Hepatobiliary Surgery Blumgart

LANDES LANDES
BIOSCIENCE V ad e me c u m BIOSCIENCE V ad e me c u m
Table of contents (excerpt)
Hepatobiliary
1. Essential Hepatic and Biliary 9. Hepatic Resection for Colorectal
Anatomy for the Surgeon
2. Imaging of the Liver, Bile
Liver Metastases: Surgical
Indications and Outcomes Surgery
Ducts and Pancreas 10. The Surgical Approach to Non-
3. Endoscopic and Percutaneous Colorectal Liver Metastases:
Management of Gallstones Patient Evaluation, Selection
and Results
4. Interventional Radiology
in Hepatobiliary Surgery 11. Surgical Techniques of Open
Cholecystectomy
5. Perioperative Care and
Anesthesia Techniques 12. Laparoscopic Cholecystectomy
and the Laparoscopic
6. Benign Tumors of the Liver: Management of Common Bile
A Surgical Perspective Duct Stones
7. Hepatocellular Carcinoma 13. Surgical Techniques for
Completion of a Bilioenteric
8. Periampullary Cancer and
Bypass
Distal Pancreatic Cancer
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I SBN 1- 57059- 630- 1 Ronald S. Chamberlain
www.landesbioscience.com
Leslie H. Blumgart
9 781570 596308
v a d e m e c u m
Hepatobiliary Surgery
Ronald S. Chamberlain, MD, MPA, FACS

Beth Israel Medical Center
Albert Einstein College of Medicine
New York, New York
Leslie H. Blumgart, MD, FACS, FRCS (Eng, Edin),

FRCPS (Glas)
Memorial-Sloan-Kettering Cancer Center
New York, New York
LANDES
BIOSCIENCE
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VADEMECUM
Hepatobiliary Surgery
LANDES BIOSCIENCE
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Library of Congress Cataloging-in-Publication Data

Hepatobiliary surgery / [edited by] Ronald S. Chamberlain, Leslie H.
Blumgart.
p.; cm. -- (Vademecum)
Includes bibliographical references and index.
Ronald S. Chamberlain ISBN 1-57059-630-1
1. Liver -- Surgery -- Handbooks, manuals, etc. 2. Biliary tract --
Surgery -- Handbooks, manuals, etc. I. Chamberlain, Ronald S. II.
Blumgart, L. H. III. Series.
[DNLM: 1. Liver Diseases -- surgery. 2. Biliary Tract Diseases --
surgery. 3. Digestive System Surgical Procedures. WI 770 H52995 2001]
RD546.H358 2001
617.5´56059 -- dc21
00-064876
While the authors, editors, sponsor and publisher believe that drug selection and dosage and
the specifications and usage of equipment and devices, as set forth in this book, are in accord
with current recommendations and practice at the time of publication, they make no
warranty, expressed or implied, with respect to material described in this book. In view of the
ongoing research, equipment development, changes in governmental regulations and the
rapid accumulation of information relating to the biomedical sciences, the reader is urged to
carefully review and evaluate the information provided herein.
Dedication
The surgical care of patients is a full commitment. As most of

you will realize, accepting any additional commitments beyond
clinical medicine is a burden that is borne by the family of the
practicing surgeon. This past year has been a tremendous 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 Courtney
and Taylor, Daddy is so proud of both you. You are all the sources
of my inspiration and contentment.
Ronald S. Chamberlain
Contents
Preface ............................................................................ xiii
1. Essential Hepatic and Biliary Anatomy
for the Surgeon ................................................................. 1
Ronald S. Chamberlain and Leslie H. Blumgart
Introduction ............................................................................................... 1
The Liver .................................................................................................... 1
Parenchyma (The Liver Substance) ............................................................. 2
Hepatic Veins (OUTFLOW) ...................................................................... 4
Hepatic Venous Anomalies ......................................................................... 6
Hepatic Arteries (INFLOW) ....................................................................... 6
The Biliary Tract ....................................................................................... 10
The Common Bile Duct ........................................................................... 11
Gallbladder and Cystic Duct ..................................................................... 12
Anomalous Biliary Drainage ..................................................................... 16
Summary .................................................................................................. 17
2. Imaging of the Liver, Bile Ducts and Pancreas ................ 20
Douglas R. DeCorato, Lawrence H. Schwartz
Test Selection ............................................................................................ 21
Hepatic Lesions ........................................................................................ 23
3. Endoscopic and Percutaneous Management
of Gallstones ................................................................... 34
Seth Richter and Robert C. Kurtz
Introduction ............................................................................................. 34
Endoscopic Retrograde Sphincterotomy ................................................... 34
Bile Duct Stone Retrieval .......................................................................... 35
Complications of Endoscopic Therapy ...................................................... 38
Percutaneous Stone Extraction .................................................................. 38
Specific Clinical Problems ......................................................................... 39
The Era of Laparoscopic Cholecystectomy ................................................ 40
4. Interventional Radiology in Hepatobiliary Surgery ........ 42
Lynn A. Brody and Karen T. Brown
Introduction ............................................................................................. 42
Diagnostic Procedures ............................................................................... 42
Therapeutic and Palliative Procedures ....................................................... 49
5. Perioperative Care and Anesthesia Techniques ................ 73
Mary Fischer, Enrico Ferri, Jose A. Melendez
Introduction ............................................................................................. 73
Preoperative Evaluation ............................................................................. 73
Hepatic Evaluation ................................................................................... 74
Intraoperative Management ...................................................................... 74
Postoperative Care .................................................................................... 76
6. Benign Tumors of the Liver: A Surgical Perspective ........ 81
Introduction ............................................................................................. 81
Evaluation ................................................................................................. 81
Benign Liver Tumors ................................................................................. 85
Additional Liver Tumors ........................................................................... 97
Conclusions .............................................................................................. 99
7. Hepatocellular Carcinoma ............................................ 101
Bryan Clary
Introduction ........................................................................................... 101
Etiology .................................................................................................. 101
Diagnosis and Pretreatment Planning ..................................................... 102
Treatment ............................................................................................... 104
Conclusion ............................................................................................. 110
8. Periampullary Cancer
and Distal Pancreatic Cancer ........................................ 111
Richard D. Schulick
Introduction ........................................................................................... 111
Pancreaticoduodenectomy for Periampullary Cancer .............................. 112
Distal Pancreatectomy for Distal Pancreatic Cancer ................................ 115
9. Hepatic Resection for Colorectal Liver Metastases:
Surgical Indications and Outcomes .............................. 121
Ronald P. DeMatteo, Yuman Fong
Introduction ........................................................................................... 121
Epidemiology .......................................................................................... 121
Preoperative Evaluation ........................................................................... 121
Physical Examination .............................................................................. 122
Laboratory Tests ...................................................................................... 122
Imaging .................................................................................................. 122
Surgical Indications ................................................................................. 123
Surgical Results ....................................................................................... 124
Survival ................................................................................................... 125
Prognostic Variables ................................................................................ 126
Recurrent Hepatic Metastases ................................................................. 127
Conclusion ............................................................................................. 127
10. The Surgical Approach
to Non-Colorectal Liver Metastases: Patient Evaluation,
Selection and Results .................................................... 129
Jonathan B. Koea
Introduction ........................................................................................... 129
Patient Selection ..................................................................................... 129
Preoperative Staging ................................................................................ 132
Techniques of Resection .......................................................................... 136
Nonoperative Techniques ........................................................................ 137
Results .................................................................................................... 138
Conclusions ............................................................................................ 143
11. Surgical Techniques of Open Cholecystectomy ............. 146
Introduction ........................................................................................... 146
Clinical Presentation ............................................................................... 146
Preoperative Studies ................................................................................ 147
Perioperative Management ...................................................................... 149
Operative Technique for Cholycystectomy .............................................. 149
Surgical Technique .................................................................................. 152
12. Laparoscopic Cholecystectomy and the Laparoscopic
Management of Common Bile Duct Stones .................. 156
Fredrick Brody
Introduction ........................................................................................... 156
Indications .............................................................................................. 156
Laparoscopic Cholecystectomy ............................................................... 156
Laparoscopic Common Bile Duct Exploration ........................................ 162
13. Surgical Techniques for Completion
of a Bilioenteric Bypass ................................................. 165
Pierre F. Saldinger, Leslie H. Blumgart
Scope of the Problem .............................................................................. 165
Anatomy ................................................................................................. 165
General Considerations ........................................................................... 169
Incisions ................................................................................................. 171
Abdominal Exploration ........................................................................... 172
Basic Anastomotic Technique .................................................................. 172
Alternative Anastomotic Techniques ....................................................... 173
Choledochojejunostomy or Hepaticojejunostomy ................................... 173
Ligamentum Teres (Round Ligament) Segment III Approach ................. 177
Choledochoduodenostomy ..................................................................... 179
14. Hilar Cholangiocarcinoma:
Surgical Approach and Outcome .................................. 183
Ronald S. Chamberlain, Leslie H. Blumgart
Etiology and Pathology ........................................................................... 183
Staging .................................................................................................... 186
Surgical Resection for Hilar Cholangiocarcinoma ................................... 187
Distal Bile Duct Tumors ......................................................................... 187
Hilar Cholangiocarcinoma (HCCA) ....................................................... 188
Liver Transplantation .............................................................................. 191
Palliative and Adjuvant Treatment for Cholangiocarcinoma .................... 191
Intrahepatic Surgical Bilioenteric Bypass ................................................. 191
Surgical Techniques ................................................................................. 192
Laparoscopy ............................................................................................ 192
Exposure and Retraction ......................................................................... 193
Palliative Approaches .............................................................................. 197
Conclusion ............................................................................................. 199
15. Surgical Management of Gallbladder Cancer ................ 201
Introduction ........................................................................................... 201
Anatomical Considerations ..................................................................... 201
Clinical Presentations .............................................................................. 202
Surgical Approach ................................................................................... 205
Summary ................................................................................................ 207
16. Techniques of Hepatic Resection .................................. 208
Sharon Weber, William R. Jarnagin, Leslie H. Blumgart
Introduction ........................................................................................... 208
Operative Technique ............................................................................... 208
Right Hepatectomy ................................................................................. 209
Extended Right Hepatectomy (Right Hepatic Lobectomy
or Right Trisegmentectomy) ................................................................. 214
Left Hepatectomy ................................................................................... 215
Left Lateral Segmentectomy (Left Lobectomy) ........................................ 218
Extended Left Hepatectomy (Left Trisegmentectomy) ............................ 218
Caudate Lobe Resection (Segment I Resection) ...................................... 222
Segmental Resection ............................................................................... 224
Wedge Resections ................................................................................... 225
Postoperative Care .................................................................................. 226
17. Technique for Placement
of the Hepatic Arterial Infusion Pump ......................... 227
N. Joseph Espat
Introduction ........................................................................................... 227
When Should HAIP Therapy Be Considered? ........................................ 228
Preoperative Patient Evaluation ............................................................... 228
Surgical Technique for the HAIP Placement ........................................... 229
Considerations for Patients with Variant Anatomy .................................. 231
Replaced Right Hepatic Artery (RRHA) ................................................. 231
Replaced Left Hepatic Artery (RLHA) .................................................... 232
Trifurcation of the Common Hepatic Artery (CHA)
into RHA, LHA and GDA .................................................................. 232
Creation of the Subcutaneous Pump Pocket ............................................ 232
Assessment of Hepatic Perfusion ............................................................. 235
Brief Comments on Technical Complications ......................................... 235
Summary ................................................................................................ 237
18. Non-Resectional Hepatic Ablative Techniques:
Cryotherapy and Radiofrequency Ablation ................... 238
Ronald S. Chamberlain and Ronald Kaleya
Introduction ........................................................................................... 238
Indications for Non-Resectional Ablative Therapies ................................ 238
Additional Indications and Contraindications ......................................... 239
Cryotherapy ............................................................................................ 239
Radiofrequency Ablation ........................................................................ 244
Results .................................................................................................... 249
Summary ................................................................................................ 253
19. Surgical Techniques in the Management
of Hepatic Trauma or Emergencies ............................... 257
H. Leon Pachter, Amber A. Guth
Introduction ........................................................................................... 257
History ................................................................................................... 257
Diagnosis of Blunt Hepatic Trauma ........................................................ 258
Diagnostic Tests ...................................................................................... 259
Nonoperative Management of Hepatic Injuries ....................................... 261
Blunt Hepatic Injuries ............................................................................ 261
Outcome of Nonoperative Management ................................................. 262
Surgical Management of Complex Hepatic Injuries ................................ 263
Operative Management of the Injured Liver ........................................... 263
Complications of Surgical Management .................................................. 267
Outcome of Hepatic Trauma .................................................................. 269
20. Liver Transplantation .................................................... 270
Patricia A. Sheiner, Rosemarie Gagliardi, D. Sukru Emre
Indications .............................................................................................. 270
Possible Contraindications to Liver Transplantation ................................ 270
Organ Allocation .................................................................................... 273
Medical Urgency ..................................................................................... 273
Timing of Transplantation ...................................................................... 273
Preoperative Planning ............................................................................. 274
Donor Selection ...................................................................................... 275
Intraoperative Considerations ................................................................. 276
The Standard Transplant Operation (Recipient) ..................................... 277
Vascular Anastomoses ............................................................................. 277
Bile Duct Anastomosis ............................................................................ 278
Piggyback Technique .............................................................................. 278
Bypass ..................................................................................................... 278
Split Livers .............................................................................................. 279
Living Donors ........................................................................................ 280
Results .................................................................................................... 281
Index ............................................................................. 283
Editors
Ronald S. Chamberlain, MD, MPA, FACS
Chief, Hepatobiliary Surgery and Pancreatic Surgery
Program Director, General Surgery
Beth Israel Medical Center
Albert Einstein College of Medicine
New York, New York
Chapters 1, 6, 11, 14, 18
Leslie H. Blumgart, MD, FACS, FRCS (Eng, Edin),

