interval is consistently an importantpredictor of outcome in all series reporting the resection of metastatic liver diseasefrom a number of primary tumors. There is little doubt that patients with synchro-nous disease have a worse prognosis than those with metachronous lesions, and ashort disease-free interval is usually indicative of a tumor with aggressive metastaticpotential (Fig. 10.2).

Extrahepatic Disease and Extent of Hepatic ResectionIn most solid tumors, the presence of untreated extrahepatic disease significantly

limits the prospect of patient cure. Great effort is typically made during preopera-tive staging examinations to detect occult disease within the chest and peritonealcavities and thus limit unnecessary surgical explorations. If hepatic resection is to beundertaken, complete resection of all intra-abdominal tumor deposits is mandatory,and in nearly all instances, noncurative resection offers no survival alternatives beyondsupportive therapy (Fig. 10.3). The exceptions to this rule are:

1. nonfunctioning neuroendocrine tumors, since the growth rate of this tu-mor is slow and significant morbidity is often related to pressure symp-toms caused by large hepatic deposits,

2. pseudomyoma peritoneii,3. peritoneal mesothelioma, and4. ovarian carcinoma, since the benefits of tumor debulking have been docu-

mented and effective adjuvant chemotherapy is available in some instances.

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

131The Surgical Approach to Non-Colorectal Liver Metastases

10

Patient Performance StatusAdequate patient performance status is an important prerequisite for hepatic

resections of any type and can be quantified using the Karnofsky Performance Score

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

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


10

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

Preoperative Staging

History and Physical ExaminationA thorough medical history and physical examination represent a critical part of

the staging process. The history should concentrate on clarifying presentation andtreatment of the primary lesion. It is important to obtain copies of the originaloperative records and the pathology. If there is doubt over the tissue diagnosis, patho-logical slides should be reviewed. It is often useful to have a preoperative discussionwith the surgeon who operated on the primary lesion. The patient’s prior medicalhistory should be elicited with particular reference to the presence and severity ofcomorbid conditions and KPS. It is also important to investigate the patient’s familyhistory with respect to familial cancer syndromes and elucidate the patient’s socialsituation in terms of support and caregivers who will be available to assist withrehabilitation.

The physical examination should be thorough while concentrating on excludingsites of extrahepatic disease (lymphadenopathy, pleural effusions, ascites and cuta-neous metastases), identifying significant comorbid conditions and detecting signsof liver disease or decompensation (spider nevi, tremor, ascites, abnormal collateralvessels).

An important part of this interview is simply to get to know the patient. Mostpatients with metastatic disease will be patients for life and while some have unreal-istic expectations of treatment goals, most simply want an honest assessment oftheir condition and sound advice about their therapeutic options. Time spent indefining the patient’s goals and expectations in this initial phase will facilitate theremainder of the preoperative and postoperative management.

Optimal staging investigations will be partially dictated by the findings on thehistory and physical examination, with any unexplained symptoms such as weak-ness or bone pain mandating specific investigation. However, even in asymptomaticpatients, a number of investigations should be carried out to define occult meta-static disease and assess the patient’s suitability for major hepatic surgery.

Investigations

Complete Blood Count and Coagulation ProfileThe presence of thrombocytopenia is important and difficult to diagnose.

Approximately 0.005% of asymptomatic patients will have unsuspected thromb-ocytopenia on preoperative testing. In addition, a hematocrit of at least 30, and ahemoglobin of 10 g/dl, is necessary for safe elective hepatic surgery.


10

Table 10.1. Karnofsky Performance Status

Score90-100 Fully active, able to carry on all pre-disease performance without

restriction.30-40 Restricted in physically strenuous activity but ambulatory and able to

do light work.30-41 Ambulatory and capable of self-care but unable to carry out work

activities.30-42 Capable of limited self care, confined to bed or chair for > 50%

waking hours.10-20 Completely disabled, cannot carry out self-care and confined to bed

or chair.

Table 10.2. Childs score for hepatic cirrhosis

Parameter Points1 2 3

Albumin (g/dl) >3.5 2.8-3.5 <2.8Bilirubin (mmol/l) <25 25-40 >40Prothrombin time <4x normal 4-6x normal >6x normalAscites None Mild ModerateEncephalopathy None Mild Moderate

Childs A = 5-6 points; Childs B = 7-9 points; Childs C = 9-15 points.

Serum Electrolytes and Liver Function TestsSerum electrolyte determinations are undertaken to define asymptomatic renal

dysfunction and unexpected electrolyte abnormalities. Serum creatinine does notrise significantly until renal function is reduced by a factor of 50%. The prevalenceof asymptomatic renal dysfunction in the general population is 0.3%.

Liver function tests (determination of circulating levels of alkaline phosphatase,aspartate transaminase, gamma glutamyl transferase and bilirubin), provide limitedinformation on hepatic functional reserve and may help define the severity of cir-rhosis. Abnormal liver function tests are present in 0.0025% of symptomatic patients.

ElectrocardiogramElectrocardiography is useful to detect evidence of previous myocardial infarc-

tion or asymptomatic rhythm disturbance. It is mandatory in any patient with ahistory of cardiopulmonary disease or age > 40 years. In patients with a history ofsignificant cardiac disease, an echocardiogram and an assessment of cardiac perfu-sion is usually indicated.

Chest RadiographPostero-anterior and lateral radiographs of the chest should be obtained preop-

eratively. The most commonly detected abnormality is cardiac enlargement or chronicobstructive pulmonary disease. The frequency of these abnormalities is related topatient age. In patients less than 5 years of age, abnormalities were found in 7.5% ofchest radiographs, while in 5% of patients over 40 years of age.


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Bone ScansWhole body radionuclide bone scanning should be undertaken in patients with

bony symptomatology to define osteolytic metastases. Plain radiographs of the areashould also be performed. There is little evidence that whole body bone scans are ofbenefit in asymptomatic patients.

Computed TomographyComputed tomographic (CT) scans of the brain are indicated in patients with

new or unexplained neurological symptoms; however, this examination has no valueas a screening examination in asymptomatic patients.

Although we have shown that CT of the chest is not useful in selecting colorectalcancer patients for hepatic resection, we feel that CT scans of the chest, abdomen andpelvis should be carried out in all patients with noncolorectal hepatic metastases. Bothbone and lung windows should be constructed for chest scans to define occult meta-static disease. Noncontrast and contrast enhanced scans of the abdominal cavity andpelvis should be performed with particular attention to demonstrating the intra-ab-dominal lymph node basins. CT portography should also be considered, as this is oftenthe most effective means to demonstrate hepatic metastases. In addition it will providevaluable information regarding the relationship of lesions to vascular structures.

Positron Emission TomographyPositron emission tomography (PET) scanning takes advantage of the glucose

avid metabolism of tumors following the administration of 2-(18F)-fluoro-2-deoxyglucose (FDG). FDG is transported into tumor cells and undergoesphophorylation by hexokinases to FDG-6-phosphate, and is selectively retainedwithin tumor cells. The sensitivity of PET scanning for most tumors is currentlyunknown. However, Fong et al have recently assessed the use of PET scanning inpatients with metastatic colorectal cancer. These investigators found that PET scansaltered clinical management in 23% of cases of metastatic colorectal carcinoma byidentifying unsuspected extra-hepatic disease. In addition, 17% of patients withpositive PET findings directed surgical biopsy that proved unresectable extra hepaticdisease. PET scanning was not as sensitive at defining small (< 1 cm in diameter)peritoneal deposits and additional intrahepatic lesions. These results imply that PETmay be a useful investigational modality for defining extrahepatic disease in patientswith metastatic colorectal carcinoma. Although its effectiveness in preoperative clinicalstaging of other solid tumors is unknown, PET scanning should be considered in allpatients with non-colorectal non-neuroendocrine metastases prior to hepaticresection.

Magnetic Resonance ImagingMRI of the liver is useful in defining unsuspected intrahepatic disease not visu-

alized on CT or CT portography. In addition, MR cholangiography and MRangiography represent noninvasive investigations that define abnormalities in thebiliary and hepatic arterial systems.


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Diagnostic Laparoscopy, Laparoscopic Ultrasound,and Peritoneal CytologyThe increased availability and sensitivity of MR and CT scanning has led to

increased reliance on these imaging modalities. Diagnostic laparoscopy has provenuseful in the staging of upper gastrointestinal malignancies, particularly gastric andpancreatic carcinoma. Its use in primary and secondary hepatobiliary cancers wasrecently assessed by Jarnagin et al. These investigators demonstrated that laparoscopyidentified 26 of 39 patients with unresectable disease in a heterogeneous group ofprimary and secondary hepatobiliary cancers. In patients who underwent only stag-ing laparoscopy rather than exploratory laparotomy, laparoscopic staging resulted ina reduced length of hospital stay (2.2 versus 8.6 days) and hospital charges in compari-son to laparotomy. Laparoscopy was most useful in detecting unexpected peritonealmetastases (9 of 10 patients), additional hepatic tumors (10 of 12 patients), and unsus-pected advanced cirrhosis (5 of 5 patients). In addition to diagnostic laparoscopy,laparoscopic ultrasound provides additional information by defining the anatomicalrelationship of metastatic lesions to intrahepatic vasculature and locating small intrahe-patic lesions that were not defined on preoperative radiological investigation. Whetherthis technique should be performed routinely is at present unclear.

The use of peritoneal cytology to define occult peritoneal metastatic diseasehas gained increased attention with regard to pancreatic cancer and gastric cancer,two diseases in which potential recurrence is common. Whatever the particularcytology, the routine use of peritoneal cytology as a potential staging tool requiresfurther investigation.

Preoperative Preparation

StagingAll patients with non-colorectal metastases should be subjected to extensive pre-

operative clinical and radiological staging. Asymptomatic patients with extrahepaticdisease are not considered for surgical resection. Patients with symptomatic hepaticmetastases can be candidates for either nonoperative treatment, such as transarterialembolization, radiofrequency ablation, alcohol injection, or in rare instances, palliativehepatic resection.

Informed consent should be obtained from all patients. This should include afull description of the nature of the procedure, anticipated benefits, possible com-plications and treatment alternatives. For many tumors (i.e., metastatic ovarian,testicular and neuroendocrine), effective adjuvant chemotherapy is available andcoordinated discussions between the treating medical oncologists, radiationoncologists, interventional radiologists and others, is a vital part of the preoperativeevaluation. Ideally, discussions relating to the care of these complex patients shouldoccur at combined medical/surgical management conferences.

Operative Technique

LaparoscopyAlthough laparoscopy can be performed under local anesthesia, staging

laparoscopic examinations should be performed using general anesthesia to allow


10

peritoneal dissection, visceral manipulation and all necessary biopsies. It is notewor-thy that many of the reported failures of laparoscopy to accurately stage gastrointes-tinal cancers have occurred in patients in whom adequate adhesiolysis was notperformed or thorough examination of the bowel or lesser sac was omitted.

With the patient supine, a 12 mm Hasson cannula is inserted into the abdomi-nal cavity under direct vision using an open technique. In the Hepatobiliary Serviceat Memorial Sloan-Kettering Cancer Center (MSKCC), the trocar is placed in theright or left upper quadrant along the line of the planned bilateral subcostal inci-sion. Intra-abdominal examination is carried out using a 30 degree angled scope. A10 mm port can be placed in the contralateral upper quadrant for the purposes ofperitoneal lavage and biopsy. If laparoscopic ultrasound is available this can directedtoward the liver. A 5 or 10 mm port can be added in the left upper quadrant forretraction and biopsy. Before undertaking formal staging, any ascitic fluid should beaspirated and sent for cytology. At our own institution, 200 ml of normal saline isthen instilled and specimens for cytology study purposes are aspirated from thepelvis and both subphrenic spaces. If present, peritoneal adhesions should be di-vided and a thorough, systematic examination of the peritoneal cavity carried out.The parietal peritoneum over the hemi-diaphragms, anterior abdominal wall andpelvis should be examined for metastatic disease and carefully inspected. With thepatient in 30˚ of reverse Trendelenburg and 10˚ of left lateral tilt, the anterior andposterior surfaces of the left lobe can be directly seen. It may be possible to performbimanual palpation of the liver using a grasping forceps inserted via a 5 mm port.Identification of deeply placed hepatic lesions can be undertaken with laparoscopicultrasound 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 thetransverse mesocolon inspected. An assessment of nodal disease along root of themesentery and the ligament of Treitz is then carried out. The small intestine and itsmesentery should be inspected for metastases. Peritoneal or liver biopsies should betaken at this point and sent for frozen section examination. An assessment should bemade 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 ligamentpermits evaluation of the caudate lobe and lymph nodes in the porta hepatitis andceliac areas.

At completion of the procedure, a 10 mm port site should be closed and subcu-ticular sutures placed on the skin. Variations in technique will be defined by clini-cian preference and the results of preoperative discussion with the patient. In general,a negative examination is immediately followed by definitive resectional surgeryunder the same general anesthetic.

Techniques of ResectionA detailed description of the techniques for liver resection is provided in Chap-

ter 16. In brief, all liver resections are performed under controlled central venouspressure (CVP) maintained at less than 5 mmHg. This permits easy control of bloodloss if a major hepatic vein or the interior vena cava is entered. Dissection is per-formed with the patient in a 15˚ Trendelenburg. A bilateral subcostal incision ismade and a midline vertical extension is used if required for adequate exposure. Thesegment of liver to be resected is mobilized by detaching all ligamentous attach-


10

ments. Alternatively, a right subcostal incision with midline extension is adequatefor most resections. The falciform ligament is dissected close to the liver to exposethe suprahepatic IVC and the hepatic veins above the liver. Hilar structures arecontrolled by extrahepatic dissection of the porta hepatitis. Intraoperative ultra-sonography is performed to assess the liver for additional lesions and to confirm thehepatic vascular anatomy in relation to the tumor.

Prior to transection of the right hepatic vein, the portal and hepatic arterial inflow are divided using the techniques discussed in more detail in Chapter 16.

For right-sided resections, the hepatic veins are divided sequentially from thelower 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. Forleft-sided resections, the left and middle hepatic veins are isolated by dissection atthe upper border of the ligamentum venosum and similarly divided after control ofthe left hepatic inflow.

Transection of the parenchyma is performed using a tissue crushing technique topermit identification of small vessels and biliary radicals which are controlled byhemoclips. Large intrahepatic veins are suture ligated. Parenchymal division is per-formed using intermittent inflow occlusion (Pringle maneuver) which is releasedevery 5-10 minutes to relieve portal venous congestion and permit hepatic perfu-sion. As alluded to above, hepatic outflow control is obtained prior to parenchymaldivision in most cases.

Tumor debulking and enucleation techniques can be utilized in the manage-ment of patients with metastatic neuroendocrine disease. Tumor debulking is car-ried out with inflow occlusion and can be undertaken by parenchymal division atthe margin of the lesion. There is often an avascular plane which, once entered,allows removal of metastatic neuroendocrine disease with a narrow surroundingmargin of normal parenchyma. This often provides long term symptomatic relieffor these patients. In addition, cryotherapy assisted resection is also useful in themanagement of metastatic lesions. This technique utilizes initial cryotherapy of thelesion, 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 amore detailed description see Chapter 18.

Nonoperative TechniquesThere are currently three techniques of nonresectional therapy widely in use.

Transarterial particle embolization has been in continuous clinical use for the last 25years. Advances in percutaneous arterial puncture technique and flexible cathetertechnology have enabled interventional radiologists to cannulate intrahepatic arte-rial branches using a femoral artery approach, and to selectively occlude these branchesusing inert particles of latex or Ivalon sponge to reduce ischemic tumor infarction.This technique is well-established and results in complete tumor necrosis inapproximately 70% of patients with hepatocellular carcinomas (HCC) or neuroen-docrine tumors. The reported mortality rate is <1% with a morbidity rate of 5%.Percutaneous ethanol injection techniques, typically performed for HCC, make useof either CT or ultrasound to guide needle placement into the tumor. It may resultin complete tumor necrosis in 60% of HCC with a low morbidity rate (~5%).Radiofrequency thermal ablation (RFA) represents a new technique for the treatment


10

of hepatic tumors and was first described in 1990. RFA utilizes an electrode con-nected to a 500 kHz radiofrequency generator placed into the center of the lesionusing ultrasound guidance. Heating of the electrode tip, when placed within a tu-mor, results in tumor ablation. Initial experience with this technique indicates thatcomplete tumor necrosis can be achieved in over 90% of patients with low mortality(<1%) and morbidity (10%). Whether radiofrequency thermal ablation of a tumortranslates into cure is less clear. Chapters 2 and 18 deal this topic in more detail.

Patients considered unsuitable for either hepatic resection due to disease relatedconcerns or significant comorbidities should be referred for some type ofnonresectional therapy preferably within a clinical trial. At present, there are noguidelines to assess the relative merits of these various techniques. However, eachtechnique does not only offer the opportunity to ablate metastatic disease, but mayalso be useful to relieve tumor-related symptoms with low rates of complication.

Results

Neuroendocrine MetastasesThe surgical management of hepatic metastases from neuroendocrine carcinoma

is currently in evolution. These tumors are rare and significant numbers are seenonly in a few centers which focus on treating hepatobiliary malignancies. Neuroen-docrine tumors generally follow an indolent course with a mean survival of 8 yearsreported in untreated patients with advanced metastatic disease. This long naturalhistory makes defining the effectiveness of therapeutic intervention difficult and hasengendered a conservative attitude toward radical treatment. However, three quar-ters of patients with advanced neuroendocrine carcinoma die within 5 years of diag-nosis. As morbidity and mortality rates for liver surgery have fallen, renewed interestin aggressive management have emerged. Recent experience has demonstrated thatcomplete surgical resection can produce significant symptom relief and a cure rateof up to 30%. The experience of a number of clinical centers with metastatic neu-roendocrine carcinoma is summarized in Table 10.3. McEntee et al presented 37patients treated with hepatic resection. Curative resection was undertaken in 17patients and palliative resection in 20; 11 were disease free at a median follow up of19 months. Palliative resection resulted in complete relief of symptoms in 60%,incomplete relief in 35%, and one postoperative death. An additional 74 patientshave been reported from the same institution with complete symptom relief ob-tained in 90% of patients and an actuarial 4-year survival of 73%. The operativemortality in this series was 2.7%.

The long natural history of these lesions has also made it acceptable to treat largetumor deposits with enucleation rather than formal hepatic lobectomy as this willoften result in long-term disease control. Soreide et al have presented the results ofrepetitive debulking in 75 patients. Only half of these patients had liver-directedsurgery and only four hepatic resections were performed. Despite seven postopera-tive deaths, this therapy resulted in a 3-fold increase in median survival (216 monthsin treated patients vs 48 months in untreated patients).

There is currently controversy regarding the importance of resection of the primarytumor in patients with neuroendocrine carcinoma metastatic to the liver. Chamberlainet al have recently reviewed the experience at MSKCC with this condition. These

139The Surgical A

pproach to Non-C

olorectal Liver Metastases

10

Table 10.3. Summary of significant reported series of hepatic resection for neuroendocrine metastases

Reference N Histology Curative Palliative Operative Relief of SurvivalMortality Symptoms

Martin14 5 Carcinoid 4 1 0% 100% 46 months(median)

Makridis15 6 Carcinoid 0 6 0% N/A 30 months(mean)

McEntee9 37 Neuroendocrine 17 20 2.7% 70% –

Soreide11 4 Carcinoid 0 4 N/A N/A 139 monthsmedian

Que10 74 Neuroendocrine 28 46 2.7% 90% 73%@ 4 yr

Dousset16 7 Neuroendocrine 12 5 5.9% 88% 62%@ 5 yr

Chen17 15 Islet Cell 15 0 0% N/A 73% @ 5 yr

Chamberlain12 34 Neuroendocrine 15 19 6% 86% 76%@ 5yr

* (N/A, not stated)


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investigators compared outcomes in patients who had concomitant resection of theprimary lesion at the time of the hepatic resection with those who had the primarytumor left in situ. Hepatic recurrence in both groups was between 70% and 80%during the follow-up period which implies that prior resection of the primary tu-mor is not mandatory.

Currently, all patients with both symptomatic and asymptomatic neuroendo-crine tumors should be considered for curative hepatic resection if all lesions can beremoved. Similarly, palliative surgical resection should be considered for symptomcontrol if at least 90% of tumor volume can be removed. Palliative resection in theabsence of symptoms should also be considered in patients with tumors locatedadjacent to or threatening vital structures. Paradoxically, these patients should comefor early resection as continued growth of strategically placed tumors often rendersthem dangerous or impossible to remove.

Patients with extensive bilobar metastases, or those who are unsuitable for resec-tion because of comorbidities, can be effectively managed with hepatic artery embo-lization and/or long acting somatostatin analogues. Brown et al have demonstrateda 96% response rate for both hormonal and pressure related symptoms followingembolization. The procedure related mortality was 6% in this series. However, it isunclear whether embolization results in improved survival in these patients.Orthotropic liver transplantation has been undertaken in patients with metastaticneuroendocrine carcinoma, but the results have been disappointing with approxi-mately 90% of patients dying as a result of recurrent disease within 12 months oftransplantation.

Non-colorectal, Non-Neuroendocrine MetastasesThe results of major clinical series reporting curative hepatic resections for non-

colorectal, non-neuroendocrine metastases are summarized in Table 10.4. Becauseof the limited experience with this type of hepatic resection, most clinical series aresmall and report results collectively rather than by tumor types. Few series specifythe total numbers of cases operated upon and concentrate on discussing long-termsurvivors. It is therefore difficult to clarify the total number of patients who areeligible for hepatic resection or the effectiveness of surgical treatment.

Head and NeckThe results for resection of metastatic squamous cell carcinoma are poor with no

long-term survivors reported. Hepatic resection for metastatic squamous cell carci-noma of the head and neck cannot be recommended. Interestingly, both Harrisonand Schwartz report survivors following resection of metastatic parotid and thyroidcarcinomas indicating that these tumors may have a more indolent biology andresection may be considered in selected cases.

LungThe results of hepatic resection for metastatic carcinoma of the lung are poor.

Schwartz reported on five patients with metastatic lung cancer who underwent liverresection. There were no long-term survivors. Lindell reported the only long-termsurvivor (185 months), a patient who underwent resection of bronchial carcinomametastatic to the liver.


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Table 10.4. Summary of significant reported series of hepatic resection for non-colorectal non-neuroendocrine metastases

Tumor Reference Number of Number of Number of Number ofCurative Survivors Survivors SurvivorsResections 1 Year 3 Years 5 Years

Parotid 3 1 1

Head & Neck 18 4

Thyroid 19,20 2 2

Lung 19-22 7 1

Esophagus 19 21 5 1

Stomach 23 18-20, 47 10 3 1124-26

Sarcoma* 3,21,22,27 63 15 618,19,25

Periampullary 20,21, 22 2 325,27

Melanoma 3,19-22, 36 4 3 1025,27

Renal/Wilms 21,25 3, 41 12 1218-20,22

Uterine 3,19-22, 15 3 125,27

Ovarian 3,19-22,27 10 1 2

Testicular 3,18 25 1

Adreno- 3,19,21, 14 1 1 5cortical 22,27

Unknown 18,20 9 1 1

Primary

Breast§ 3,18-22,25 89 2 11

*Includes gastric and intestinal leiomyosarcoma, § includes 14 unreported casesfrom Memorial Sloan-Kettering Cancer Center.


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EsophagogastricOchiai et al analyzed the results of gastric resection for hepatic metastases in 29

patients out of a total of 284 patients (10%). Synchronous hepatic resection andgastrectomy were performed in 21 patients. The median interval between gastricand hepatic resection in the remaining 8 patients was 21 months. Four patients (4/29%) survived more than five years following gastric resection. Among patientsundergoing synchronous resection, the presence of serosal invasion was the singleprognostic factor that could be assessed during surgery. Among patients undergoingmetachronous resection, the authors found that if lymphatic and venous invasionby the primary tumor was present, hepatic resection was unlikely to be of benefit.These investigators emphasized that metastatic disease restricted to the liver is rarein gastric cancer in the absence of significant lymph node involvement and perito-neal disease. Miyazaki et al also emphasized the importance of an adequate surgicalmargin and number of lesions in the resection of gastric metastases. The majority ofpatients (69%) in their series who developed recurrent hepatic disease had multiplelesions that were resected with margins of < 10 mm. Bines et al demonstrated that enbloc resection of large gastric tumors which directly invade the liver may result inlong-term survival. Two of three patients in their series survived 10 years. Theseauthors argued strongly against hepatic resection for synchronous or discontinuousmetastases under any circumstance.

Pancreas/PeriampullaryHepatic resection of metastatic adenocarcinoma of the pancreas has not resulted

in any documented long-term survivors. In comparison, Berney has reported twosurvivors following hepatic resection for metastatic ampullary cancer and cystad-enocarcinoma of the pancreas at 70 and 84 months, respectively. Malt and Eliashave emphasized that in patients who present with hepatic metastases of unknownprimary, the majority will harbor a primary tumor in the pancreas or colon.

Renal Carcinoma/Wilms TumorA number of investigators have demonstrated that long term survival is possible

following hepatic resection for both renal cell carcinoma and Wilms tumor. Schwartzreported that four patients out of a total of 13 who underwent hepatic resection formetastatic renal cell cancer survived longer than 5 years. In 20 patients with Wilmstumor, seven were alive and free of disease 5 years after hepatic resection. Foster hasalso reported nine patients with Wilms alive between 18 months and 7 years follow-ing hepatic resection. Elias et al have emphasized that the results of hepatic resectionfor metastatic renal cell carcinoma and Wilms tumor are very similar to those formetastatic colorectal carcinoma. Consequently, hepatic resection for solitary meta-static lesions from primary renal carcinoma and Wilms tumor should be stronglyconsidered in all patients. In addition, metastases from renal carcinoma are gener-ally cystic and can also be safely treated with RFA. However, at present, there are nooutcome data available for this technique.

MelanomaThe results for hepatic resection of metastatic melanoma are poor. However,

Harrison has reported two 5 year survivors following hepatic resection. In contrast,


10

Schwartz found that only one of 11 patients who underwent resection for meta-static cutaneous melanoma survived 5 years. Hepatic metastases from ocular mela-noma is very common and, in rare instances, may be useful in patients with localizeddisease. Schwartz has reported a survival of between 3 and 6 years for this condition.Foster has reported two survivors of 59 and 72 months respectively. Hepatic resec-tion should be considered in patients with solitary lesions. However, intensive inves-tigation should be undertaken preoperatively to define other sites of metastases.Consideration should also be given to combining hepatic resection with adjuvantimmunotherapy.

SarcomaThe most common sarcoma to metastasize to the liver is a gastrointestinal stro-

mal tumor. If localized to the liver, resection appears worthwhile. Harrison reported27 patients with metastatic sarcoma, the majority being gastrointestinal stromal tu-mors, with a median survival of 31 months with one 5-year survivor.

OvarianHepatic resection for metastatic genitourinary tumors is generally associated with

a favorable outcome. In the series reported by Harrison et al, hepatic resection wasperformed in 34 patients with metastatic genitourinary tumors and was associatedwith a 60% 5-year survival with seven actual 5-year survivors. These included tes-ticular, ovarian, cervical and uterine carcinomas (Fig. 10.4). It is important toemphasize that most ovarian carcinomas are actually extrahepatic lesions which growinto the liver, and in these patients, the primary aim of surgery is operative debulkingto enhance the effects of postoperative chemotherapy.

AdrenocorticalResection of metastatic adrenocortical carcinoma is associated with a 20-30%

long term survivorship. Harrison et al reported seven resections with two long-termsurvivors. Schwartz reported two long-term survivors (131 and 132 months,respectively) out of eight patients undergoing resection.

BreastSystemic chemotherapy remains the mainstay of therapy for patients with local-

ized and advanced breast cancer. Hepatic resection has been undertaken in highlyselected patients with solitary breast metastases. Nineteen patients with metastaticbreast carcinoma have been considered for hepatic resection at MSKCC with a medianof 46 months from resection of the primary to hepatic resection. Laparoscopy revealedextrahepatic disease in five patients, 14 were resected. Six patients have died of re-current disease a median of 11 months after resection. Both the number of hepaticlesions (> 2) and the presence of positive resection margins were adverse prognosticfactors. Elias et al point out that metastases should be isolated and chemosensitive ifresection is to be considered, while also noting that up to 30% of patients will alsohave involved hilar lymph nodes.

ConclusionsAlthough there is no prospective data or published randomized trials, there are

sufficient retrospective studies to demonstrate that hepatic resection for metastatic


10

cancer is safe and can be undertaken with acceptable morbidity and mortality. Littleis currently known about the natural history of treated metastases since, historically,patients with metastatic disease were regarded as incurable and managed symptom-atically. However, it is clear that aggressive resection does, in some cases, result insignificant survival advantage. Overall, the survival rates for melanoma and stomachprimaries are close to 30% at three years although less than 20% at five years. Forcarcinoma of the testis, renal cell carcinoma, Wilms tumor, gynecological tumors,and gastrointestinal stromal tumors, survival is close to 50% at three years. Theindications for hepatic resection should be cautiously expanded to include patientswith these tumors. Careful patient selection should be undertaken with preopera-tive staging investigations prior to resection. All patients should become part ofprospective clinical protocols. In addition, every attempt should be made to treatpatients postoperatively with any available adjuvant therapies to optimize their chanceof disease-free survival.

Selected Reading1. Foster JH, Berman M. Solid liver tumors. Ebert P. Philadelphia: WB Saunders Co.

Major problems in clinical surgery. 1977.2. Fong Y, Fortner J, Sun RL et al. Clinical scores for predicting recurrence after

hepatic resection for metastatic colorectal cancer. Analysis of 1001 consecutivecases. Ann Surg 1999; 230:309-321.

3. Harrison LE, Brennan MF, Newman E et al. Hepatic resection for noncolorectalnonneuroendocrine metastases: A fifteen year experience with ninety-six patients.Surgery 1997; 121:625-632.

4. Fong Y, Saldinger P, Akhurst T et al. Utility of 18F-FDG positron emissiontomography scanning on selection of patients for resection of hepatic colorectalmetastases. Am J Surg 1999; 178:282-287.

Fig. 10.4. Comparison of survival after liver resection for genitourinary cancers, softtissue tumors (including melanoma) and gastrointestinal tumors. * p < 0.05 log ranktest. Reprinted with permission from Harrison LH, Brennan MF, Newman E et al.


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5. Jarnagin WR, Bodniewicz J, Dougherty E et al. Prospective analysis of staginglaparoscopy in patients with primary and secondary hepatobiliary malignancies. JGastrointestinal Surg 2000; 4:34-44.

6. Billingsley KG, Jarnagin WR, Fong Y et al. Segment-orientated hepatic resectionin the management of malignant neoplasms of the liver. J Am Coll Surg 1998;187:471-481.

7. Polk W, Fong Y, Karpeh M et al. A technique for the use of cryosurgery to assisthepatic resection. J Am Coll Surg 1995; 180:171-176.

8. Norton JA, Doherty GM, Fraker DL et al. Surgical treatment of localized gastrinomawithin the liver: A prospective study. Surgery 1998; 124:1145-1152.

9. McEntee GP, Nagorney DM, Kvols LK et al. Cytoreductive hepatic surgery forneuroendocrine tumors. Surgery , 1990; 108:1091-1096.

10. Que FG, Nagorney DM, Batts KP et al. Hepatic resection for metastatic neuroen-docrine tumors. Am J Surg 1995; 169:36-43.

11. Soreide O, Berstad T, Bakka A et al. Surgical treatment as a principle in patientswith advanced abdominal carcinoid tumors. Surgery 1992; 111:48-54.