FRCPS (Glas)
Chief, Hepatobiliary Service
Enid A. Haupt Chair in Surgery
Memorial Sloan-Kettering Cancer Center, New York
Chapters 1, 13, 14, 16
Contributors
Fredrick Brody Ronald P. DeMatteo
Department of Surgery Department of Surgery
Cleveland Clinic Foundation Memorial Sloan-Kettering Cancer Center
Cleveland, Ohio New York, New York
Chapter 12 Chapters 9, 15
Lynn A. Brody Sukru Emre

Division of Interventional Radiology Miller Transplantation Institute
Memorial Sloan-Kettering Cancer Center Mount Sinai Medical Center
New York, New York New York, New York
Chapter 4 Chapter 20
Karen T. Brown N. Joseph Espat

Division of Interventional Radiology Department of Surgery
Memorial Sloan-Kettering Cancer Center University of Illinois at Chicago
New York, New York Chicago, Illinois
Bryan Clary Enrico Ferri

Department of Surgery Department of Anesthesiology
Duke University Medical Center Memorial Sloan-Kettering Cancer Center
Durham, North Carolina New York, New York
Chapter 7 Chapter 5
Douglas R. DeCorato Mary Fischer

Department of Radiology Department of Anesthesiology
Memorial Sloan-Kettering Cancer Center Memorial Sloan-Kettering Cancer Center
Chapter 2 Chapter 5
Yuman Fong H. Leon Pachter
Department of Surgery Department of Surgery
Memorial Sloan-Kettering Cancer Center New York University School of Medicine
New York, New York Director, Division of Shock and Trauma
Chapters 9, 15 Bellevue Hospital Center
New York, New York
Amber A. Guth Chapter 19
New York University School of Medicine
Surgical ICU Seth Richter
Bellevue Hospital Center Department of Gastroenterology
New York, New York Memorial Sloan-Kettering Cancer Center
Chapter 19 New York, New York
Chapter 3
Rosemarie Gagliardi
Miller Transplantation Institute Pierre F. Saldinger
Mount Sinai Medical Center Danbury Hospital
New York, New York Danbury, Connecticut
William R. Jarnagin Patricia A. Sheiner

Department of Surgery Miller Transplantation Institute
Memorial Sloan-Kettering Cancer Center Mount Sinai Medical Center
Ronald N. Kaleya Richard D. Schulick

Department of Surgery Department of Surgery and Oncology
Montefiore Medical Center The Johns Hopkins Hospital
Bronx, New York Baltimore, Maryland
Jonathan B. Koea Lawrence H. Schwartz

Hepatobiliary Service Department of Radiology
Department of Surgery Memorial Sloan-Kettering Cancer Center
Memorial Sloan-Kettering Cancer Center New York, New York
New York, New York Chapter 2
Chapter 10
Sharon Weber
Robert C. Kurtz Hepatobiliary Service
Gastroenterology Department of Surgery
Memorial Sloan-Kettering Cancer Center Memorial Sloan-Kettering Cancer Center
Jose A. Melendez
Department of Anesthesiology
Memorial Sloan-Kettering Cancer Center
New York, New York
Chapter 5
Preface
Hepatobiliary Surgery is a technical manual and not a textbook. Although
some chapters are robust in their discussion of anatomic and physiologic
detail, others are written in a purely “how to” style. At its core, the book is
written as a reference and guidebook for practicing surgeons, gastroenter-
ologists, and interventional radiologists with an interest in hepatobiliary dis-
eases. However, we believe it will also be of great value to medical students
on 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, knowledgeable
gastroenterology collaborator, and skilled interpreter of radiologic images.
No one medical discipline has a patent on knowledge and opinion, and
most complex hepatobiliary problems are best managed by securing the opin-
ion of experts in all disciplines before embarking on a treatment plan. This
book attempts to parallel that dialogue by collating the expertise, experience
and opinion of all of these disciplines and distilling it down into one vol-
ume. Please note, this book is not gospel about how unique patients should
be managed, nor does it claim to present the only way in which various
operative procedures and interventions can be performed. Rather, this book
presents a strategy that works for us and can hopefully be utilized to enhance
your practice and the care of your patients.
Acknowledgments
This book represents a group project. There are many people whose efforts
we acknowledge here and many others whose names we may fail to mention
but to whom we remain grateful. We acknowledge …
Our contributing authors, whose generosity in compiling, collating and
writing up their experience has made this effort possible.
The committed editorial, organizational, and proofreading expertise pro-
vided by Judy Lampron. Judy’s tremendous energy and tireless efforts in
communicating and cajoling contributors, devoting hours to late night and
weekend manuscript review sessions, and providing constant support made
it all possible.
Maria Reyes whose professionalism and expertise in the editorial process
have contributed greatly to the successful and timely completion of this work.
Tireless efforts from Kim Mitchell, Cynthia Dworaczyk, and Ron Landes
from Landes Bioscience have made this all possible.
Leslie H. Blumgart
CHAPTER 1
CHAPTER 1
Essential Hepatic and Biliary Anatomy

for the Surgeon
Ronald S. Chamberlain and Leslie H. Blumgart
Introduction
That every surgeon will experience complications is a certainty. Yet, major 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 normal
anatomy and function, 2) a failure to recognize anatomic variants when they present,
and 3) a failure to ask for help when uncertain or unsure. All but the last of these
errors are remediable with study and effort. In regard to the last error, most surgeons
learn humility through their failures and at the expense of their patients, while some
never learn.
The importance of a precise knowledge of parenchymal structure, blood supply,
lymphatic drainage, and variant anatomy on outcome is perhaps nowhere more
apparent then in hepatobiliary surgery. Though the liver was historically an area
where few brave men dared to tread, and even fewer returned a second time, recent
advances in anesthetic technique and perioperative care now permit hepatic surgery
to be performed with low morbidity and mortality in both academic and commu-
nity hospitals. That said, surgeons are duly cautioned to inventory their own skills
and knowledge before venturing forward into the right upper quadrant. This chap-
ter will review functional biliary and hepatic anatomy necessary for the conduct of
safe and successful hepatic operations.
The Liver
Surface Anatomy
The liver is situated primarily in the right upper quadrant, and usually benefits
from complete protection by the lower ribs. Most of the liver substance resides on
the right side, although it is not uncommon for the left lateral segment to arch over
the spleen. The superior surface of the liver is molded to and abuts the undersurface
of the diaphragm on both the right and left sides. During normal inspiration, the
liver may rise as high as the 4th or 5th intercostal space on the right.
The liver itself is completely invested with a peritoneal layer except on the poste-
rior surface where it reflects onto the undersurface of the diaphragm to form the
right and left triangular ligaments. The liver is attached to the diaphragm and ante-
rior abdominal wall by three separate ligamentous attachments, namely the falci-
form, round, and right and left triangular ligaments. (Figure 1.1) The falciform
ligament, which is situated on the anterior surface of the liver, arises from the ante-
Hepatobiliary Surgery, edited by Ronald S. Chamberlain and Leslie H. Blumgart.