12. Chamberlain RS, Canes D, Brown KT et al. Hepatic neuroendocrine metastases:Does intervention alter outcome. J Am Coll Surg Submitted for publication. 2000.

13. Brown KT, Koh BY, Brody LA et al. Particle embolization of hepatic metastases forcontrol of pain and hormonal symptoms. J Vascular Interventional Radiol 1999;104:397-403.

14. Martin JK, Moertel CG, Adson MA et al. Surgical treatment of functioning meta-static carcinoid tumors. Arch Surg 1983; 118:537-542.

15. Makridis C, Oberg K, Juhlin C et al. Surgical treatment of mid-gut carcinoidtumors. World J Surg 1990; 14:377-385.

16. Doussett B, Saint-Marc O, Pitre J et al. Metastatic endocrine tumors: medicaltreatment, surgical resections or liver transplantation. World J Surg 1996;20:908-915.

17. Chen H, Hardcare JM, Uzar A et al. Isolated liver metastases from neuroendocrinetumors: does resection prolog survival. J Am Coll Surg 1998; 187:88-93.

18. Elias D, Cavalcanti de Albuquerque A, Eggenspieler P et al. Resection of livermetastases from a noncolorectal primary: Indications and results based on 147monocentric patients. J Am Coll Surg 1998; 187:487-493.

19. Lindell G, Ohlsson B, Saarela A et al. Liver resection of noncolorectal secondaries.J Surg Oncol 1998; 69:66-70. 98 A.D.

20. Savage AP, Malt RA. Survival after hepatic resection for malignant tumours. Brit JSurg 1992; 79:1095-1101.

21. Schwartz SI. Hepatic resection for noncolorectal nonneuroendocrine metastases.World J Surg 1995; 19:72-75.

22. Iwatsuki S, Starzl TE. Personal experience with 411 hepatic resections. Ann Surg1988; 208:421-434.

23. Ochiai T, Sasako S, Mizuno S et al. Hepatic resection for metastatic tumors fromgastric cancer: analysis of prognostic factors. Brit J Surg 1994; 81:1175-1178.

24. Miyazaki M, Itoh H, Nakagawa K et al. Hepatic resection of liver metastases fromgastric carcinoma. Am J Gastroenterology 1997; 92:490-493.

25. Foster JH. Survival after liver resection for secondary tumors. Am J Surg 1978;135:389-394.

26. Bines SD, England G, Deziel DJ et al. Synchronous, metachronous, and multiplehepatic resections of liver tumors originating from primary gastric tumors. Surgery1993; 114:799-805.

27. Berney T, Mentha G, Roth AD et al. Results of surgical resection of liver me-tastases from noncolorectal primaries. Brit J Surg 1998; 85:1423-1427.

CHAPTER 11

Surgical Techniques of OpenCholecystectomy


IntroductionGallstones are extremely common throughout the Western world and are found

in approximately 10% of the adult population. Gallstones occur twice as commonlyin females as in males, with the prevalence peaking in the sixth and seventh decade.Interestingly, several cultural and ethnic groups demonstrate an extremely high inci-dence of gallstones compared to other populations. For example, in Peru, the PimaIndians have a reported incidence of gallstones that may approach or surpass 50% ofthe adult population.

The majority of gallstones remain asymptomatic and silent throughout the lifeof an affected individual and it is estimated that only 20-30% of all patients everdevelop symptoms. The risk of a patient with asymptomatic gallstones developingbiliary-related symptoms is estimated at 1-2% per year, with a risk of 0.1% per yearof developing severe complications such as gallbladder perforation or empyema.

In nearly all cases, cholecystectomy is the treatment of choice for symptomaticgallstones. At present, cholecystectomy is the most common elective operation per-formed worldwide, with approximately 500,000 cholecystectomies performedannually (1990 figures). It seems reasonable to surmise that this number has increasedwith the advent and widespread application of laparoscopic cholecystectomy tech-niques. The indications for cholecystectomy are variable. In most series, 70-80% ofpatients undergo elective cholecystectomy for chronic cholecystitis or biliary colicin conjunction with ultrasonographic evidence of gallstones. Only 10-30% of patientsundergo cholecystectomy due to complications of acute cholecystitis.

Clinical PresentationThe most common clinical presentation for gallstone disease is acute cholecysti-

tis, which occurs in 90-95% of cases. The disease course normally begins as a resultof inflammation due to cystic duct obstruction by a gallstone impacting in Hartmann’spouch. Interestingly, although bile remains stagnant within the gallbladder over longperiods of time, bacterial contamination of the gallbladder is not routine. Indeed, atthe time of operative cholecystectomy, 60-70% of gallbladder cultures are sterile. Iforganisms are identified, they are most commonly anaerobic or aerobic enteric bac-teria such as E. coli, Klebsiella sp and Enterococcus sp. The long-held belief that acutegallbladder inflammatory changes were due to coincident bacterial infection is prob-ably false. Indeed, the current consensus is that the initial cascade of events leading


147Surgical Techniques of Open Cholecystectomy

11

to acute biliary colic and acute cholecystitis is mucosal damage due to trauma froman impacted gallstone that sets off an inflammatory cascade and resultant symp-toms. Classically, biliary colic is characterized by the acute onset of right upperquadrant pain, with or without radiation to the back or right scapular area. Clinicalinterview can frequently elicit a history of less severe episodes of similar pain oftenpreceded by nausea and vomiting. In the case of acute cholecystitis, patients areoften febrile and may demonstrate some degree of abdominal rigidity and a Murphy’ssign indicating an underlying peritoneal irritation from the distended and inflamedgallbladder. Jaundice is rare in the setting of both acute and chronic cholecystitisand, when present, should suggest the presence of choledocholithiasis, secondarycholangitis, or partial obstruction of the common duct by either edema or a stone(Mirizzi’s syndrome). Physical exam may demonstrate right upper quadrant painand at times abdominal rigidity. A palpable gallbladder or mass in the right upperquadrant is present in up to 25% of cases. In general, making the diagnosis of acutecholecystitis is not difficult with the differential generally limited to peptic ulcerdisease, gastroenteritis, acute pancreatitis, retrocecal appendicitis, or right-sideddiverticulitis. Laboratory evaluation is generally nonspecific and demonstrates onlya leukocytosis. In the setting of choledocholithiasis or cholangitis, elevation of theserum bilirubin and alkaline phosphatemia are present. An elevated amylase level ispresent in the setting of gallstone pancreatitis and may help exclude other diagnoses.

Chronic cholelithiasis typically presents with severe pain characteristic of biliarytract origin, but there is a broad spectrum of mild to severe recurrent pain syn-dromes that may make the diagnosis of chronic cholecystitis difficult. Typical painarising from chronic cholecystitis, or “biliary colic,” is manifested by right upperquadrant abdominal pain occurring in association with eating a fatty meal. As withacute cholecystitis, pain often radiates to the scapular area and is associated withnausea and occasional vomiting. However, these symptoms are not specific and thedifferential diagnosis is broad and includes peptic ulcer disease, gastroesophagealreflux, hepatitis, pancreatitis, renal calculi, irritable bowel disease, and diverticulitis.The physical exam is usually normal, although there may be mild right upper quad-rant pain or tenderness. Rarely, there is a palpable gallbladder.

Preoperative StudiesThe initial diagnostic study obtained in the setting of acute and chronic chole-

cystitis is usually a plain abdominal x-ray taken in the emergency department. Radi-olucent gallstones can be detected in 10-20% of patients on plain radiographs, andin the setting of complicated acute cholecystitis, evidence of emphysematous chole-cystitis with air in the gallbladder wall may also be appreciated. Pneumobilia, or airin the biliary tree, normally indicates the presence of a cholecystoenteric fistula andif appropriate, the diagnosis of gallstones ileus may be entertained.

Ultrasonography should be the initial study performed if the diagnosis of eitheracute or chronic cholecystitis is considered. Ultrasound is quick, noninvasive andeasily obtainable. Characteristic ultrasound findings of acute cholecystitis include athickened gallbladder wall with the presence of posterior acoustical shadowing fromstones contained within the gallbladder. Occasionally, no stones are seen and mate-rial described as biliary sludge or mucosal sloughing may be noted. These findingsare common in the setting of acalculous cholecystitis. Air in the gallbladder wall,


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gallbladder wall thickening, and pericholecystic fluid are also common with severedisease. Calcifications of the entire gallbladder wall, the so-called “porcelaingallbladder,” or the presence of gallbladder polyps, should raise a concern of apossible malignancy.

Gallbladder scintigraphy is commonly used to confirm the diagnosis of acutecholecystitis. In this setting, aminodiacetic acid derivatives (HIDA) are used to dem-onstrate a functioning or nonfunctioning gallbladder. This test has a sensitivity andspecificity in the range of 97% and 87%, and is regarded by many as most accuratetest. The absence of isotope uptake within the gallbladder is generally regarded as anindication of cystic duct obstruction (Fig. 11.1). The presence of isotope in thepericholecystic area outside the gallbladder is a valuable secondary benefit of anHIDA scan and often correlates with the presence of gangrenous cholecystitis orgallbladder perforation. Note the results of an HIDA scan may be inaccurate in thesetting of significant hyperbilirubinemia (>5 mg/dl), in which case cholecystitis limitsbiliary flow.

Additional imaging modalities that may be useful in select circumstances includecomputed tomography scans, intravenous cholangiography, and oral cholecystogra-phy. Currently, these studies are utilized when the diagnosis is in doubt and haveonly limited indications.

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


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Perioperative ManagementAs with any acute intra-abdominal process, the initial perioperative manage-

ment of a patient with acute cholecystitis involves intravenous fluid resuscitation,electrolyte replacement and the administration of a broad-spectrum antibiotic. Asecond-generation cephalosporin is usually sufficient aerobic coverage, although inthe setting of positive anaerobic blood cultures or evidence of gangrenous cholecys-titis, an antibiotic that provides coverage for Bacterioides and Clostridium is indi-cated. Once the diagnosis is confirmed, adequate analgesia should be provided tokeep the patient comfortable, as peritoneal irritation from acute cholecystitis can besignificant. The patient should be kept fasted to reduce cholecystokinin release andboth gallbladder and bile duct stimulation.

Timing of SurgeryThe timing of surgery is generally dictated by the severity of the symptoms.

Indications for emergency or urgent cholecystectomy include deterioration of thepatient’s clinical condition or physical signs of generalized peritonitis with aninflammatory abdominal mass, gas in the gallbladder lumen or biliary tree, and theonset of intestinal obstruction. Note, despite the fact that several of these signs orsymptoms may be present, if comorbidities exist that would otherwise make anoperation prohibitive, a percutaneous tube cholecystostomy is often the initial treat-ment of choice. Although patients with acute and chronic cholecystitis have tradi-tionally 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 alaparoscopic cholecystectomy and bile duct exploration. The remainder of this Chap-ter will summarize the technical approach to performing an open cholecystectomy.

Whether to proceed early to cholecystectomy (within the first 24-48 hours ofdiagnosis), or to perform an interval cholecystectomy six to eight weeks after resolu-tion of an acute attack, remains relatively controversial. Despite the fact that at leastsix controlled prospective trials of treatment have all shown a clear benefit for earlycholecystectomy, a delayed approach is still frequently practiced. It is our experiencethat the edema which develops during an episode of acute cholecystitis permits aneasier operation, both open and laparoscopically, if performed within the first 24-48hours of diagnosis.

Operative Technique for CholycystectomyPrecise knowledge of normal and variant anatomy of the biliary tree is para-

mount to performing a safe and successful cholycystectomy. Inadvertent iatrogenicinjury to the biliary tree is associated with tremendous morbidity and mortality, andthe importance of proper visualization, exposure, and identification of all structuresprior to ligation cannot be overemphasized.

A Brief Review of Biliary AnatomyChapter 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 experiencedbiliary surgeon.


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The gallbladder is normally adherent to the undersurface of Segment V of theliver. The gallbladder runs transversely from beneath the free edge of Segment Vmedially and inferiorly towards the hepatoduodenal ligament. Peritoneal folds thatalso cover the major structures within the hepatoduodenal ligament envelop theneck of the gallbladder and cystic duct. The junction of the cystic duct with thecommon 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

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


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and cystic artery (Fig. 11.1). Exposure and identification of these anatomic struc-tures prior to ligation and gallbladder removal is the key to a safe operation.

Although biliary anomalies are among the most frequent anatomic variants, theanatomy of the gallbladder itself is typically constant. Note however, agenesis of thegallbladder, 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 pres-ence of a variety of anatomic variants involving the insertion of the cystic duct, oraberrant entry of a right or left sided hepatic duct, are the sources of nearly all biliaryinjuries. Figure 11.2 depicts the more common means by which the cystic ductenters the common bile duct. Normally, the cystic ducts takes a fairly serpigenouscourse prior to entry into the mid to distal common bile duct. However, cystic ductlength is variable and may be quite short or even absent. At other times, the cysticduct may be long and enter the common bile duct on the left side by coursing eitherabove or beneath it. Finally, though separate from the common bile duct, the cysticduct may share a fibrous septum with the duct making it appear short and predis-posing to potential injury.

In our experience, failure to recognize an abnormal confluence of the hepaticducts is the single most common surgical error leading to biliary injury. Theseabnormalities may occur in 30-45% of patients, so adherence to surgical techniqueand vigilance in properly recognizing these anomalies cannot be stressed enough.The more common anomalies encountered are discussed in Chapter 1 (Fig. 1.9 Aand B). The most common abnormalities typically involve aberrant or low entry ofone or both right-sided sectoral ducts; however, abnormalities involving the cysticduct are not infrequent. In our experience, injury to a right posterior sectoral duct

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


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

Surgical TechniqueWith the advent of laparoscopic cholycystectomy (Chapter 12), experience in

performing open cholecystectomy is rapidly vanishing. The view obtainedlaparoscopically is different than the view at open operation. Moreover, the perfor-mance of an open cholecystectomy is today typically performed only as an en passantoperation (where too little attention to technique may occur), or when laparoscopicoperation is deemed unsafe, in which case difficult anatomy and dangerous pathol-ogy preside. Though historically an operation for the general surgery resident to“cut his or her teeth on”, the infrequency with which it is currently performednecessitates proper supervision.

IncisionOpen cholycystectomy has traditionally been performed through a right subcos-

tal or Kocher incision, and this is the incision we recommend. However, a midlineincision also provides good access to the right upper quadrant, and may be preferredif cholecystectomy is to be performed as part of another operation. The advent ofminimally invasive surgery has led some surgeons to describe “keyhole” cholecystec-tomy during which 2-3 cm incisions are utilized to improve postoperative cosmesisand shorten postoperative recovery. While it may be possible to perform a cholecys-tectomy through these small incisions, it is justifiable only when the limited expo-sure does not hinder precise visualization of biliary anatomy or other intra-abdominalorgans that need proper evaluation.

ExposureUpon initial entry into the peritoneal cavity, careful assessment of all intra-

abdominal organs should be completed whenever possible. Although special careshould certainly be made to carefully examine the liver, gallbladder, bile duct andpancreas, palpation of all intra-abdominal organs frequently identifies additionalpathology or resolves clinical questions that arose on preoperative imaging studies.When examining the gallbladder, palpation should not be overly vigorous to avoidpushing stones down into the common bile duct. Often, a dense fibro-inflamma-tory reaction limits identification of the gallbladder, and an extensive effort may berequired to carefully dissect the omentum, stomach, duodenum, small bowel, andcolon off the gall bladder. Dense adherence of the colon or duodenum to the gall-bladder may actually represent a cholecystcolic or cholecystodudodenal fistula. Dis-section 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. Incases of chronic cholecystitis or biliary colic, the gallbladder may be difficult toidentify due to scarring or an intrahepatic location. In this scenario, the supraduodenalbile duct should be exposed with recognition of the cystic duct followed by anantegrade cholecystectomy.

Decompression of the Gall BladderIn 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’sability to adequately identify the structures in Calot’s triangle. In this setting, de-compression of the gallbladder is necessary. The technique utilized to decompressthe gallbladder is generally dependent upon available instruments but need not becomplex. 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 areaspirated, cultures obtained (mandatory in the setting of cholecystitis and cholangi-tis), and the suture tied to avoid the annoying leak of bile which typically follows.

Choice of Retractor and ExposureAs 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. Thismaneuver allows air to enter that space and permits mobilization of the right liverout of the right upper quadrant. Two rolled up laparotomy sponges may be placedabove the liver to further mobilize it down into the operative field. Regardless ofwhich incision is utilized, a body wall retractor is placed in the right upper quadrantto aid exposure for the operating surgeon. Although this has historically been therole of the medical student, junior housestaff or surgical assistant, we favor the place-ment of a retractor that can be fixed to the operating table to provide steady con-stant retraction. A Buckwalder, Thompson, or Goligher retractor is suitable for thispurpose. An operative towel or sponge is placed over the right colon and smallbowel that is used to pack the viscera inferiorly within the abdominal cavity. Thefirst assistant’s left hand is then used to provide gentle but constant caudal retractionon the hepatoduodenal ligament. Once initial mobilization of the gallbladder hasbegun, a second hand-held retractor is frequently placed over the free edge of theliver to provide exposure to the cystic duct-common bile duct junction.

Antegrade TechniqueWe favor performance of an antegrade cholecystectomy whenever possible. Careful

attention to surgical technique when performing this operation significantly limitsthe potential for biliary injury. The fundus of the gallbladder is typically graspedwith a long Kelly clamp and retracted inferiorly. Scissors or the electrocautery areused to incise the gallbladder serosa 5 mm from the liver edge. Using sharp dissec-tion, a plane is developed on both the anterior and posterior surfaces of the gallbladderallowing it to become separated from the liver. When the gallbladder is not acutelyinflamed this can be accomplished readily using the Metzenbaum scissors; however,when acute inflammation is encountered, electrocautery is preferred. Small surgicalclips can be used to ligate rare arterial branches or small bile ducts that run directlyfrom the liver to the gallbladder. At the level of the gallbladder infundibulum, thecystic artery is identified as it enters the gallbladder, typically on the anterior serosalsurface. This should be carefully dissected circumferentially in order to visualize theterminal arterial branches entering the gallbladder prior to ligation. This maneuveris 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. Careshould be directed to avoid significant manipulation of the gallbladder to preventthe migration of stones into the cystic duct or common bile duct. If stones are feltwithin 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 chole-cystectomy is typically performed only for the “most difficult” gallbladders, a cho-langiogram is typically indicated. A cholangiogram should be performed if thereis any question that a biliary anomaly exists. Chapters 2 and 3 provide a detaileddiscussion on the role of endoscopic retrograde cholangiopancreatography (ERCP)as well as the interpretation of cholangiographic findings. Therefore the discussionhere will be limited to operative technique alone.

Once the infundibulum-cystic duct junction is identified, a clamp or ligature issecured proximally to prevent bile and stones from leaking out of the gallbladder. Asecond ligature is placed more distally around the cystic duct, but not secured. Asmall 2-3 mm transverse incision is made at the level of the infundibulum—cysticduct junction. A variety of cholangiogram catheters are currently in use; the authorprefers the Ponsky cholangiogram catheter that has a 1 cc balloon that can be inflatedto hold the catheter in position. If the surgeon encounters difficulty introducing thecholangiogram catheter, this is typically due to the presence of a stone, a valve or thetortuous course of the cystic duct. Manual palpation can usually exclude the pres-ence of a stone, after which a fine tipped clamp can be carefully inserted into thecystic duct to permit gentle dilatation. Once the catheter is positioned, the distalsuture is tied snug to hold the catheter in place. All retractors are removed and thepatient is rotated slightly to the right for better exposure. For similar reasons asdiscussed in Chapter 12 it is our current practice to perform all cholangiogramsusing C-arm fluoroscopy. If contrast passes rapidly into the duodenum (which oftenoccurs after ERCP and papillotomy), and obscures exposure of the intrahepatic bileducts, a vessel loop can be placed about the hepatoduodenal ligament preventingdistal flow. Once the cholangiogram is performed, the catheter is removed and thecystic duct is divided between the ties.

The gallbladder should always be opened and inspected in the operating roomfor the presence of tumors and aberrant biliary anatomy. Any doubt as to the biliaryanatomy should prompt a cholangiogram if one has not already be obtained.

Mild to moderate hemorrhage from the gallbladder fossa is a common and an-noying problem. In nearly all instances, this can be controlled by use of the electro-cautery in conjunction with sufficient pressure and patience. If a liver laceration hasoccurred, Surgicel or Gelfoam may be required and in very rare instances, directparenchymal suturing is required.

Debate continues as to whether one should routinely drain an open cholecystec-tomy. The experience gained with laparoscopic cholecystectomy, in which drains arerarely placed, would suggest a drain is unnecessary in most cases. However, as notedpreviously, today open cholecystectomies are typically performed for laparoscopicfailures in which case the same “rules” may not apply. Simply stated, the surgeonmust exercise his or her best judgment based on experience and prior teaching. Ifone is more comfortable leaving a drain, one should do so. The drain is typicallyremoved the next day if drainage is less than 50 cc, but should remain if drainage isexcessive or bile stained.

Retrograde TechniqueMuch 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 cholecystec-tomy, historically performed less often, has now become commonplace in the era oflaparoscopic cholecystectomy (which is performed retrograde). A large Kelly clampis initially placed on the fundus and/or body of the gallbladder to provide superiorand lateral retraction. The thin layer of peritoneum covering the hepatoduodenalligament is incised at the level of the infundibulum of the gallbladder anteriorlytowards the cystic plate (and the base of the quadrate lobe (Segment IV)), and pos-teriorly towards the Segment V and the caudate process. Carefully teasing the peri-toneal tissue off of the infundibulum with sharp or blunt dissection (using a Kitneror peanut) exposes the cystic duct and allows development of Calot’s triangle. Thecystic 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 tothe cystic duct and is usually readily identified. Once again, this artery should befollowed to its terminal branches on the gallbladder prior to ligation. At this pointthe infundibulum-cystic duct junction is typically well exposed, and the cystic ductcan be doubly ligated and divided. If a cholangiogram is to be performed, the sametechnique as described above should be used.

After the cystic duct and cystic artery are divided, superior and lateral retractionon the gallbladder is applied, and the serosa of the gallbladder is excised in a retro-grade fashion. Occasionally, a posterior cystic artery lying behind and medial to themain cystic artery may be encountered. This should be carefully inspected to seethat 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 directlyfrom the liver and enter the gallbladder. As when performing a laparoscopiccholycystectomy, these are typically easily handled with the use of the electrocau-tery. Upon removal of the gallbladder, the surgeon is reminded once again to inspectit carefully for tumors and normal anatomy. Issues relating to whether a drain shouldbe left have been discussed previously.

ClosureIf 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 perma-nent or semi-permanent suture, and typically close with a #1 double loop PDSsuture. If a right subcostal incision is used, the question always arises as to whetherone 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 beguided by judgment and experience. This author favors a two-layer closure usingtwo #1 double looped PDS sutures. The skin can be closed with skin staples or asubcuticular suture.

CHAPTER 12

Laparoscopic Cholecystectomyand the Laparoscopic Managementof Common Bile Duct Stones

Fredrick Brody

IntroductionIn less than a decade, laparoscopy has significantly effected general surgical pro-

cedures for a variety of pathologic indications. Approximately 85% of all cholecys-tectomies are now completed laparoscopically. This translates into improved cosmesis,less postoperative pain, and faster recovery times. The price for these advantages isan increased rate of biliary duct injuries. This devastating injury is avoided by adher-ing to a systematic approach to laparoscopic cholecystectomy regardless of patientor disease acuity.

IndicationsPatients with cholecystitis present with a broad range of symptoms depending

on the severity of their disease. The majority of patients present with right upperquadrant or epigastric abdominal pain with radiation to the right flank associatedwith right upper quadrant tenderness on physical examination. Ultrasound findingsof gallbladder wall thickness greater than 4 mm, echogenic gallbladder contents,and pericholecystic fluid collections are consistent with acute cholecystitis. Afterconfirming the diagnosis, the patient is kept NPO and started on intravenous fluidsand a second generation Cephalosporin. Though somewhat controversial, earlyoperative intervention is generally indicated within the first 24-72 hours of admis-sion. The majority of patients are candidates for a laparoscopic cholecystectomy.Previous absolute contraindications including pregnancy, obesity, acute cholecysti-tis, bleeding disorders, and prior abdominal surgery are all now relativecontraindications.

Laparoscopic CholecystectomyAfter 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 thepatient voids prior to induction. Abdominal access is performed through the umbi-licus. An open technique with a Hasson trocar as opposed to a closed techniquewith a Veress needle decreases major complications while enabling high flow ratesimmediately after insertion. Three subsequent ports are placed after exposing thegallbladder. The epigastric port is placed 2 cm below the xiphoid process correlating


157Laparoscopic Cholecystectomy

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with the level of the cystic duct and gallbladder infundibular junction. The patientis then placed at 40˚ of reverse Trendelenburg and rotated 15˚ to the left. This allowsthe colon and small intestine to fall into the pelvis while elevating and rotating theplane of dissection perpendicular to the surgeon (Fig. 12.1).

The final two ports are placed in the midclavicular and anterior axillary linesrespectively. These ports should be at least 2 cm below the costal margin. If theseports are misplaced, they should err laterally and inferiorly. Medially displaced trocarsinterfere with laparoscopic visualization while superiorly displaced trocars inhibitlateral and inferior retraction of the gallbladder infundibulum.

An inline grasper (Karl Storz, Charlton, MA) is introduced through the anterioraxillary trocar and the gallbladder fundus is grasped and elevated over the liver edge.Blunt stripping of multiple adhesions extending from the colon, duodenum, orpyloric region may be required. Cautery is never used to release these adhesions ascurrent can easily conduct to these structures. Delayed duodenal perforations twoto three days postoperatively are well documented in the literature following ill advisedcautery at this juncture of this procedure. Another inline grasper is introduced throughthe midclavicular port and the gallbladder infundibulum is grasped and retractedlaterally and posteriorly towards the spine. This simple maneuver places the cysticduct at right angles to the common bile duct and ensures that the cystic duct is outof alignment with the common bile duct (Fig. 12.2).

Prior to dissecting Calot’s triangle, a preliminary examination through the over-lying peritoneum is performed. Several structures including the gallbladder infundibu-lum, cystic duct, cystic artery, and Calot’s node, are identified by the surgeon andfirst assistant. Identification by both surgeons at this stage enables critical commu-nication throughout the entire procedure. By identifying Calot’s node and theinfundibular-cystic duct junction, the inferior aspect of the biliary dissection isascertained. A safe dissection revolves around the infundibular-cystic duct junctionat the level of Calot’s node.

Dissection begins with a Maryland dissector (Karl Storz, Charlton, MA) alongthe lateral aspect of the gallbladder infundibulum. The peritoneum overlying thisregion is stripped in a downward fashion along the course of the cystic duct. As thisperitoneum is gradually stripped, the infundibular-cystic duct junction becomesapparent. The dissection proceeds medially along the anterior surface of the cysticduct. Calot’s node is gently pushed medially exposing the entire anterior surface ofthe cystic duct. Minimal manipulation of Calot’s node avoids persistent and annoy-ing bleeding.

The posterior cystic duct surface is exposed by retracting the gallbladderinfundibulum across its longitudinal access towards Segment IV of the liver usingthe midclavicular inline grasper. This maneuver exposes the posterior peritoneumoverlying the cystic duct and gallbladder infundibulum. Using a Maryland dissec-tor or hook cautery, the posterior peritoneum is carefully stripped. This dissectionexposes the posterior surface of the cystic duct and gradually “lengthens” the ductby several millimeters. The infundibulum is then returned to its original lateraland posterior position.

The concave surface of the Maryland dissector is then positioned along the medialaspect of the cystic duct. The tips of the instrument should now point towardsSegment 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 cholecystec-tomy.

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


12After achieving the anterior-posterior window along the cystic duct, the perito-

neum adherent to the medial aspect of the cystic duct is divided with the hookcautery. This is performed in a cephalad direction on top of the cystic duct towardsthe infundibular-cystic duct junction. The peritoneum along the lateral portion ofthe cystic artery is released simultaneously during this maneuver. By dissecting theperitoneal elbow of the cystic artery, the artery is released and straightened facilitat-ing clip application (Fig. 12.3). The crotch of the infundibular-cyst duct junction isdeveloped by gently sliding the hook cautery beneath each peritoneal layer and lift-ing towards the anterior abdominal wall while applying short bursts of current.After several peritoneal layers are divided, the heel of the hook cautery is placedagainst the medial side of the cystic duct without current. Gentle pressure with theheel against the duct opens the anterior-posterior window and helps expose theremaining 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 arterydissection is completed with the hook cautery and Maryland dissector. The dissectionremains at or above the level of Calot’s node. The peritoneum overlying the cysticartery is divided and the Maryland dissector is used to gently encircle the cysticartery. The nuzzling technique with the dissector tips is utilized again. When the

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


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cystic artery is approached at or above the level of Calot’s node, posterior branchesof the cystic artery may not be apparent. It is safer to assume that posterior branchesof the cystic artery are present until completing further dissection.

The cystic duct and artery are now separated by a clear window without anyintervening tissue (Fig. 12.4). This window was previously described by Soper andStrasberg as the “critical view.” With the critical view completed, one clip is placedacross the cystic duct-infundibular junction. A 3 mm ductotomy is made 4 mmfrom this clip. The cystic duct is milked proximally with a Maryland dissector toextrude any stones or debris through the ductotomy. The inline grasper is thenremoved from the midclavicular port and reinserted through the epigastric port.The infundibulum is regrasped and retracted laterally so the cystic duct is alignedwith the shaft of the midclavicular trocar.

An Olsen clamp with a Ponsky cholangiocatheter is introduced through themidclavicular port. The clamp and infundibulum are aligned to ensure easy passageof the cholangiocatheter through the ductotomy. Utilizing dynamic fluoroscopy, ascout film is obtained localizing the tip of the cholangiocatheter. Initially, only 2-3 ccof 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 isshifted caudally a few centimeters and the course of the distal common bile duct isidentified by injecting another 5 cc of contrast. Contrast should flow easily throughthe distal common bile duct with imaging of the duodenum. The fluoroscopy arm

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


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is shifted cephalad and another 5 cc of contrast is injected to visualize the commonhepatic duct and the proximal hepatic radicals. Filling of the proximal radicals isenhanced by placing the laparoscope on top of the second portion of the duodenumand applying gentle pressure towards the spine while injecting contrast. This ma-neuver compresses the distal common bile duct and forces contrast proximal intothe hepatic radicals. It is critical to image the hepatic radicals of Segments V and VIto ensure the absence of any accessory ducts communicating with the gallbladder. Ifthe gallbladder is demonstrated during fluoroscopy, a clip is needed for the duct drain-ing directly into the gallbladder. If the cholangiogram is within normal limits, theclamp 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 alongthe gallbladder and liver confluence. The infundibulum is lifted towards the ante-rior abdominal wall creating tension on the peritoneal bands within the gallbladderfossa. These bands are isolated individually with the hook cautery as opposed to thespatula. Continuous cautery in a horizontal motion with the spatula risks injury toa torturous right hepatic duct or right hepatic artery. Individual dissection of theseperitoneal bands with a hook cautery may prolong the operative procedure, but ithelps avoid inadvertent injury to these particular structures. Similarly, delicate dis-section with the hook identifies any posterior cystic artery branches requiringhemoclips. The gallbladder is removed through the umbilicus and the three portsare removed under direct vision to verify hemostasis. It is our practice to first placethe gallbladder in a specimen bag within the abdomen prior to removal.