©2003 Landes Bioscience.
2 Heptobiliary Surgery
Fig. 1.1. Surface anatomy of the liver. (A) Anterior surface, (B) inferior surface of the
liver viewed in vivo, and (C) inferior view of the liver, viewed ex vivo. Reprinted with
permission from: Surgery of the Liver and Biliary Tract (3rd Edition), Blumgart LH,
Fong Y and WH Jarnigan (Eds.) W.B. Saunders, London, UK (2000).
rior leaflets of the right and left triangular ligaments and terminates inferiorly where
the ligamentum teres enters the umbilical fissure. The gallbladder is normally at-
tached to the undersurface of the right lobe and directed towards the umbilical
fissure. At the base of the gallbladder fossa, is the hilar transverse fissure through
which the main portal structures to the right lobe course. Additional important
landmarks on the posterior liver surface include a deep vertical groove in which the
inferior vena cava is situated and a large bare area (i.e. no peritoneal coating) that is
normally in contact with the right hemidiaphragm and right adrenal gland. The left
lateral segment of the liver arches over the caudate lobe that is situated to the left of
the vena cava. The caudate lobe is demarcated on the left by a fissure containing the
ligamentum venosum (a remnant of the umbilical vein). Additional left-sided im-
portant surface features include the gastrohepatic omentum located between the left
lateral segment and the stomach. The gastrohepatic omentum may contain replaced
or accessory hepatic arteries. Finally, there is usually a thick fibrous band that envel-
ops the vena cava high on the right side and runs posteriorly towards the lumbar
vertebrae. This band, which is sometimes referred to as the vena caval ligament,
must be divided to allow proper visualization of the suprahepatic cava and right
hepatic veins.
Parenchyma (The Liver Substance)
The liver is comprised of two main lobes, a large right lobe and a smaller left
lobe. Although the falciform ligament is often thought to divide the liver into a
Essential Hepatic and Biliary Anatomy for the Surgeon 3
right and left lobe, the true “anatomic” or “surgical” right and left lobes of the liver
are defined by the course of the middle hepatic vein that runs through the main
scissura of the liver. Although various descriptions of the internal anatomy of the
liver have been proffered over the last century, Couinaud’s (1957) segmental anatomy
of the liver is the most useful for the surgeon.
Couinaud’s classification system divides the liver into four unique sectors based 1
upon the course of the three major hepatic veins. Each sector receives its blood
supply from a separate portal pedicle. Within the main scissura lies the middle he-
patic vein that courses from the left side of the suprahepatic vena cava to the middle
of the gallbladder fossa. Functionally, the main scissura divides the liver into 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 left
hemilivers is known as Cantlie’s line. The right hepatic vein runs within the right
segmental scissura and divides the right lobe into a right posterior and anterior
sector, while the left hepatic vein follows the path of the falciform ligament and
divides the left lobe into a medial and lateral segment.
The right and left lobes of the liver are further divided into eight segments based
upon the distribution of the portal scissurae. At the hilus, the right portal vein pur-
sues a very short course (1-1.5 cm) before entering the liver. Once entering the
hepatic parenchyma, the portal vein divides into a right anterior sectoral branch
that arches vertically in the frontal plane of the liver and a posterior sectoral branch
that follows a more posteriorlateral course. The right portal vein supplies the anterior
(or anteriormedial) and posterior (or posteriorlateral) sectors of the right lobe. The
branching pattern of these sectoral portal veins subdivides the right liver into four
segments—Segments V (anterior and inferior) and VIII (anterior and superior) form
the anterior sector, and Segments VI (posterior and inferior) and VII (posterior and
superior) form the posterior sector.
In contrast to the right portal vein, the left portal vein has a long extrahepatic
length (3-4 cm) coursing beneath the inferior portion of the quadrate lobe (Seg-
ment VIB) enveloped in a peritoneal sheath (the hilar plate.) Upon reaching the
umbilical fissure, the left portal vein runs anteriorly and superiorly within the liver
substances, and gives off horizontal branches to the quadrate lobe medially (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 it
lies mostly on the left side (Fig. 1.4). More precisely, it is the most dorsal portion of
the liver situated behind the left lobe and embracing the retrohepatic vena cava from
the hilum to the diaphragm. The portion of the caudate lobe that is within the right
liver is usually quite small and lies posterior to Segment IVB. Figure 1.3 illustrates
the location of the caudate lobe which lies between the left portal vein and vena cava
on the far left, and the middle hepatic vein and vena cava within the right liver. The
caudate lobe receives blood vessels and biliary tributaries from both the right and
left hemilivers. The right side of the caudate lobe, and the caudate process, receives
its blood supply from branches of the right or main portal vein, while the left side of
the caudate receives a separate vessel from the left portal vein.
Fig. 1.2. Segmental and sectoral anatomy of the liver. The liver is divided into three
main scissurae by the right, middle, and left hepatic vein branches. The middle
hepatic courses through the main scissura (or Cantlie’s line) and divides the liver
into right and left lobes. The right hepatic vein divides the right liver into anterior
(Segments V and VIII) and posterior (Segment VI and VII) sectors, while the left
hepatic vein divides the left lobe into medial (Segments IV A and B) and lateral
segments (Segments II and III). The intrahepatic branching of the right and left
hepatic ducts, arteries and portal veins (shown) in the horizontal plane of the liver
divides the liver into eight separate segments. The caudate lobe (Segment I) is nei-
ther part of the right or left lobe. Rather the caudate lobe receives venous and arterial
branches from both the right and left side of the liver, and drains directly into the
inferior vena cava. Reprinted with permission from: Surgery of the Liver and Biliary
Tract (3rd Edition), Blumgart LH, Fong Y (Eds.) W.B. Saunders, London, UK (2000).
Aberrant segmental anatomy of the liver is uncommon. The presence of a di-

minutive left lobe is the most common anomaly reported and is important only
because it may serve as a limitation to the performance of extended right hepatecto-
mies. Although reports of “accessory” hepatic lobes are not uncommon, these do
not represent separate segments with independent intrahepatic vascular supply, but
rather elongated tongues of normal liver tissue. Riedel’s lobe is the most common of
these “accessory” lobes and is reality an extended piece of liver tissue hanging 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 always
present as direct communications between the vena cava and the posterior surface of
Fig. 1.3. Couinaud’s segmental anatomy of the liver. (a) in vivo appearance; (b) ex
vivo appearance. Reprinted with permission from: Surgery of the Liver and Biliary
the right lobe. Uniquely, the caudate lobe (Segment I) drains principally through
direct communication with the retrohepatic cava.
The hepatic veins lie within the three major scissurae of the liver dividing the
parenchyma into the right anterior and posterior sectors, and the right and left
lobes. (Figs. 1.2 and 1.3) The right hepatic vein lies within the right scissura (or
segmental fissure) and divides the right lobe into a posterior (Segments VI and VII)
and anterior (Segments V and VIII) sector. The middle hepatic vein lies within the
main hepatic scissura (or main lobar fissure) separating the right anterior sector
(Segments V and VIII) from the quadrate lobe (Segment IV). Anatomically, the
main scissura separates the liver into right and left lobes. The left hepatic vein lies
within the left scissura (or the left segmental fissure) in line with or just to the right
of the falciform ligament. The right hepatic vein drains directly into the suprahe-
1 patic cava, while the middle and left hepatic veins coalesce to form a short common
trunk prior to entry. The umbilical vein represents an additional alternative site of
venous efflux. It is located beneath the falciform ligament and eventually terminates
in the left hepatic vein, or less commonly in the confluence of the middle and left
hepatic veins.
Hepatic Venous Anomalies
Although the outline above should suffice as cursory knowledge of hepatic venous
anatomy, it is far from exhaustive. For example, large accessory right hepatic veins
are commonly found, and an appreciation of these structures on axial imaging can
be important for operative planning. If a large accessory right hepatic vein is present,
it may be possible to divide all three major hepatic veins in the performance of an
extended left hepatectomy. Most importantly, the surgeon embarking on hepatic
resection should have a thorough knowledge of the internal course of the hepatic
veins, as the danger posed by hepatic venous bleeding cannot be overestimated.
Hepatic Arteries (INFLOW)
Extrahepatic Arterial Anatomy
“Normal” hepatic arterial anatomy is anything but normal. Indeed standard ce-
liac arterial anatomy as described in most major anatomic treatise is found in only
60% of cases. An accessory hepatic artery refers to a vessel that supplies a segment of
liver that also receives blood supply from a normal hepatic artery. An aberrant he-
patic artery is called a replaced hepatic artery as it represents the only blood supply
to a specific hepatic segment. Precise knowledge of normal hepatic arterial anatomy
is necessary to appreciate abnormal anatomy and will be the focus of this section.
The celiac artery arises from the aorta shortly after it emerges through the dia-
phragmatic hiatus. The celiac trunk itself is typically very short and divides into the
left gastric, splenic, and common hepatic arteries shortly after its origin. (Figure
1.5). The common hepatic artery typically passes forward for a short distance in the
retroperitoneum where it then emerges at the superior border of the pancreas and
left side of the common hepatic duct. The common hepatic artery supplies 25% of
the liver’s blood supply, with the portal vein supplying the remaining 75%.
After arising from the celiac axis, the common hepatic artery turns upward and
runs lateral and adjacent to the common bile duct. The gastroduodenal artery that
supplies the proximal duodenum and pancreas is typically the first branch of the
common hepatic artery. The right gastric artery takes off shortly thereafter and con-
tinues within the lesser omentum along the lesser curve of the stomach. At this
point the common hepatic artery is referred to as the proper hepatic artery. The
proper hepatic artery courses towards the hilum and soon divides into the right and
left hepatic arteries. Prior to the bifurcation, a small cystic artery branches off to
provide blood supply to the gallbladder. While coursing through the hepatoduodenal
ligament the hepatic artery proper, common bile duct, and portal vein are enveloped
Fig. 1.4. Caudate lobe anatomy. The caudate lobe is situated to the left of the
inferior vena cava (IVC). Superiorly the caudate lobe is covered by Segments II and
III which are reflected laterally in this diagram. The ligamentum venosum, a rem-
nant of the fetal umbilical vein, courses across the anterior surface of the caudate
lobe to enter the left hepatic vein. The caudate lobe runs along the retrohepatic vena
cava from the common trunk of the middle and left hepatic veins (MHV, LHV) to the
portal vein (PV) inferiorly (Left (LPV) and right portal vein (RPV)). Small venous tributar-
ies drain the caudate lobe directly into to the IVC. On its medial surface, the caudate
lobe is attached to the right liver by the caudate process. Reprinted with permission
from: Surgery of the Liver and Biliary Tract (3rd Edition), Blumgart LH, Fong Y (Eds.)
W.B. Saunders, London, UK (2000).
in a peritoneal sheath within the hepatoduodenal ligament. The proper hepatic ar-
tery bifurcates earlier than the common bile duct and portal vein. In 80% of cases
the right hepatic artery courses posterior to the common hepatic duct before 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 right
hepatic artery branches into right anterior (Segments V and VIII), and right poste-
rior sectoral branches (Segments VI and VII). The posterior sectoral branch initially
runs horizontally through the hilar transverse fissure (of Gunz) normally present at
the base of Segment V and adjacent to the caudate process. The left hepatic artery
runs vertically towards the umbilical fissure where it gives off a small branch (often
called the middle hepatic artery) to Segment IV, before continuing on to supply
Segments II and III. Additional small branches of the left hepatic artery supply the
Fig. 1.5. Normal celiac axis anatomy. The presence of the right hepatic (RH), middle
hepatic (MH) to Segment IV, and left hepatic (LH) artery are demonstrated. Reprinted
with permission from: Surgery of the Liver and Biliary Tract (3rd Edition), Blumgart
LH, Fong Y (Eds.) W.B. Saunders, London, UK (2000).
caudate lobe (Segment I), although caudate arterial branches may also arise from the
right hepatic artery. The sectoral and segmental bile ducts and portal veins follow
the course of the hepatic artery branches. Intrahepatic branching of these structures
will be discussed in more detail below.
The blood supply to the common bile duct is varied and multiple. Branches of
the common hepatic, gastroduodenal, and pancreaticoduodenal arteries have all been
shown to provide arterial supply at various levels.
Hepatic Arterial Anomalies
Variations in the arterial blood supply to the liver are common. Although the
hepatic artery typically arises from the celiac axis, complete replacement of the main
hepatic artery or its branches occur with variable frequency. Similarly, duplication
or accessory hepatic arterial branches, particularly an accessory left hepatic artery,
may be more the norm than an anomaly. The most common hepatic arterial anomaly
involving a replaced vessel is a replaced right hepatic artery (25%). In this situation,
the replaced right hepatic artery usually arises from the superior mesenteric artery
and runs lateral and posterior to the portal vein within the hepatoduodenal 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 Anatomy
The portal vein is formed by a union of the superior mesenteric vein (SMV)
and splenic vein behind the neck and body of the pancreas. In up to 1/3rd of all
Fig. 1.6. Hepatic arterial anomalies. (a) Replaced main hepatic artery arising from
the superior mesenteric artery (SMA), (b) Independent origin of the right and left
hepatic artery from the celiac axis, (c) Replaced right hepatic artery arising from
the SMA, (d) Replaced left hepatic artery arising from the left gastric artery (LGA),
(e) Accessory right hepatic artery arising from the SMA, (f) Accessory left hepatic
artery arising from the LGA. Reprinted with permission from: Surgery of the Liver
and Biliary Tract (3rd Edition), Blumgart LH, Fong Y (Eds.) W.B. Saunders, London,
UK (2000).
individuals the inferior mesenteric vein may also join this confluence. Venous tribu-
taries from the pancreas may also drain directly into the portal vein, and generally
correspond to the arterial supply. More precisely, there are anterior, posterior, superior
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 may
enter the portal vein directly. Surgical dogma states that there are no venous branches
on the anterior surface of the portal vein and, for the most part this is true–most
veins enter the portal vein tangentially from the side. However, having paid homage
1 to surgical dogma, the reality is that small anterior venous branches may exist, and
any manipulation posterior to the pancreatic neck and anterior to the portal vein
should be performed with maximum operative exposure and care.
Access to the portal vein is typically obtained by identifying the superior 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 follow
it inferiorly to the SMV. The length of the SMV is highly variable, and may range
from only a few millimeters up to 4 cm. In many circumstances the SMV is made
up of two to four venous branches that coalesce shortly before joining the portal
vein rather than a single dominant vein. The inferior pancreaticoduodenal vein,
which can be quite prominent, is the only vein that normally enters the SMV 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 vein
rather 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 portal
vein and facilitates the creation of a “tunnel” above the portal vein and beneath the
pancreas. Once a determination has been made regarding the resectability of the
pancreatic lesion, we favor early transection of the common bile duct. If the tumor
later proves unresectable, a palliative end to side bilioenteric bypass can be performed.
In addition to those variants described above, there are additional (but rare)
congenital anomalies of the portal vein with which the surgeon should be aware.
The two most common are an anterior portal vein that lies above the pancreas and
duodenum, and direct entry of the portal vein into the inferior vena cava—a con-
genital “portocaval” shunt. The importance of careful dissection around the portal
vein cannot be overemphasized. Inadvertent injury or transection of the portal vein
or a main tributary is difficult to correct and remains among the most lethal of
surgical errors.
Intrahepatic Arterial and Portal Venous Anatomy
Throughout the course of the liver, the sectoral and segmental bile ducts, hepatic
arteries and portal venous branches run together. (Fig. 1.8) Whereas knowledge of
precise intrahepatic biliary anatomy is of most practical value to the operating surgeon,
further detail about intrahepatic anatomy will be discussed below.
The Biliary Tract
Extrahepatic Hepatic Biliary Anatomy
The extrahepatic biliary system consists of the extrahepatic portions of the right
and left bile ducts that join to form a single biliary channel coursing through the
posterior head of the pancreas to enter the medial wall of the second portion of the
duodenum. The gallbladder and cystic duct form an additional portion of this ex-
trahepatic biliary system that typically joins with the terminal portion of the common
hepatic duct to form the common bile duct. In most instances, the confluence of
the right and left bile ducts lies to the right of the umbilical fissure and anterior to
the right branch of the portal vein. The right hepatic duct is typically short (< 1cm)
and branches into a right posterior sectoral duct (Segments VI/VII) and a right
anterior sectoral duct (Segments V/VIII) shortly after entering the hepatic paren-
chyma. In contrast, the left hepatic duct has a relatively long extrahepatic course 1
(2-3 cm) along the base of the quadrate lobe (Segment IV) and enters the hepatic
parenchyma at the umbilical fissure. Lowering the hilar plate (i.e., connective tissue
enclosing the left hepatic elements and Glisson’s capsule) at the base of the quadrate
lobe provides great exposure to both the biliary hilum and the extrahepatic portion
of the left hepatic duct. (Figure 1.7)
The Common Bile Duct
By convention, the entry point of the cystic duct divides the main extrahepatic
biliary channel into the common hepatic duct (above) and the common bile duct
(below). The common bile duct continues inferiorly positioned anterior to the por-
tal vein and lateral to the common hepatic artery. If the hepatic artery bifurcates
early, the right hepatic artery may be seen coursing below (80% of the time) the
Fig. 1.7. Lowering of the hilar plate and exposure of the left hepatic duct. The left
hepatic duct runs at the base of the quadrate lobe (Segment 4) and is covered by
the hilar plate (a layer of connective tissue running between the hepatoduodenal
ligament and the Glissonian capsule of the liver). Dividing this layer demonstrates
the extrahepatic portion of the left hepatic duct arising from the umbilical fissure.
(Numbers 2,3,4 and refer to segmental liver anatomy). Reprinted with permission
Fig. 1.8. Portal pedicles. This cutaway view of the right and left portal pedicles
demonstrates the course of the right and left portal veins, hepatic ducts, and he-
patic arteries as they enter the hepatic parenchyma. Reprinted with permission
common bile duct (see details above). At the junction of the 1st and 2nd portions of
the duodenum, the common bile duct ducks behind the duodenum posterior to the
pancreatic head in order to enter the medial wall of the duodenum (2nd portion) at
the sphincter of Oddi.
Gallbladder and Cystic Duct
The gallbladder is situated on the undersurface of the anterior inferior sector
(Segment V) of the right lobe of the liver. Though often densely adherent, it is
separated from the liver parenchyma by the cystic plate, a layer of connective tissue
arising from Glisson’s capsule and in continuity with the hilar plate at the base of
Segment IV. In rare instances, the gallbladder is only loosely attached to the
undersurface of the liver by a thinly veiled mesentery and may be prone to volvulus.
Variations in gallbladder anatomy are rare. These variations include (a) bilobed or
double gallbladders, (b) septated gallbladders, or (c) gallbladder diverticula.
(Fig. 1.9A).
The cystic duct arises from the infundibulum of the gallbladder and runs me-
dial and inferior to join the common hepatic duct. The cystic duct is typically 1-3
mm in diameter and can range from 1 mm to 6 cm in length depending upon its
union with the common hepatic duct. Spiral mucosal folds, referred to as valves of
Heister, are present in the mucosa of the cystic duct. Cystic duct abnormalities are
uncommon and include (a) double cystic ducts (very rare), (b) aberrant cystic duct
entry sites, and (c) aberrant cystic duct union with the common hepatic duct. (Fig-
ure 1.9 A and B) Aberrant entry points for the cystic duct include a low entry into
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).
the common hepatic duct retroduodenal or retropancreatic and anomalous entry