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


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Laparoscopic Common Bile Duct ExplorationIf the cholangiogram identifies gallstones greater than 3 mm in diameter, their

location determines the next step. If the stones are located in the common hepaticduct or above the cystic duct-common bile duct junction, a choledochotomy isperformed. Another 5 mm port is placed in the right upper quadrant to completethis dissection. The cystic duct is traced down to its junction with the common bileduct. The anterior surface of the common bile duct is dissected while avoiding injuryto the 3 and 9 o’clock vessels. Using microscissors, a 1 cm longitudinalcholedochotomy is made 1 cm below the junction of the cystic duct and commonbile 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 towardsthe stone. Continuous normal saline irrigation for the choledochoscope and a sec-ond video system are required. With the stone in view, a wire basket is advancedbeyond the stone (Fig. 12.5). The basket is opened and slowly withdrawn towardsthe stone. When the stone eventually falls between the wires of the basket, the wiresare closed and the entire choledochoscope is removed keeping the stone under di-rect vision at all times. This procedure is repeated until the duct is cleared of allstones and debris greater than 3 mm. A cholangiogram is obtained by injectingcontrast through the working channel of the choledochoscope to ensure completestone extraction. The choledochoscope is removed and a 14F T-tube catheter isplaced through the choledochotomy. Ideally, the draining arm of the T-tube exitsthrough the cystic duct making closure of the choledochotomy easier. Interrupted4-0 vicryl sutures are used to close the ductotomy. A completion cholangiogram isobtained through the T-tube to verify stone extraction and a water tight closure ofthe ductotomy. Finally, a 10 mm Jackson Pratt drain is placed.

If the initial cholangiogram identifies stones within the cystic duct or below thejunction of the cystic duct and common bile duct, a transcystic exploration is per-formed (Fig. 12.6). Approximately 90% of choledocholithiasis are found below thecystic duct junction in the distal common bile duct. The cystic duct may need dila-tation with sequential Fogarty catheters to accommodate the choledochoscope. Awell lubricated 3.3 mm choledochoscope is introduced through the cystic duct andadvanced to the offending stone. Baskets are used for retrieval and a completioncholangiogram 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 aredischarged from the recovery room. Patients undergoing duct explorations areadmitted and advanced to a regular diet. Patients with T-tube catheters undergo acholangiogram on postoperative day 21. If the cholangiogram is normal the T-tubeis removed. Following a transcystic exploration, the Jackson Pratt 10 mm drain isremoved on postoperative day 1 if the patient is tolerating regular food and there isno 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 belowthe cystic duct junction. Wire baskets are used to extract the stones.

Selected Reading1. Berci G, Cuschieri. Bile Ducts and Bile Duct Stones 1997 Philadelphia PA: W.B.

Saunders Company.2. Hunter JG. Avoidance of the bile duct injury during laparoscopic cholecystec-

tomy. Am J Surg 1991; 162:71-76.3. 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 andbaskets are passed for stone extraction.

4. Strasberg S, Hertl M, Soper NJ. An analysis of the problem of biliary injury duringlaparoscopic cholecystectomy. J Am Coll Surg 1995; 180:101-124.

5. Trus TL, Hunter JG. Laparoscopic bile duct techniques. 1995; 2 (2):118-127.

CHAPTER 1CHAPTER 13

Surgical Techniques for Completionof a Bilioenteric Bypass

Pierre F. Saldinger, Leslie H. Blumgart

Scope of the ProblemSurgical 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 aremost commonly seen after injury to the common hepatic duct during cholecystec-tomy. A biliodigestive anastomosis of a jejunal Roux-en-Y loop to normal extrahe-patic 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 hasto perform a hepaticojejunostomy to one or several intrahepatic bile ducts whichcan present a technical challenge. A biliodigestive bypass to an intrahepatic bile ductwill provide excellent biliary decompression and palliation in the case of anunresectable bile duct cancer. Lastly, a biliodigestive anastomosis can be of use incomplex stone disease.

This chapter will outline the anatomical aspects, technical details, and generalconsiderations with respect to performing a biliodigestive anastomosis.

AnatomyIt is essential to be cognizant of the anatomical details and variants of the extra-

and intrahepatic biliary tree as well as adjacent hepatic arterial and portal venousstructures. The normal biliary and vascular anatomy is depicted in Figures 13.1 and13.2. The important ductal anomalies are nearly all related to the manner ofconfluence 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 acquaintedwith their range and should always expect the unusual.

The most common variation is an abnormal junction between the cystic ductand the main extrahepatic biliary channel. The cystic duct may join the commonhepatic duct high, almost at the hilus of the liver (Fig. 13.3). The right hepatic ductas such may be absent and the major ducts draining the anterior and posterior sec-tors of the right liver may join the left hepatic duct separately to form the commonhepatic duct. In some cases, the right anterior or right posterior sectoral duct mayrun a long extrahepatic course to join the common duct, and the cystic duct maydrain directly into such a duct. However, while these variations are common, thereis 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 ductalways has an extrahepatic course (Fig. 13.4), the length of which reflects the width



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Fig. 13.1. Normal extra- and intrahepatic segmental biliary anatomy. Reprintedwith 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).

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

167Surgical Techniques for Completion of a Bilioenteric Bypass

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of the quadrate lobe at the base of the liver. If the quadrate lobe has a broad longbase, then the left hepatic duct has a longer rather transverse course, whereas if thequadrate lobe has a narrower more pyramidal base, the left hepatic duct has a shortersomewhat more oblique course. The duct traverses to the left together with the leftbranch 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).

Fig. 13.3. Cystic duct and gallbladder anomolies. A, Bilobed gallbladder; B, septum ofthe 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).


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The left duct and left branch of the portal vein are joined by the left branch ofthe hepatic artery, enter the umbilical fissure of the liver within which division ofvessels to and confluence of ducts from the left lobe (Segments II and III) and thequadrate lobe (Segment IV) occur. The left hepatic duct receives major tributariesfrom each of these segments which converge in the umbilical fissure dorsocranial tothe left portal vein. Hepatic ductal tributaries from the quadrate lobe (Segment IV)and hepatic arterial and portal venous branches supplying it re-curve to SegmentsIVA and IVB (Fig. 13.6).

The ligamentum teres, in the lower edge of the falciform ligament, traverses theumbilical fissure of the liver which is usually, but not always, bridged in its lower-most 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 anteriorlyand caudally, giving off branches to Segments II and III of the left lobe and toSegment IV (Fig. 13.6).

The most common vascular anomaly is an accessory or replaced right hepaticartery originating from the superior mesenteric artery. This anomaly is present inabout 20-25% of patients. The right hepatic artery runs posterolateral to the rightof the common bile duct in close proximity to the cystic duct. The artery is prone toinjury during cholecystectomy particularly if injury to the common bile duct occurs.

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 WHJarnigan (Eds.) W.B. Saunders, London, UK (2000).


13Its presence has to be ascertained prior to any isolation of the common bile duct inorder to avoid injury.

The techniques to be described rely upon a firm understanding of those ana-tomical features. Anastomoses are usually carried out either to the common, majorright or left hepatic duct, or to the Segment III duct of the left lobe.

General ConsiderationsIt 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 ofteneasier to perform an anastomosis on a bile duct that is dilated secondary to obstruc-tion. However, preoperative biliary drainage is advised in patients with sepsis fromcholangitis in order to stabilize the patient prior to surgery.

It is of utmost importance to obtain as much information as possible on both thelevel and etiology of biliary obstruction prior to surgery. With the advent of highquality magnetic resonance cholangiopancreatography (MRCP), there is limited needfor preoperative percutaneous or endoscopic cholangiography to determine the level

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).


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of biliary obstruction. This holds true for both benign and malignant biliary stric-tures. 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 liverresection.

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 theportal venous branch; D, ligamentum teres. Reprinted with permission from: Surgeryof 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. 13.7. An MRCP image demonstrating a cholangiocarcinoma. A large tumor is seenat the confluence of the right and left hepatic ducts. The gallbladder is distended whichsuggests origin or spread to the mid-bile duct causing cystic duct occulusion.

IncisionsAdequate 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 lowhepaticojejunostomy. While being less morbid than a bilateral subcostal incision, itdoes not allow appropriate access to the hilus and should not be used if a hilardissection is anticipated.

If in doubt, a right subcostal incision is a better choice as it can be extendedupwards to the xyphoid or across the midline as a bilateral subcostal incision, whichallows excellent exposure of the extrahepatic bile duct and liver. If a bilateral subcos-tal incision is employed, the use of a broad-bladed retractor fixed to an overheadsupport elevating the costal margin is valuable.

In cases of right lobar atrophy with posterior rotation of the hilar structures, itmight be necessary to extend a bilateral subcostal incision into the right chest toprovide safe access to the hilus.


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Abdominal ExplorationUpon 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 theligamentum teres and freeing of the falciform ligament from the abdominal wallback to the diaphragm. If previous surgery has been carried out, adhesions are care-fully 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 work-ing medially so as to expose the area of the hilus. The duodenum will frequently befound adherent to the base of the liver; the colon may be densely adherent to thescar 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 orunresectable 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 Roux-

en-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 makeits blind end subcutaneous (Fig. 13.8). If this technique is selected, the Roux loopmust be made long enough to allow the blind end of the jejunum to reach theabdominal wall without tension. This technique will allow percutaneous access tothe loop which may be necessary for adjuvant biliary tree intervention. When this isdone, a silastic tube is left across the anastomosis and brought out through the loopin order to provide initial access. It should be emphasized, however, that in the usualcircumstance, where an anastomosis is obtained between the mucosa of the bileduct and the jejunum, there is usually no need for transanastomotic tubes and noevidence that intubation assists long-term patency. The authors now advocate a simplesutured anastomosis in the average case. Indeed, transanastomotic stents carry theirown complications and these are thus avoided.

Basic Anastomotic TechniqueIt is valuable to have an established routine for biliary-enteric anastomosis. Al-

though some anastomoses are low and easily performed, a regular technique thatfacilitates the completion of the anastomosis, even in cases of high difficult stric-tures, should be developed.

In brief, after the bile duct has been encircled and dilated, a Roux-en-Y loop ofjejunum 70 cm in length is prepared and brought up (preferably in a retrocolicfashion) for completion of an end-to-side anastomosis. The end-to-side anastomosisis 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 theposterior row. If more than one ductal orifice is visible at the hilus, these are bestapproximated with a row of sutures so that they can be treated as a single duct foranastomotic purposes (Fig. 13.9). If this cannot be done, then the entire anteriorrow to all exposed ducts is inserted first so that the separated orifices can be treated


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as if single. Attempts to complete one anastomosis and then another are difficult,and sometimes impossible. These sutures are serially introduced starting from theleft and working to the right (Fig. 13.10). We recommend using a mono- orpolyfilament 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 alsofacilitates precise placement of the posterior layer (Fig. 13.11), which is likewiseplaced 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 TechniquesIn some cases, where the bile duct is large and easily exposed, a simpler tech-

nique using a running suture can be employed. This technique is less time consum-ing than the above and can be used in most instances where the bile duct isanastomosed just proximal to the duodenum such as after a Whipplepancreaticoduodenectomy.

Choledochojejunostomy or HepaticojejunostomyThis operation is usually performed in an end-to-side fashion; however, a side-

to-side hepaticojejunostomy can be performed using techniques similar to thosedescribed for choledochoduodenostomy (see below).

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


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

TechniqueThe 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 ductis dissected well above the obstruction, and care is taken to avoid an accessory orreplaced right hepatic artery, if present. The duct is divided and the lower end of thecommon bile duct is closed with a running suture. The exposed common bile ductis now sutured into the jejunum using either technique described above.

Approaches to the Left DuctApproaches 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 casesecondary 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 systemfrom the undersurface of the quadrate lobe (Hepp – Couinaud approach).


13Fig. 13.10. Placement of the posterior row for hepaticojejunostomy. Reprinted withpermission from: Surgery of the Liver and Biliary Tract (3rd Edition), Blumgart LH, FongY and WH Jarnigan (Eds.) W.B. Saunders, London, UK (2000).

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

Hepp–Couinaud ApproachThis technique allows performance of an anastomosis to the extrahepatic left

bile duct in cases of high benign strictures, provided there is an intact communica-tion between the right and the left liver.

The ligamentum teres is transected and a firm tie is placed so that it may beelevated and used as a retractor. The liver is elevated to display its undersurface. Thebridge 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’scapsule 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. Reprintedwith 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).

Fig. 13.12. Cutting of the bridge of tissue connecting the left lobe of the liver to thequadrate 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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left portal triad (Figs. 13.13A, 13.13B). This maneuver allows exposure of the extra-hepatic left duct.

Stay sutures are placed in the left hepatic duct which is then incised longitudi-nally. A Roux-en-Y loop of jejunum is brought up. Side-to-side anastomosis is thenperformed by the technique illustrated previously.

Ligamentum Teres (Round Ligament) Segment III ApproachWhile 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 ductbeneath the quadrate lobe. This may be due to dense adhesions, bleeding, or a large

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


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and overhanging quadrate lobe. On occasion, the extrahepatic length of the lefthepatic duct may be relatively short and oblique, making the approach difficult. Inthe setting of a carcinoma of the bile duct, a tumor extending into the left duct fromthe confluence area may preclude the use of the main left duct. In any event, pallia-tive 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 theumbilical fissure.

It is important to note that unilateral drainage of the left hepatic duct, in thepresence of a tumor which completely excludes the right liver and right hepaticducts from the anastomosis, is effective in the relief of jaundice provided the leftlobe of the liver is not atrophic.

Fig. 13.13B. Lowering of the hilar plate. Reprinted with permission from: Surgery ofthe 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 ligamentum teres is elevated and the bridge of liver tissue joining the quad-rate lobe to the left liver is divided as described above (Figs. 13.13A, 13.13B). Theliver to the left of the ligamentum teres is split and a small segment of liver tissue isremoved thus exposing the duct to Segment III (Fig. 13.14). A side-to-side anasto-mosis to a loop of jejunum is then carried out by the techniques described above

CholedochoduodenostomyA choledochoduodenostomy is infrequently used for the relief of biliary tract

obstruction in malignant disease, and much more frequently for the patient withbiliary obstruction due to gallstones. In the latter case, side-to-sidecholedochoduodenostomy is preferable.

A choledochoduodenostomy is usually performed at the conclusion of a com-mon bile duct exploration in lieu of T-tube placement.

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


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IndicationsThe single most important condition allowing the performance of a

choledochoduodenostomy is an enlarged common bile duct. A duct measuring lessthan 12 mm in diameter is an absolute contraindication. The following are situa-tions which are amenable to a choledochoduodenostomy. Contraindications includeduodenal ulcer and acute pancreatitis.

1. Retained or recurrent stones in the common bile duct2. Cholangitis3. Ampullary stenosis4. Primary common duct stones calculi or stasis bile5. Tubular stricture of the transpancreatic portion of the choledochus usu-

ally due to chronic pancreatitis6. A combination of these above7. Low iatrogenic stricture8. Malignant obstruction in the periampullary area

TechniqueTwo 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 develop-

ment of a standard technique for the rapid construction of a stoma that allows freeentry and egress from the common bile duct.

While attempts are made to remove stones and particulate matter from the com-mon bile duct, impacted stones at the distal common bile duct that are not easilyretrieved, and stones in the hepatic duct are not pursued vigorously prior to theanastomosis.

The duodenum is fully mobilized by a Kocher maneuver and thus approximatedtoward the common bile duct. A duodenotomy is performed perpendicular to thecholedochotomy. The anastomosis is performed either in an interrupted fashion oras a continuous suture. The interrupted technique is illustrated (Figs. 13.15-13.17).


13Fig. 13.15. Lines of incision. Choledochoduodenostomy performed using an inter-rupted technique. Reprinted with permission from: Surgery of the Liver and BiliaryTract (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 theLiver and Biliary Tract (3rd Edition), Blumgart LH, Fong Y and WH Jarnigan (Eds.) W.B.Saunders, London, UK (2000).

CHAPTER 1CHAPTER 14

Hilar Cholangiocarcinoma: SurgicalApproach and Outcome

Ronald S. Chamberlain, Leslie H. BlumgartCholangiocarcinoma is an uncommon malignancy with an incidence of

1.2/100,000. This neoplasm accounts for less than 2% of all cancer diagnoses withequal sex distribution. The incidence of cholangiocarcinoma increases with age, withtwo-thirds of all cases occurring in patients over 65. Jaundice is the presenting com-plaint in 90-98% of patients with cholangiocarcinoma. Additional complaints includeweight loss (29%), abdominal pain (20%), and occasionally fever (9%). Jaundicemay be absent if the tumor is intrahepatic or involves only the right or left hepaticduct. In these cases, the resultant lobar obstruction leads to ipsilateral hepatic lobaratrophy whose only manifestation may be an elevated alkaline phosphatase. Despitea high incidence of bactobilia in patients with both complete and incomplete ob-struction due to cholangiocarcinoma, cholangitis is a rare presentation. However, atwo-fold increase in postoperative infectious complications has been reported inassociation with preoperative instrumentation and stenting.

Cholangiocarcinoma can arise anywhere along the biliary tree from the ampullaof 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 bifurca-tion into right and left hepatic ducts. Middle third tumors (17%) are located fromthe upper border of the duodenum and extending to the cystic duct junction. Lowerthird or distal bile duct tumors (18-27%) arise between the ampulla of Vater and theupper border of the duodenum. Intrahepatic cholangiocarcinoma (IHC) are rareneoplasms accounting for 6-10% of all cholangiocarcinoma and are managed simi-larly to other hepatic neoplasms. This chapter will focus on the surgical manage-ment of upper third or hilar cholangiocarcinoma. Chapter 8 details the surgicalapproach to distal bile duct tumors, namely pancreaticoduodenectomy.

Etiology and PathologyThe etiology of cholangiocarcinoma is unknown; however conditions resulting

in acute or chronic biliary epithelial injury may predispose its development. Theseconditions include primary sclerosing cholangitis in which occult cholangiocarcinomahas 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 ofmalignant transformation. Oriental cholangiohepatitis, a rare form of pyogenic cho-langitis, also has a 5-12% lifetime incidence of cholangiocarcinoma. Additional riskfactors include biliary tract infection with parasites (e.g., Clonorchis sinensis and



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Opisthorchis viverrin), chronic typhoid carrier states, and exposure to various chemi-cal carcinogens, including asbestos, digoxin, and nitrosamines.

Cholangiocarcinomas are generally well-differentiated slow-growing adenocar-cinomas which may be mucin producing. Hematogenous spread is rare, but nodalmetastases occur in up to one-third of all cases. Extensive subepithelial tumor spreadbeyond the gross margin is common, and may extend 1-2 centimeters in each direc-tion. Cholangiocarcinoma are classified as papillary, nodular-sclerosing, or diffusetype based upon its macroscopic appearance. The papillary variant is least commonbut carries the most favorable prognosis. Papillary tumors commonly involve thedistal bile duct and grow as intraluminal soft, polypoid tumors. The nodular variantoccurs most commonly in the upper and mid-duct and presents as a fibrotic masswith intraductal projections. The sclerosing variant is most commonly seen in hilartumors, and appears as annular thickening of the duct wall with both longitudinaland radial tumor infiltration. The diffuse type, which involves the entire extrahe-patic bile duct, is both rare and universally fatal.

Fig. 14.1. Anatomic distribution of cholangiocarcinoma based on site-specificpercentages.

185Hilar Cholangiocarcinoma: Surgical Approach and Outcome

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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 forcurative 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

Preoperative EvaluationThe 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 beenutilized in the work-up of these patients, it is our practice to perform a combinationof duplex ultrasonography and magnetic resonance cholangiopancreatography(MRCP) which we believe provides more comprehensive and relevant informationthan any other combination of studies. Duplex ultrasonography is noninvasive andcan identify the site of biliary obstruction and the presence or absence of portalvenous involvement with a high degree of sensitivity and specificity (Fig. 14.2). Theefficacy of MRCP as a noninvasive means of acquiring reliable and precise informa-tion about the anatomy of both the intra- and extrahepatic biliary tree, and the levelof tumor involvement has been well documented, and has all but replaced the needfor 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 theyidentify a malignancy (sensitivity < 50%), and excessive reliance upon negative resultsmay miss the opportunity to resect an early lesion. Whereas the vast majority ofextrahepatic strictures are the result of cholangiocarcinoma, histologic diagnosis isnot mandatory prior to exploration. In the absence of clear evidence of unresectability,all suspected cholangiocarcinoma should be considered for resection (Table 14.1).


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StagingThe two most commonly utilized staging systems for cholangiocarcinoma are

the American Joint Committee on Cancer (AJCC) TNM system and the modifiedBismuth-Corlette classification for HCCA (Tables 14.2 and 14.3). A new proposedT staging which takes into consideration both vascular involvement by local tumorextension, 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 nodalor distant metastases, and overall survival.

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


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

Surgical Resection for Hilar Cholangiocarcinoma

Treatment ResultsIrrespective 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 TumorsTumors of the distal bile duct require either a pancreaticoduodenectomy, or less

commonly, a local bile duct excision. Technical details related to these tumors areaddressed in Chapter 8. Very few surgical series of distal bile cancers have beenreported. Zerbi et al reported on 27 patients with distal bile duct cancer who under-went pancreaticoduodenectomy. Operative mortality was 3.7%, and morbidity was44%. All patients had negative histologic margins. The vast majority of patientswere stage IVA (81.5%, N = 22) due to pancreatic invasion, and 48% of patientshad lymph node metastases. Only 7.4% (N = 2) of patients had tumors limited tothe bile duct without either nodal, lymphatic or neural invasion identified. Despitethe addition of adjuvant therapy in 48% of patients, the authors report a meansurvival of 22 months and actuarial 3- and 5-year survival of 20 and 13% respec-tively. Fong et al reported on 104 patients with distal bile duct cancer of which 45patients were resected (43%). Thirty-nine patients underwent apancreaticoduodenectomy, 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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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 andare generally indistinguishable from reports on survival following resection for pan-creatic adenocarcinoma and periampullary neoplasms.

Hilar Cholangiocarcinoma (HCCA)Table 14.5 details 11 surgical series of HCCA with 10 or more patients pub-

lished since 1990. Nearly all groups, with one exception, are now performing liverresection for HCCA in 50-100% of cases. Using this approach, a negative histologicmargin was achieved in more than 56% of cases and at a minimum was associatedwith a trend towards increased survival in all studies. The operative mortality rate inthese aggressive series are zero to 14%. Madariaga et al performed liver resection in100% 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

Fig. 14.3B. Percutaneous transhepatic cholangiogram of the same tumor dem-onstrating hilar obstruction and delineation of the intrahepatic anatomy andextrahepatic anatomy.


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Table 14.2. AJCC staging systems for cholangiocarcinoma

Stage 0 Tis N0 M0Stage I T1 N0 M0Stage II T2 N0 M0Stage III T1,2 N1,2 M0Stage IVA T3 Any M0Stage IVB Any Any M1Tis - Carcinoma in situT1 - Tumor invades subepithelial connective tissue (T1a) or fibromuscular

layer (T1b)T2 - Tumor invades perifibromuscular connective tissueT3 - Tumor invades adjacent structures: liver, pancreas, duodenum, stomach,

gallbladder, colon or stomach.N0– No lymph node metastasesN1 - Metastasis in the cystic duct, pericholedochal and/or hilar lymph nodesN2 - Metastasis in the peripancreatic (head only), periduodenal, periportal,

celiac, superior mesenteric, and/or posterior pancreaticoduodenallymph nodes.

M0 - No distant metastasesM1 - Distant Metastases

Table 14.3. Modified Bismuth–Corlette classification for hilarcholangiocarcinoma

Type I Below the confluenceType II Confined to confluenceType IIIa Extension into right hepatic duct

IIIb Extension into left hepatic ductType IV Extension into right and left hepatic ducts

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

Table 14.4. Proposed modified T stage criteria for hilar cholangiocarcinoma

T1 Tumor confined to the confluence and/or right or left hepatic ductwithout portal vein involvement or liver atrophy

T2 Tumor confined to the confluence and/or right or left hepatic duct withipsilateral liver atrophy. No portal vein involvement demonstrated.

T3 Tumor confined to the confluence and/or right or left hepatic duct withipsilateral portal vein branch involvement with/without associatedipsilateral lobar liver atrophy. No main portal vein involvement(occlusion, invasion, or encasement)

T4 Any of the following:i) Tumor involving both right and left hepatic ducts up to secondarybiliary radicals bilaterallyii) Main portal vein encasement

190H

eptobiliary Surgery

14

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

Author Study Resected Liver Histologic 3-year Operativeyears N = resection margin survival mortality

% status (%) (%) (after liverpositive Negative Margin + Margin - resection)

Hadjis, 8 27 60% 44% 56% 17.5 mo* 22 mo* 7.4%1990Bismuth, 30 23 57% 61% 39% 12% 50% 0%1992Baer, 1992 4 21 43% 33% 67% 21 mo * 40 mo* 5%Suigura 18 85 100% 43% 57% 11% 41% 8.4%1994Pichlmayr, 18 125 76% 27% 73% 12.2% 40.1% 10.5%1996Nakeeb, 23 109 7% 74% 26% 9%** 19%** 6.7%1996Madariaga, 14 28 100% 50% 50% 18% 40% 14%1998Figueras, 8 16 50% 37% 63% N/A 43% 0%1998Nagino, 19 138 90% 22% 78% N/A 42.7% 5.6%1998Miyasaki, 14 76 86% 25% 75% 8% 40% 4.6%1998Burke, 1998 6 30 73% 17% 83% 0%** 56%** 6%

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


14

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

Liver TransplantationThe role of orthotopic liver transplantation (OLT) for cholangiocarcinoma

remains very controversial. Although OLT has been performed for both resectableand unresectable HCCA, the high incidence of lymph node metastases associatedwith this disease has limited adoption of this approach. Pichlmayr et al have reporteda series of 249 patients with HCCA in which 125 patients underwent resection, and25 patients underwent OLT. Resectional therapy yielded equivalent or superior overall5-year survival (27.1% versus 17.1%) at all stages of disease. Klempnauer et al havesubsequently reported on four (12.5%) 5-year survivors out of a total of 32 patientsthat underwent OLT for HCCA. During this same time period 151 HCCA patientswere resected with curative intent, and 28 patients (18.5%) survived 5 years ormore. These results led the authors to conclude that radical resection offers the bestpossibility of prolonged survival with a good quality of life. Although additionalreports of OLT for HCCA have appeared, OLT should not be considered a standardform of therapy for patients with HCCA.

Palliative and Adjuvant Treatment for CholangiocarcinomaIn the setting of advanced local disease or obvious nodal or distant metastases,

therapeutic intervention should be directed towards the relief of biliary obstructionand its associated symptoms. Biliary decompression for jaundice in the absence ofsymptoms is not justified. Biliary decompression is indicated for relief of symptoms,facilitation of biliary access for investigational palliative therapies, and as a means toallow recovery of hepatic parenchymal function in patients who might be candi-dates for chemotherapeutic protocols. Percutaneous or endoscopic biliary stent place-ment is the preferred method of decompression if unresectability is determined priorto surgery. If unresectability or the presence of metastatic disease is identified atlaparotomy, palliative options include postoperative placement of transhepatic orendoscopic stents, surgically placed transhepatic stents, or a surgical bilioentericbypass. When deciding among these options, the general physical condition and ageof the patient, in addition to projected short life expectancy must be considered.Procedure related morbidity, including the need for prolonged or frequent hospitalor physician visits, limits the quality of remaining life and consumes valuable time.

In expert hands, percutaneous biliary drainage can be placed in almost all patientsand circumstances. In many instances multiple stents may be required. We prefermetallic wall stents to plastic stents for long-term palliative relief of malignant bil-iary obstruction. These stents are completely internal, require no catheter care, andhave a longer duration of patency than plastic stents (6-8 months). In the absence ofinfectious symptomatology, the entire liver need not be drained, as it is has beenshown that only 30% of the functioning hepatic mass needs to be decompressed forrelief of jaundice.

Intrahepatic Surgical Bilioenteric BypassIf patients are identified at laparotomy to be unresectable, we favor performing

an intrahepatic bilioenteric bypass to the Segment III hepatic duct. This procedure


14

provides excellent palliation, eliminates the need for frequent hospital visits for stentchange, and can be performed with low operative morbidity and mortality. In arecent series of 20 patients undergoing Segment III bilioenteric bypass there was nooperative mortality, and a one-year patency rate of 80% was observed.

Surgical TechniquesCareful 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 clear-ance of the supraduodenal tissues of the hepatoduodenal ligamentincluding 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 aright, left or extended hepatectomy: A liver resection is mandatory whenthe tumor extends unilaterally either into the right or left liver, but leavesthe contralateral portion of the liver free of tumor with an intact biliarydrainage and blood supply.

A detailed description of the operative technique for resection of a hilarcholangiocarcinoma follows. The technique for liver resection will not be describedsince it is addressed in detail in Chapter 16.

LaparoscopyIt is our current practice to perform a diagnostic laparoscopy prior to a laparo-

tomy for hilar cholangiocarcinoma. In our experience, laparoscopy has identifiedunsuspected intra- or extrahepatic disease altering the surgical decision to proceedto laparotomy in 25% of cases. We begin by marking our proposed laparotomyincision on the anterior abdominal wall with a felt pen. In general, we utilize abilateral subcostal (Chevron) incision that can be extended in the midline foradditional exposure if a concomitant liver resection is to be performed. Other surgi-cal groups perform this operation through a midline, but this is limiting if a hepate-ctomy is required. A 10-mm Hussan trocar is initially inserted in the right subcostallocation along the lateral edge of the proposed incision. A 30˚ camera is used toenable complete visualization over the dome of the right and left liver. A second10-mm trocar is introduced in the left subcostal location through which additionalinstruments for retraction or biopsy are inserted. All segments of the liver are evalu-ated carefully. Exposure of the caudate lobe is difficult, but can be facilitated byplacing the patient in a step reverse Trendelenberg position with slight rotation tothe left. The lesser omentum is incised and the caudate lobe inspected. Any suspi-cious hepatic lesions should be biopsied. The hepatoduodenal ligament is carefullyinspected, and suspicious nodes unlikely to be encompassed in the resection areexcised or biopsied. All peritoneal surfaces should be carefully inspected similarly.The greater omentum, lesser omentum, and gastrocolic omentum should also beinspected If no contraindications to laparotomy are identified, an initial right sub-costal incision is made. This limited incision permits bimanual palpation of theliver, a more complete abdominal evaluation, and the performance of an intraoperativehepatic ultrasound. The ultrasound should focus primarily on identifying unsuspected


14

intrahepatic metastases. Unilobar metastases that would be encompassed with anipsilateral hepatectomy are not a contraindication to surgical resection. All suspectedliver lesions should be biopsied with histologic confirmation of malignancy. If nocontraindications are encountered, a Chevron incision or right subcostal incisionwith midline extension is completed.

Exposure and RetractionUpon initial entry into the peritoneal cavity, exposure of the region of the

hepatoduodenal ligament is of primary importance. Although manual retractionwith handheld retractors has historically been the role of the medical student, juniorhouse staff, or surgical assistant, we favor the placement of a retractor that can befixed to the operating table to provide steady constant retraction. A Buckwalder,Thompson, or Goligher retractor is suitable for this purpose. If there are no signifi-cant adhesions, an operative towel or sponge may be placed over the right colon andsmall bowel that can be used to pack the viscera inferiorly within the abdominalcavity. Usually, division of the hepatocolic ligament and mobilization of the hepaticflexure is required to aid exposure.

Once the right colon and abdominal viscera are retracted inferiorly, the firstassistant’s left hand is used to provide gentle but constant caudal retraction on thehepatoduodenal 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 theliver. In order to facilitate access to the biliary confluence and related vessels, theCBD is transected below the cystic duct and above the duodenum. This maneuveris mandatory, as it is impossible to differentiate vascular invasion by tumor from adense fibroblastic response unless the bile duct is reflected upward to reveal thesestructures. Dividing the thin layer of peritoneal tissue which envelopes thehepatoduodenal ligament usually allows easy identification of the CBD. If there isany 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 ofthe CBD is oversewn, and a suture is left in the proximal duct to permit retractionon 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 tech-niques. In most instances, the hilar plate is lowered as described in detail in Chap-ters 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 bydividing the tongue of liver tissue bridging the base of the quadrate lobe (SegmentIV) to the left lobe (Fig. 14.5).

Alternatively, or in combination with the above technique, the liver may be splitin the Glissonian plane with division of the substance of the parenchyma down tothe hilus. Pursuance of these techniques results in mobilization of the quadrate lobethat can then be retracted upwards. In our experience this is rarely indicated, but insome 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 resecteden bloc. The common bile duct is carefully swept upward off the underlying portalvein. The lymphatic tissue, which always lies lateral to the portal vein (and in some


14 cases contains a replaced right hepatic artery), should similarly remain attached tothe 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 itsinsertion in the CBD and left attached. Elevation of the common bile duct, togetherwith the gallbladder and related connective tissue exposes the vessels, allowingdissection in a plane posterior to the tumor and anterior to the portal vein andhepatic artery (Fig. 14.6). It is now, only after performing this extensive dissection,that differentiation between vascular involvement by tumor as opposed to merely adense fibroblastic response, can be accomplished. Ipsilateral vascular involvementwould necessitate a hepatic resection for cure. Contralateral vascular involvementwould render the tumor unresectable, or require vascular resection and reconstruction.

Fig. 14.4. Resection of a hilar cholangiocarcinoma. Initial approach to a hilarcholangiocarcinoma is made through the distal common bile duct and access tothe 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).


14Though practiced infrequently by the authors, the utility of vascular resection for hilarcholangiocarcinoma is very controversial and will not be addressed in this chapter.

When local resection is to be performed, exposure of the left hepatic duct ispursued. 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 tumorclearance. The proximal end of the left hepatic duct is reflected to the right togetherwith the tumor, the mobilized common hepatic channel, and the gallbladder. Thisallows continuation of the dissection towards the right hepatic duct which is alwaysshorter. This right hepatic duct is now cleared, marked with sutures and similarlytransected. The specimen is now removed. Once again, a thin rim of tissue is takenfor histological examination in order to establish tumor clearance. If a liver resectionis to be performed, this is completed prior to division of the right hepatic duct, andthe liver and biliary complex are removed together.

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


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

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


14and Kelly (Fig. 14.8). This technique is extensively described in Chapter 13. It isimportant 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 pre-ferred method is to place the entire anterior sets of sutures to all exposed ducts andthen separately place the entire posterior row of sutures. The jejunum is then rail-roaded up on the posterior sutures. The posterior layer of sutures to all exposedducts are tied first and then individual anterior layers are completed sequentially. A10 F Jackson Pratt drain is routinely left through a separate stab wound incision.

Palliative ApproachesThe 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

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 Liverand Biliary Tract (3rd Edition), Blumgart LH, Fong Y and WH Jarnigan (Eds.) W.B.Saunders, London, UK (2000).


14 treatment at all or percutaneous biliary stenting if indicated for symptoms or tofacilitate access to other treatment. If the tumor is found unresectable at laparotomy,available options are either a biliary-enteric anastomoses (we prefer a Segment IIIbypass described in Chapter 13) or transtumoral tube. The technique for a palliativebypass or intubation may be combined with radiotherapeutic approaches in someinstances, but no prolongation of survival for this technique has been demonstrated. Inrare 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 com-bined biliary and hepatic resection and therefore constitute a better risk group, whilein other instances patients were possibly too ill to tolerate any form of treatment atall. In many series, histological confirmation of the nature of the stricture is notavailable, and in many instances it is not sought. In contradistinction, the wide-spread availability of percutaneous and endoscopic biliary decompression techniques

Fig. 14.8. Resection of a hilar cholangiocarcinoma. A Roux-en-Y limb of jejunum isbrought 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).


14

and expertise has in some cases led to the application of these palliative approachesprior to due consideration of resection, or whether biliary-enteric bypass might pro-vide a better form of palliation.

In some centers, the U tube technique, initially described by Praderi and popu-larized by Terblanche, continues to be the preferred palliative approach. In this pro-cedure, a long tube with side holes is passed transhepatic through the tumor andinto the intrahepatic ducts exiting through the anterior abdominal wall. The lowerend of the tube is also delivered at the skin. The tube thus traverses the tumor andallows drainage of bile into the gut. The tube can be readily washed out and can bereplaced by attaching a second tube to one end and pulling it through the estab-lished sinus track. The procedure may be combined with a Roux-en-Yhepaticojejunostomy rather than bring the lower end out through the common bileduct—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 takento confirm a malignant diagnosis before claims of long term survival after intuba-tion or indeed any other treatment option can be accepted. In our opinion, recentadvances in the development of percutaneous and endoscopic intubational tech-niques and endoprostheses have made operative tubal placement rarely necessary.

Adjuvant TherapyAt 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 of21.4% using a regimen of 5-FU, leucovorin, and carboplatin. In more recent reportshowever, minimal response and PR rates far less than 20% are the norm. We havereported on the management of 12 HCCA patients treated with 2000 cGy deliveredvia intraductal brachytherapy catheters afterloaded with Iridium, and followed by5000 cGy of external beam radiation over 5-6 weeks. Mean survival among thegroup was 14.5 months with all patients surviving 6 months. Similar promising resultsutilizing external beam radiotherapy alone and neoadjuvant chemoradiotherapy havebeen reported; however all approaches are considered investigational and should beapplied selectively if at all.

Photodynamic therapy has recently been applied in the palliative managementof HCCA. Unresectable patients treated intravenously with a hematoporphyinderivative, followed two days later by intraluminal cholangioscopic photoactivationhave shown a precipitous fall in serum bilirubin and a subjective improvement inquality of life. No procedural related morbidity or mortality was reported. Mediansurvival was 14.5 months. Although this new modality appears promising, validationof these results awaits further investigation.

ConclusionCholangiocarcinoma is an uncommon malignancy that almost uniformly pre-

sents with obstructive jaundice. Complete resection with negative histologic mar-gins provides the only hope for long-term survival and perhaps cure, but is attainableonly in the minority of patients (< 30%). Distal bile duct cancer is treated bypancreaticoduodenectomy or local bile duct excision with survival rates similar to thoseseen with pancreatic cancer. In regards to the management of HCCA, data now exist


14

to justify a radical surgical approach in attempt to achieve negative histologic mar-gins, which usually requires partial hepatectomy.

Palliative biliary decompression performed surgically, endoscopically, or percu-taneously provides effective relief of jaundice-related symptoms, but fails to prolongsurvival. No effective adjuvant therapy can be recommended. In sum, radical surgeryremains the mainstay of therapy for all forms of cholangiocarcinoma. The rarity ofthis neoplasm and the expertise required for its management should prompt physi-cians and patients to seek care at specialized hepatobiliary referral centers.

Selected Readings1. Nakeeb A, Pitt HA, Sohn TA et al. Cholangiocarcinoma: A spectrum of intrahe-

patic, perihilar, and distal tumors. Ann Surg 1996; 224:463-475.2. Stain SC, Baer HU, Dennison AR et al. Current management of hilar

cholangiocarcinoma. SGO 1992; 175:579-588.3. Burke E, Jarnagin WR, Hochwald SN et al. Hilar cholangiocarcinoma patterns of

spread, the importance of hepatic resection for curative operation, and a presurgicalclinical staging system. Ann Surg 1998; 228:385-394.

4. Blumgart LH, Benjamin IS. Cancer of the bile ducts. In: Blumgart LH, ed.) Sur-gery of the liver and biliary tract, 2nd ed. London: Churchill Livingstone1994:1051-1067.

5. Schwartz LH, Coakley FV, Sun Y et al. Neoplastic pancreaticobiliary duct obstruc-tion; evaluation with breath-hold MR cholangiopancreatography. AJR 1998;170:1491-1495.

6. Bismuth H, Nakache R, Diamond T. Management strategies in resection for hilarcholangiocarcinoma. Ann Surg 1992; 215:31-8.

7. Fong Y, Blumgart LH, Lin E et al. Outcome of distal bile duct cancer. Br J Surg1996; 83:1712-5.

8. Nagorney DM, Donohue JH, Farnell M et al. Outcomes after curative resectionsof cholangiocarcinoma. Arch Surg 1993; 128:871-79.

9. Blumgart LH, Benjamin IS, Hadjis NS et al. Surgical approaches tocholangiocarcinoma at the confluence of hepatic ducts. Lancet 1984; 1:66-70.227:821-833.

10. Chamberlain RS, Blumgart LH. Hilar cholangiocarcinoma: A review and com-mentary. Ann Surg Oncol 2000 Jan-Feb; 7(1):55-66.

CHAPTER 1CHAPTER 15

Surgical Managementof Gallbladder Cancer

Ronald P. DeMatteo, Yuman Fong

IntroductionGallbladder adenocarcinoma is a treacherous entity. It produces symptoms late

in the course of the disease, disseminates rapidly from the primary site, and respondsinfrequently to nonsurgical therapy. The overall median survival for all patients isless than 6 months. The disease is up to five times more common in females. It isusually associated with gallstones, although few patients with gallstones actuallydevelop gallbladder cancer. It is the most common biliary tract cancer and is thefifth leading gastrointestinal malignancy in the United States. Nevertheless, gall-bladder adenocarcinoma is seldom encountered and, consequently, its diagnosticevaluation and management are not widely appreciated.

Anatomical ConsiderationsThe management of gallbladder cancer requires a thorough knowledge of the

common variations in the biliary tract and hepatic vasculature and the normalanatomy of the gallbladder with its relation to surrounding structures. The gallblad-der is situated in the inferior aspect of the liver at the junction of Segments IVb andV. It lies in proximity to the major portal structures and often abuts the duodenumor transverse colon. Terminal branches of the middle hepatic vein are adjacent to thegallbladder bed. The right anterior portal pedicle lies deeper in the substance of theliver and branches into the Segment V and VIII pedicles.

A thorough understanding of the patterns of tumor dissemination is essential tothe management of gallbladder cancer. The disease spreads through the lymphaticsvia the bloodstream or by direct invasion. The lymphatic drainage of the gallbladderhas been well-defined. The immediate (N1) drainage comprises the cystic duct nodeand the pericholedochal nodes. From there, drainage proceeds to the N2 nodes thatinclude the posterior pancreatic, periduodenal, periportal, superior mesenteric, com-mon hepatic artery, interaortocaval, and celiac lymph nodes. All other nodes areconsidered M1. Hematogenous metastases most commonly occur to the liver andlung and, less commonly, the brain. Direct spread occurs by local invasion, spreadthrough the peritoneum, or extension along the wounds. Local invasion of the liveroccurs readily in gallbladder cancer because the normal gallbladder wall is quite thinand gallbladder cancer is known to disseminate early within the peritoneal cavity.Consequently, the subserosal plane of gallbladder dissection that is commonly utilizedin routine cholecystectomy should be avoided when a gallbladder cancer is suspected.



15

Iatrogenic sites of tumor spread occur in laparoscopic port sites, percutaneous bi-opsy tracts, drain sites, and surgical wounds.

There are several staging systems for gallbladder cancer. The most commonlyaccepted is the American Joint Committee on Cancer (AJCC) TNM staging criteriawhich is outlined in Table 15.1.

Preoperative Evaluation

SymptomsPatients with gallbladder cancer are often initially asymptomatic. Nonspecific

symptoms of abdominal pain and weight loss may mimic the symptoms of benigngallbladder 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 compres-sion by tumor, or involved lymph nodes. It suggests that the tumor is advanced ororiginated in the gallbladder neck or cystic duct and is therefore more likely toinvolve the portal vascular structures. It should be remembered that Mirizzi syn-drome may be associated with a gallbladder cancer.

Diagnostic EvaluationA variety of radiologic tests are available for the preoperative evaluation of a

patient suspected or known to have gallbladder cancer. Duplex ultrasound is espe-cially accurate in demonstrating mucosal abnormalities. It is imperative that thesurgeon review the sonographic images prior to planning biliary surgery, even whenbenign biliary disease is suspected. Magnetic resonance cholangiopancreatography(MRCP) may be used to define ductal anatomy and avoids contamination of thebile that is associated with direct cholangiography. In a patient without jaundice, acomputerized tomography (CT) of the abdomen and pelvis may be sufficient tosearch for intra-abdominal dissemination. If percutaneous transhepatic cholangiog-raphy (PTC) or endoscopic retrograde cholangiopancreatography (ERCP) is per-formed, then cytology or brushings should be obtained. It should be emphasizedthat a tissue diagnosis is not necessary prior to surgical exploration. Percutaneousbiopsy should be avoided, especially given the chance of tumor spread along theneedle tract or in the peritoneum and should be reserved solely to confirm a malig-nant diagnosis in unresectable disease.

A few specific radiologic findings should be assessed. In particular, the presenceof liver invasion or liver metastases should be sought. Lymphadenopathy may repre-sent metastatic disease or local inflammation. A calcified “porcelain” gallbladdermay indicate the presence of an underlying gallbladder cancer. The finding of amid-common bile duct stricture should always raise the suspicion of a gallbladdercancer. Gallbladder tumors that arise in the neck of the organ may be difficult todistinguish from hilar cholangiocarcinoma.

Clinical PresentationsPatients 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).

203Surgical Management of Gallbladder Cancer

15

Table 15.1. TNM staging criteria for gallbladder cancer

Stage I T1 N0Stage II T2 N0Stage III T1-2 N1

T3 N0-1Stage IVA T4 N0-1Stage IVB Any N2 or M1

T1 tumor invades lamina propria or muscleT2 invasion of perimuscular connective

tissueT3 liver invasion <2 cm or involves 1

adjacent organT4 liver invasion >2 cm or involves 2

adjacent organs

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

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

Gallbladder Mass Identified PreoperativelyA gallbladder mass identified preoperatively enables referral to a specialty center

if necessary. It allows for a complete discussion with the patient regarding the rangeof operations (cholecystectomy to radical resection) that may be performed. Thor-ough radiologic evaluation is also possible. Unfortunately, a mass may be visible butoverlooked in the presence of gallstones. A gallbladder polyp that is less than 1 cm insize may be observed with serial imaging. Larger masses should be considered to bemalignant until proved otherwise, although only a fraction of them will actuallycontain cancer. A “porcelain” gallbladder should also be resected. To avoid the pos-sibility of dissemination to port sites or the peritoneum during insufflation atlaparoscopy, open abdominal exploration is recommended when a gallbladder can-cer is suspected. In this way, the entire gallbladder, including the serosa, may be re-moved from the liver bed. During cholecystectomy, particular attention should bemade to avoid inadvertent entry into the gallbladder and potential tumor spillage. Ifthe mass is found to penetrate into the liver, the operation should be adjusted accordingly.

Gallbladder Cancer Identified IntraoperativelyA gallbladder cancer may be detected at the time of operation. If it is recognized

at exploration during laparoscopy or laparotomy, then the procedure should usuallybe aborted if radical resection is required. In this way, the patient can be furtherevaluated and appropriately consented. If there is doubt about the diagnosis, thenfine needle aspiration with minimal manipulation of the tumor may be performed.However, it is paramount not to compromise resectability. Cholecystectomy shouldbe avoided as a means to make the diagnosis when the surgeon is not prepared toperform radical resection if the cancer is greater than Stage I.


15

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

A gallbladder cancer may also become known immediately after the removal ofthe gallbladder. Because of the possibility of an occult gallbladder cancer, all speci-mens should be examined intraoperatively for the presence of mucosal abnormali-ties. If the cholecystectomy was performed via laparoscopy, the surgeon should convertto laparotomy only if he is able to carry out a radical resection if one is indicated. Ifan open cholecystectomy was performed, and the surgeon is not prepared to per-form a radical resection, the cystic duct node should be taken and the cystic ductmargin proved to be negative by frozen section.

Gallbladder Cancer with Prior OperationWith the advent of laparoscopic cholecystectomy, a frequent occurrence is the

incidental finding of an occult gallbladder cancer in the pathologic specimen. Ifanother surgeon operated upon the patient, emphasis should be placed upon gain-ing as much information as possible about the primary tumor because its locationmay dictate the type of operation that is now necessary. Consultation with the primary


15

surgeon and review of the operative and pathologic reports are advocated. The pres-ence of a cystic duct node, the margin status of the gallbladder itself, and the cysticduct are also important. The initial tests performed prior to the first operation shouldalso be reviewed. The presence of a mass may often be found retrospectively, especiallyon ultrasound studies.

A re-operation for gallbladder cancer should include excision of all prior surgicalwounds (port sites, drain sites, laparotomy wounds) because of the frequency oflocal tumor recurrence. Often, the duodenum or transverse colon is densely adher-ent to the gallbladder bed and should be resected en bloc with the specimen. There-fore, a preoperative bowel preparation is mandatory. The major difficulty in are-resection is distinguishing tumor from scar tissue that has developed from theinitial procedure. For this reason, many patients will require a bile duct and liverresection to guarantee adequate clearance. A re-resection should be performed inpatients with Stage II to IV A disease (see below). The patient should be aware of thepossibility that no additional disease may be found in the pathologic specimen evenif a radical operation is undertaken.

Surgical ApproachA 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 chanceof cure and long-term survival. The treatment of gallbladder cancer is based on thestage (radiologic or pathologic) of disease and the prior therapeutic interventions.

Treatment by Tumor StageThe treatment of a Stage I tumor confined to the mucosa is simple cholecystec-

tomy. If it is discovered intraoperatively, the cystic lymph node should be excisedand the portal nodes should be carefully evaluated although they are unlikely to be

Fig. 15.2. Treatment algorithm for patients discovered to have gallbladder can-cer after previous operation.


15

involved. Often, these tumors are discovered incidentally at pathologic examina-tion. No further therapy is indicated because few of these patients will recur. Patientswith Stage II tumors are the most likely to benefit from radical resection (orre-resection) that includes an en bloc lymphadenectomy and liver resection with orwithout bile duct resection. These patients will have a 50-70% 5-year survival ratewith complete resection. Stage III and IVA patients should have similar treatmentand most of them will require extended hepatic resection. This group of patients canbe expected to have about a 20-40% 5-year survival rate after complete resection.

Stage IVB patients should undergo palliation for symptomatic jaundice. Therapyshould be minimized given their short survival. In most cases, interventional radio-logic procedures can provide biliary drainage with the use of Wallstents. In patientswho were explored with the presumption of less advanced disease, a Segment IIIenteric bypass may be indicated.

LaparoscopyLaparoscopy is advocated to identify occult peritoneal or hepatic metastases that

would preclude resection and obviate laparotomy. Often, the port sites can be posi-tioned in the line of the intended laparotomy incision. The finding of gross ascitesshould prompt cytological evaluation which, if positive, would make a resectioncontraindicated.

Lymphatic DissectionIf laparoscopy reveals no evidence of tumor dissemination, then a laparotomy is

undertaken. The preferred approach is through a right subcostal incision. After peri-toneal and liver metastases are excluded, a Kocher maneuver is then performed topalpate the retropancreatic lymph nodes. The hepatic artery nodes should also beinspected. N2 nodal disease is considered inoperable, although some surgical groupsadvocate combined pancreaticoduodenectomy and hepatectomy. In the absence ofN2 disease, the incision should be extended to the xiphoid and the retractors posi-tioned. A Goligher retractor is preferred with blades that retract both costal marginslaterally and upward. Alternatively, a Buchwalter retractor may be used. The lym-phatic dissection begins with sweeping the superior retropancreatic nodes upwardto the hilus of the liver. The bile duct is identified at the superior border of thepancreas and is divided and lifted forward to further expose the lymphatic tissue inthe porta and improve the completeness of lymphadenectomy. Some prefer to avoidbile duct transection (and thus reconstruction) for patients with T2 tumors withoutprevious surgical intervention or those with tumors located in the fundus. The gas-troduodenal artery is dissected free and usually preserved. The dissection continueswith skeletonization of the hepatic artery and portal vein up to the hilus and then tothe duct that is being preserved (usually the left hepatic duct).

Liver ResectionThe extent of hepatectomy necessary in the resection of gallbladder cancer is

somewhat controversial. It depends on the location of the primary tumor and whetheran operation has already been performed. For tumors with minimal (T3) liver inva-sion, a formal anatomic Segment IVB and V resection is preferred over a wedgeresection to guarantee adequate tumor clearance and minimize bleeding and biliaryleak. The Segment IVB vessels can be controlled just to the right of the umbilical


15

fissure through a hepatotomy that is performed during a Pringle maneuver. TheSegment V portal triad is identified within the parenchyma with care given to pre-serve the Segment VIII structures. The middle hepatic vein is divided at the junc-tion of Segments IVB and V.

Patients with tumors in proximity to the hilus, or who have already had a chole-cystectomy, are more likely to require a right hepatic lobectomy to achieve tumorclearance. Actually, an extended right lobectomy is often necessary inferiorly. Mean-while, the plane of a right hepatic lobectomy is followed cephalad (which is at somedistance from the tumor), thus sparing Segment IVA. There are rare instances whenan extended left lobectomy may be indicated to remove a gallbladder cancer.

Bile Duct Resection and ReconstructionWhether 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 usu-ally done to facilitate a thorough portal lymphadenectomy. In certain patients, suchas those who are thin or those with tumors of the fundus, biliary resection (with itsincreased morbidity) may be avoided. However, it is usually performed for resectionof T2 or greater tumors. When bile duct resection is necessary, a standardhepaticojejunostomy is created to the common hepatic duct or lobar duct (almostalways the left hepatic duct) using a 60-70 cm Roux-en-Y limb. This is described indetail in other chapters.

SummaryGallbladder cancer continues to be a challenging disease. A detailed knowledge

of biliary anatomy and familiarity with the dissemination pattern of gallbladdercancer prepares the surgeon to perform a variety of operations depending on thelocation of the tumor and the patient’s previous treatment.

Suggested Reading1. Bartlett DL, Fong Y, Fortner JG et al. Long-term results after resection for gall-

bladder cancer. Implications for staging and management. Ann Surg 1996;224:639-646.

2. Matsumoto Y, Fujii H, Aoyama H et al. Surgical treatment of primary carcinomaof the gallbladder based on the histologic analysis of 48 surgical specimens. Am JSurg 1992; 163:239-245.

3. Fong Y. Submitted. Ann Surg.

CHAPTER 16

Techniques of Hepatic Resection

Sharon Weber, William R. Jarnagin, Leslie H. Blumgart

IntroductionHepatic 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 isthe only treatment with curative potential. Over the past 30 years, improvements inperioperative care and surgical technique have dramatically decreased the morbidityand mortality of major hepatic resection, thus making it a viable treatment optionfor many patients.

The risk of hemorrhage has been the major obstacle to the safety of hepaticresection. While this remains a concern, blood loss and transfusion requirementshave been markedly reduced as a result of changes in operative technique. Althoughportal triad clamping reduces hepatic arterial and portal venous bleeding duringparenchymal transection, this has no effect on bleeding from the hepatic veins whichare usually the major source of blood loss. Inflow and outflow vascular control be-fore parenchymal transection, low central venous pressure anesthesia, and anatomi-cally based resections, are all important components of contemporary hepatic resectionand play a role in minimizing operative blood loss. Total vascular isolation, a funda-mentally different approach that is required in few cases, has not been shown tolower intraoperative blood loss or transfusion requirements.

Operative TechniqueIn patients with malignant disease, complete resection requires a negative histo-

logic margin; resection with a positive margin is a well-known predictor of recur-rence and poor survival. Although 1 cm of normal parenchyma around the tumorwas previously considered to be essential, recent studies have shown that a resectionmargin of a few millimeters is probably adequate. Regardless, anatomically basedsegmental resections are the best means of achieving a negative margin. Wedge re-sections have a higher incidence of positive margins, are associated with greaterblood loss, and should be avoided except for small peripheral lesions.

Major intraoperative bleeding is generally the result of injury to the hepatic veinsor vena cava. To minimize venous bleeding, early control of the hepatic veins isperformed before dividing the liver, and the venous outflow is divided after control-ling the inflow blood supply. A low central venous pressure (CVP) of 5 mm Hg orless minimizes bleeding from disrupted hepatic veins, which may occur duringmobilization or parenchymal transection. Early fluid restriction is maintained toachieve both low CVP and the minimal volume necessary for renal perfusion, but


209Techniques of Hepatic Resection

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low urine output during the resection is accepted. To minimize the risk of air embo-lism 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 insuffi-ciency, the impact of low CVP anesthesia on postoperative renal function is minimal.

In selected cases, laparoscopy is performed immediately prior to laparotomy. Ifthe patient appears to be resectable, a right subcostal incision is made with extensionof the incision as necessary. Exploration for extrahepatic disease is performed. Theround ligament is divided, leaving a long suture on the hepatic side for traction. Thefalciform ligament is divided up toward the hepatic veins, and the right triangularligament and the coronary ligament are partially divided with cautery (Fig. 16.1).Once fully mobilized, the liver is examined with bimanual palpation and intraop-erative ultrasound (IOUS) both to identify the tumor(s), the presence of additionaldisease, 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 diaphragmaticattachments by completely dividing the right triangular ligament and exposing thebare 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 dia-phragm laterally. The peritoneum at the inferior border of the liver is divided lateralto medial, taking care to avoid injury to the right adrenal gland. Small veins drain-ing from the liver into the IVC are separated from the caudate process all the way upto the hepatic venous confluence (Fig. 16.2). During this dissection, a ligamentousband is encountered which arises from the caudate lobe on the left, passes posteriorto the IVC, and attaches to Segment VII. This ligament may contain small vessels orhepatic 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 triangularligament and left coronary ligament to the lateral margin of the IVC, avoiding injuryto the left hepatic vein. The lesser omentum should be incised and the ligamentumvenosum, which runs along the anterior surface of the caudate lobe to enter the lefthepatic vein, should be ligated and divided.

Right HepatectomyRight hepatectomy involves removing all hepatic parenchyma to the right of the

middle hepatic vein (Segments V, VI, VII, and VIII). If necessary, the middle he-patic vein can be sacrificed during right hepatectomy since the umbilical and lefthepatic veins will provide adequate drainage of the remaining left liver. After fullmobilization, vascular inflow and outflow control should be achieved. Three generalapproaches have been described for achieving vascular inflow control: extrahepaticdissection within the porta hepatis with division of the right hepatic artery and rightportal vein prior to division of the parenchyma (Fig. 16.3); intrahepatic control ofthe main right pedicle within the substance of the liver prior to parenchymal transec-tion (pedicle ligation); or intrahepatic control of the pedicle during parenchymaltransection. For the overwhelming majority of resections, we control the inflowextrahepatically with either a hilar dissection or, if possible, the pedicle ligation tech-nique. Proceeding with liver resection before inflow control is achieved is not advised.

Extrahepatic vascular control begins with cholecystectomy. If the gallbladder isinvolved by the tumor, it should not be removed, but the cystic duct and cysticartery ligated and divided. The common hepatic artery should then be dissected


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


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sufficiently to reveal the right and left branches after which the right branch can bedivided with suture ligatures. The portal vein is then exposed. Again, the right andleft branches should be clearly identified. A small branch from the right portal veinto the caudate process is a constant finding and should be controlled early in thedissection. This maneuver facilitates exposure of an additional length of the rightportal vein making it easier to divide. Once adequately dissected, the right portalvein 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 todeal with them. The common variations of arterial anatomy are well-described.However, variant anatomy of the portal vein is also encountered, the most commonof which is a separate origin of the right anterior and posterior branches. For allmajor hepatic resections, it is essential to fully define the vascular anatomy in orderto avoid potentially disastrous injury to the contralateral branch.

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


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When possible, we perform a pedical ligation maneuver to control the partialstructures. This technique has several advantages over hilar dissection. After remov-ing the gallbladder, two hepatotomy incisions are made medially at the base of thegallbladder 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 thesubstance of the liver to encircle the main right pedicle (Fig. 16.5), which is encasedin a tough, fibrous sheath (Fig. 16.6). Bleeding from terminal branches of the middlehepatic vein may occur but is readily controlled. Residual liver tissue is then clearedaway to expose the pedicle and identify the anterior or posterior branches to theindividual segments for segmental resections. Before dissecting the pedicle, it isessential to divide all posterior venous branches entering the IVC (Fig. 16.2); other-wise, these veins may be torn and significant hemorrhage will occur. Once the rightpedicle is isolated, it should be occluded temporarily and the portal triad clamp

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 peritoneumoverlying the common bile duct is incised. The cystic duct and cystic artery are ligatedand divided. A tie has been left on the cystic duct for retraction. C. The right hepaticduct is dissected. D. The right hepatic duct has been ligated and divided with absorb-able suture. The right hepatic artery is dissected, ligated and divided. E. The right portalvein is dissected, doubly clamped and divided. The branch from the caudate process iseither divided prior to dividing the right portal vein. F. The proximal end of the portalvein 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, 2dEdition. LH Blumgart, ed. 1994. © Churchill Livingstone.


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Fig. 16.4. Approach to pedicle ligation during right hepatectomy. The gallbladderhas been removed and the cystic and hilar plates lowered. Hepatotomy incisionsare made in the caudate process (1) and in the gallbladder fossa (2) to allow controlof the right pedicle. Reprinted with permission from LH Blumgart. Liver resec-tion—liver and biliary tumours (with comments by B Launois and C. Huguet. He-patic cryosurgery addendum by Y Fong. Surgery of the Liver and Biliary Tract, 2dEdition. LH Blumgart ed. 1994. © Churchill Livingstone.

released to reveal the line of demarcation along the principal plane. Performance ofa pedicle ligation eliminates the need for hilar dissection, thereby saving time andreducing 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 encroachon the hilus, since the resection margin will be compromised.

When hilar dissection is used, it is not necessary to attempt to encircle and di-vide the right hepatic duct after the vascular pedicle is isolated. This maneuver risksinjury to the biliary confluence. Control of the right hepatic duct can be obtainedduring parenchymal transection.

With the inflow controlled, outflow control of the right hepatic vein is achievednext (Fig. 16.7). Although the right hepatic vein is visible after initial mobilization,complete control requires further dissection of the avascular tissue along the supra-hepatic vena cava, between the right and middle hepatic veins. The right vein canthen be encircled and divided with a vascular stapler (preferably) or divided betweenvascular clamps and oversewn. Alternatively, the right vein may also be controlledand 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 middlehepatic vein, depending on the location of tumor. The surgeon should not hesitate


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to divide the middle vein if necessary, since the umbilical vein will provide adequatedrainage of Segment IV. Parenchymal division begins by marking the line of transec-tion with the electrocautery and cutting the capsule with scissors. Stay sutures of 0chromic catgut are placed on either side of the transection plane and used for trac-tion as dissection proceeds. A Kelly clamp is used to crush the liver parenchyma, andexposed vessels are controlled with clips, ligatures or the vascular stapler. Althoughthe liver can tolerate warm ischemia for up to 60 minutes, intermittent portal triadclamping during the parenchymal transection phase allows decompression of themesenteric veins. After transection is complete, the raw surface of the liver is exam-ined for hemostasis and bile leaks. The argon beam coagulator is used to control rawsurface oozing. Biliary leaks should be clipped or suture ligated.

The authors do not use closed suction drainage after routine hepatic resectionunless concomitant biliary resection and reconstruction have been performed, if aportion of the diaphragm has been resected and repaired, or if there is obvious bileleakage that cannot be fully controlled with suture ligation.