into the main right hepatic duct or sectoral duct. Aberrant union of the cystic duct
and common hepatic duct can take multiple forms including (a) absence of a cystic
duct (< 1%) , (b) parallel course of the cystic duct and common hepatic artery with
a shared septum (20%), and (c) an anomalous passage of the cystic duct posterior to
1 the common hepatic duct with entry on the medial wall (5%). (Figure 1.9A and B)
Typically the cystic artery is a single vessel that courses lateral and posterior to
the cystic duct. However, variations in the anatomy of the cystic artery are common.
(Figure 1.10) Multiple cystic arteries, origin of the cystic artery from a segmental or
lobar hepatic artery, aberrant course of the cystic artery over the cystic duct, and
various other anomalies have been reported. A careful intraoperative determination
of cystic artery anatomy is important to prevent unnecessary hemorrhage during
cholycystectomy.
Intrahepatic Bile Duct Anatomy
An understanding of intrahepatic ductal anatomy is obviously important and
vital to the performance of high biliary anastomoses for cholangiocarcinoma (Klatskin
tumors), an intrahepatic bilioenteric bypass, and complex hepatic resections such as
caudate lobectomy, and left and right trisegmentectomy. The right and left lobes of
the liver are drained separately by the right and left hepatic ducts. In contrast, 1–4
smaller ducts from either the right or left hepatic ducts drain the caudate lobe.
Within the liver parenchyma, the intrahepatic biliary radicals parallel the major
portal triad tributaries directed toward each hepatic segment of the liver. More spe-
cifically, bile ducts are usually situated superior to its complementary portal vein
branch, while the hepatic artery lies inferiorly.
The left hepatic duct drains all three segments of the left liver. (Segment II, III,
and IV). In some textbooks Segment IV, the quadrate lobe, is futher sub-divided
into sub-segments (IVa, superior, and IVb, inferior) so conceptually both the right
and left hepatic ducts each drain four segments. Although the left hepatic duct
originates within the liver and terminates in the common hepatic duct, it is easier to
describe its’ path in reverse since the extrahepatic areas are readily visible to the
operating surgeon. After the bifurcation into the right and left hepatic ducts, the left
duct courses towards the umbilical fissure along the undersurface of Segment IVb
above and behind the left branch of the portal vein. Access to this area can be gained
by lowering the hilar plate (described above). Several small branches from the quad-
rate lobe (Segment IV) and the caudate lobe (Segment I) may enter the left duct at
this location. The left hepatic duct is formed within the umbilical fissure by the
Segment III (lateral) and Segment IVb (medial) ducts. Following the course of the
umbilical fissure vertically towards the falciform ligament, the Segment II (lateral),
and Segment IVa (medial) branches are formed. Although a careful and tedious
dissection is required to access the segmental biliary ducts for anastomoses, (e.g., a
Segment III bypass), control of the segmental portal triads to all areas of left lobe is
readily achievable within the umbilical fissure. (see Fig. 1.11)
The right hepatic duct emerges from the liver at the base of Segment V just to
right of the caudate process. This duct drains Segments V, VI, VII, and VIII and
originates at the junction of the right posterior (Segments VI and VII), and anterior
(Segments V and VIII) sectoral ducts. The right posterior sectoral duct follows an
Fig. 1.10. Cystic artery anomalies. (A) Typical course, (B) double cystic artery, (C) cystic
artery crossing anterior to the main bile duct, (D) cystic artery originating from the right
branch of the hepatic artery and crossing the common hepatic duct anteriorly, (E) 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).
almost horizontal course at the base of Segments V and VI that can often been seen
lying within a transverse fissure on the superficial surface of the liver. Segmental
biliary branches from Segments VI (inferior) and VII (superior) converge to form
the main right posterior sectoral duct. Segmental branches from Segments V and
VIII form the right anterior sectoral duct. While the right posterior sectoral duct fol-
lows a horizontal course, the right anterior sectoral duct runs almost vertical within
Segment V, and receives branches from both Segment V (inferior) and VIII (superior).
Fig. 1.11. Left portal vein pedicle. The union of the Segment IV, II, and III portal
veins within the umbilical fissure forms the left portal vein. A separate Segment I
portal vein also enters the left portal vein before it coalesces with the right portal
vein at the hilus. Lines A, B, C, D demonstrate the lines of portal vein transection
which are required to complete various hepatic resections. Line A is the line of
transection for completion of a left hepatectomy and caudate lobectomy. Line B is
the line of transection for completion of a left hepatectomy. Line C is the line of
transection for a Segment II resection. Line D is the line of transection for a Seg-
ment III resection. Reprinted with permission from: Surgery of the Liver and Biliary
Biliary drainage of the caudate lobe is less predictable. Conceptually, the