Extended Right Hepatectomy (Right Hepatic Lobectomyor Right Trisegmentectomy)The additional removal of Segment IV during right hepatectomy (V, VI, VII,

VIII) constitutes an extended right hepatectomy or right trisegmentectomy. Theinitial steps are similar to right hepatectomy, with division of the right hepatic vein

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


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and portal pedicle. The bridge of tissue connecting Segments III and IV, which maybe well-developed hepatic parenchyma in some patients, is divided to reveal thelower part of the umbilical fissure. The ligamentum teres can be seen within theumbilical fissure, joining the left portal vein.

After the right pedicle is divided, the recurrent vessels from the umbilicalfissure to Segment IV are controlled (Fig. 16.8). This may be achieved withinthe umbilical fissure or during parenchymal transection. The right hepatic veinis divided as described above.

The liver is transected just to the right of the falciform ligament using the stan-dard parenchymal crushing technique. The middle hepatic vein is encountered as dis-section 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 themiddle hepatic vein. This is of particular concern for tumors involving Segment IVa.

Left HepatectomyRemoval of Segments II, III and IV constitutes a left hepatectomy. After full

mobilization of the left triangular ligament, inflow control is achieved outside of theliver at the base of the umbilical fissure (Fig. 16.9). The bridge of tissue connecting

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


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Fig. 16.7. Isolation of the right hepatic vein. The right liver has been fully mo-bilized and the inferior vena cava completely exposed up to the right hepaticvein. A. Vascular clamps have been applied to the right hepatic vein. B. A sec-ond vascular clamp is applied to the caval side of the vein. C. The right hepaticvein had been divided and the stump oversewn with vascular suture. It is gen-erally not necessary to control the vena cava above and below the liver. Re-printed with permission from LH Blumgart. Liver resection—liver and biliarytumours (with comments by B Launois and C. Huguet. Hepatic cryosurgeryaddendum by Y Fong). Surgery of the Liver and Biliary Tract, 2d Edition. LHBlumgart ed. 1994. © Churchill Livingstone.


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Segments III and IV on the undersurface of the liver must be divided. The hilarplate is lowered and the left hepatic artery identified and divided. The portal vein isidentified at the base of the umbilical fissure. If the caudate is to be preserved, thenthe portal vein is controlled beyond the origin of the principal caudate branch whichusually arises from the left portal vein. The long extrahepatic course of the left bileduct can be identified behind the portal vein and divided at the umbilical fissure, orcontrolled from within the hepatic parenchyma.

The left and middle hepatic veins are controlled after mobilizing the left lobeand lifting it anteriorly and to the right (Fig. 16.10). The gastrohepatic ligament isinitially divided exposing the ligamentum venosum, which itself is divided just priorto entry into the left hepatic vein. Control of the veins is obtained by careful dissec-tion from above and below the liver; a passage is developed from just to the right ofthe middle hepatic vein from above and the superior border of the caudate lobefrom below. The middle and left hepatic veins most often enter the IVC as a singletrunk (Fig. 16.10), but may be independent in some cases. The veins are dividedand stay sutures placed along either side of the principal plane, followed by paren-chymal transection.

Fig. 16.8. Extended right hepatectomy. A. Recurrent vessels from the umbilical fissureto 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 careto avoid injuring the main left pedicle. B.Division of the liver parenchyma proceedstoward the inferior vena cava to the right of the falciform ligament. Reprinted from LHBlumgart. Liver resection—liver and biliary tumours (with comments by B Launois andC. Huguet, Hepatic cryosurgery addendum by Y Fong). Surgery of the Liver and BiliaryTract, 2d Edition. LH Blumgart ed. 1994. © Churchill Livingstone.


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Fig. 16.9. The main left portal pedicle as it courses along the undersurface of Seg-ment IV into the umbilical fissure. A. Division at this level will devascularize theentire left liver including the caudate lobe. B. Division above the caudate branchwill 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 todivide the Segment III pedicle. Note: The pedicles to IVa and IVb branch off theright side of the left portal triad with the umbilical fissure and can be controlledhere 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 Bil-iary Tract, 2d Edition. LH Blumgart ed. 1994. © Churchill Livingstone.

Left Lateral Segmentectomy (Left Lobectomy)Removal of Segments II and III constitute a left lateral segmentectomy. The

bridge of tissue overlying the umbilical fissure, and running between Segments IIIand IV, is divided after mobilization. For tumors lying close to the fissure, the pediclesto Segments II and III can be dissected individually within the umbilical fissure(Fig. 16.9). An alternate approach for peripheral lesions is splitting the liveranteroposteriorly just to the left of the falciform ligament. The Segment II and IIIpedicles can then be divided during parenchymal transection. The left hepatic veincan be controlled and divided within the liver substance posteriorly, thus obviatingthe need for extrahepatic dissection. However, if the tumor approximates the lefthepatic 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 com-pletely mobilized and lifted anteriorly and to the right (open arrow). The gastrohe-patic 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 justto the right of the middle hepatic vein from above and the superior border of thecaudate lobe (A to B). The veins are clamped, ligated and divided. IVC = inferiorvena cava; MHV = middle hepatic vein; LHV = left hepatic vein; GB = gallbladder.Reprinted with permission from LH Blumgart. Liver resection—liver and biliarytumours (with comments by B Launois and C. Huguet, Hepatic cryosurgery adden-dum by Y Fong). In: LH Blumgart ed. Surgery of the Liver and Biliary Tract, 2ndEdition. 1994. Edinburgh UK.

and IV). This is among the most challenging of hepatic resections; the difficulty liesin defining the plane of transection (Figs. 16.11 and 16.12). Injury to the posteriorsectoral 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 importantfinding, especially for tumors encroaching on the main right hepatic vein origin,and may allow sacrifice of the main right hepatic vein for tumor clearance. Dissec-tion proceeds as with a left hepatectomy, with the portal triad approached from theleft side. If the caudate lobe is to be included in the resection (Fig. 16.11, inset), theleft hepatic artery and portal vein should be ligated close to their origins in order todisconnect the blood supply to both caudate and Segments II and III (Fig. 16.9). Ifthe caudate is preserved, the left portal triad is transected at the base of the umbilicalfissure, preserving the blood supply to the caudate (Fig. 16.9). If possible, the ante-rior pedicle supplying Segments V and VIII should be controlled before parenchy-mal 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 hori-zontal 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 isalong the ligamentum venosum, the base of the quadrate lobe and hilus, and alongthe 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 theirorigins (inset). Reprinted with permission from LH Blumgart. Liver resection—liverand biliary tumours (with comments by B Launois and C. Huguet, Hepaticcryosurgery addendum by Y Fong). In: LH Blumgart ed. Surgery of the Liver andBiliary Tract, 2d Edition. 1994. © Churchill Livingstone.

Controlling the middle and left hepatic veins extrahepatically is important to reduceblood 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 thegallbladder fossa. If the inflow has been completely divided, the line of transectionwill be shown extending from the anterior border of the right hepatic vein to an areato the right of the gallbladder fossa. If the right anterior sectoral pedicle has not beencontrolled, 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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Using intermittent portal triad occlusion, the parenchyma is divided from theinferior surface upwards and from right to left in a horizontal plane. In order tofacilitate the dissection, the liver is rotated clockwise to convert the horizontal planeto 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 oftransection is often dictated by the tumor, since tumors close to the posterior pedicleor the right hepatic vein will limit the resection.

Extended left resections can be done safely with mortality rates only slightlyhigher than other resections. Postoperative morbidity is significant, however, withbiliary leak and abdominal abscess being the major complications. Because of thesmall remnant, significant postoperative liver dysfunction may result and patientsare more likely to develop significant ascites.

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


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

Caudate Lobe Resection (Segment I Resection)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 caudateresection. Damage to the middle or left hepatic veins is a major risk of isolatedcaudate lobectomy (Figs. 16.13 and 16.14). The caudate may be approached fromthe 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 fromthe left or when the caudate is excised en bloc with the right liver. After division ofthe gastrohepatic omentum and the ligamentous attachments from the caudate tothe IVC, the right liver is mobilized with division of the posteriorly draining veinsalong the entire retrohepatic cava. The dissection then proceeds along the anteriorsurface of the IVC, lateral to medial with control of the caudate veins. Some of theseveins may be more easily controlled from the left side. The branches to Segment Ifrom the left portal vein and hepatic artery are then dissected close to the base of theumbilical fissure just before the entry of the left portal triad. The caudate is thenseparated from its attachment to the right liver with inflow occlusion.

A principal approach from the left side may be possible with smaller tumors orwhen the caudate is to be removed en bloc with the left liver. The left lateral marginof 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 splitalong the principal plane to allow detachment of the right side of the caudateunder direct vision of the middle hepatic vein. This approach may help reduce therisk of inadvertent injury to the middle vein, which can result in significant hemor-rhage. Reprinted with permission from LH Blumgart, Liver resection for benigndisease and for liver and biliary tumors. In: LH Blumgart, Y Fong eds. Surgery of theLiver and Biliary Tract, 3d Edition. 2000. © W.B. Saunders.

diaphragm, exposing the veins draining the caudate into the cava. The approach tothe inflow vessels remains the same.

An alternative approach to an isolated Segment I resection involves mobilizationof the caudate as described above, followed by splitting of the hepatic parenchymaalong the principal plane (Fig. 16.14). This approach provides access to the rightborder of the caudate, which can be disconnected under direct vision of the middlehepatic vein and may prevent uncontrolled bleeding.


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

Segmental ResectionBecause they are defined by anatomic structures with their own pedicles, each

hepatic segment can be resected individually (Fig. 16.15), or in combination withother segments as part of a larger resection. This section describes some of the morecommonly performed anatomical sub-lobar hepatic resections.

Right Posterior Sectorectomy (Segments VI and VII)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 hepaticvein will provide adequate drainage of Segments V and VIII (anterior sector). Evenif the right hepatic vein is to be preserved, it should be fully dissected and exposed toallow rapid control if injured during parenchymal transection. The right portal pedicleis exposed and the anterior and posterior branches identified. The posterior pedicleis clamped and the line of demarcation between the anterior and posterior sectors isdemonstrated. The pedicle may be divided and parenchymal dissection performed.The line of transection is horizontal and posterior to the right hepatic vein, but maybe extended into the anterior sector with sacrifice of the right hepatic vein, if necessary.


16

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 sacri-ficed. The right lobe must be fully mobilized and the right hepatic vein completelyexposed. The approach is similar to that used for posterior sectorectomy except thatthe anterior pedicle is divided, and the line of transection indicated between theright and middle hepatic veins. The line of transection can be extended into Seg-ment IV if necessary for complete tumor clearance.

Segment IV ResectionSegment IV is divided into a posterosuperior portion (IVa) and an anteroinferior

portion (IVb), which can be resected together or separately. The left branches of theportal vein and hepatic artery supply the inflow to Segment IV. The middle hepaticvein provides venous drainage via medial branches. The umbilical vein providesadditional drainage and may drain into the middle or left vein. Division of thebridge of tissue overlying the umbilical fissure is performed and the hilar plate low-ered. 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 dividedjust to the right of the falciform ligament and along the principal plane. Control ofthe Segment IV feedback vessels is as described for extended right hepatectomy.Initial division of these vessels will delineate the extent of the resection. The middlehepatic vein may be preserved or divided.

Central ResectionRemoval of Segments IV, V, and VIII (Segment IV plus an anterior sectorectomy)

constitute a central resection. This seemingly complex procedure is used to maxi-mize the amount of remnant liver left after resection because both the posteriorsector and the left lateral segment are preserved. The approach to a central resectionis similar to that used for a posterior sectorectomy and left lateral segmentectomy,except these are preserved rather than removed. The right anterior and posteriorsectoral portal triads are identified and the anterior pedicle clamped. Transection isperformed with intermittent Pringle, carefully preserving the right posterior pedicleand the right hepatic vein. Segment IV is devascularized and resected as describedfor a Segment IV resection. The middle hepatic vein must be divided; a vascularclamp may be used to occlude the vein during parenchymal transection.

Wedge ResectionsWedge resections are associated with a higher incidence of positive margins and

greater blood loss and should therefore be avoided in most cases. However, they maybe appropriate in selected cases. Small, peripheral lesions can be safely excised withadequate margins using an intermittent Pringle maneuver. After dissection of theporta hepatis to place an umbilical tape, intraoperative ultrasound is performed toconfirm the lesion, identify other lesions, and define the relationship of the lesion tomajor 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


16

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

Postoperative CareAs discussed above, drains are not necessary for routine hepatic resection with-

out concomitant biliary resection and reconstruction; in fact, drains are associatedwith an increased complication rate in patients undergoing hepatic resection. Post-operatively, intravenous fluids should include phosphorus because liver regenera-tion requires large amounts of high-energy phosphates and serum phosphorus levelscan drop quite low without supplementation. For large-volume liver resections, elec-trolytes, blood count and coagulation profiles are checked postoperatively and dailyfor three days, with particular attention to the prothrombin time (PT) and hemo-globin. Hypoglycemia is not a major concern after hepatic resection. In our experi-ence, administration of 10% dextrose solutions (which is commonly practiced) isnever necessary and only serves to raise the serum glucose levels and induce anosmotic diuresis. In general, packed red blood cells are administered if the hemoglo-bin falls to 8 mg/dL or lower and fresh frozen plasma is given if the PT is greaterthan 17 sec. An understanding of the decreased clearance of hepatic-metabolizeddrugs is important in selecting pain medication as small doses may linger. Unex-plained fever or rising bilirubin with normalization of other hepatic functionparameters suggests an intra-abdominal bile collection and should be investigatedwith a CT scan. Such collections usually resolve within a few days with percutane-ously placed drains; reoperation is rarely necessary.

Selected Reading1. Melendez JA, Arslan V, Fischer ME et al. Perioperative outcomes of major hepatic

resections under low central venous pressure anesthesia: blood loss, blood transfu-sion, and the risk of postoperative renal dysfunction. J Am Coll Surg 1998;187:(6)620-5.

2. Belghiti J, Noun R, Zante E et al. Portal triad clamping or hepatic vascular exclu-sion for major liver resection. A controlled study. Ann Surg 1996; 224:(2)155-61.

3. DeMatteo RP, Palese C, Jarnagin WR et al. Anatomic segmental hepatic resectionis superior to wedge resection as an oncologic operation for colorectal liver me-tastases [In Process Citation]. J Gastrointest Surg 2000; 4:(2)178-84.

4. Launois B, Jamieson GG. The posterior intrahepatic approach for hepatectomy orremoval of segments of the liver. Surg Gynecol Obstet 1992; 174:(2)155-8.

5. Povoski SP, Fong Y, Blumgart LH. Extended left hepatectomy. World J Surg 1999;23:(12)1289-93.

6. Bismuth H, Dennison AR. Segmental liver resection. Adv Surg 1993; 26:189-208.7. 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)171-6.8. Fong Y, Brennan M, Brown K et al. Drainage is unnecessary after elective liver

resection. Am J Surg 1996; 171:158-162.

CHAPTER 1CHAPTER 17

Technique for Placement of the HepaticArterial Infusion Pump

N. Joseph Espat

IntroductionColorectal 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. Inbrief, patients with hepatic metastases considered for surgical resection must be freeof extrahepatic disease. Although bilobar hepatic metastases are no longer consid-ered to be a contraindication to resection, the resection should be anatomic withpreservation of portal vein inflow and hepatic vein outflow to the residual liver. Amore detailed discussion on the concepts relevant to the assessment of these patientsas operative candidates is contained elsewhere in this text.

The relatively limited population of patients who are appropriate for curativehepatic resection implies that the majority of patients (70-80%) will be treated withsystemic adjuvant chemotherapy. Yet, although systemic chemotherapy is the main-stay of treatment for patients with metastatic disease, less than one-third of patientsdemonstrate a response to this therapy and, historically, the five-year survival forthese patients is less than 3%.

Systemic chemotherapy for the treatment of hepatic disease has evolved intoliver-directed chemotherapy. Hepatic artery infusion pumps (HAIP) using animplantable, automatic drug delivery mechanism is one approach. 5-flurode (FUDR)based regimens administered through HAIP have been utilized successfully withimproved median survival in selected patients. However, other drug regimens withand without FUDR have also shown promise. Chemotherapy delivered via a HAIPelicits superior clinical response rates and limited toxicity when compared to stan-dard systemic treatment.

The use of regional hepatic artery chemotherapy delivered via HAIP is based onthree key concepts:

1. Hepatic metastases > 3 mm in size derive their blood supply from thehepatic artery and not the portal vein

2. A 4-fold increase in concentration of chemotherapy (e.g., FUDR) isachieved when injected through the hepatic artery as opposed to systemicinfusion.

3. Certain chemotherapeutic agents are almost completely extracted duringthe first pass through the liver allowing for large doses to be given withminimal side effects.



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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 treat-ment 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 withsynchronous colon and hepatic disease, hepatic metastases within 24 months of theprimary tumor, or patients undergoing hepatic resection with minimal free marginsor demonstrated persistent disease.

Nonresectional hepatic ablative therapies (e.g., radiofrequency ablation,cryoablation), for patients not otherwise candidates for surgical resection, have beenpopularized by the early promising results demonstrated in small series. In thesepatients, 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 EvaluationThis section will be necessarily brief, as the topic of metastatic work-up for patients

with colorectal cancer is covered elsewhere. Patient eligibility for enrollment intoclinical trial is specifically defined by the study protocol. In general, the followingcriteria are common to most HAIP clinical trials:

• History of histologically confirmed colorectal adenocarcinoma metastaticto 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 anatomyfor HAIP placement.

HAIP placement requires that a catheter (Fig. 17.1) be introduced into the gas-troduodenal artery (see following section, technique for placement of HAIP), sothat 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 angiogra-phy (MRA), which is noninvasive and devoid of the angiography-associated mor-bidities, is being developed. At the present time, the radiographic images obtainable

229Technique for Placement of the Hepatic Arterial Infusion Pump

17

by MRA provide at least equivalent anatomic information (Fig. 17.2), althoughtheir routine use awaits validation.

Our preferred operative technique for HAIP placement in patients with stan-dard vascular anatomy is presented.

Surgical Technique for the HAIP PlacementPatients should receive prophylactic preoperative gram-positive antibiotic cover-

age and this should be continued for 24 hours following the operation. Operativedraping of the patient for this procedure should extend cranially to the nipple lineand inferiorly to the symphysis. The skin is prepared with a bactericidal such as aBetadine or Hibiclens solution. The skin is dried with an absorbent sterile towel anda providone-iodine adhesive drape is placed on the operative field. We prefer the useof a right subcostal incision extended slightly beyond the midline. This approachprovides ample exposure to the right upper quadrant and spares the left side of theabdomen for the creation of the pump pocket (Fig. 17.3).

Intra-abdominal adhesions will be present in patients who have previouslyundergone colectomy. Some of these adhesions will need to be cleared to preventinadvertent injury during retraction, dissection, or when passing the pump catheteracross the abdomen from within the peritoneum.

Cholecystectomy is routinely performed to prevent chemical cholecystitis. Thehepatic artery is easily identified in the porta hepatis, both by location and palpabletell-tale arterial thrill. Favorable anatomy for pump placement has been verifiedprior to coming to the operating room by angiogram or MRA.

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


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

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


17

The gastroduodenal artery (GDA) is located immediately inferior to the properhepatic artery coursing inferiorly towards the proximal duodenum (Figs. 17.1 and17.2). Sharp dissection to isolate the GDA is performed, taking care to ligate or clipthe surrounding lymphatic vessels. The common bile duct (CBD) lies lateral to theGDA, and injury to the CBD must be avoided during the dissection. Medially anddeep to the GDA lies the portal vein, and again, great care is needed while dissectingin this area.

After circumferentially dissecting the GDA, a right angle instrument is used tofacilitate the passing of a suture ligature around this vessel. This suture will be usedfor traction as arterial branches are cleared off for approximately 1 cm towards theduodenum and head of the pancreas, 1 cm toward the proximal common hepaticartery, and 1 cm towards the bifurcation of the hepatic artery (but proximal to theright and left divisions).

Up to 15% of patients may have an accessory left hepatic artery arising from theleft gastric artery, which should be (but is not always) identified by the preoperativeimaging. In order to maintain drug-only arterial blood flow to the liver, this vesselmust be identified and ligated. Elevation of the left lobe of the liver to assess for thepresence of a nonvisualized left hepatic artery is mandatory. This is best accomplishedby 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 towardsthe liver via the common hepatic artery and the liver should receive only drugscontaining blood flow.

Considerations for Patients with Variant AnatomyThe technique previously described is applicable only for patients with standard

arterial anatomy. As discussed, it is important to identify any aberrant arterial archi-tecture. By definition, accessory vessels are present, in addition to the normal ana-tomic structures, such that ligation and division of an accessory right or left hepaticartery can be performed without ischemic consequences. In contrast, replaced arter-ies may represent the sole arterial supply to a given lobe of the liver.

Prior to ligation and division, replaced arteries should be clamped with anoncrushing vascular clamp to assess for potential liver ischemia. If no obviousischemia is noted, the vessel can be ligated. However, at least one artery to eitherlobe of the liver arising from the hepatic artery after the take-off of the GDA mustbe preserved. Crosshepatic arterial perfusion to the contralateral lobe of the liverdevelops rapidly after ligation of the replaced lobar artery in the patient with anontoxic liver. In contrast, if ischemic changes are observed during “trial-clamping”,then that vessel should be preserved and cannulated separately to maintain adequatehepatic 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 bypalpation as it exits from behind the duodenum, courses lateral to the common bileduct, and posteriorly within the hepatoduodenal ligament. The RRHA has no sidebranches that can be used to insert the catheter; however, arteriotomy or directpuncture under vascular control can be used for placement of a polyethylene or 22


17

gauge “angiocatheter” with subsequent connection to the HAIP catheter. Placingthe catheter directly in the RRHA, and ligating the LHA, results in the develop-ment of crossover perfusion of the left lobe of the liver. Another approach is theplacement of a double-catheter pump where one catheter is placed into the LHAfrom the GDA and the second catheter is inserted directly into the RRHA to assurebilateral 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 thereis a normal RHA. In this setting, the HAIP catheter can be inserted into the GDA toperfuse the RHA with ligation of the RLHA. Another technique is the placement of adouble-catheter pump, where one catheter is inserted into the LGA to perfuse theRLHA and the other catheter is inserted into the GDA to perfuse the RHA.

Trifurcation of the Common Hepatic Artery (CHA)into RHA, LHA and GDATrifurcation of the CHA into a RHA, LHA and GDA is another described ana-

tomic variant that can be managed by inserting the HAIP catheter into the GDA1 cm proximal to the takeoff of the GDA from the CHA to allow for adequate drug-blood mixing. The GDA is then ligated. Although feasible, this approach is associ-ated with an increased risk for CHA thrombosis. Alternatively, insertion of the HAIPcatheter into the splenic artery, advancing it into the CHA with ligation of the GDAand left and right gastric arteries, will obtain bilateral perfusion. A more complexapproach to deal with this anatomy is to construct a conduit using a short segmentvein graft for catheter insertion into a selected artery with subsequent ligation of theother vessels. We do not recommend this latter approach.

These variant arterial anatomies underscore the importance of preoperativeassessment of vascular anatomy in order to be prepared at the time of operation.Failure to appropriately identify and ligate aberrant arteries and arterial branchesmay result in malperfusion.

Creation of the Subcutaneous Pump PocketThe 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 toprevent patient discomfort from the hard metal pump abutting against the ribs. Theskin incision is transverse and should measure no more than 1 cm wider than thewidth of the actual pump to be placed (Fig. 17.4). The subcutaneous tissues aredivided using electrocautery up to, but not into, the abdominal wall fascia. Continuinginferiorly along the adipose-fascial interface, the pocket is extended for about 8-10cm (actual pocket size should be planned based on the size of the actual model ofpump to be implanted). Strict attention to hemostasis must be maintained duringthe dissection of the subcutaneous pocket to minimize the risk of hematoma andlessen 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


17

at body temperature to activate it. Flow through the catheter is driven by hydro-static pressure secondary to internal expansion from thermal activation. The deliv-ery mechanism is graduated to deliver a set rate of flow, and adjustment of thesolution 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 varyaccording to manufacturer and model; however, all designs will have a catheter withan internal component that exits through the pump body (Fig. 17.5). This cathetermust be inserted into the abdominal cavity through the anterior abdominal walland subsequently placed into the GDA. In performing this maneuver, care shouldbe taken to avoid injury to vessels coursing through the posterior surface of therectus abdominus muscle.

Pumps have anchoring “loops” (Fig. 17.5) fused to the pump body housing toprevent “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 theceiling; interrupted nonabsorbable sutures are placed into the fascia of the anteriorabdominal wall and passed through each anchor loop. The two distal anchors aresutured first and not tied until the two proximal sutures are placed. Until the suturesare tied, the ends of the cut suture are held in place by individual clamps. Theinferior pump pocket edge is elevated and the distal anchor sutures are tied, pullingthe pump down into the pocket as it is fastened down. Care should be taken toinsure that the pump catheter does not become twisted or damaged during thismaneuver. With the pump in place, the catheter is free within the abdomen.

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


17

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

The catheter is measured and cut sharply such that the tip has an oblique angleand only one of the flanged catheter hubs remains. The catheter length should belong enough to reach the junction of the GDA with the hepatic artery but notextend beyond it. In this manner, flow-out of the catheter will necessarily go onlytowards the liver.

The GDA is ligated in continuity as it enters the duodenum. The position ofthis suture will determine the length of artery available for catheter insertion. Oncethe catheter is prepared as described above, and the branches off of the GDA andother arteries have been cleared, proximal and distal control of the hepatic artery isobtained using pediatric vascular clamps. A #11 scalpel blade is used to incise theanterior wall of the GDA in a transverse fashion. An arteriotomy introducer is in-serted into the GDA lumen to facilitate passing of the catheter tip into the vessellumen. The catheter is advanced using nontoothed forceps and the previously placedcircumferential traction suture ligature is tied down onto the catheter behind theflanged hub. Care is needed to insure that the knot is not too tight as to impede orocclude flow through the catheter. We advocate the use of an additional separatesuture to prevent inadvertent arterial dislodgement. We place a 4-0 prolene suturethrough the adventitia of the GDA behind the flanged hub of the catheter andcircumferentially encompassing the vessel, again not encroaching on the catheterlumen. The distal (outflow) vascular clamp is removed, followed by the proximal(inflow) clamp.


17

Assessment of Hepatic PerfusionIntraoperative fluorescein test is generally performed after pump placement to

assure liver-only perfusion. Using the side port of the pump, approximately 3-5 ccof fluorescein (nondiluted) are injected, followed by illumination with a Wood’slamp. If all the arterial branches have been properly ligated or clipped, only the livershould demonstrate fluorescence. Do not aspirate into the pump when injecting itas this will result in small clot formation and subsequent pump malfunction. Subse-quently, the pump is flushed with 10 cc of heparinized saline. The pump pocket isclosed in two layers using absorbable suture material. The abdominal incision isclosed in standard fashion.

Postoperative hepatic perfusion and extravasation (i.e., stomach, duodenum, andspleen) via HAIP is assessed three days postoperatively by a Technetium-labeledmacroaggregated albumin hepatic scan. This will confirm liver-only pump perfu-sion and is necessary prior to the initiation of HAIP therapy (Fig. 17.6).

Brief Comments on Technical ComplicationsAnalysis of the technical complications associated with hepatic artery infusion

pump placement, reveals that HAIP complications can be divided into those occur-ring either early (< 30 days postpump placement), or late (>30 days) (Table 17.1).Furthermore, complications are divided into arterial, catheter, perfusion or pumprelated.

Arterial complications include intimal dissection and thrombosis. Arterial throm-bosis 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 cath-eter from its original site or out of the artery with or without hemorrhage. Catheterdislodgement is a rare occurrence in the early postoperative period; most dislodgementoccurs late. Catheter dislodgement may be accompanied by hemorrhage that can belife-threatening. Catheter occlusion is a late occurrence and can be salvaged by lytictherapy.

Malperfusion is defined as the identification of organ perfusion other than theliver (i.e., stomach, duodenum or spleen). Extrahepatic perfusion can occur withcatheter misplacement or failure to identify and ligate the appropriate arterial branchesoff the GDA. If malperfusion is apparent, a patent branch of the common hepaticarterial system that continues to perfuse the distal stomach or duodenum is oftenidentified. Once localized, this complication is corrected by laparotomy with liga-tion of the patent branches of the GDA or CHA. More recently, patent vessel brancheshave 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 prematuretermination of therapy. However, pump salvage rates of approximately 25% areobtainable for both early and late pump infections.

Complications related to local and regional toxicity of the therapeutic agents arewell characterized elsewhere.1,5


17

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

Table 17.1. Early and late technical complications of HAIP ( n=391)6

Complication Early Terminated Late TerminatedArterial thrombosis 10 (1%) 6 (2%) 15 (4%) 14 (4%)Catheter dislodgement 3 (1%) 2 (1%) 22 (6%) 12 (3%)Catheter occlusion 0 — 9 (2%) 4 (1%)Pump infection 4 (1%) 3 (1%) 8 (2%) 6 (2%)Malperfusion 10 (3%) 0 3 (1%) 0Total 27 (7%) 11 (3%) 57 (15%) 36 (9%)

The technical complications following HAIP placement between 1986 and 1995(N=391). Complications were defined as early (<30 days ) and late (>30 days)following pump placement. These data represent a median follow-up interval of16 months (range 1-110). A total 3% early and 9% late technical failure rates wereobserved. The prevention of late arterial thromboses and catheter dislodgementwould prevent the majority of premature treatment terminations related to pumpcomplications.


17

SummaryIn the absence of efficacious systemic chemotherapy regimens to treat hepatic

colorectal metastases, regional therapies will continue to be investigated. HAIP place-ment has a low associated mortality; however, the challenge for the surgeon in themanagement of these patients is to provide a reliable system for the administrationof regional chemotherapy. The efficacy of hepatic artery infusion pump (HAIP)chemotherapy for metastatic colorectal cancer confined to the liver is currently thesubject of several national multi-center randomized trials.

Selected Reading1. Allen Mersh, TG, Earlam S, Fordy C, Abrams K, Houghton J. Quality of life and

survival with continuous hepatic-artery floxuridine infusion for colorectal livermetastases [see comments]. Lancet 1994; 344:1255-6000.

2. Chang AE, Schneider PD, Sugarbaker PH et al. A prospective randomized trial ofregional versus systemic continuous 5-fluorodeoxyuridine chemotherapy in thetreatment of colorectal liver metastases. Ann Surg 1987; 206:685-933.

3. Ensminger WD, Rosowsky A, Raso V et al. A clinical-pharmacological evaluationof hepatic arterial infusions of 5-fluoro-2'-deoxyuridine and 5-fluorouracil. Can-cer Res 1978; 38:3784-3922.

4. Grage TB, Vassilopoulos PP, Shingleton WW et al. Results of a prospective ran-domized study of hepatic artery infusion with 5-fluorouracil versus intravenous5-fluorouracil in patients with hepatic metastases from colorectal cancer: A Cen-tral Oncology Group study. Surgery 1979; 86:550-555.

5. Kemeny N, Daly J, Reichman B et al. Intrahepatic or systemic infusion offluorodeoxyuridine in patients with liver metastases from colorectal carcinoma. Arandomized trial. Ann Intern Med 1987; 107:459-655.

6. Dudrick PS, Picon A, Paty PB et al. Technical Complications Associated withHepatic Arterial Infusion Pumps for Metastatic Colorectal Cancer. (In Prepara-tion)

7. Sigurdson ER, Ridge JA, Kemeny N et al. Tumor and liver drug uptake followinghepatic artery and portal vein infusion. J Clin Oncol 1987; 5:1836-400.