caudate lobe has three distinct areas—a right part, a left part, and the caudate
process. In some instances three separate bile ducts may be present. The cau-
date process represents a narrow bridge of tissue that connects the caudate to
the right lobe (Segment V). In more than 75% of cases the caudate drains into
both the right and left hepatic ductal system, but isolated drainage into the
right (< 10%), or left hepatic duct (~15%) can occur.
Anomalous Biliary Drainage
Normal intra- and extrahepatic biliary anatomy is present in approximately 75
percent of cases. (Fig. 1.12) Every effort should be made to define existing intrahe-
patic anatomy based on preoperative imaging since failure to do so may result in
devastating complications. Anomalies in both sectoral and segmental anatomy may
exist together or separately. The more common type of each of the anomalies will be
described in detail below.
Anomalous Sectoral Biliary Anatomy
Although the union of the right and left hepatic duct typically occurs at the
hilum, a triple confluence of the right posterior and anterior sectoral ducts with the 1
left hepatic duct may exist in up to ~15% of cases. (Fig. 1.12) In 20% of cases one of
the right sectoral ducts, more commonly the anterior sectoral duct, may enter the
common hepatic duct distal to the confluence. If this situation is not recognized it
can be very dangerous, and represents a common cause of injury during laparoscopic
cholecystectomy. Less commonly (~5%) the right posterior sectoral duct (and rarely
the right anterior sectoral duct) may cross to enter the intrahepatic portion of the
left hepatic duct. Failure to appreciate this anomaly prior to right or left hepatec-
tomy can lead to significant postoperative problems. Note some authorities believe
that this anomaly represents the most common intrahepatic biliary variation.
Anomalous Segmental Biliary Anatomy
A large number of segmental biliary anomalies have been reported. Most are
unimportant to the surgeon and of anatomical interest only. Figure 1.13 illustrates
the more common anomalies that have been reported within the right lobe and the
medial segment of the left lobe.
Summary
A comprehensive understanding of normal and aberrant anatomy is the corner-
stone of surgery. The truth of this statement is nowhere more apparent than in the
performance of complex hepatobiliary surgery. Mastery of the segmental anatomy
of the liver, as well as a comprehensive understanding of both normal and anoma-
lous arterial, venous and biliary anatomy are the sine qua non for performing safe
hepatic resections. Recent advances in perioperative management of patients with
hepatobiliary diseases (detailed elsewhere) permit the surgeon to perform increas-
ingly radical hepatic procedures (upon sicker patients.) Although the expertise of-
fered by our radiology and anesthesiology colleagues is important, it is incumbent
upon every surgeon who performs liver resection to be well prepared. An age-old
surgical axiom states “98% of the surgical outcome is determined in the operating
room.” A good outcome in the performance of hepatic resections requires one to
become a student of the game.
Selected Readings
1. Cameron J L. In discussion of Hanks J B, Meyers W C, Filston H C et al. Surgical
resection for benign and malignant liver disease. Annals of Surgery 1980
191:584-592
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).
Fig. 1.12. Normal and aberrant sectoral ductal anatomy. (A) Typical ductal anatomy,
(B) triple confluence, (C) ectopic drainage of a right sectoral duct into the common
hepatic duct (C1), right anterior duct draining into the common hepatic duct; (C2),
right posterior duct draining into the common hepatic duct, (D) ectopic drainage
of a right sectoral duct into the left hepatic ductal system (D1, right posterior sectoral
duct draining into the left hepatic ductal system; D2, right anterior sectoral duct
draining into the left hepatic ductal system, (E) absence of the hepatic duct
confluence, (F) absence of right hepatic duct and ectopic drainage of the right
posterior duct into the cystic duct. Reprinted with permission from: Surgery of the
Liver and Biliary Tract (3rd Edition), Blumgart LH, Fong Y (Eds.) W.B. Saunders,
London, UK (2000).
Fig. 1.13. Normal and aberrant segmental ductal anatomy. (A), variations of Segment
V, (B) variations of Segment VI, (C) variations of Segment VIII, (D) variations of Segment
IV. Note there is no variation of drainage of Segments II, III, and VII. Reprinted with
permission from: Surgery of the Liver and Biliary Tract (3rd Edition), Blumgart LH,
Fong Y (Eds.) W.B. Saunders, London, UK (2000).
CHAPTER 2
Imaging of the Liver, Bile Ducts

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

Imaging of the Liver, Bile Ducts and Pancreas 21
displaying anatomic information. Certain MR contrast agents, such as gadolinium

chelates, are administered with T1-weighted images (mostly gradient echo images, a
sequence that can be adjusted to generate rapid T1-weighted images). T2-weighted
images generate bright (hyperintense) fluid and are generally used to identify patho-
logic processes.
Imaging of the hepatobiliary system is dependent on the suspected underlying 2
disease, pretest likelihood of a positive study, and clinical suspicion of concurrent
underlying disease process (for example, cirrhosis). The initial study, if chosen prop-
erly, may be able to both identify the underlying disease process and provide staging
information at the same time. In a patient with a low pretest likelihood of disease,
initial screening of the liver is best accomplished with US due to its wide availability
and relatively low cost. A patient with a negative ultrasound, and low pretest likeli-
hood of disease, may need no further workup. However, patients with a high pretest
likelihood of disease may require a different initial examination. Once a lesion or
unsuspected underlying parenchymal disease is identified on US, a second imaging
test may be necessary. A comparison between the three main imaging modalities is
summarized in Table 2.1.
Test Selection
The choice of initial imaging test is influenced by several factors, including patient
population, prevalence of certain disease processes, test availability, cost restraints,
radiologic equipment and the pretest likelihood of a positive study. For example, US
is an excellent screening test for many patients; however, body habitus, underlying
hepatic disease, and overlying bowel gas can limit an otherwise diagnostic 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 limits
identification of small lesions and hinders characterization. MRI routinely acquires
multiple sequences that aid in lesion identification and characterization. MRI has a
set of absolute contraindications for scanning (Table 2.2). Additionally, since no
radiation is administered, precontrast images are routinely obtained. MRI scanners
are variable in both speed and quality. Low field strength systems and “open” mag-
nets may not afford the resolution necessary for preoperative planning.
Contrast administration is an important aspect of both CT and MRI. CT scans
principally use iodinated contrast material, while MRI has a variety of contrast agents
available of which gadolinium is the most common. Patients allergic to iodine will
usually not cross-react with gadolinium-based agents and, thus, may be safely referred
for MRI. A variety of newer MRI contrast agents, including tissue specific antigens,
are currently under investigation.
A more detailed analysis of the best test for each specific hepatic, biliary and
pancreatic abnormality is beyond the scope of this Chapter, but general guidelines
are discussed below and summarized in Table 2.3.
Evaluation of the liver is best done with MRI, as it provides improved lesion
detection and characterization. In addition, MRI can precisely define underlying
liver processes, such as fatty infiltration, which can sometimes be confused with other
diagnoses on both CT and US. An additional advantage of MRI is the development of
Table 2.1. Comparison of imaging modalities
MRI CT Ultrasound
Resolution Superior contrast Superior spatial Spatial resolution
resolution resolution dependent on
2 transducer selected
Contrast material Superior safety High safety profile No contrast
profile than CT of nonionic administered
and lower volumes contrast. Requires
are administered relatively high
doses of iodinated
contrast for study
Radiation None Ionizing radiation None
used
Speed Rapid imaging Rapid imaging Imaging time
time available time. Entire exam operator dependent
may be performed
in under a minute
Technique Variable depending More uniform than Standard images
on hardware and MR, while still with additional
software somewhat variable images acquired
depending on the
clinical situation
Cost Relatively high High Moderate
Availability Less than CT Readily available, Generally available,
usually 24 hrs/day but may be limited
at certain periods
due to staffing
Table 2.2. Contraindications for MR imaging*

Absolute contraindications Relative contraindications
Pacemaker Pregnancy
Neurostimulator Recent intravascular stent
Cerebral aneurysm clip of unknown composition. Claustrophobia
Possible metallic foreign body in the globe. Critically ill patients
* Note: This table is not meant to be a complete list of all contraindications and
any question should be referred to an MR imaging specialist.
new contrast agents, such as ferumoxides (Feridex), which have been shown to im-
prove lesion detection in certain cases.
The selection of an ideal imaging technique for abnormalities of the biliary tree
is somewhat more complex. In the evaluation of cholelithiasis or choledocholithiais,
US is clearly first choice due to its low cost, availability and accuracy. If an evalua-
tion is performed for suspected malignant disease, MRI is superior to both CT and
Table 2.3. Test selection based on body part

CT MR Imaging Ultrasound
Liver 2 1 3
Biliary Tree 3 1 1 2
Pancreas 1 2 3
Ranking is in order of preference (1 being the most preferred). When two

modalities are ranked first, it depends on the clinical indication for the study as to,
which is chosen as discussed in the text.
US since bowel gas will not interfere with evaluation of the distal common bile duct
or the identification of periportal and retroperitoneal adenopathy (Fig. 2.5). 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 is
the next test of choice. MRI and CT are equivalent with regard to vascular encase-
ment and adenopathy in the setting of pancreatic adenocarcinoma. Microcystic
adenomas may be better delineated with MRI, as the small cysts are more easily
depicted (Fig. 2.6). Pancreatitis is best evaluated with CT especially if the patient is
unstable or in critical condition.
The next section will review the more commonly encountered lesions of the
liver, biliary tree and pancreas and their associated imaging features.
Hepatic Lesions
Hepatic cysts are commonly encountered on all imaging studies. On US, they
are hypoechoic, with increased through transmission and thin or imperceptible walls.
If these criteria are met, the lesion is considered a simple cyst (Fig. 2.1A). On CT, a
cyst is a nonenhancing lesion with low HU typically under 10 (Fig. 2.1B). On MRI,
cysts are hyperintense on initial T2-weighted imaging and remain hyperintense on
heavily T2-weighted images (TE> 180). The lesion is typically hypointense on
T1-weighted images and, as with CT, does not enhance with contrast administration.
Hemangiomas are the most common benign hepatic tumors. These lesions are
typically hyperechoic on US and are either well defined or have lobulated borders
(Fig. 2.2A). Hemangiomas typically reveal low attenuation on the noncontrast CT
study and peripheral nodular enhancement following contrast administration
(Fig. 2.2B). On MRI, hemangiomas display similar signal intensity to cysts and are
hyperintense on T2 and heavily T2-weighted images (Fig. 2.2C). Initial peripheral
nodular enhancement is seen after contrast administration, and the lesion may or
may not completely fill on delayed contrast imaging.
The enhancement patterns of particular lesions are often critical to their 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 underlying
cirrhosis and a hypervascular lesion are considered to have hepatocellular carcinoma
(HCC) until proven otherwise (Fig. 2.3B). In addition to arterial dominant
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 increased
through transmission.
Fig. 2.1B. A CT image of the same patient demonstrates two lesions. Although
these lesions are low attenuation, Hounsfield units were greater than 10 and thus
nondiagnostic for a cyst. (Note a noncontrast CT was performed prior to the con-
trast-enhanced scan to evaluate for enhancement.)
Fig. 2.2A. Hepatic hemangioma: Ultrasound examination demonstrates a

hyperechoic mass (arrows) in the liver. Although hemangiomas are hyperechoic, a
definitive diagnosis is often difficult.
Fig. 2.2B. A CT examination of the same patient demonstrates a lesion (arrow) with
peripheral nodular enhancement (curved arrow), characteristic for a hemangioma.
Fig. 2.2C. An MRI examination in a different patient demonstrates a mass (m) which
is hyperintense on T2 weighted images. The fluid is bright (please note CSF arrow).
Gadolinium enhanced MRI (not shown) will also demonstrate the classic periph-
eral nodular enhancement pattern when present.
Fig. 2.3A. Metastatic disease ultrasound examination of a patient with a prior hepatic
resection demonstrating a mass (arrow) in the residual left lobe. The mass demon-
strates a partial hypoechoic rim (arrowhead), a slightly hyperechoic portion, and a
central region which is hyperechoic (target).
Fig. 2.3B. A T2-weighted image demonstrates a mass (m) with a peripheral portion that
is slightly hyperintense to liver, and a central portion that is markedly hyperintense.
Fig. 2.3C. Contrast enhanced T1-weighted MRI demonstrates heterogeneous