8. Wagner J S, Adson MA, Van Heerden JA et al. The natural history of hepaticmetastases from colorectal cancer. A comparison with resective treatment. AnnSurg 1984; 199:502-588.

9. Weiss GR, Garnick MB, Osteen R et al. Long-term hepatic arterial infusion of5-fluorodeoxyuridine for liver metastases using an implantable infusion pump. JClin Oncol 1983; 1:337-444.

10. Wingo PA, Ries LA, Rosenberg HM et al. Cancer incidence and mortality, 1973-1995: a report card for the U.S. Cancer 1998; 82:1197-2077.

CHAPTER 18


Non-Resectional Hepatic AblativeTechniques:Cryotherapy and Radiofrequency Ablation

Ronald S. Chamberlain and Ronald Kaleya

IntroductionThe liver is a frequent site of both primary and metastatic tumors. Surgical resec-

tion, and in rare instances liver transplantation, remain the only treatments associ-ated with prolonged survival and in some cases cure. Unfortunately, less than 25%of patients with either hepatocellular cancer (HCC) or metastatic colorectal cancerpresent with liver-only disease and are candidates for surgical resection. The inabil-ity of surgery to impact on the survival of most patients with malignant tumors ofthe liver has been the impetus behind the development of multiple alternative treat-ment modalities. Tumor histology, stage and site of the primary tumor, extent ofhepatic parenchymal involvement, presence of extrahepatic disease, and the clinicalcondition of the patient influence the appropriateness of the various alternative treat-ments. Available alternatives include hepatic artery chemotherapy (Chapter 17) he-patic arterial embolization or chemoembolization (Chapter 4), percutaneous ethanolablation (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 mini-mally invasive techniques. This Chapter will focus on the indications, techniques,and complications associated with cryotherapy and radiofrequency thermal abla-tion. Suffice it to say the clinical efficacy of both techniques remains unproven, andthe subject of considerable on-going study. Based upon this data, several prospectiveand retrospective analyses have demonstrated that liver failure is the primary causeof death in up to 90% of these patients. Non-resectional hepatic ablative strategieshave been developed in an attempt to alter either the course of the disease and/orcause of death in patients with unresectable liver tumors.

Indications for Non-Resectional Ablative Therapies

Histology

Hepatocellular CarcinomaPrimary liver cancer is the most common malignancy in Southeast Asia and

Africa and remains the leading causes of cancer-related deaths world wide. Each yearthere 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

239Ablative Techniques in the Management of Hepatobiliary Malignancies

18

nevertheless greater than 90%. Among patients with HCC, only 15 to 25% areoperable at presentation and even fewer patients are resectable with curative intent.Despite this fact, the majority of patients with unresectable disease have tumor con-fined to the liver. In a report by Farmer et al from the Dumont-UCLA Liver Trans-plant Center, 70% of patients with HCC had disease localized to the liver and only24% were candidates for hepatic resection; these figures clearly demonstrate thecentral role that ablation therapy can play in the treatment of hepatic tumors.

Metastatic DiseaseThe liver is one of the most common sites of metastatic spread for many cancers,

particularly gastrointestinal malignancies. Unfortunately, most malignancies thatspread to the liver also spread elsewhere making regional ablative therapies unsuit-able. Colorectal cancer represents a unique exception to this rule, in that up to one-third of patients with metastatic colorectal cancer may have liver only metastases.Despite occasional reports of high rates of resectability (> 50%), in reality only asmall proportion of patients with metastases confined to the liver are operable dueto limitations imposed by tumor characteristics and patient co-morbidities. Severalauthors have estimated that only 8 to 12% of all patients who develop liver me-tastases from colorectal primaries are resectable for cure. While the percentage ofpatients 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 vari-ety of other tumor histologies in addition to colorectal cancer. These include, butare not limited to, metastases from gastric, pancreatic, esophageal, thyroid, neu-roendocrine, melanoma, renal cell, and sarcoma. The application of ablative thera-pies to treat these tumors should be considered extremely experimental and cannotbe advocated outside of a clinical trial. The only exception to this rule may be theuse of radiofrequency ablation for the treatment of metastatic neuroendocrine tu-mors for which a considerable body of literature is emerging.

Additional Indications and ContraindicationsAbsolute indications and contraindications for cryotherapy and RFA remain

undefined. As a general rule, most experienced centers advocate treating not morethan 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 notcandidates for ablative therapy alone. Non-resectional ablative strategies are par-ticularly attractive approaches for the treatment of many patients with HCC whohave limited functional hepatic reserve due to cirrhosis. These techniques permitpinpoint tumor ablation while maximizing the preservation of normal liver. In someinstances, ablative modalities may be used in conjunction with resective therapy totreat a “close” or “positive” margin of resection.

Cryotherapy

The Physiology of Cryoinjury: Deep FreezeThe 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 ofcooling. Factors such as the depth of hypothermia, rate of decline in tempera-ture, and number of freeze-thaw cycles are all important variables in regards tothe percent of cell death achieved.

When a cryoprobe is inserted into the liver, three overlapping zones of injurydevelop within the iceball. The rate of freezing decreases in proportion to thedistance from the probe and creates zones of intermediate and slow cooling. Simi-larly, a grading of temperature develops in the iceball, falling 3 to 10˚C per milli-meter (from -170˚C near the probe to just below the 0˚C at the periphery of thecryolesion). The dynamics of the freezing process cause different mechanisms ofinjury to occur in these three zones.

Cooling RatesCooling 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 cellsurvival is seen with intermediate cooling rates. Cellular dehydration causes the lethalinjuries when slow cooling rates are used, while rapidly cooled cells are destroyed by themechanical action of ice crystallization.

Intra- and extracellular fluids are complex solutions containing varying amounts ofprotein, macromolecules and electrolytes. The presence of these solutes depresses thefreezing 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 theextracellular space, solutes are excluded leaving a hyperosmotic extracellular environ-ment. Cellular dehydration occurs as the unfrozen intracellular water flows out of a cellalong the osmotic gradient. As a consequence of cellular dehydration, the intracellularpH and ion concentrations are altered, proteins denature and membrane bound en-zyme systems are destroyed. Although many cells die as a direct result of dehydration,others succumb to isotonic rehydration during the thaw cycle. When the cryolesionthaws, the extracellular fluid thaws first creating a relatively hypotonic environment.Water flows into the hyperosmolar and hypertonic cells causing them to burst. Thistype 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 mecha-nism. Cooling rates on the order of 50˚C per minute cause intracellular fluid tofreeze before cellular dehydration takes place. Intracellular ice is particularly le-thal. Small ice crystals coalesce, resulting in a physical grinding action that dis-rupts cellular organelles and membranes leading to reproducible and certain celldeath. 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 theextracellular fluid turns to ice. However, the temperature falls fast enough to freeze theintracellular water before cellular dehydration reaches a critical level. Intracellular iceformation excludes solute, thereby increasing intracellular osmotic concentration, equal-izing the osmotic gradient, and preventing further cellular dehydration. In this setting,the critical level of dehydration allowing influx of solute is not reached, thus protectingthe cell from the lethal injury caused by water influx during the thaw cycle. Cells in thezones of intermediate cooling therefore have improved survival, and several freeze-thaw cycles are necessary to effect complete cell death.


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Hypothermia and the Thawing ProcessThe sensitivity of different tissues to hypothermia varies considerably. Most nor-

mal hepatocytes exposed to temperatures below –15 to -20˚C die, whereas nearly allhepatocytes cooled to -10˚C survive. Bile ducts, connective tissue and vascular struc-tures tolerate lower temperatures than hepatocytes. Unfortunately, liver tumors areeven more robust than normal hepatocytes and tend to require even deeper hypoth-ermia for complete and certain destruction. As a general rule, a temperature of lessthan -40˚C is sought. In practice, assuring that all tumor cells reach this temperaturerequires 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 ofrecrystalization. In brief, as the tissue warms ice crystals reform, coalesce and en-large, 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 ablatedin one freeze/thaw cycle, multiple cycles are necessary to ensure that tumor cells atthe periphery reach the depth of hyperthermia required for reliable cell kill.

Technical Aspects of CryotherapyHepatic cryotherapy can be performed through a variety of approaches, includ-

ing the percutaneous, laparoscopic and open method. The open approach allowsthe most flexibility and permits treatment of lesions not accessible by other meth-ods, albeit with increased operative morbidity. Minimally invasive cryotherapy tech-niques should be limited to highly selected patients.

Preoperative PreparationPrecise radiologic evaluation of the volume, location, and proximity of the liver

tumors(s) to the hepatic vasculature and biliary structures is the key to performanceof successful cryotherapy and RFA. Patients with more than 40% of the liver re-placed with tumor are typically not candidates for either ablative approach. In gen-eral, the same preoperative preparations instituted prior to liver resection are employedprior to either cryotherapy or RFA. This is most important in those rare instancesduring which a conversion to resection is necessary due to unexpected resectabilityor intraoperative complications. A unique, but rare, complication of cryotherapythat must be anticipated is “cryoshock.” This complication is typically manifestedby profound systemic hypotension, pulmonary failure, renal failure, andcoagulopathies. 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 treatedwith appropriate blood products.

Operative (Open) ApproachThe abdomen may be approached through a subcostal, bilateral subcostal (Chev-

ron-type), or mid-line incision. The peritoneal cavity is carefully inspected for anyevidence of extrahepatic metastases. Enlarged lymph nodes, particularly those in thehepatoduodenal ligament, should be evaluated by frozen section. The falciform liga-ment is divided up to the level of the hepatic veins to permit careful bimanualpalpation. A 5 MHz intraoperative ultrasound transducer is used to evaluate each seg-ment 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 shouldbe confirmed by intraoperative ultrasound and/or biopsy.

Once an intraoperative strategy is defined, a Penrose drain or vessel loop is placedaround the porta hepatis should inflow occlusion be required later. The cryoprobe isintroduced into the center of each lesion under ultrasound guidance. The place-ment is confirmed sonographically by viewing the probe in two or three perpen-dicular planes. When at all possible, the cryoprobe should be introduced throughthe anterior surface of the liver. By placing the ultrasound transducer on the poste-rior surface of the liver, the introduction of the cryoprobe and the subsequent for-mation of the ice ball can be carefully monitored. In order to minimize tumor spillageand to avoid “cracking” the surface of the tumor, the probe should ideally be in-serted through normal liver before entering the tumor. Direct introduction of theprobe into the tumor or a wire-guided Seldinger-style localization may be used de-pending upon the depth of the lesion. The Seldinger technique is preferred for deepintraparenchymal and poorly palpable tumors. After identification of the tumor byintraoperative ultrasound, an echogenic needle is passed into the center of the lesionand is subsequently exchanged for a J-wire. Once the J-wire is in place, the tract isdilated with a coaxial dilator and peel away sheath. The dilator is withdrawn afterproper position is established and the cryoprobe is inserted through the sheath intothe center of the tumor. The correct positioning of the cryoprobe should be re-evaluated in two or three different axes. Ideally the probe is placed through thetumor with the tip near the opposite margin.

The size and location of the tumor governs the type of cryoprobe used. Thesurgeon must be familiar with the physiology of cryotherapy in order to determinewhich shape of probe is most suitable for the situation. The most commonly usedcryo-system employs vacuum insulated probes and supra-cooled liquid nitrogen re-frigerant. 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 an8 mm trocar probe creates a freeze zone up to 6 cm. Probes may be used in tandemto create larger lesions. Flat-faced probes which form a “half-moon” lesion may beapplied 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 sur-rounding tissue. Laparotomy sponges are usually sufficient for this purpose. Thefreezing process then commences. At -100˚C, the cryoprobe becomes stuck in thehepatic parenchyma, and additional probes may be safely placed. When one is justbeginning to perform cryotherapy we recommend using one probe at a time inorder to ensure adequate monitoring of the cryoablation and reduce the risk ofintraoperative hypothermia. The freeze front appears as a hyperechoic rim with pos-terior acoustic shadowing on intraoperative sonography (Fig.18.2). Cooling contin-ues until the freeze front extends 1 cm beyond the margin of the tumor. This processusually takes 8 to 15 minutes to complete depending upon the efficiency of thecryosystem and the size of the tumor.

Following completion of the first freeze cycle, the tissue is thawed passively. Com-plete thawing may take up to 20 to 30 minutes. Since cryotherapy failure usuallyoccurs at the periphery of the ice ball, we recommend thawing only the most periph-eral centimeter before initiating the second freeze cycle. This technique reduces opera-


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tive time without compromising clinical efficacy. Additional freeze-thaw cycles areaccomplished in a similar fashion.

Following completion of the second freeze-thaw cycle, the probe is actively re-warmed allowing it to disengage before the tumor completely thaws. The probetract is packed with Surgicel™ or a similar hemostatic material and gentle pressureis applied to the liver to prevent delayed hemorrhage. The thawing ice ball should behandled gently to prevent a cleavage plane from developing between of the iceballand the normal liver parenchyma that can result in massive bleeding. Bleeding inthe probe site is common but generally stops promptly as the coagulation cascadeactivates at body temperature.

Postoperative CareDrains 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 secondpostoperative day. A transient elevation of liver enzymes, leukocytosis, drop in theplatelet count, and high fever are common in the early postoperative period. Therise in the liver transaminases is directly related to the volume of liver treated andusually resolves within one week. Platelet count typically bottomout in the first fewdays and then stabilize and returns to normal or supranormal levels in 7 to 10 days.Less commonly, the coagulation profile deteriorates with increased partial thrombo-plastin and prothrombin times; however the development of clinically disseminatedintravascular coagulopathy is rare.

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


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Radiofrequency Ablation

The Physiology of Thermal InjuryThe 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 useof heat in a therapeutic fashion to treat tumors. Throughout the last century, bothwhole-body and local hyperthermia have been extensively evaluated for their me-dicinal value in the treatment of a variety of neoplastic and non-neoplastic disor-ders. Yet despite anecdotal reports on the efficacy of whole body hyperthermia, noreproducible clinical results have been generated and there is no current medicalindication for systemic hyperthermia treatment. Local hyperthermia, which refersto heat applied directly to the tumor resulting in coagulation and tumor destruc-tion, has been used for decades in the palliative management of a variety of malig-nancies. Electrocautery or laser ablation has demonstrable palliative benefit inproviding both symptom relief and restoration of function for tumors that block the

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


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bronchus, esophagus, colon or rectum. Unfortunately, techniques, which are usefulto recannulate hollow viscus organs or parts of the respiratory tree, have no clinicaluse for most solid organ metastases. Recent technologic advances, however, havenow made it feasible to induce thermal injury in precise anatomic locations whileavoiding injury to surrounding tissue. Radiofrequency, microwave, and laser abla-tion are three such modalities that may have both curative and palliative roles in thetreatment 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. Thisdiscovery provided the framework for the development of medical diathermy andthe application of the electrocautery in surgery. The clinical utility of RF ablativetechniques to induce controlled lesions with anatomic precision has already beenexploited in the fields of cardiology and neurology where it has been used to treatcardiac arrhythmias, seizures, and movement disorders. The application of this tech-nology in the treatment of hepatic tumors did not occur until 1990. These initialreports detailed the use of ultrasound guided RF ablation to induce deep thermalinjury in hepatic tissue while sparing normal parenchyma. Since that time RF tech-nology has also been used to treat neoplastic processes including breast tumors,prostate tumors, soft tissue sarcomas, head and neck tumors, osteoid osteomas, ce-rebral metastases, and lung tumors.

Although the clinical value of RFA for any tumor remains unknown, clinicalreports and indications for its use continue to expand. At present, a variety of equip-ment-related and technical approaches to RF technology are being explored. Thesestudies include reports detailing the superiority of bipolar versus monopolar elec-trodes, pronged versus straight electrodes, and new cooled-tip electrodes. A detailedanalysis of these new approaches is beyond the scope of this chapter.

The Physiology of RFA: Energy TransferRF ablation refers to the induction of thermal injury due to frictional heat gen-

erated by the ionic agitation of particles within tissue following the application ofalternating current in the radiofrequency range (200-1200 mHZ). The frictionalheat that occurs desiccates the surrounding tissue leading to the evaporation of in-tercellular water and coagulation necrosis. In point of fact, radiofrequency wavesplay no role in the induction of tissue injury during RF ablation. The agitation ofions within the tissue occurs only around the needle or electrode through which thealternating current is applied. Unlike other forms of local hyperthermia, the elec-trode does not become hot. The anatomic precision of the zone of injury variesbased on the size, position, and shape of the electrode used. Heat (i.e., ionic agita-tion), which concentrates around the tip of the electrode, is rapidly dissipated withfurther distance from the electrode. McGahan has reported that a minimal tempera-ture threshold of 49.5˚C, and an optimum temperature of 80-100˚C are requiredfor coagulation of hepatic tissue to occur. Although the degree of injury around theneedle increases with both rising temperature and length of time over which theheat 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 electricalimpedance. At present, this remains a major limitation on the size of lesion that canbe treated with this modality.

Technical RFA Issues: Generators and ElectrodesThree RF generators are commercially available for clinical or experimental use

in the Unites States. All three units provide alternating current within theradiofrequency range and function based upon the same principles. They differ pri-marily 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. (Moun-tain Valley, CA), and consists of an RF generator operating at 460-kHZ frequencysupplied by a 50 RF watt power output (Fig. 18.3). The electrode is a 15-guagestainless needle insulated by thick plastic, with a 1.0 cm active tip and four to eightnickel-titanium retractable hooks. The maximum deployment diameter for the hooksis currently 7 cm, and each hook is equipped with an individual thermistor to moni-tor 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 elec-trode. The electrode itself is hollow with two to three side ports. Continuous perfus-

Fig. 18.3. RITA Medical Systems RFA Generator.


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ing of the inner chamber of the electrode with cooled saline is believed to increasethe zone of thermal injury via two distinct mechanisms. Cooling the tip of theelectrode potentially prevents charring of adjacent tissues (keeping resistance low),and thereby increasing the zone of thermal injury. The continuous perfusion of thesurrounding tissue with saline via the side ports in the electrode theoretically in-creases the number of ions in the target tissue resulting in more ionic agitation andthermal injury. Unlike the RITA device, the length of the active tip is variable, between1 and 3 cm, and can be changed based on the size of the lesion being treated. The RFdevice manufactured by Radiotherapeutics is a 90 W alternating current generatorwith a multiple array electrode with 10 curved prongs which deploy from the end ofthe electrode. The large number of prongs is thought to provide a more spherical injurythan the straight probe (Radionics). Unlike the RITA electrode, the Radiotherapeuticselectrode does not have individual thermistors at the end of each prong. Comparisondata between these three devices is currently not available.

Indications and ContraindicationsAt 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

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


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recommend that RFA use be limited solely to those patients who are not candidates forsurgical resection. Although significant research is currently underway to optimizeRF thermal ablation technology, only tumors up to 5 cm in diameter can be effec-tively treated by a single ablation. Although multiple adjacent ablations can be per-formed to encompass larger lesions, overlapping of ablation fields increases tissuecharring and impedance thereby limiting effectiveness. A 7 cm ablative probe fromRITA is due to come to market shortly.

As with cryotherapy, the complication rate increases, and the likelihood ofachieving a therapeutic benefit decreases as the number and size of the treatedlesions increase. Although there are no absolute contraindications to RF thermalablation, most authors advocate limiting treatment to those patients with less thanfour lesions. Patients with obvious extrahepatic disease, and those with limited lifeexpectancies (< 6 months), are similarly unlikely to benefit from ablative therapiesand should not be treated.

Table 1. Indications and contraindications for hepatic ablative therapy

Indications

Patients with four or fewer, small (< 5 cm) primary hepatocellular ormetastatic colorectal tumors who are not candidates for surgical resectiondue 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 me-

tastases. Tumor biology and the natural history of the malignant tumorshould be considered carefully before treatment for non-colorectalmetastases is offered.

Contraindications

• 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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TechniqueRF thermal ablation can be performed percutaneously, laparoscopically, or at the

time of laparotomy. Technically, the performance of RF thermal ablation is the sameregardless of which method is utilized. However, hepatic exposure, access to tumorlocations, as well as patient monitoring are different depending upon the approach.Significant controversy currently exists as to the optimal way to perform RFA. Thelowest risk of recurrence (or persistence) is associated with open laparotomy, butacceptable recurrence rates (though higher) have also been reported with thelaparoscopic approach. Percutaneous RF thermal ablation represents another viableoption. However, prior to referral to an interventional radiologist for treatment, allpatients with liver metastases should be discussed at a multidisciplinary tumor boardmeeting to optimize treatment. For the sake of consistency we shall describe theopen technique.

Operative Technique The abdomen is opened using a subcostal, bilateral subcostal (Chevron) or mid-

line incision. A careful exploration for extrahepatic disease is carried out, and aftercomplete mobilization, bimanual and ultrasound examination of the liver is per-formed. Once the decision is made to proceed with RFA, the needle is introducedinto the selected area of the tumor using sonographic guidance. We utilize the RITAdevice at our institution. Using this device, the tip of the needle is positioned at thedeepest part of the tumor prior to deploying the electrodes. The prongs are initiallydeployed approximately two-thirds of their maximum length, and the ablation isstarted 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 de-ployed fully. The temperature is kept at 90–110˚C for 6 minutes to complete theablation process. Overlapping ablations are completed to encompass the entire le-sion if necessary. In general, lesions less than 3 cm require only one or two treat-ments. Lesions larger than 4 cm may require multiple (> 6) overlapping fields toencompass the entire tumor with a satisfactory margin of normal tissue. As withsurgical resection of hepatic tumors, a margin of 1 cm is ideal, but often not attain-able. At the completion of the ablation process, the prongs are retracted and theneedle tract is cauterized as it is removed (Fig. 18.5).

Results

Cryotherapy

Hepatocellular CarcinomaCryotherapy of primary liver cancer has been reported in approximately 250

patients to date (Table 18.2). These numbers include patients who have undergonecryotherapy alone or in combination with resection, percutaneous alcohol injection(PEI), chemotherapy, or hepatic arterial ligation. Among patients treated with cryo-therapy alone, the five-year survival rate was 28%, and as expected this correlatedwell 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. Thepattern 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 tumorin the left lateral segment of the liver. B, Post-op contrast-enhancing CT scan dem-onstrated a hypodense area in the left lateral segment, and a second in the rightlobe (not seen in A).


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Table 18.2. Published series of cryotherapy for hepatic tumors

Author (Year) Histology Patients (N = ) ResultsZhou (1996) HCC 167 Combined series of cryo

alone plus cryo combinedwith other treatment 32%5-year actuarial survival

Haddad (1998) CRM 31 Combined series 7 moPLC median disease freeOther survival

Seifert & Morris (1998) CRM 116 Combined series 13%5-year survival 26 momedian survival

Yeh (1997) CRM 24 Combined series 85%3-year actuarial survival31 mo median survival

Adam (1997) HCC 34 Combined series 52%CRM 5-year survival

Korpan (1997) CRM 63 Combined series 4%5-year actuarial survival

Shafir (1996) CRM 39 Cryo alone 65%HCC 3-year actuarial survivalOther

Crews (1997) CRM 40 Cryo alone 30%HCC 5-year actuarial survivalOther

Weaver (1995) CRM 140 Combined seriesOther 62% 2-year actuarial

survival 22 mo mediansurvival

Wrens (1997) HCC 12 Cryo alone 19 momedian survival

Ravikumar (1991) CRM 32 Combined series 63%HCC overall actuarial survival

Onik (1991) CRM 18 Combined series 33%survival at 29 mos

Lezoche (1998) CRM 18 Cyro alone 78% NEDOther at 11 months

McKinnon (1996) CRM 11 Combined series 73%PLC alive at 18 months

Heniford (1998) CRM 12 Cryo alone 83% aliveOther 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, sur-vival following cryoablation for HCC is reasonable when compared to other thera-peutic approaches. For the present however, it seems unlikely that cryotherapy willreplace PEI as first line therapy for unresectable HCC.

Liver MetastasisCurrently, long-term studies of patients treated with cryotherapy are inadequate

as few provide follow-up beyond 2 years. More concerning, cryotherapy has typi-cally been utilized as a salvage procedure or in combination with other treatmentmodalities which limits any ability to draw conclusions about its efficacy. Ravikumaret al have reported the best results with overall and disease free actuarial survivals of78% and 39%, respectively, among 18 patients undergoing an R0 cryoablation ofliver metastasis. Although encouraging, these results have not been duplicated inmore recent studies in which survival rates remain highly variable. Note, however,despite the wide variation in outcome following cryotherapy, approximately 20% ofpatients in nearly all published studies have achieved a durable survival.

We believe that current data support the ongoing use of cryosurgery in clinicaltrials only. Cryotherapy should not be used in cases of resectable disease. As withother regional therapies, survival appears closely related to the size of the lesionstreated 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 orwithout extrahepatic disease, and underscores the need for multi-modality approaches.

Radiofrequency Ablation

Hepatocellular Carcinoma and Liver MetastasesTo 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) ormetastatic tumors (N=11). The histology of the metastatic tumors was varied andincluded six colorectal metastases, one breast tumor, one gastric tumor, one gastrinomaand one thymoma. Tumor size was 3.5 cm in less than all but one case. The 1-, 3-and 5-year survivals in patients with HCC were 94, 68 and 40% respectively. Fifty-nine percent of patients remain disease free at 12 months, while 41% of patientsrecurred. Among the 16 patients that recurred, only two recurred in a previouslytreated area. The outcome in patients with metastatic disease was less favorable with50% of patients recurring within the first year and only two patients remainingdisease free at 11 months on follow-up. There were no procedure-related complica-tions. Rossi et al (1998) has subsequently reported an additional 37 patients treatedwith RFA. In this group there were 26 patients with HCC and 14 patients withhepatic metastasis, all tumors were less than 3.5 cm. In the HCC patient group100% tumor ablation was achieved when assessed by CT scan. Seventy-one percentof patients remain tumor free at a follow-up of 10 months. These results are compa-rable to those reported for both surgical resection and percutaneous ethanol injec-tion for small hepatocellular cancers. Among the 14 patients with metastatic diseasethe 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 diseaseby 14 months of follow-up.

Solbiati et al (1997) reported on 16 patients with a variety of metastatic livertumors 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 fol-low-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 under-went surgical resection (15 to 60 days after RFA) and four had residual tumors. In aseparate study, Solbiati et al (1997) reported on the treatment of an additional 29patients. Ninety-four percent of patients were alive at one year and 50% of patientsremained disease free. There were no serious complications in either study.

Livraghi et al (1997) treated 15 patients harboring 25% separate metastatic livertumors with RFA. Seventy-four percent (N=11) of patients had colorectal metastases,with the remaining having a variety of other tumor histologies. A complete radio-logic response was obtained in 52% of patients at six months; however, only onecomplete 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 compensatedliver cirrhosis with Child-Pugh A or B classification. Exclusion criteria were tumorsgreater than 5 cm, portal vein thrombosis, refractory ascites or dilated bowel ducts.Eleven patients had solitary tumors and one patient had two tumors. Eighty-threepercent had complete necrosis by CT assessment; however, only 52% had no evi-dence of viable tumor on CT six months later. Curley et al (1999) have reported on125 patients with metastatic liver disease managed with open RFA and have dem-onstrated it to be an effective approach in selected cases of unresectable disease.

Complications after RFA are rare. Major complications include liver hemor-rhage, pyogenic abscess formation, enterotomy, and diaphragmatic injury.

SummaryMinimally invasive ablative treatments for inoperable hepatic metastasis are a

promising technique that can be performed with low morbidity. Recent advances inthe technology have made it possible to treat more and larger lesions using theseapproaches. Given the simplicity of RFA, we prefer it to cryotherapy, though com-parison studies are lacking. However, the absence of strong data supporting theefficacy of either approach in prolonging overall survival, informed consent andjudicious patient selection are paramount. Neither RFA nor cryotherapy should beused as an alternative to curative resection. Hepatocellular cancer, colorectal me-tastases, and hepatic neuroendocrine metastases remain the only histology for whichsubstantial 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 po-tential to impact on a large percentage of patients with liver only tumors for whomcurrent treatments offer no hope. Future trials will demonstrate whether our hopesare to be confirmed, or remain in vain.


18 Suggested Readings1. Allgaier HP, et al. Percutaneous radiofrequency interstitial thermal ablation of small

hepatocellular carcinoma. Lancet 1999;353:1676-7.

Table 18.3. Clinical results of radiofrequency thermal ablation (RFA) for hepatictumor

Author (Year) Histology Patients (N = ) ResultsRossi (1996) HCC 50 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 hepaticrecurrence. No treatmentrelated complications.

Mets 11 50% recurrend @ < 12 mo2/11 NED (mean F/U 11months)

Solbiati (1997) Mets 16 67% of tumors table (mean18.1 mo) 67% 1-yr tumor-free survival One minimal IPbleed

Solbiati (1997) HCC (N=19) 29 26/28 HCC completelyablated on CT

Mets (N=10) 19/23 tumor-free by CT 3/3liver explants had viable oftumor at ablation marginOne serious IP bleed

Rossi (1998) HCC Mets 23 36/37 had CR on CT No14 major complications

Allgaier (1999) HCC 12 10/12 complete ablationon CT. All patients tumor-free(mean F/U 5 mos.) No majorcomplications

Lencioni (1998) HCC 80 Randomized to RFA or PEICR by CT—91% RFA

85% PEIRecurrence ratesRFA-2% PEI-13%

Rhim (1999) HCC Mets 25 69% complete ablation onCT13% recurrence

17 Four complications2 IP bleeds1 needle track seeding1 diaphargm injury

Siperstein (1999) NET Mets 66 88% demonstrated shrinkageafter ablation12% recurrence (N = 22)

Bauer (1999) Mets 20 92% experience > 50%increase in pre-op CEA Nocomplications

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


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2. Allgaier HP, et al. Percutaneous treatment of liver tumors using interstitialradiofrequency thermoablation. A new therapeutic strategy. Dtsch Med Wochenschr.1998;123:907-11.

3. Boaz TL, et al. MR monitoring of MR-guided radiofrequency thermal ablation ofnormal liver in an animal model. J Magn Reson Imaging 1998;8:64-9.

4. Buscarini L, et al. Laparoscopic ablation of liver adenoma by radiofrequencyelectrocauthery. Gastrointest Endosc 1995;41:68-70.

5. Cheng YC, et al. Calculated RF electric field and temperature distributions in RFthermal ablation: comparison with gel experiments and liver imaging. J Magn ResonImaging 1998;8:70-6.

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7. Chung YC, et al. Generation and observation of radio frequency thermal lesion ab-lation for interventional magnetic resonance imaging. Invest Radiol 1997;32:466-74.

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9. Elias D, et al. Intraoperative use of radiofrequency treatment allows an increase inthe rate of curative liver resection. J Surg Oncol 1998;67:190-1.

10. Fischbach P, et al. Transhepatic access to the atrioventricular ring for delivery ofradiofrequency energy. J Cardiovasc Electrophysiol 1997;8:512-6.

11. Goldberg SN, et al. Percutaneous radiofrequency tissue ablation: does perfusion-mediated tissue cooling limit coagulation necrosis? J Vasc Interv Radiol 1998;9:101-11.

12. Goldberg SN, et al. Large-volume tissue ablation with radio frequency by using aclustered, internally cooled electrode technique: laboratory and clinical experiencein liver metastases. Radiology 1998;209:371-9.

13. Goldberg SN, et al. Percutaneous radiofrequency tissue ablation: does perfusion-mediated tissue cooling limit coagulation necrosis? J Vasc Interv Radiol 1998;9:101-11.

14. Goldberg SN, et al. Radio-frequency tissue ablation: effect of pharmacologicmodulation of blood flow on coagulation diameter. Radiology 1998;209:761-7.

15. Goldberg SN, et al. Transluminal radiofrequency tissue ablation with use of metallicstents. J Vasc Interv Radiol 1997;8:835-43.

16. Goldberg SN, et al. Radiofrequency tissue ablation: importance of local temperaturealong the electrode tip exposure in determining lesion shape and size. Acad Radiol1996;3:212-8.

17. Goldberg SN, et al. Radiofrequency tissue ablation: increased lesion diameter witha perfusion electrode. Acad Radiol 1996;3:636-44.

18. Goldberg SN, et al. Tissue ablation with radiofrequency using multiprobe arrays.Acad Radiol 1995;2:670-4.

19. Goldberg SN, et al. Tissue ablation with radiofrequency: effect of probe size, gauge,duration, and temperature on lesion volume. Acad Radiol 1995;2:399-404.

20. Jiao LR, et al. Clinical short-term results of radiofrequency ablation in primaryand secondary liver tumors. Am J Surg 1999;177:303-6.

21. Kainuma O, et al. Combined therapy with radiofrequency thermal ablation andintra-arterial infusion chemotherapy for hepatic metastases from colorectal cancer.Hepatogastroenterology 1999;46:1071-7.

22. Lencioni R, et al. Radio-frequency thermal ablation of liver metastases with a cooled-tip electrode needle: results of a pilot clinical trial. Eur Radiol. 1998;8:1205-11.

23. Livraghi T, et al. Small hepatocellular carcinoma: treatment with radio-frequencyablation versus ethanol injection. Radiology 1999;210:655-61.

24. Livraghi T. Physical and chemical locoregional therapy in liver metastasis. Ann ItalChir 1996;67:799-804.

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26. Lorentzen T. A cooled needle electrode for radiofrequency tissue ablation: thermo-


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dynamic aspects of improved performance compared with conventional needledesign. Acad Radiol 1996;3:556-63.

27. Lorentzen T. The loop electrode: in vitro evaluation of a device for ultrasound-guidedinterstitial tissue ablation using radiofrequency electrosurgery. Acad Radiol1996;3:219-24.

28. Marone G, et al. Echo-guided radiofrequency percutaneous ablation of hepatocel-lular carcinoma in cirrhosis using a cooled needle. Radiol Med (Torino)1998;95:624-9.

29. Mazziotti A, et al. An appraisal of percutaneous treatment of liver metastases. LiverTranspl Surg 1998;4:271-5.

30. McGahan JP, et al. Hepatic ablation using bipolar radiofrequency electrocautery.Acad Radiol 1996;3:418-22.

31. McGahan JP, et al. Hepatic ablation with use of radio-frequency electrocautery inthe animal model. J Vasc Interv Radiol 1992;3:291-7.

32. McGahan JP, et al. Hepatic ablation using radiofrequency electrocautery. InvestRadiol 1990;25:267-70.

33. Miao Y, et al. Ex vivo experiment on radiofrequency liver ablation with salineinfusion through a screw-tip cannulated electrode. J Surg Res 1997;71:19-24.

34. Nativ O, et al. Percutaneous ablation of malignant liver tumor in rabbits using lowradio frequency energy. J Exp Ther Oncol 1996;1:312-6.

35. Patterson EJ, et al. Radiofrequency ablation of porcine liver in vivo: effects ofblood flow and treatment time on lesion size. Ann Surg 1998;227:559-65.

36. Rhim H, et al. Radiofrequency thermal ablation of liver tumors. J Clin Ultrasound1999;27:221-9.

37. Rossi S, et al. Percutaneous RF interstitial thermal ablation in the treatment ofhepatic cancer. AJR Am J Roentgenol 1996;167:759-68.

38. Rossi S, et al. Percutaneous Radiofrequency Interstitial Thermal Ablation in theTreatment of Small Hepatocellular Carcinoma. Cancer J Sci Am. 1995;1:73.

39. Rossi S, et al. Thermal lesions induced by 480 KHz localized current field in guineapig and pig liver. Tumori 1990;76:54-7.

40. Scudamore CH, et al. Radiofrequency ablation followed by resection of malignantliver tumors. Am J Surg 1999;177:411-7.

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CHAPTER 1CHAPTER 19

Surgical Techniques in the Managementof Hepatic Trauma or Emergencies

H. Leon Pachter, Amber A. Guth

IntroductionThe liver is the most frequently injured intraperitoneal organ, at risk by virtue of

its location and size for both penetrating and blunt thoracoabdominal trauma. Whilecomplex hepatic injuries carry a 20% mortality rate, the routine use of high-speedcomputed tomographic (CT) scanning in the evaluation of bluntly-injured traumapatients has resulted in the detection of minor, asymptomatic injuries that wouldnot have been diagnosed in the past. The frequent recognition of these lesser hepaticinjuries has prompted the adoption of nonoperative management of liver traumaover the last decade. In this Chapter, the indications for operative and nonoperativemanagement, surgical techniques, and outcomes of hepatic injuries are reviewed.

HistoryModern surgical treatment of hepatic injuries dates back to 1870, with Bruns’

description of the first successful operative debridement of a gunshot wound to theliver. The next major surgical advance was Pringle’s report in 1908 of his techniqueto occlude hepatic blood flow by compressing the porta hepatis, allowing repair ofhepatic injuries before death from exsanguination.

During World War I, the reported mortality from liver injuries was 66%. ByWorld War II, with improvements in anesthesia and patient support, this had droppedto 27%. In the decade following the war, liver stitches placed through the wound toapproximate the injured liver and provide hemostasis by compression was described;however, the technique of packing massive hepatic injuries was condemned. By thetime 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 inju-ries were popularized including direct control of hemorrhage by ligation of bleedingvessels rather than anatomic resection or the use of large liver stitches to compressthe site of bleeding. By the 1980s, the techniques of finger-fracture exposure ofvascular injuries, the selective use of perihepatic packing, and improvements in criti-cal care support of the severely injured patient had become routine components oftrauma management.

First published in 1989 (and subsequently revised in 1994), the Liver InjuryScale developed by the American Association for the Surgery of Trauma (AAST) hasbecome the standard describing hepatic injuries (Table 19.1).



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Diagnosis of Blunt Hepatic TraumaMotor vehicle accidents (MVAs) account for the majority of blunt hepatic inju-

ries, with unrestrained drivers and passengers at greatest risk, and pedestrians struckby vehicles, falls and assaults accounting for the remaining injuries.

Advances in prehospital care, such as intubation and fluid resuscitation in thefield coupled with rapid transport times, have resulted in increasingly critically in-jured patients reaching the hospital alive. Hemodynamically unstable patients withobvious hemoperitoneum should be quickly resuscitated and immediately trans-ferred to the operating room as further work-up only delays definitive treatmentand results in death from exsanguination (Fig. 19.1).

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

Grade Injury DescriptionI Hematoma

Subcapsular, nonexpanding, < 10 cm surfacearea

Laceration Capsular tear, nonbleeding, < 1 cm parenchy-mal depth

II Hematoma Subcapsular, nonexpanding, 10-50% surfacearea: intraparenchymal nonexpanding< 10 cm diameter

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

III Hematoma Subcapsular, > 50% surface area or expand-ing; ruptured subcapsular hematoma withactive bleeding; intraparenchymal hematoma> 10 cm or expanding

Laceration > 3 cm parenchymal depth

IV Hematoma Ruptured intraparenchymal hematoma withactive bleeding

Laceration Parenchymal disruption involving 25-75% ofhepatic lobe or 1-3 Couinaud’s segmentswithin a single lobe

V Laceration Parenchymal disruption involving > 75% ofhepatic lobe or > 3 Couinaud’s segmentswithin a single lobe

Vascular Juxtahepatic venous injuries

VI Vascular Hepatic avulsion

*J Trauma 1995; 38:323

259Surgical Techniques in the Management of Hepatic Trauma

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The hemodynamically stable patient can undergo further diagnostic studies andsubspecialty consultation as needed. However, the trauma surgeon must recognizethe limits of physical exam in detecting intra-abdominal injuries. Data from the1970s demonstrated that up to 43% of patients thought to have a normal abdomi-nal exam at initial presentation were subsequently found at laparotomy to havesignificant intra-abdominal injuries. Particularly treacherous, are patients withdeacceleration injuries, who may present without obvious changes in vital signs oron physical exam but, due to unrecognized ongoing bleeding, can suddenly collapsehemodynamically. This scenario is particularly dangerous when the patient is un-dergoing radiologic evaluation such as CT and is relatively inaccessible to the traumateam. Thus, the trauma surgeon must be in continuous attendance of the patient,despite hemodynamic stability, until the evaluation is complete and the presence orabsence of injuries definitively established.

Diagnostic TestsFour major diagnostic modalities are currently used to detect intra-abdominal

injuries:1. diagnostic peritoneal lavage (DPL),2. CT scanning,3. ultrasound, and4. laparoscopy (Table 19.2).

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


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Diagnostic Peritoneal Lavage (DPL)First popularized by Root in 1965, the adoption of DPL as a diagnostic inter-

vention played a major role in the elimination of mandatory celiotomy for sus-pected intra-abdominal trauma and remains a reliable test performed at the bedsideutilizing local anesthesia. A small opening is surgically created in the anteriorabdominal wall just below the umbilicus (supraumbilical in patients with pelvicfractures) and if no free blood is noted, the peritoneal cavity lavaged with a liter oflactated Ringers, and the effluent examined for RBC and WBC counts, amylase,and particulate matter. Diagnostic peritoneal lavage reliably detects intraperitonealblood (98% accurate), and has been particularly useful in patients with altered men-tal status due to head injury or drug and alcohol use or those who cannot be fol-lowed by serial physical exam. That said, the technique has a number of shortcomings,including:

1. oversensitivity in detecting even small amounts of clinically insignificantintraperitoneal 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)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 advan-tage of accurately detecting solid organ and retroperitoneal injuries, although stillnot very sensitive for diaphragmatic injuries. With increased use of CT in hepaticinjuries, it became clear that small amounts of free blood in the peritoneum was notassociated with significant injuries, and thus, numerous patients have been spared

Table 19.2. Diagnosis of hepatic injury

Technique Pros Cons

Diagnostic Peritoneal Bedside procedure Does not distinguishLavage Rapid serious from trivial

Extremely low injuriesfalse-negative rate Procedural

complications

CT Scan Complete evaluation Expensiveof intra-abdominal Removes patient fromorgans monitored setting

Ultrasound Rapid bedside Less specific informationprocedure regarding individual

organ injuries than CTscan

Laparoscopy Accurately detects Role of comprehensiveperitoneal intra-abdominalpenetration evaluation not

established


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nontherapeutic exploratory surgery which would have been performed based on thepresence of RBCs in the DPL fluid.

However, CT scanning has its own drawbacks, and is contraindicated in thehemodynamically unstable patient.

Ultrasonography (US)First popularized in Europe, bedside US has become a powerful tool in the evalu-

ation of blunt abdominal trauma. Within minutes of arrival in the EmergencyDepartment (ED), the presence of free blood can be detected during a rapid bedsidescan of the hepatorenal space, left subdiaphragmatic space, and pelvis. This hasproved especially useful in the hemodynamically unstable, multiply injured patientin whom the site of bleeding is not immediately evident.

The technique is operator-dependent, but the radiologic skills can be acquiredby trauma surgeons. It is currently used to detect free blood, but experience withscanning the liver parenchyma is accumulating, and this technique may reduce de-pendence on costly CT scanning in the future.

LaparoscopyIn an effort to minimize the performance of nontherapeutic trauma laparoto-

mies, diagnostic laparoscopy for stable penetrating abdominal trauma has been usedwith increasing frequency. There are scattered reports of hepatic injuries diagnosedand managed with laparoscopic techniques such as intracorporeal suturing and ap-plication of hemostatic agents. However, its reliability in detecting hollow viscusinjuries has not been established, and the ability of laparoscopy to establish thepresence or absence of peritoneal violation from penetrating abdominal traumaremains undefined.

Nonoperative Management of Hepatic InjuriesIn 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 questionsabout what is appropriate management of these injuries. The sensitivity of thesetechniques resulted in a significant increase in diagnosis and laparotomy for trivial,nonbleeding hepatic injuries. The recognition that up to 67% of celiotomies per-formed for blunt abdominal trauma were nontherapeutic, and that up to 86% of allblunt hepatic injuries had stopped bleeding by the time surgery was performed,prompted a re-evaluation of the indications for surgical management of the stablepatient with blunt hepatic injury, especially in light of the success of nonoperativemanagement in pediatric patients. Early concerns about the inability of hepatic in-juries to stop bleeding spontaneously, and missed concomitant intra-abdominal in-juries, have proven to be unfounded.

Blunt Hepatic InjuriesAs per Figure 19.1, hemodynamic stability is the crucial factor in selecting pa-

tients for nonoperative management. Additional qualifying criteria include absenceof peritoneal signs on physical exam, delineation and American Association for theSurgery of Trauma (AAST) grading of hepatic injury by CT scan, and lack of asso-ciated 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


19

nonoperative management. Initially, nonoperative therapy was considered appro-priate only for AAST grade I to III injuries. With experience, it now appears thathemodynamic stability supersedes injury grade, and approximately 21-38% of selectedpatients with grade IV or V injuries can be safely managed nonoperatively. How-ever, in a recent multi-institutional study authored by Pachter, only 14% of gradeIV or V injuries were managed nonoperatively, and this group accounted for 67% ofall patients who failed and required surgical control of bleeding. Thus, while hemo-dynamically stable patients with grade IV and V injuries can be candidates for ob-servation, this course of management should be undertaken only with theunderstanding that they are at greater risk for failure, and must be monitored closelyin a critical care setting with immediate availability of the operating room.

The current approach to nonoperative therapy relies heavily on CT imaging toboth define the extent of hepatic injury, as well as evaluate the rest of the abdomenfor associated injuries. While early reports highlighted missed hollow viscus injuries(the true incidence ranges from 0.22-3.5%), these injuries should be detected byclinical monitoring of the patient, even if they are not demonstrated on initialabdominal CT evaluation.

While initial CT grading of hepatic injuries does not always correlate with intra-operative findings or outcome, certain findings mandate immediate intervention. Acontrast “blush”, or pooling of contrast within the liver parenchyma, represents freearterial bleeding, leaving the patient at risk for sudden hemodynamic decompensa-tion. However, since surgical identification and control of these injuries can be elu-sive, it is preferable in the hemodynamically stable patient to manage these injuriesutilizing the radiologic techniques of selective hepatic angiography and emboliza-tion of the bleeding vessel. In the rare case where embolization fails to control bleed-ing, the angiogram does provide a road map of the injury for the surgeon, allowingfor rapid intraoperative identification and management of the lacerated artery.

Outcome of Nonoperative ManagementThe overall success rate for nonoperative management is 96%. The mean trans-

fusion rate is 1.9 units, half the operative requirement in matched patients. Latehemorrhagic complications occur infrequently, and the overall rate of hepatic-relateddeaths in adult patients appears to be approximately 0.3%.

The complications of bile leaks and abscesses are uncommon, with frequenciesof 3 and 0.7% respectively. In the septic, jaundiced patient, these collections can beinitially approached by radiologic-guided percutaneous drainage, with the caveatthat 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 improv-ing, immediate surgery should be undertaken for drainage and debridement. Analternative approach to bilomas is endoscopic sphincterotomy and stenting of thecommon bile duct. By facilitating outflow at the ampulla of Vater, bile flows prefer-entially into the duodenum rather than through the peripheral, higher resistanceduct injury.

Follow-up CT scanning is not necessary after an uncomplicated course ofnonoperative management for grades I-III injuries, and its role is still being evalu-ated for complex grade IV and V injuries.


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Penetrating Hepatic TraumaThe role of nonoperative management of penetrating hepatic injuries in the

hemodynamically stable patient has not been established, although its success inselected cases of penetrating splenic injury suggests a possible role in liver injuries aswell. This is a scenario where one can foresee laparoscopic evaluation defining theextent of hepatic injury in addition to its current role in the mere detection of peri-toneal violation.

Surgical Management of Complex Hepatic InjuriesWhile 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 theliver parenchyma. These injuries present a formidable challenge to the trauma sur-geon. The algorithm outlined in Figure 19.2 summarizes the techniques needed tosuccessfully manage these potentially lethal injuries.

Profuse hemorrhage results in hypothermia, acidosis and coagulopathy, a deadlycombination. Intraoperative management by both the anesthesia and surgical staffsmust be directed at correcting these parameters; otherwise death is imminent. Ifnormothermia, correction of acid-base status and coagulopathy cannot be achieved,the operation must be aborted and “damage control” employed. Prior to laparo-tomy, which can release the tamponade of bleeding provided by the abdominal wall,the anesthesiologist should have all resuscitative tools in place, including high-flowfluid warmers, bed and Bair-Hugger™ heating blankets, heated ventilator circuits,wide bore intravenous access, blood and blood products, and appropriate hemody-namic monitoring. Upon opening the abdomen, hematoma is evacuated andbimanual compression of the liver performed to control bleeding and allow ongoingresuscitation 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 hepaticartery, 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 mustbe employed (see below).

How long can the human liver tolerate normothermic ischemia? While 20 min-utes is the commonly accepted time period, data from elective hepatic resections formalignancy 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 numberof reasons. Collateral blood supply is common in large tumors; additionally, theseresections are performed under controlled conditions with optimization of thepatient’s hemodynamics, both preoperatively and intraoperatively, unlike the traumapatient whose medical history may not be known, and whose liver is often exposedto significant periods of hyperprofusion before reaching the operating room. Thus,at Bellevue Hospital, there has been a long interest in manipulating the local hepaticenvironment to provide hepatocyte protection and minimize the risk of ischemic


19

injury to the liver. While the use of high-dose steroids (previously considered to playa role in hepatocyte protection) has recently been shown in an animal model to be ofno benefit, cooling the liver to 32˚C, while maintaining systemic normothermia bythe techniques outlined above, may provide cryoprotection. While some authorsadvocate reperfusion of the liver after 15-20 minutes by releasing the cross-clampfor 5 minutes, data from Pachter et al detailed 81 consecutive patients who under-went cross-clamping with hepatocyte protection for a mean period of 32 minutes(up to 75 minutes) without adverse sequelae.

Table 19.3. Principles of initial intraoperative management of complex hepaticinjuries

A. Bimanual compression of liver and anesthesia resuscitationB. Portal triad occlusion (Pringle maneuver)C. Finger fracture hepatotomy to expose lacerated blood vessels and bile ducts

for repairD. Debridement of nonviable hepatic tissueE. Vascularized omental pedicle pack of injury siteF. Closed suction drainage

Fig. 19.2. Surgical management of complex hepatic injuries


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Additional Techniques of Vascular ControlJuxtahepatic Venous Injuries. In cases where the Pringle maneuver does not pro-

vide adequate hemostasis to explore the liver parenchyma, bleeding from the he-patic veins or retrohepatic cava must be controlled. Multiple surgical approacheshave been described including insertion of atriocaval shunts, sequential total vascu-lar isolation of the liver with or without venous bypass, direct exposure of the injuryby the finger-fracture technique, “damage-control” tamponade of the injury by pack-ing the liver with laparotomy pads, and subsequent re-exploration of the liver oncethe patient has stabilized. Isolated case reports describe emergent hepatectomy andtransplantation for the shattered nonsalvagable liver.

Hepatic HemostasisOnce bleeding has been minimized by the Pringle maneuver, the injury is explored

and local hemostasis achieved.

Deep Liver StitchesThis technique is mentioned only to be condemned. Large simple absorbable

liver sutures on a blunt-tipped needle are passed through normal liver parenchymasurrounding the injury and tied snugly to provide compressive hemostasis. Prob-lems with this approach include inadequate occlusion of lacerated hepatic artery,vein, and portal vein branches which result in ongoing bleeding, hematoma forma-tion, and subsequent infection and abscess formation. Mass closure of the liverparenchyma can also result in hepatic necrosis.

Finger Fracture HepatotomyThis technique addresses the shortcomings of deep liver stitches, allowing expo-

sure of the injured vascular and biliary system, and precise repair or ligation of thesestructures. After portal triad occlusion, the liver is mobilized by division of the coro-nary and triangular ligaments. The mobilized liver is brought forward into the woundand stabilized by the first assistant’s left hand. Next, the injury is opened by dividingthe hepatic parenchyma in a nonanatomic fashion following the direction of theinjury. A suction catheter or clamp is used to gently divide the liver, and fine suturesor clips to divide the bridging blood vessels and bile ducts. Care must be taken notto inadvertently injure the main right and left hepatic ducts, or to extend the area ofthe 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 for-mation.

DebridementRemoval of all devascularized hepatic parenchyma is necessary to prevent devel-

opment of postoperative septic complications. Although counterintuitive, the injurysite must be debrided back to well-vascularized bleeding tissue, recognizing that anintact Glisson’s capsule may hide an extensive zone of deeper devitalized liver.

Omental PackNext, 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 edgesare then brought gently together over the omentum using 0 or 00 chromic liver


19

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

DrainsRoutine drainage of hepatic injuries remains controversial. While open drainage

using passive Penrose drains is clearly associated with increased rates of perihepaticpostoperative sepsis, the evidence regarding closed suction drainage is debatable.Recent studies have implicated independent factors such as hypotension, blood trans-fusions, and the presence of additional intra-abdominal injuries (all indicators ofthe severity of injury), rather than the mere presence of closed suction drains.

Additional Techniques of Hepatic Hemostasis

Hepatic ResectionFormal hepatic resection is associated with a prohibitively high mortality (up to

43%) and is rarely indicated except in occasional cases where the extent of injuryrequires lobectomy.

Mesh HepatorrhaphyExperience 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 widedecapsularization with bleeding which is difficult to control with the techniquesdescribed above. However, the major mechanism of hemostasis is by local tampon-ade of the liver, unlike hepatic packing with laparotomy pads which, by displace-ment and compression, can result in an “abdominal compartment syndrome”, andwhich requires reoperation for lap pad removal and definitive management of inju-ries. The major technical pitfall of this procedure is possible compromise of bloodflow through the porta hepatis and vena cava.

Perihepatic Packing and “Damage-Control” LaparotomyExtensive hepatic injury can rapidly result in exsanguinating hemorrhage with

resultant uncorrectable acidosis and coagulopathy. Continued efforts to obtain sur-gical hemostasis in this setting can be lethal. A 20-year experience has establishedthe 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 sur-geon must recognize the futility of proceeding with surgery early in the course of theoperation, quickly packing the liver closing the laparotomy incision with towel clips,and transferring the patient to a critical care area for resuscitation and correction ofhemodynamic and hematologic parameters. When the decision to abort surgeryand pack the abdomen is delayed and the technique applied as a last desperate mea-sure, 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 betweenthe liver and lap pads. Other injuries that require immediate attention are quicklyaddressed (for example, hollow viscus injuries stapled closed and vascular injuriesshunted), and the abdomen closed with towel clips. Jackson-Pratt drains are placed


19

on the skin and attached to external suction to evacuate fluid after the entire abdo-men has been covered with Betadine Steri-drapes to maintain sterility.

The technique is indicated in only about 5% of hepatic trauma, as the majorityof injuries can be managed with the techniques described above. Liver packing ap-pears to be especially efficacious in juxtahepatic injuries, whereas other approachessuch as atriocaval shunting carry a 50% mortality rate. If bleeding from these inju-ries can be controlled by packing the liver with laparotomy pads, no attempt at venacaval shunting should be made, but rather the operation terminated and the patientfully resuscitated. It is not unusual for the bleeding to have ceased at the time ofre-exploration and pack removal. If there is bleeding from a juxtahepatic injury atthe time of reoperation, the patient is stable and appropriate surgical staff are avail-able for insertion of the shunt and management of the vascular injury.

The inevitable increase in intra-abdominal pressure due to packing can result inthe “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 theFoley catheter which measures pressure within the bladder and reflects the intra-abdominal pressure. If abdominal hypertension is present, it must be released byopening the abdominal incision and utilizing prosthetic material (sterile urologyirrigation bags, Gortex) to bridge the gap between the skin edges.

Return to the operating room is predicated upon reversal of the patient’s hypo-thermia, acidosis and coagulopathy, which can usually be accomplished within 24-36hours. Leaving the abdomen packed for greater than 72 hours is associated withperihepatic sepsis rates of up to 83%.

Selective Hepatic Artery LigationSince the previously described techniques are usually adequate to provide hemo-

stasis, this is a rarely used technique with recent reports suggesting a 1-2% inci-dence. The major role of hepatic artery ligation is the management of hepatic arteryinjuries, when ligation results in a 42% survival compared to 14% for primary arte-rial repair.

Complications of Surgical Management

Recurrent BleedingThis is uncommon, with an incidence of 2-7%. In stable patients, angiography

and selective embolization is the preferred initial approach. The unstable patientmust return immediately to the operating room, with intraoperative resuscitationoccurring simultaneously with re-exploration of the injury, identification and con-trol of the source of bleeding.

HemobiliaIatrogenic injuries from percutaneous liver biopsy and transhepatic stents are the

most common etiologies. Only 30% of patients present with the classic triad ofright upper quadrant pain, gastrointestinal bleeding, and jaundice. Since the bleed-ing is often intermittent, endoscopy may not be diagnostic as there may not beactive bleeding noted at the ampulla of Vater at the time of endoscopic evaluation.Angiography is both diagnostic and therapeutic, identifying the traumatic hepatic


19

artery aneurysm, as well as providing access for selective embolization of the injuredvessel. Surgical management is rarely needed, except in cases with a very large intra-hepatic aneurysm cavity, or if angiographic access for embolization cannot be pro-vided. In cases of large intrahepatic cavities, vascular control must be secured beforeopening the aneurysm, as exsanguinating hemorrhage can result before the internalsurface of the aneurysm can be oversewn.

Intra-abdominal AbscessWhile 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 describ-ing 3663 cases of hepatic trauma from the late 1980s, the overall abscess rate was9.7% and abscess-associated mortality was 41%. More recent reports place the cur-rent sepsis-related mortality rate at 9.5%.

Risk factors for abscess development include associated enteric injuries, exten-sive destruction of hepatic parenchyma, ongoing hemorrhage, and the use of openpassive drains. Thus, the rate of perihepatic sepsis and its high attendant mortalitycan be minimized by careful surgical technique including debridement of nonviabletissue, meticulous hemostasis, and avoidance of passive drains.

Most abscesses are diagnosed by CT imaging of the liver. If a well-defined collec-tion is present, percutaneous drainage can be attempted under radiologic guidancewith a caveat that failure of the patient to improve within 24-48 hours mandatesre-exploration.

Bile FistulaeWhile not uncommon, bile leaks usually resolve spontaneously and rarely pose a

management problem. If the drainage persists at 50 mL/day for greater than twoweeks, a biliary fistula is present. The incidence ranges from 7-10%. With adequateexternal drainage (to prevent biloma formation) and free flow of bile through theampulla of Vater into the duodenum, the fistula should close spontaneously.

High output fistulae of 300 mL/day or greater must be managed more aggres-sively. A fistulogram, performed by injecting contrast material through the drain,will provide a roadmap of the injured biliary system. Major right or left ductal inju-ries usually require surgical repair. However, percutaneous transhepatic stenting ofthe lacerated bile duct is a useful temporizing intervention, particularly in the mul-tiply injured critically ill patient. Sometimes the ductal injury will heal over thestent, eliminating the need for surgical repair.

Recently, the use of self-expanding endoprosthesis stents has also been describedin the management of major bile duct injuries.

ERCP is another useful tool in the diagnosis and management of major bile ductleaks. Sphincterotomy, stent placement, and nasobiliary stent insertion all increasethe rate of bile flow through the ampulla of Vater, decreasing pressure in the intrahe-patic ducts and thus favoring bile flow into the duodenum rather than out the fis-tula. This reduction in bile flow allows the site of injury to heal.

Arterial-Portal Venous FistulaeThese 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 bleed-ing, ascites, and high-output cardiac failure can result.

Small peripheral fistulae usually resolve spontaneously and can be observed. Forlarge fistulae, or those located in the portal triad, embolization has a 42% successrate. Surgical approaches include ligation, primary repair, or bypass grafting. Some-times the aneurysmal sac must be approached directly by opening it and oversewingthe orifices of all entering vessels, a situation where complete vascular control can bedifficult to obtain, and in which use of a cell-saver can be life saving.

Outcome of Hepatic TraumaIn summary, the majority of hepatic injuries are minor grade I and II injuries

diagnosed by CT imaging of the abdomen in the hemodynamically stable bluntlyinjured 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 vastmajority of hepatic-related deaths. The mortality rate from complex hepatic inju-ries has decreased from 50-20% over the last decade, due in part to the widespreadapplication of nonoperative management, and the use of damage-control laparo-tomy and ERCP. In addition, the interventional radiologist, with the ability to per-form selective angiography and embolization, percutaneously drain abscesses andbilomas, and stent biliary tract injuries, has become a crucial member of the teamcaring for the patient with complex hepatic injuries.

Selected Reading1. Pachter HL, Spencer FC, Hofstetter SR et al. Significant trends in the treatment

of hepatic trauma: Experience with 411 injuries. Ann Surg 1992; 215:492.2. 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 Trauma1996; 40:31.

3. Pachter HL, Hofstetter SR. The current status of nonoperative management ofblunt hepatic injuries. Am J Surg 1995; 169:442.

4. Morris JA, Eddy VA, Blinman TA et al. The staged celiotomy for trauma: issues inunpacking and reconstruction. Ann Surg 1993; 217:576.

5. Denton JR, Moore EE, Coldwell DM. Multimodality treatment for grade V he-patic injuries: Perihepatic packing, arterial embolization, and venous stenting. JTrauma 1997; 42:964.

6. Pachter HL, Feliciano D.V. Complex hepatic trauma. Surg Clin N Amer 1996;76:763.

7. Guth AA, Pachter HL. Laparoscopy for penetrating thoracoabdominal trauma:Pitfalls and promises. J Soc Laparoend Surg 1998; 2:123.

CHAPTER 20


Liver Transplantation

Patricia A. Sheiner, Rosemarie Gagliardi, D. Sukru EmreIn 1963, Thomas Starzl performed the first successful orthotopic liver transplan-

tation in a human being. Until the 1980s, however, liver transplantation was associ-ated with poor survival rates. Then, with the introduction of new antirejectionmedications and organ preservation solutions, survival rates began to improve, andorthotopic liver transplant (OLT) became an accepted therapy for advanced liver dis-ease. In 1983, a National Institutes of Health (NIH) consensus conference concludedthat OLT for end-stage liver disease “deserves broad application.” Presently, 1-yearpatient survival rates of 85-90% and 5-year patient survival rates of 70% are verycommon.

IndicationsPatients 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 VirusUntil recently, human immunodeficiency virus (HIV) was an absolute contrain-

dication to liver transplant. With multidrug therapy permitting long-term survivalin HIV patients, the issue is being readdressed. A few programs have already trans-planted patients under strict protocols. These individuals are HIV antibody positivebut have had no opportunistic infections, have a normal CD4 count, and are nega-tive for circulating virus by PCR. Long-term outcomes are still unknown.

Extrahepatic SepsisExtrahepatic sepsis remains an absolute contraindication. With immunosuppres-

sion after transplant, uncontrolled infection becomes deadly.