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

hypervascular lesion (arrows) biopsy proven to be HCC.
Fig. 2.4B. An axial T2-weighted image with fat suppression from an MRI exam
performed 9 months earlier demonstrates the same lesion (curved arrow).
Fig. 2.4C. Equilibrium phase postcontrast T1-weighted image demonstrates the lesion
(arrow) but also demonstrates significant underlying siderotic nodules.
Fig. 2.5A. Hilar cholangiocarcinoma (Klatskin tumor): Ultrasound examination

demonstrates a small soft tissue tumor (arrowheads) surrounding an endoscopically
placed stent (curved arrow).
Fig. 2.5B. Axial image from a T2-weighted MRI demonstrates eccentric soft tissue
(curved arrow) surrounding a narrowed common bile duct. Note the plastic stent is
not appreciated as it is on the ultrasound.
Fig. 2.6. Pancreatic mass: Ultrasound examination demonstrates a normal appearing

pancreatic head with a hypoechoic mass in the body/tail region (curved arrows).
Fig. 2.7A. Microcystic adenoma: A CT examination demonstrates a mass in the

body of the pancreas with cystic components (arrow).
Fig. 2.7B. MR image of the same patient demonstrates this mass to be comprised of
multiple small cysts (arrow).
Selected Reading
1. 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 2
MRI Correlation. 3rd ed: Lippincott Williams and Wilkins; 1998.
CHAPTER 3
Endoscopic and Percutaneous Management

of Gallstones
Seth Richter and Robert C. Kurtz
Introduction
Management of gallstone disease has changed dramatically in the last two decades.
Before the use of laparoscopic techniques, conventional surgical methods of open
laparotomy were used to remove the diseased gallbladder. If common bile duct 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 bile
duct and pancreatic duct. An iodinated contrast agent was injected into the biliary
system, and tumors or gallstones could be seen on fluoroscopy. The continued im-
provement in instrument development and the expansion of endoscopic training
programs has made ERCP universally available. The skilled endoscopist working
with a cooperative patient can often perform a diagnostic ERCP in 15 to 20 min-
utes. Success rates for cannulating the common bile duct and pancreatic duct are
well over 90%. Now, side-viewing electronic duodenoscopes are used to afford ex-
cellent visualization of the ampulla. As an adjunct to ERCP, the development of
endoscopic sphincterotomy (ERS) in 1973 enabled therapeutic maneuvers in the
biliary system to be routinely performed. Endoscopic sphincterotomy gave the 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. These
important clinical situations previously either required surgical correction or a per-
cutaneous, transhepatic catheter. ERCP has allowed for less invasive diagnostic and
therapeutic maneuvers to be performed.
Today, laparoscopic cholecystectomy is the procedure of choice for removing a
diseased gallbladder. If there is concern that there may also be concomitant 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 Sphincterotomy
Endoscopic retrograde sphincterotomy (ERS) refers to the division of the circu-
lar muscles of the biliary sphincter using diathermy current delivered through an
endoscopically positioned sphincterotome. The initial step in sphincterotomy is se-
Endoscopic Management of Hepatobiliary and Pancreatic Disorders 35
lective cannulation of the common bile duct. This is achieved by cannulating the
duodenal papilla and under fluoroscopic guidance maneuvering the sphincterotome
into the common bile duct. It is imperative that selective cannulation of the bile
duct is confirmed fluoroscopically to avoid pancreatic trauma due to the electrocau-
tery, and subsequent acute pancreatitis. The electrical incision is made by controlled
application of a blended cutting/coagulating current through the exposed
sphincterotome wire. Complete control of wire tension and electrosurgical current
is maintained at all times. On occasion, deep cannulation of the common bile duct 3
by the sphincterotome may be difficult and a “pre-cut” of the ampulla is needed.
With an adequate sphincterotomy, most stones less than 1 cm in diameter will pass
spontaneously. However active stone extraction is favored to avoid stone impaction,
biliary obstruction, and cholangitis.
Several authors have recently advocated the use of endoscopic papillary dilata-
tion instead of ERS to allow the endoscopic removal of small common bile duct
stones. They cite a lower complication rate, with fewer episodes of post-ERS 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 favor
endoscopic sphincterotomy.
Bile Duct Stone Retrieval
Common duct stones less than 15 mm can usually be removed by standard
extraction methods using either balloon catheters or wire baskets. Stones that are
larger in size usually need to be broken up prior to removal. Under fluoroscopic
guidance, a balloon catheter is inserted into the common bile duct, above the level
of the stone. It is then inflated and withdrawn, pulling the stone out of the bile duct
ahead of the balloon. If there are multiple bile duct stones, the lowest stone should
be removed first. The balloon catheters used for stone extractions do not carry the
risk of stone impaction that a Dormia basket does. The balloon will burst or slide by
a stone that is difficult to extract.
The Dormia basket offers an advantage over balloon catheters in that it is often
easier to entrap the stone in the basket, and it will also allow more traction force to
be used when extracting the stone. The technique used with the basket is similar to
that used with the balloon catheters. The basket is advanced beyond the stone to be
removed. This is done with the basket in the closed position. As with the balloon
catheters care must be taken not to push the stone more proximal into the intrahe-
patic ducts as this makes extraction much more difficult. Once past the stone, the
basket is opened and maneuvered to entrap the stone. After the stone is entrapped it
is removed by withdrawing the basket while applying traction to the basket catheter.
After completion of stone extraction by either balloon catheter or basket method, a
cholangiogram is performed to confirm that no stones remain in the biliary duct
system. With these techniques, about 85% to 90% of bile duct stones can be re-
moved successfully. Failure to remove bile duct stones can be due to several reasons
which include the inability to get to the ampulla because of anatomic problems, the
inability to cannulate the bile duct, and large bile duct stones.
Large Bile Duct Stones

Stones that are greater than 15 mm in diameter are considered to be large. The
technical difficulty of stone extraction increases as the size of the stone increases.
These large stones represent a significant challenge to even the very skilled endoscopist.
In addition, there is a finite limit to the size of the endoscopic sphincterotomy that
can be safely produced. As mentioned previously, stones less than 15 mm can be
removed by standard methods, using balloon catheters or retrieval baskets. Larger
3 stones, in general, require fragmentation prior to removal. The common endoscopic
methods for stone fragmentation are mechanical lithotripsy and intracorporeal lithot-
ripsy using either laser or electrohydraulic probes to cause stone fragmentation.
Mechanical Lithotripsy
Mechanical 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 especially
useful when the retrieval basket containing the large gallstone can not be withdrawn
from the bile duct through the sphincterotomy site. When impaction of the stone in
the basket occurs, the handle of the basket is cut off, the endoscope is removed over
the basket sheath, and then the outer Teflon sheath covering the wires of the basket
is also removed. A flexible metal tube is then threaded over the basket wires, under
fluoroscopic guidance, into the bile duct, to the level of the basket and stone. It acts
as a solid surface onto which the basket and stone are pulled tightly using the
lithotripter crank handle. Generally, the stone fragments as a result of the force of
tightening the basket wires. If the stone does not fragment, the basket itself, will
break, enabling its withdrawal from the bile duct. Other methods will then be needed
to deal with the stone. This technique has made it possible for patients to avoid
surgery because of a stone that has become impacted in a retrieval basket.
Mechanical lithotripters that can pass through the endoscope have also facili-
tated stone fragmentation. These consist of a wire basket within a Teflon sheath
attached to a handle that passes through the endoscope instrument channel. Endo-
scopic sphincterotomy is also necessary before inserting the lithotripter into the bile
duct. The basket within the teflon sheath is inserted above the stone. The basket is
then opened and the stone is trapped in the basket. After the entrapment of the
stone, it can be crushed on a metal sheath, which is extended over the inner Teflon
catheter which in turn is attached to a winding mechanism used to increase pressure
on the stone in the basket. When cranked, the system retracts the basket and stone
against the metal sheath, causing the stone to fragment. The stone fragments can
then be removed with a basket or balloon catheter. Overall, mechanical lithotripsy
has a success rate of approximately 85%-90% for crushing and removing bile duct
gallstones that are refractory to standard extraction techniques.
Laser Lithotripsy
Laser lithotripsy devices rely on the conversion of the laser energy to thermal and
mechanical energy in order to produce gallstone fragmentation. Concerns of bile
duct injury and incomplete stone fragmentation were associated with these systems.
Newer laser lithotripters have been investigated, and the United States Food and
Drug Administration has approved only the 504 nm Coumarin Flashlamp Pulsed
Dye laser for use in the biliary system. This system produces a unique laser pulse
that is absorbed on the stone surface and creates a plasma cloud that rapidly expands
and contracts, resulting in a shock wave causing stone fragmentation. Recently laser
lithotripsy has been possible under fluoroscopic guidance. This so called “smart
laser” resulted from the development of a device that can identify duct stones by
analyzing back scattered light and interrupting the laser pulse in case of bile duct 3
tissue contact.
Electrohydraulic Lithotripsy
Similar 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 of
two coaxial isolated electrodes at the tip of a flexible catheter. The catheter is capable
of delivering electric sparks in short rapid pulses. This leads to a hydraulic shock
wave which creates a shearing force that ultimately leads to stone fragmentation.
The main advantage of EHL over laser lithotripsy is in its lower cost. However the
potential risk for bile duct injury appears to be greater with EHL.
Complete duct clearance rates with laser lithotripsy and EHL is approximately
85%. Both of these procedures are also limited by the fact that they are both highly
specialized procedures that are not available in all centers. In addition they require a
very high level of expertise to be used safely and successfully.
Biliary Endoprosthesis
In the small number (about 5%) of cases where either gallstone extraction is
incomplete or not possible, the endoscopic insertion of a biliary endoprosthesis is
recommended. This maneuver will buy time and allow for improvement in the
patient’s condition until complete stone extraction is achieved either by using addi-
tional endoscopic techniques or by subsequent surgical intervention. Endobiliary
stents 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 through
the patient’s nose. Other polyethylene stents have either straight or “pig-tailed” ends.
The “pig-tailed” variety has at least a theoretical advantage in that the rounded end
may prevent the bile duct stone from impacting in the ampulla. Metal endobiliary
stents are a more permanent solution and should not be used if surgery or additional
stone removal techniques are to be employed. Endobiliary stents are used to provide
biliary decompression, treat or prevent cholangitis and sepsis, and to prevent stone
impaction in the distal common bile duct and ampulla. The insertion of an
endobiliary stent can help change an emergent surgical situation into a more 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 acceptable
long-term solution, when attempts at endoscopic stone removal are unsuccessful.
Rendezvous Technique
If the ampulla and common bile duct can not be cannulated, a combined 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
guide wire is then passed through the percutaneously placed catheter and out the
bile duct opening in the ampulla. Endoscopy is performed at the same time. The
guide wire is identified, grasped, and pulled through the endoscope. A wire-guided
sphincterotome is inserted over the percutaneously placed guide wire, and ERS is
performed in the usual fashion.
Complications of Endoscopic Therapy
3 Complications 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 is
almost always as a result of the endoscopic sphincterotomy. Unfortunately, bleeding
can be massive and life threatening. It is important to recognize that significant
bleeding can present several days after endoscopic sphincterotomy. Treatment ranges
from electrocautery or sclerotherapy if the bleeding occurs during the endoscopic
procedure, to angiography and embolization, or surgical intervention in patients
who fail endoscopic therapy.
Retroperitoneal perforation occurs in less than 1% of cases. It is more likely to
occur when either the endoscopic sphincterotomy is too large or when the electrical
cut deviates from the recommended orientation in the ampulla. The diagnosis can
be made at the time of procedure on fluoroscopy and x-ray, if air or contrast is seen
outside the bile duct or duodenum. Most cases of retroperitoneal perforation can be
managed conservatively if the diagnosis is made promptly.
Pancreatitis is the most common complication of ERS and occurs in approxi-
mately 3%-6% of cases. It is more likely if there has been injection of contrast into
the pancreatic duct, especially if the pancreatic duct is filled under pressure and so-
called pancreatic acinarization occurs. ERCP-related pancreatitis is usually mild and
manifested by abdominal pain, nausea, and vomiting that occurs within several hours
of the procedure. Most cases are self-limited, but on occasion, severe pancreatitis
can occur with all of its inherent complications. Serum amylase levels are not 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 complication
occurs when an obstructed biliary system is not adequately drained at the end of the
endoscopic procedure. Cholangitis and sepsis can be minimized by assuring adequate
biliary drainage if there is a question of incomplete stone clearance and by using pre-
and post-procedure antibiotics for patients with evidence of biliary obstruction.
Percutaneous Stone Extraction
There are occasions when the ampulla can not be reached by endoscopic means.
This may be as a result of a previous surgical procedure such as a distal subtotal
gastrectomy with gastrojejunostomy for gastric cancer. The afferent loop is often
long, and the ampulla cannot be approached by endoscopy. Other common 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 and
access the biliary tree. Dilating catheters are used to dilate the ampulla, and small
biliary stones can then be pushed through into the duodenum. The large bile duct
stones are fragmented first, either with a mechanical lithotripter in a fashion similar
to that employed with ERCP, or other methods of stone fragmentation are used,
similar to those described with ERCP. Once the large stones are broken up they can
be pushed by catheters through the ampulla and into the duodenum. If multiple
intrahepatic stones are present, the percutaneous tract can be dilated, and the stones
may be removed by the use of Dormia baskets through the dilated tract. This proce-
dure can be tedious and frequently must be done in several stages. Percutaneous bile 3
duct 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 a
means to enter the biliary tree and deal with bile duct stones. The complication rate
of percutaneous stone extraction is somewhat higher that endoscopic stone removal
and approaches 10%. As with endoscopic methods, bleeding, pancreatitis, and 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 Sepsis
Cholangitis and sepsis are the result of a bacterial infection in an obstructed bile
duct. This condition is most commonly caused by common bile duct stones but
may rarely be secondary to either benign or malignant bile duct strictures, especially
if the biliary system has been previously instrumented. The majority of patients will
present with a clinical picture of right upper quadrant abdominal pain, fever, and
jaundice: the so-called “Charcot’s triad”. However patients can also present with
fulminant, life-threatening sepsis.
Patients without complete biliary obstruction may respond to conservative
measures, intravenous hydration, and antibiotics. If patients do not show a rapid
clinical response, and for those that develop generalized sepsis, urgent drainage of
the obstructed biliary tree is required. Biliary drainage can be performed by several
techniques which in part depend on the experience of the medical staff and the
severity of the patient’s illness. In patients with multiple stones in the biliary system
extending well up into the liver, an open surgical procedure, stone extraction, and T-
tube placement may be the best approach. If there is a high-grade stricture at the
hilus of the liver, percutaneous biliary drainage would be most appropriate. 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 rate
of up to 40%. Endoscopic drainage has become the favored modality if the expertise
is available and the biliary abnormality is appropriate.
Endoscopic biliary decompression may be achieved by endoscopic sphinctero-
tomy and stone extraction, nasobiliary drainage, or by placement of a biliary stent
depending on the nature and cause of the obstruction. For obstruction secondary to
stone disease, sphincterotomy with stone extraction is the procedure of choice, as it
resolves the problem in one endoscopic session. However the insertion of an
endobiliary stent may be the best option for the seriously ill patient or for the pa-
tient with a large common bile duct gall stone. In addition, ERCP can delineate the
cause of the obstruction and can provide a sample of bile for bacterial culture or
cytology if a malignant stricture is suspected.
The effect of biliary decompression is often dramatic with a rapid resolution of
pain, fever, and other signs of sepsis. Once the infection is controlled, repeat ERCP
can be performed, and if any stones were left during the initial procedure, they can
then be removed.
3 Acute Gallstone Pancreatitis

Gallstone disease is a leading cause of acute pancreatitis in Western countries
accounting for 34%-54% of cases. Initially endoscopists were reluctant to perform
ERCP in patients with acute pancreatitis for fear of exacerbating the pancreatitis.
However ERCP has been shown to be a safe and effective procedure in patients with
severe acute gallstone pancreatitis. Endoscopic sphincterotomy with stone extrac-
tion has been compared with conventional treatment in patients with suspected
gallstone pancreatitis. Common bile duct stones were found on ERCP in 63% of
patients with severe attacks compared with 26% of patients with mild attacks. Com-
plications of pancreatitis were significantly less frequent in the group who had early
ERCP, ERS, and stone extraction, and the benefit was more marked in those pa-
tients with severe pancreatitis. This demonstrated that ERCP can be performed in
acute pancreatitis and that there was significant benefit from early stone extraction,
especially in patients with severe pancreatitis.
The Era of Laparoscopic Cholecystectomy
Laparoscopic cholecystectomy has revolutionized the management of gallblad-
der disease. Laparoscopic cholecystectomy has replaced open cholecystectomy as
the 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 and
presumed common bile duct stones. However, the laparoscopic management of com-
mon duct stones is more complicated then laparoscopic cholecystectomy alone. This
procedure requires advanced surgical expertise and instrumentation. Thus
laparoscopic cholecystectomy is still frequently coupled with ERCP, ERS, and stone
extraction when common bile duct stones are suspected.
Generally, in the patient with gallbladder disease, if there is a low suspicion of
common duct stones, there appears to be little if any value in performing routine
ERCP prior to laparoscopic cholecystectomy. Studies have shown that there is a low
yield of detecting unsuspected common duct stones and clinically important biliary
duct anatomic variants compared with the known complication rate of ERCP. Pa-
tients in whom there is a high suspicion of common duct stones, than is those that
have a history of jaundice or abnormal liver function studies, are more likely to
benefit from preoperative ERCP, ERS, and stone extraction. Patients identified as
having a medium risk of a common bile duct stone create a clinical dilemma. Some
have suggested routine intravenous cholangiography and selective ERCP in these
patients. These issues may also be resolved based on the skills of the endoscopists
and surgeons at each institution. A patient with a history of mild pancreatitis, nor-
mal liver function studies, and no evidence of common bile duct stones on non-
invasive imaging should not routinely have a preoperative ERCP.
Selected Reading
1. 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. 1995
Jul;109(1):252-63.
3. Cotton PB. Endoscopic retrograde cholangiopancreatography and laparoscopic
cholecystectomy. Am J Surg. 1993 Apr;165(4):474-8.
4. Johnson AS, Ferrara JJ, Steinberg SM, Gassen GM, Hollier LH, Flint LM. The 3
role of endoscopic retrograde cholangiopancreatography: sphincterotomy versus
common 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 retrograde
cholangiopancreatography 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: a
prospective 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. Percutaneous
treatment of bile duct stones in patients treated unsuccessfully with endoscopic
retrograde 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 bile
duct 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 in
patients undergoing laparoscopic cholecystectomy. Gastrointest Endosc. 1998
Jan;47(1):50-6.
11. Freeman ML, Nelson DB, Sherman S, Haber GB, Herman ME, Dorsher PJ, Moore
JP, Fennerty MB, Ryan ME, Shaw MJ, Lande JD, Pheley AM. Complications of
endoscopic biliary sphincterotomy. N Engl J Med. 1996 Sep 26;335(13):909-18.
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 Hepatobiliary

Surgery
Lynn A. Brody and Karen T. Brown
Introduction
The interventional radiologist performs many procedures which facilitate the
diagnosis and treatment of patients being cared for by the hepatobiliary surgeon.
Procedures may be diagnostic, therapeutic, or palliative. A close working relation-
ship between the hepatobiliary surgeon and the interventional radiologist benefits
both doctors and patients, and is best accomplished in the background of a team
comprised of surgeons, gastroenterologists, radiologists and appropriate medical spe-
cialists such as oncologists and hepatologists.
This chapter will provide a guide to the procedures performed by interventional
radiologists that may be useful when caring for the hepatobiliary surgery patient.
Diagnostic Procedures
Needle Biopsy
General Considerations
Percutaneous needle biopsy may be performed to diagnose primary or secondary
neoplasms, or in cases of diffuse hepatic disease and/or hepatic dysfunction. Fine
needle aspiration (FNA), biopsy, and core biopsy, can be performed depending on
the indication. Fine needle aspiration is typically performed using a 20-25 gauge
needle and provides material for cytological analysis and/or culture. A wide variety
of needles are available. At our institution, a 22 or 20 gauge side notched (Westcott)
needle is most commonly used (Fig. 4.1A). Procedures are best performed in the
presence of a cytotechnologist who determines whether adequate material has been
obtained in order to maximize the likelihood that the procedure is not terminated
prematurely. FNA is typically adequate for diagnosing metastatic disease, particu-
larly when the original material is available for comparison. Further examination
using 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 in
cases when tissue from the primary tumor is unavailable for comparison. Fine
needle biopsy of primary neoplasms may also be diagnostic dependent on local
cytopathologic expertise.
Core specimens provide tissue for surgical pathology and allow for architectural
evaluation of the specimen. In the liver, this is utilized most often to distinguish well-
differentiated hepatocellular carcinoma (HCC) from normal liver. Core specimens are
Interventional Radiology in Hepatobiliary Surgery 43
Fig. 4.1A. Percutaneous biopsy. Representation of two biopsy needles.
also often helpful in classifying sarcomas and lymphomas. Cores of tissue can be
obtained with needles as small as 22 gauge, although these biopsies are performed
most commonly using 18 gauge needles or larger. At our institution, core specimens
are generally obtained using an 18-gauge needle. Tissue coring needles come in a
wide variety of designs, including automated devices, and, in general, needle selection
should be based on operator familiarity and preference.
Indications
Many primary hepatic neoplasms, both benign and malignant, can be confi-
dently diagnosed by cross sectional imaging. Hemangiomas in the liver often have a
characteristic appearance with both ultrasound and magnetic resonance imaging
(MRI), with MRI being most likely to afford a confident diagnosis. MRI can also
accurately identify focal nodular hyperplasia (FNH) and may be helpful in supporting
44 Hepatobiliary Surgery
a diagnosis of a hepatic adenoma. Needle biopsy is rarely requested to diagnose