Hepatocellular CarcinomaPatients with small hepatocellular carcinoma (HCC) (<5 cm), without evidence

of portal vein thrombosis, have long-term results after liver transplant equal to thoseachievable in transplant recipients without tumors. Patients with larger tumors havea high incidence of recurrence. We have found that tumor size >8 cm or majorvenous invasion is associated with rapid recurrence and unacceptable patient andgraft survival after transplantation. At our center, patients with tumors between 5-8cm undergo transplantation under a multimodality protocol that includespretransplant chemoembolization and intra- and postoperative systemic chemotherapy

271Liver Transplantation

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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

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 antimitochondrialautoantibody. Transplant appropriate with bilirubin >10 mg/dl or upondevelopment of portal hypertension.

• Primary sclerosing cholangitis (PSC) - Usually affects men. Associated withinflammatory bowel disease. Patients develop recurrent cholangitis and are atrisk for developing cholangiocarcinoma.

• Fulminant hepatic failure - Encephalopathy within 2 months of onset ofjaundice. Involves massive necrosis in previously healthy liver.Causes include HBV, HAV, drug toxicity (e.g., from acetaminophen orisoniazid), Wilson’s disease, autoimmune hepatitis. Multiorgan failuredevelops. Before availability of transplant, mortality from cerebral edema orsepsis was 80%. Decision to transplant emergently is based on predictors ofspontaneous recovery, including Factor V level, etiology, age, and intervalfrom jaundice to encephalopathy >1 week. Some die on waiting list.

• Budd chiari syndrome - Caused by hepatic vein obstruction, most oftenassociated with myeloproliferative disease. Transplant indicated for hepaticfailure.

• 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’sdisease, antitrypsin deficiency). Others do not (e.g., hemophilia, oxalosis) andmay indicate auxiliary segmental orthotopic or heterotopic transplant.

• Postnecrotic cirrhosis and fulminant hepatic failure• Hepatoblastoma - Better results than for hepatoma.


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with adriamycin. Results of this protocol are still being evaluated. An importantconcern is how to manage patients with small tumors while they wait for transplant.In the current United Network for Organ Sharing (UNOS) allocation system, thepresence 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 inoper-able if the tumor grows to an unacceptable size or if portal vein thrombosis devel-ops. At our center, patients are closely followed, with imaging studies done every 3months. If the tumor grows or if other small lesions develop, we attempt to controltumor growth with alcohol injection, radiofrequency ablation (for tumors <5 cm),or chemoembolization (for tumors >5 cm). Recent advances in living-donor trans-plants for adults may have a major impact on our ability to provide transplants totumor patients while their tumors are relatively small.

CholangiocarcinomaCholangiocarcinoma (CCA), a complication of long-standing primary scleros-

ing cholangitis (PSC), is a contraindication to transplant at many centers because ofhistorically high recurrence rates, even with small and in situ carcinomas discoveredincidentally. In a patient with PSC, a new dominant stricture, an acute rise in biliru-bin, or rapid deterioration may be a sign of CCA and may indicate extensive re-evaluation (e.g., with ERCP with brushing and imaging studies). A few centers haveachieved promising results with protocols in which patients receive pre-transplant ra-diation and adjuvant therapy, but only a few patients are eligible for such protocols.

Nonhepatic TumorsIn most cases, the presence of metastatic tumors (e.g., colorectal, breast, GI tract,

etc.) is an absolute contraindication to liver transplant. Such tumors recur rapidlyafter transplant and there are no known long-term survivors. Patients with certainslow-growing tumors such as metastatic neuroendocrine tumors and carefully se-lected patients with leiomyosarcomas confined to the liver have undergone trans-plantation with good 5-year survival.

Pulmonary HypertensionThe association of pulmonary hypertension and end-stage liver disease is well

described, with reported incidences ranging from 2-4%. The etiology of pulmonaryhypertension in end-stage liver disease is unclear, but one frequently proposed hy-pothesis is that in patients with portal hypertension, the pulmonary vasculaturemay be exposed to vasoactive mediators normally metabolized by the liver. Whenthese patients undergo major surgery, anesthetics, hypoxemia, and acidosis may con-tribute to further increases in pulmonary vascular pressures, which will further re-duce the venous return to the left heart and further decrease the cardiac output. Thiseffect will in turn exacerbate the problems of acidemia and hypoxemia, leading to acuteright heart failure and an inability to maintain perfusion pressures to the left heart.

Advanced AgeGiven 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 withtheir age. A 70-year-old patient in the ICU with renal failure is not likely to survivelong-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 toyounger patients. The shortage of organs has made waiting times very long, andpatients deteriorate while they wait for transplant. This fact has affected the eligibil-ity of older patients. Now, because living-related transplants allow US to bypass thewaiting list and schedule transplants electively, we are able to transplant older pa-tients successfully.

Psychosocial ContraindicationsActive drug or alcohol use is an absolute contraindication to transplant. Although

rules regarding drug or alcohol abstinence vary, most transplant programs require a6-month abstinence period as well as participation in a rehabilitation program. Be-cause demand for donor organs is greater than the supply, the patient’s social sup-port system is also an important consideration. A recipient with poor support maynot be able to manage his/her medications and frequent hospital visits, thus riskingthe success of the transplant and possibly wasting the organ.

Organ AllocationCurrently, organ allocation in the United States is determined by both medical

urgency and time on the waiting list, within 11 geographic regions. The waiting listis dynamic, in that a patient’s status can change over time. Within each region, andthen 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 theperson with the most time accrued on the waiting list.

Medical UrgencyUnder the current UNOS system, there are four medical urgency statuses for

each blood group. Each patients status is determined mainly on the basis of theChild-Turcotte-Pugh (CTP) score (Table 20.3). The advantage of the CTP score isthat it is objective; it provides a uniform standard for programs at all centers. Thedisadvantage is that it does not permit subjective evaluation by the physician of anindividual patients degree of illness. In order of increasing urgency, the four levels arestatus 3, status 2B, status 2A and status 1. To meet waiting list criteria, a patient musthave at least 7 points on the CPT score. Point requirements are shown in Table 20.4.

Timing of TransplantationThe 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 performtransplantation 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 ofthe hepatologist is to optimize patient’s medical conditions on the waiting list andto identify life-threatening complications that afford higher priority on the list. Un-fortunately, due to the discrepancy between demand and supply of livers, transplan-tation can rarely be optimally timed. Some patients are too sick at baseline to becomeliver transplant candidates. For example, an elderly bed-bound patient with lowalbumin and no muscle mass is unlikely to survive a transplant. Early involvementof nutritionists and physical therapists is becoming increasingly important.


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Preoperative Planning

Liver VolumeAlthough blood type is the primary determinant of who a donor liver can be

used for, size can sometimes be an issue. A 2 kg liver will not fit into a small womanwith an 800 cc liver volume, and a liver from a small child will not support an adultwith an 1800 cc liver. (Occasionally, the presence of massive ascites can allow alarger liver to be put into a smaller person.) In living-donor liver transplants, it isparticularly important to know in advance the liver volumes of the donor and re-cipient to ensure adequate volume. The size of the recipient’s liver can be deter-mined by use of CT scan, with a calculation of liver volume. The estimated volumerequired is calculated on the basis of donor liver weight to recipient body weight(DLRW) ratio. A DLRW ratio >0.8 is suggested for successful transplantation.

Correction of ElectrolytesEnd-stage cirrhotics, especially those with massive ascites and renal insufficiency

who are taking diuretics, may have low sodium levels. Postoperatively, approximately1% of liver recipients exhibit clinical findings ranging from mental status changes tostupor to death. These findings have been ascribed to the presence of central pontine

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

Points 1 2 3

Encephalopathy None 1 - 2 3 - 4

Ascites Absent Slight At leastmoderate(or controlleddespite diuretictreatment bydiuretics)

Bilirubin (mg/dl) <2 2-3 >3

Albumin (g/dl) 2.8-3.5 <2.8

Prothrombin time <4 4-6(secs. prolonged) >6 or (INR)

<1.71.7-2.3>2.3

For primary biliary cirrhosis, primary sclerosing cholangitis, or other cholestaticliver diseases:

Bilirubin (mg/dl)* <4 4-10 >10


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myelinolysis (CPM), a known complication after liver transplant. While the etiol-ogy may be multifactorial, a known risk factor is rapid change in serum sodiumlevel. 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 madeto 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 AbnormalitiesPatients with end-stage liver disease often have low platelet counts (due to hy-

persplenism) and elevated prothrombin times. Preoperative correction or partial cor-rection with fresh frozen plasma and platelets is important to diminish the risk ofbleeding during the placement of large-bore central venous catheters as well as dur-ing the hepatectomy itself.

Antibiotics; Spontaneous Bacterial PeritonitisAll patients receive antibiotics preoperatively, usually for three doses only. In

some cases, a longer course of antibiotics may be needed. For example, a patientwith spontaneous bacterial peritonitis (SBP) who has received 3 days of therapy andhas a normal tap may undergo transplant, but the full course of antibiotics shouldbe completed. Patients who have received long-term antibiotic therapy pretransplantare 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.

TumorsWhen 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 fromthe porta hepatis are biopsied. A back-up recipient is usually waiting, in case thetumor patient is no longer a candidate for transplant.There are a variety of protocolsfor larger HCCs. One consists of intraoperative infusion of adriamycin during theanhepatic phase to prevent spread of tumor during mobilization of the liver. Postop-eratively, if the pathology report indicates vascular invasion by the tumor, a courseof adjuvant chemotherapy may be indicated.

Hepatitis BPatients with hepatitis B, especially DNA-positive patients, were once consid-

ered poor transplant candidates due to high rates of severe recurrence and death, butuse of long-term passive immunization with hepatitis B immune globulin (HBIg)has improved their outcomes. Prophylaxis consists of approximately 45 million UHBIg intraoperatively, followed by 25 million U on postoperative days 1, 2, and 3and monthly thereafter. Because the hepatitis B virus can develop resistance, manyprograms also add a second agent, lamivudine, to the regimen.

Donor SelectionIdentification of good donor livers is key to successful outcomes. Today, there

are few absolute contraindications to liver donation. These include active intrave-nous drug abuse, infection with the human immunodeficiency virus, increasinglyabnormal 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 criteriahave been broadened at many centers. We now know that the quality of the donorliver is based on many factors that must be considered together. The presence ofantibody to hepatitis C virus in donor serum is not necessarily a contraindication.We now know that hepatitis C virus commonly recurs after transplant, even whenthe donor is hepatitis C negative. Furthermore, the outcome and severity of recur-rence in hepatitis C patients who receive grafts from hepatitis C positive donors isno different from that in patients who receive hepatitis C negative livers. Liversfrom hepatitis C positive donors are biopsied, however, and organs with chronicactive hepatitis are discarded. Use of hepatitis B core antibody (HBcAb) positivelivers for hepatitis B recipients with hepatitis B immune globulin (HBIg) prophy-laxis is also accepted.

Intraoperative Considerations: Monitoring, PatientPositioningDuring the transplant, central venous or pulmonary artery monitoring is neces-

sary for monitoring pressures and cardiac output. A Swan-Ganz catheter may helpdetect previously undiagnosed pulmonary hypertension. An arterial line is essentialfor monitoring of blood pressure, and adequate venous access is mandatory in casemassive transfusions are needed. The patient is placed supine on the OR table andprepped with the left arm extended, in case bypass is needed. The right arm may beleft by the patients side.

Selection of Operation and Cadaveric Donor OperationsThe liver is normally brown, smooth, and sharp-edged and producing viscous,

golden bile. Steatotic livers are large and yellow, with round edges. The presence andseverity of steatosis is best confirmed with frozen section biopsy. Livers that are firmand edematous in the absence of high CVP and with poor intraoperative bile pro-duction often have severe ischemic injury and are not used. Liver graft survival de-pends on in situ perfusion with preservation solution and cold storage. In stabledonors, dissection is traditionally performed before the organs are flushed of blood.A rapid-flush technique, used in unstable donors, involves perfusion before most ofthe dissection. In either case, the hepatic arterial supply must be carefully delin-eated. The portal vein is cannulated via the inferior mesenteric vein. The distal aortais cannulated after systemic heparinization. When all teams are ready, the supraceliacaorta is cross-clamped, cold preservation solution is flushed through the portal andarterial systems, and crushed ice is placed in the abdomen. Exsanguination andperfusate 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 aortaand divided with an aortic patch. The portal vein is dissected to the confluence anddivided. The diaphragm, supra/infrahepatic IVC and remaining peritoneal attach-ments are divided. The liver is removed and preserved in UW solution. Iliac arteryand 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 exten-sion is made. In many patients with portal hypertension, large blood vessels can beencountered even in the muscle and fascial layers. The abdomen is opened, andascites, if present, is drained. The falciform ligament is divided. The left triangularligament is divided. Control of the hepatoduodenal ligament is obtained by openingthe gastrohepatic ligament. The hepatic arteries are carefully dissected and divided.The common bile duct is divided. The portal vein is cleared of remaining tissue inthe hepatoduodenal ligament. The right side of the liver is mobilized. The infrahepaticvena cava is exposed circumferentially. The right adrenal vein is divided and the barearea dissected off the retroperitoneum. The caudate lobe is freed from theretroperitoneum. The suprahepatic cava is cleared circumferentially. When the liveris attached by only three structures—the portal vein, infrahepatic cava, and supra-hepatic 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 thewarm ischemic time. There are variations in the recipient operation, but the follow-ing is a standard approach.

Vascular Anastomoses

Caval AnastomosisThe native suprahepatic caval cuff is fashioned and the end-to-end anastomosis

is performed with heavy running suture. The infrahepatic caval cuffs are fashionedand similarly anastomosed.

Portal Vein Anastomosis and ReperfusionThe portal vein cuffs are fashioned and anastomosed end-to-end with fine su-

ture. Running technique is usually used, and the sutures tied with so-called growthfactor (an air knot), to avoid purse stringing and stricturing this delicate anastomo-sis. The graft is then reperfused with portal blood. Approximately 500 cc of blood isvented from the cava before removing the caval clamps in order to rinse out coldhyperkalemic preservation solution, acidotic blood, and air. Hemostasis is secured.In cases of complete portal vein thrombosis an interposition graft from the spleno-mesenteric confluence is employed, using donor iliac vein. Another alternative is ajump graft from the SMV that is tunneled through the mesocolon and lesser sac.

Hepatic Artery AnastomosisThe recipient common hepatic artery is anastomosed end-to-end to the

donor celiac axis with fine suture using delicate technique. If hepatic arteryinflow is inadequate, as occurs when there is an intimal dissection or hepatic arterythrombosis, 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 AnastomosisThe 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 T-tube brought out through the distal recipient duct. The T-tube is removed 3 monthslater, after a normal cholangiogram has been obtained. Many surgeons no longeruse T-tubes routinely. If there is a major size discrepancy between the donor andrecipient ducts, or if the recipient bile duct is diseased (as in PSC) or too small (asin pediatric cases), a choledochojejunostomy is performed. The duct is anasto-mosed to a Roux-en-Y limb of jejunum using a stented end-to-side technique.

Piggyback TechniqueIn 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, theshort hepatic veins are ligated, and the hepatic veins are identified. The right hepaticvein is clamped and divided and oversewn with 5-0 prolene. The left and middlehepatic veins are clamped and the liver removed. The left and middle hepatic veinsare opened to make one cuff. Performing a piggyback maintains venous return tothe heart but does not affect portal hypertension. The donor suprahepatic cava isanastomosed 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 witha 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. Thecaval clamp is removed and the donor infrahepatic cava is ligated with 2-0 silk ties.

BypassVeno-venous bypass (VVB) was originally introduced in an attempt to modify

the hemodynamic changes that occur during the anhepatic phase of liver transplan-tation. During this period, venous flow through the portal vein and inferior venacava is interrupted and may cause major hemodynamic changes.The standard tech-nique involves cannulation of the transected portal vein, the axillary vein, and thefemoral vein, which is cannulated via the saphenous vein. This system diverts bloodfrom the lower extremities and the splanchnic bed into the suprahepatic systemiccirculation. Modifications of the VVB technique have been described and may beconsidered as alternatives to the standard technique. Recently, cannulation of theinferior mesenteric vein, rather than the portal vein, has been described for use withVVB. This method offers the advantage of early decompression of the portal systembefore dissection of the hepatoduodenal ligament and may significantly reduce earlyblood loss, particularly in patients with a history of previous upper abdominal sur-gery. On the other hand, there are disadvantages associated with this procedure. Itprolongs operative time, air and thrombotic emboli have been reported, and flowsmust be maintained at 1000 ml/min or greater. At lower flow rates, clots and plate-let aggregation are more likely. The heparinless VVB system cannot use a heatexchanger. Such heat loss from the bypass circuit contributes to the hypothermiaand subsequent coagulopathy. The routine use of VVB is now controversial. Whenthe Mount Sinai Medical Center began its liver transplant program in 1988, VVBwas used routinely. As the program grew and we gained anesthetic and surgical


20

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 reduc-tion in venous return. In the blood pressure drops significantly, by pass or the piggy-back technique may be needed. Bypass should also be used in patients with a historyof recent variceal bleed, in whom clamping of the portal vein can cause acute varicealbleeding in the OR.

Split LiversThe increasing gap between supply and demand has resulted in higher mortality

among candidates on the waiting list. In attempts to narrow this gap, besides broad-ening their donor selection criteria, transplant centers have begun to employ inno-vative surgical techniques, such as living-related and split-liver transplantation.Split-liver transplantation is appealing because it provides two allografts from a singledonor liver. The liver can be split through the falciform ligament, creating left lateralsegment and extended right lobe grafts, or splitting can be done through the mainscissura, to create left lobe and right lobe grafts (Figure 20.1). Donor selection forsplit transplant is extremely important. Fifty years is the upper age limit for donorsfor 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

Fig. 20.1. Split liver transplantation. In this example, the liver is split through the falci-form ligament creating left lateral segment and extended right lobe graft. Reprintedwith 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).


20

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

Living DonorsLiving donor liver transplantation is another innovative technique. Hepatic grafts

from living donors were first used for pediatric recipients. More recently, with excel-lent results in children and with established donor safety, living donor liver transplantshave been performed for adult recipients as well. In pediatric recipients youngerthan age 5, an adult’s left lateral segment usually provides adequate liver volume. Forteenage recipients, a left lobe should be used. For adults, right lobe grafts are neces-sary to ensure enough liver volume for recipient. Because this procedure subjects a

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 WHJarnigan (Eds.) W.B. Saunders, London, UK (2000).


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healthy individual (donor) to major surgery, donor safety is essential, and informedconsent is crucial. The risks and benefits of the living donor operation must beexplained to the donor, the recipient, and their immediate families. In addition,donors should be thoroughly evaluated by an unbiased physician. The examinationsshould include a history and physical, chest x-ray, EKG, blood work (including liverfunctions and viral serologies), and MRI with calculation of liver volume. In ourexperience with pediatric and adult living donor liver transplants, the donor opera-tion has been asssociated with low rates of morbidity and mortality. The procedureprovides many advantages to the recipient. The transplant operation can be sched-uled electively (without having to wait for a cadaveric organ), before the recipientdevelops serious complications of end-stage liver disease. Furthermore, since thedonor is healthy and the ischemia time is short, graft quality is better than withcadaveric liver allografts. The recipient and donor operations are performed simulta-neously, to minimize ischemia time. Technical problems in the recipient, such as he-patic artery thrombosis and biliary leaks, were seen initially but have decreaseddramatically with increasing experience in technique and recipient selection.

Recipient Operation for Split and Living Donor GraftsThe 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 graftsand all living donor liver grafts, the allograft does not have the vena cava, and there-fore 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 theright or left portal vein) and the recipient portal vein using 6/0 prolene continuoussuture. The hepatic artery anastomosis is performed between the allograft hepaticartery (either right or left) and the recipient right or left hepatic artery using 8/0prolene interrupted sutures. For anastomoses in pediatric recipients, an operatingmicroscope is necessary. When the entire length of the recipient portal vein andhepatic artery are dissected into the hilum, extension grafts are rarely needed. In themajority of the cases, bile duct anastomosis is done by Roux-Y hepatico-jejunos-tomy using interrupted 6/0 PDS sutures.

ResultsWith improvement in pretransplant patient care, evolution of surgical techniques,

better preservation fluids, modern immunosuppressive medications, and state-of-the-art postoperative care, results of liver transplantation have dramatically improved,with 1-year patient survival averaging 85-90% at large transplant centers. New, in-novative techniques such as split livers and living-donor liver transplantation havehelped to alleviate the severe organ shortage, although the number of patients wait-ing for transplants still far outweighs the number of donors. Despite these improve-ments, our understanding of the disease processes that affect outcome remainsincomplete. For example, recurrence of hepatitis C after transplantation still re-mains a major problem, causing graft damage and long-term graft loss. Patient sur-vival 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-


20

lems early after transplantation. Long-term studies are needed to determine the ef-fects of recurrence of these diseases on outcome.

In the early 1990s, before the introduction of hepatitis B immune globulin pro-phylaxis, hepatitis B was a relative contraindication to transplant, due to high ratesof morbidity and mortality associated with recurrence. With the use of HBIg, to-gether with other antiviral agents such as lamivudine, hepatitis B has become one ofthe favorable indications for liver transplantation, with 1-year disease-free survivalreaching 90%.

283

Inde

x

Index

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, 180Adrenal gland 2, 209Adrenocortical 143Alpha fetoprotein (AFP) 44, 83, 93,

102, 104, 106American Association for the Surgery

of Trauma Liver Injury Scale 259Aminopyrine breath test 74Angiomyelipoma 83, 98Antacids 79Antithrombin III 79Arterial-Portal Venous Fistulae 268Ascites 44, 52, 57, 67, 78, 79, 102,

104, 125, 132, 206, 221, 228,253, 269, 270, 274, 275, 277

B

Bile Fistulae 268Biliary calculi 28Biliary endoprosthesis 37Biliary hamartomas 97, 98Bilioenteric Bypass 165, 191Bilioenteric bypass 10, 14, 191, 192Biloma 58, 268Biopsy 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, 190Blunt hepatic trauma 258, 260Bone scan 123Brachytherapy 54, 56, 199Breast cancer 143Breast carcinoma 143Buckwalder retractor 153, 193

C

CA-19-9 83, 94Calot’s triangle 150, 153, 155, 157,

159, 160

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, 223Celiac artery 6Central resection 225Charcot’s triad 39Child’s classification 63, 74, 102, 105,

107-110, 132, 253, 273, 275Child-Turcotte-Pugh scoring system

(CTP) 273, 275Cholangiocarcinoma (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, 147Choledochoscope 162, 164Cholelithiasis 22Cirrhosis 21, 44, 59, 92, 101, 102,

104-108, 110, 123, 132, 133,135, 239, 249, 253, 256, 270,275

Cisplatin 107Colorectal adenocarcinoma 121, 228Colorectal cancer 121, 122, 123, 129,

134, 227, 228, 237-239Colorectal liver metastases 124, 125,

127, 128, 129Common 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

Coronary artery disease (CAD) 73Couinaud’s classification 174Cryoablation 66, 107, 110, 228, 242,

252Cryoinjury 239Cryoprobe 107, 240, 241, 242 CT arterial portography 46Cystic artery 6, 14, 15, 150, 151, 153,

155, 160, 161, 194, 209, 213Cystic 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

D

Deep liver stitches 265Diagnostic peritoneal lavage (DPL)

259-261Diaphragm 1, 3, 65, 98, 153, 172,

209, 214, 223, 249, 276Disseminated intravascular coagulation

(DIC) 79Distal pancreatectomy 112, 115, 120Dopamine 78Dormia basket 35Doxorubicin 107 Drain 7, 9, 10, 14, 52, 53, 114, 115,

154, 155, 162, 165, 197, 202,205, 225, 242, 268, 269

Duodenojejunostomy 115, 119

E

Electrohydraulic lithotripsy (EHL) 37Embolization 38, 52, 61-71, 90, 96,

103, 108-110, 123, 124, 128,135, 137, 140, 238, 262,267-269

Embolotherapy 61End-stage liver disease 270, 272, 275,

281Endoscopic retrograde

cholangiopancreatography(ERCP) 34, 38-41, 154, 202,268, 269, 272

Endoscopic sphincterotomy (ERS)34-36, 38-40, 262

Extended left hepatectomy 6, 124,

218, 220, 221Extended right hepatectomy 124, 214,

225External beam radiation 87, 109, 199

F

Feridex 22Fibrinogen deficiency 79Fine needle aspiration (FNA) 42, 203Finger fracture hepatotomy 265Fluoropyrimidines 109Focal nodular hyperplasia 23, 28, 43,

81, 83, 91, 93-95

G

Gallbladder adenocarcinoma 201Gallbladder fossa 2, 3, 113, 154, 161,

172, 212, 220, 221Gallbladder scintigraphy 148Gastroduodenal 6, 8, 15, 108, 113,

206, 228, 231Gelfoam 62, 154Gemcitabine 109Genitourinary cancers 145Glisson’s capsule 11, 12, 85, 167, 168,

175, 193, 265Goligher retractor 153, 193, 206

H

H2 blockers 79 HbsAg 101Hemangiomas 23, 24, 43, 81, 85-87,

89, 90-92, 123Hemobilia 267Hepatic adenomas 23, 81, 91, 93, 94,

96, 97Hepatic artery infusion pumps (HAIP)

227-229, 232, 235, 237Hepatic artery ligation 89, 91, 267Hepatic encephalopathy 79, 228Hepatic 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

Inde

x

Index

Hepatitis C 101, 270, 276, 281Hepatocellular carcinoma 23, 42, 44,

59, 62, 64, 83, 92, 94, 101, 104,107, 110, 270

Hepatorenal syndrome 78Hepp-Couinaud approach 174, 175HIDA scan 148Hilar plate 3, 11, 12, 14, 175, 176,

179, 193, 194, 217, 225

I

Indocyanine green clearance 74Inferior mesenteric vein 9, 10Intra-abdominal abscess 268

J

Jackson Pratt drain 162, 197Jaundice 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 132Klatskin tumor

see CholangiocarcinomaKocher maneuver 113, 114, 180, 206Kupffer cells 84, 92-94

L

Laparoscopic cholecystectomy 17, 34,40, 146, 149, 154, 155, 156,159, 162, 204

Laser lithotripsy 36, 37Left gastric vein 10Left hepatectomy 6, 16, 17, 124, 215,

218-221Left hepatic duct 11, 14, 16, 17, 56,

165, 167-169, 171, 176-178,183, 188, 193, 195, 206, 207

Left lateral segmentectomy 218, 225Left lobectomy 207, 219Left trisegmentectomy 218Lienorenal ligament 116Ligamentum teres 2, 168, 171, 172,

175, 179, 211, 215Lipoma 83, 98

Liver abscess 58, 108Living donor liver transplantation 280Low central venous pressure anesthesia

(LCVP) 74, 75, 77, 80, 208Lung 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 6Maryland dissector 157-160Mechanical lithotripsy 36Melanoma 62, 141-145, 239Mesenchymal hamartomas 98Mesh hepatorrhaphy 266Metastases 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 102Myelolipoma 83, 98Myxoma 99

N

Na+-K+ ATPase 79Neuroendocrine carcinoma 138, 140

O

Obstructive jaundice 52, 76, 111,113, 165, 169, 199

Okuda staging 104Olsen clamp 160Omental pack 265Ovarian carcinoma 130

P

Pancreatic cancer 115, 135, 199Pancreatic imaging 23, 28Pancreaticoduodenectomy 111-115,

118, 119, 173, 183, 187, 199,206

Pancreaticojejunostomy 111, 115,117, 120


Index

Percutaneous abscess drainage 56Percutaneous cholangiography 38Percutaneous cholecystostomy (PC)

39, 49, 52Percutaneous ethanol injection therapy

(PEIT)/percutaneous ethanolinjection (PEI) 64, 65, 109,110, 137, 252-254

Percutaneous hepatic cyst drainage 60Percutaneous portal venogram 68, 71Percutaneous transhepatic cholangiog-

raphy (PTC) 46, 47, 49, 52,202

Periampullary cancer 111, 112Perihepatic Packing 266Perihepatic packing 257, 266Photodynamic therapy 199Ponsky cholangiocatheter 160Portal 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 79Protein S 79Pulmonary function tests 73Pulmonary hypertension 272, 276

Q

Quadrate lobe 167, 168, 174, 175,177-179, 193, 221

R

Radioembolization 109Radiofrequency ablation 135, 228,

239, 252, 272Radionics 247Radiotherapeutics 247

Recurrent Bleeding 267Renal failure 78, 125, 241, 272, 281Rendezvous technique 37Replaced right hepatic artery (RRHA)

231, 232Right gastric artery 6, 114Right hepatectomy 124, 209,

212-214, 217, 225Right hepatic duct 11, 14, 18, 161,

165, 188, 195, 213Right hepatic lobectomy 207Right scissura 5, 220, 221Right trisegmentectomy 14, 66, 69,

214RITA Medical Systems, Inc. 246Round ligament 177, 209Roux-en-Y 115, 118, 165, 172, 177,

192, 196, 199Roux-en-Y reconstruction 115, 118

S

Sarcoma 141, 143, 239Segment I resection 222, 223Sengstaken-Blakemore tube 79Sepsis 37-40, 46, 52, 53, 75, 76, 79,

209, 266, 267, 268, 270Solitary fibrous tumors (SFT) 98Splenectomy 115, 120Splenic artery 46, 116, 232Split-liver transplantation 279Squamous cell carcinoma 140Steatosis 276, 279Superior mesenteric vein 8, 10, 114Surface anatomy 2Surgicel 154, 243

T

Teratoma 99Thompson retractor 153, 193Thorotrast 102Thrombocytopenia 44, 64, 79, 85,

86, 91, 132Transjugular intrahepatic

portosystemic shunts (TIPS) 67Triangular ligaments 1, 2, 265

287

Inde

x

Index

U

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, 56Wedge resections 124, 208, 225Whipple procedure 112, 113

V m


a d e m e c uV a d e m e c u m

Table of contents1. Essential Hepatic and Biliary

Anatomy for the Surgeon

2. Imaging of the Liver, BileDucts and Pancreas

3. Endoscopic and PercutaneousManagement of Gallstones

4. Interventional Radiologyin Hepatobiliary Surgery

5. Perioperative Care andAnesthesia Techniques

6. Benign Tumors of the Liver:A Surgical Perspective

7. Hepatocellular Carcinoma

8. Periampullary Cancer andDistal Pancreatic Cancer

The Vademecum series includes subjects generally not covered in other handbookseries, especially many technology-driven topics that reflect the increasinginfluence of technology in clinical medicine.

The name chosen for this comprehensive medical handbook series isVademecum, a Latin word that roughly means “to carry along”. In the MiddleAges, traveling clerics carried pocket-sized books, excerpts of the carefullytranscribed canons, known as Vademecum. In the 19th century a medical publisherin Germany, Samuel Karger, called a series of portable medical booksVademecum.

The Landes Bioscience Vademecum books are intended to be used both in thetraining of physicians and the care of patients, by medical students, medical housestaff and practicing physicians. We hope you will find them a valuable resource.

All titles available at

www.landesbioscience.com


I SBN 1- 57059- 630- 1

9 7 8 1 5 7 0 5 9 6 3 0 8


HepatobiliarySurgery

9. Hepatic Resection for ColorectalLiver Metastases: SurgicalIndications and Outcomes

10. The Surgical Approach to Non-Colorectal Liver Metastases:Patient Evaluation, Selectionand Results

11. Surgical Techniques of OpenCholecystectomy

12. Laparoscopic Cholecystectomyand the LaparoscopicManagement of Common BileDuct Stones

13. Surgical Techniques forCompletion of a BilioentericBypass

(excerpt)

hepatobiliary surgery blumgart

Documents

chamberlain leslie

biliary tract surgery

chamberlain isbn

new york leslie

chamberlain contentspreface

blumgart introduction

liver diseases

biliary anatomy