these entities and is best avoided in suspected hemangioma as bleeding complica-
tions may occur. In addition, in those select cases, needle biopsy rarely adds much
information beyond that observed from imaging studies and an excisional biopsy is
often indicated if uncertainty remains.
HCC can be confidently diagnosed based on an appropriate constellation of
clinical, laboratory and radiographic criteria. Patients with hepatic neoplasm(s) in
the setting of cirrhosis and/or hepatitis B or C, with an elevated alpha-fetoprotein
level, can be assumed to have primary hepatocellular carcinoma. At our institution,
an AFP level >500 ng/dl is considered diagnostic. In the absence of these criteria,
4 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 prior
hepatic 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 patients
being evaluated for diffuse hepatic disease whose thrombocytopenia or coagulopathy
renders standard percutaneous techniques more dangerous. The liver is accessed
from a hepatic vein, using an automated device advanced from a jugular approach.
The needle is advanced from an intravascular approach within the liver taking care
not to puncture the hepatic capsule.
Technique
Needle biopsy is performed under imaging guidance, using either ultrasound or
computed tomography (CT) (Figs. 4.1B, 4.1C). MRI may be utilized more frequently
in the future. Operator preference and equipment availability generally determine
the modality for guidance which is used. Procedures are generally performed on an
out-patient basis using local anesthesia with or without conscious sedation.
Complications
Complications of needle biopsy are rare. Bleeding is quite uncommon in our
experience and is typically self-limited when it does occur. Small subcapsular
hematomas are most common. Pneumothorax may occur during biopsy of high
hepatic lesions. Fortunately, the majority of these pneumothoraces are small and do
not require placement of a chest tube. Tumor seeding has been reported but is
extremely uncommon. Percutaneous pancreatic biopsy may incite pancreatitis.
Diagnostic Angiography
With the enormous recent advances in cross sectional imaging techniques, diag-
nostic angiography is rarely performed today. Tumor characterization and vascular
involvement are better demonstrated by many other modalities. At our institution,
diagnostic angiography is performed most commonly in conjunction with CT angio-
portography or to evaluate arterial anatomy prior to placement of hepatic arterial
infusion pumps. Studies are under way to determine whether equivalent informa-
tion may be obtained using triple phase CT or contrast enhanced MRI. Early data
suggest that arterial anatomy can be accurately depicted by these less invasive means.
Fig. 4.1B. Non-contrast CT image shows a 1.5 cm mass in Segment V.
Fig. 4.1C. Non-contrast CT image shows a 22 gauge notched needle within the
mass. The notch is directed anteriorly at the edge of the lesion.
CT Arterial Portography
There are some surgeons who still feel that CT arterial portography (CTAP)
represents the “gold standard” for evaluating the liver for tumor(s). As mentioned
previously, studies are being conducted to determine the value of CTAP relative to
other less invasive imaging modalities.
Technique
A selective catheter is typically placed from a right femoral artery approach using
the Seldinger technique. The type of selective catheter utilized is based on operator
preference. Catheters as small as 4F may be used. At our institution, a 5F catheter is
4 generally used. Contrast is injected into the celiac and superior mesenteric arteries
to document arterial anatomy and to guide placement of the catheter for the CTAP.
The catheter should be positioned in either the splenic artery or the superior mesen-
teric artery (SMA). In the case of replaced or accessory hepatic vessels arising from
the SMA (most commonly an accessory or replaced right hepatic artery), the cath-
eter is positioned in the splenic artery or very distally in the SMA in order to avoid
reflux to the hepatic arterial branch during scanning. Once the catheter is posi-
tioned, the patient is transferred to the CT scanner for the CTAP. The study should
be performed on a spiral CT scanner (Figs. 2.2A-H). Contrast is injected into the
arterial catheter at a rate of approximately 3 cc per second. After an appropriate
delay to allow filling of the portal vein (typically 40-60 seconds for catheters in the
SMA, slightly shorter for catheters in the splenic artery), spiral scanning is per-
formed from the dome to the tip of the liver. After a second delay (20-30 seconds) to
allow for some filling in of perfusion artifacts, spiral scanning is then performed in
the reverse direction. The catheter is then removed and the patient returns 3-4 hours
later for delayed imaging.
Interpretation
CTAP demonstrates areas of diminished portal perfusion very well. While it is
quite sensitive for identifying tumor, it is far less specific. The initial images are the
most sensitive for demonstrating areas of decreased portal perfusion. The later im-
ages, in particular the delayed, or hepatic excretion phase images, are then used to
differentiate tumor from perfusion artifact. In general, tumors are visible on each of
the three sets of images while perfusion artifacts will disappear over time. It is im-
portant to understand that there are locations in which perfusion artifacts typically
occur, which may be unrelated to tumor. These areas occur most commonly at the
back of Segment IV and along the umbilical fissure.
Percutaneous Transhepatic Cholangiography
Like diagnostic angiography, percutaneous transhepatic cholangiography (PTC)
has largely been replaced by improved noninvasive imaging. High quality 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. Multiplanar
reconstruction 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 be
reserved for those cases in which noninvasive imaging is inconclusive or where
Fig 4.2A. Early phase image through the upper liver shows two lesions in the lateral
segment and one in Segment VIII.
Figs. 4.2A-J. CT portogram in a patient with metastatic colorectal carcinoma. The
angiographic catheter is in the superior mesenteric artery. The study consists of
three phases. The early images are acquired in a cephalad to caudad direction,
immediately following the injection of iohexol 140 radiographic contrast into the
superior mesenteric arterial catheter. A total of 185 cc are given at 3 cc per second.
Axial images are acquired from the dome of the liver to the tip of the liver. The
middle phase images are obtained after approximately 20 to 30 seconds and are
acquired in the reverse direction. The final phase is obtained approximately 4 hours
later, without additional contrast.
functional information is needed. At our institution, this is done most commonly to

evaluate the status of bilioenteric anastamoses in cases of suspected partial or
intermittent occlusion.
Technique
The procedure is generally performed using conscious sedation and local anes-
thesia. Prophylactic antibiotics are administered. A right or left-sided approach is
chosen based on anatomic considerations and operator preference. Punctures may
be performed using fluoroscopic or sonographic guidance. Sonographic guidance
affords the advantage of allowing a duct to be targeted directly, thus minimizing the
number of needle passes; however, it requires the availability of a good quality ultra-
sound machine and a high degree of operator skill. Left-sided punctures are easier to
perform under ultrasound guidance since intercostal imaging is avoided.
PTC techniques will be described further in the section on percutaneous biliary
drainage.
Fig. 4.2B. Middle phase image at the same level looks similar. The three lesions are
demonstrated.
Fig. 4.2C. Late phase images. The three lesions are seen on these two images. The
lesion in Segment VIII and the lesion in the lateral aspect of Segment II/III are very
low attenuation and likely to represent cysts. The small mass medially in the left
liver (arrows) is most likely a metastasis.
Fig. 4.2D. Early phase image at the level of the porta. There is an area of low
attenuation anteriorly in Segment IV, abutting the umbilical fissure.
Therapeutic and Palliative Procedures

Percutaneous Cholecystostomy
Percutaneous cholecystostomy (PC) is generally performed in patients with acute
cholecystitis who are too ill to undergo cholecystectomy. The procedure is most often
performed in acute acalculous cholecystitis. Acalculous cholecystitis typically occurs in
elderly and/or extremely ill patients, frequently in the intensive care unit. Definitive
diagnosis may be difficult, but should be suspected in this patients in whom there is no
other explanation for fever and leukocytosis, or when the gallbladder is distended and
tender. PC may represent definitive treatment in these patients. Given the relative ease
and safety, of performing PTC, most interventional radiologists have a low threshold
for performing this procedure in the appropriate clinic situation.
PC may also be performed in cases of calculous cholecystitis in patients consid-
ered poor operative candidates. When gallstones are present, the ultimate treatment
depends on the clinical situation. The procedure may be temporizing in patients
whose condition improves enough to allow for definitive cholecystectomy. In pa-
tients who remain poor surgical candidates, stones may be removed percutaneously
from the gallbladder or common bile duct, and balloon sphincterotomy may be
performed. Rarely, PC may be performed to provide biliary drainage in cases of
distal obstruction.
Fig. 4.2E. Late phase image at the same level. No mass is demonstrated. This is a
characteristic location for a perfusion artifact, which is what this “lesion” represented.
Fig. 4.2G. Early phase image in the lower liver demonstrating a metastasis in
Segment VI.
Fig. 4.2H. Middle phase image in the lower liver demonstrating a metastasis in
Segment VI.
Fig. 4.2I. Late phase image in the lower liver demonstrating a metastasis in Segment VI.
Technique
PC may be performed under ultrasound or CT guidance or even at the bedside
in patients too ill to be transported to the interventional suite. In most cases of
acalculous cholecystitis, thick dark bile is aspirated at the time of drainage. As 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 be
capped until the tract has matured (we generally wait at least 3 weeks), at which
point the tube can be removed.
Percutaneous Biliary Drainage
4
Indications
Percutaneous biliary drainage is indicated in cases of obstructive jaundice caus-
ing cholangitis or intractable pruritus, or where an elevated bilirubin precludes other
treatment. 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 solely
to reduce a high bile duct obstruction (at or above the confluence) may cause many
more problems than it solves. We usually try to avoid treating patients when cross
sectional imaging suggests subsegmental isolation, as the goals of drainage can rarely
be accomplished. Preoperative biliary drainage remains controversial except for the
treatment of biliary sepsis.
The hepatobiliary disease management team should evaluate each patient to
determine the need for drainage. Once the need for drainage is determined, con-
sideration should be given as to whether an endoscopic or percutaneous drainage
approach is more appropriate. In general, patients with low bile duct obstruction
are managed endoscopically by the gastroenterologists. Percutaneous drainage is
reserved for cases of high bile duct obstruction or for patients whose biliary tree
cannot be accessed endoscopically (e.g., previous bypass procedure or gastric or
duodenal tumors).
Technique
As with PTC, the optimal approach to the biliary tree is determined by many
factors. Good quality diagnostic imaging is essential for proper planning of a percu-
taneous biliary drainage. It is important to identify the level of obstruction, the
status of the portal vein, the presence of hepatic atrophy or ascites, and the extent of
parenchymal disease. Operator preference, while important, is secondary to the need
to maximize the safety and efficacy of the procedure.
Punctures are generally performed using 21 or 22 gauge needles. Right-sided
drainage is performed from a lower intercostal or, when possible, subcostal approach.
Left-sided drainage is generally performed from an epigastric approach (Figs. 4.3A-F).
We use a 21-gauge diamond tipped, two-part needle for the initial punctures. After
the needle is inserted into the liver, contrast is injected until the biliary tree is opaci-
fied. Multiple passes may be necessary until a duct is visualized. If the initial duct
punctured is not optimal for placement of a drainage catheter, a second needle is
used to puncture a suitable duct once the ducts have been filled with contrast. The
optimal duct for drainage should be peripheral so as to avoid large, central vessels,
and also to provide enough intraductal space above the level of obstruction for an
adequate number of catheter side holes through which the bile will drain.
Once a suitable duct is punctured, the needle is exchanged over a small (.018)
guide wire for a three part system consisting of a thin metal stiffener, a thin inner
introducer sheath, and a 7F outer introducer sheath. The inner two pieces are re-
moved leaving the outer portion of the introducer, through which catheters and
wires of appropriate size to perform the drainage can be placed. Generally, every
attempt is made to cross through the obstruction in order to allow placement of an
internal-external drainage catheter that has a loop in the duodenum and side
holes above and below the level of obstruction. The interventionalist has a
large armamentarium of catheters and guidewires to facilitate passage through various
4
types of obstructions. At times, an obstruction cannot be negotiated nor is it preferable
to minimize manipulation in the setting of sepsis; in these cases an external catheter
is placed initially. Attempts are generally made at a later time to convert the initial
catheter to an internal-external catheter. At the time of initial drainage, bile specimens
are obtained for culture and, if necessary, cytology. Brush biopsy can also be performed,
either initially or as a second procedure.
Depending on the level of obstruction, the goals of drainage may not be accom-
plished with one catheter. The higher the obstruction, the less likely it is that one
drainage will suffice. It is unnecessary to drain every hepatic segment in order to
normalize bilirubin and relieve pruritus. Unfortunately, the need to drain multiple
segments seems more common in the setting of cholangitis, where isolated systems
are contaminated and continue to cause symptoms in the absence of drainage. As
mentioned previously, we ardently avoid treating patients where cross sectional 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 anterior
sector and one in the right posterior sector). Whereas each catheter is difficult for
the patient to tolerate, every effort is made to use as few catheters as possible.
Complications
With the advent of micropuncture technology, targeted punctures, and improved
antibiotics, biliary drainage is much safer now than when first developed. Major
complications include bleeding and sepsis. Coagulopathy must be addressed prior
to drainage and all patients should receive prophylactic antibiotics. Complications
such as pneumothorax and biliary-pleural fistula are very uncommon.
Internal Stent Placement
Internal stents may provide drainage with improved quality of life compared to
percutaneous drainage catheters. Most interventionalists place self-expanding, flexible
metallic stents. Metal stents cannot be changed, and because of limited duration of
patency (generally 5-7 months) they are rarely employed in benign disease (Figs.
4A-D). Plastic stents can be placed percutaneously and may be appropriate in
certain situations.
While most patients and referring physicians are anxious to have percutaneous
drainage catheters converted to internal stents as quickly as possible, it is important
Figs. 4.3A-F. Percutaneous biliary drainage catheter placement and subsequent

conversion to Wallstent® (Boston Scientific, Watertown, MA) in a patient with meta-
static pancreatic carcinoma. The patient had undergone a gastrojejunostomy and
could not be approached endoscopically.
Fig. 4.3A. Contrast enhanced CT image showing hepatic metastases, more pronounced
in the right hemiliver. Both the right and left portal veins are patent.
to consider each case carefully to determine the appropriate timing for internaliza-
tion. In general, when one is confident that no future drainage procedures will be
necessary or possible, it is appropriate to place an internal stent. In cases of low bile
duct obstruction, stent placement may be primarily performed. In cases where a
stent would extend above the confluence, the stent may interfere with future inter-
ventions and placement should be delayed until all necessary drainage procedures
have been performed. Multiple stents may be placed at the same time. Nearly all
metallic biliary stents are self expanding. Balloon dilatation is extremely painful,
and is rarely, if ever, indicated. In general, if a stent is not fully expanded immedi-
ately (as is often the case), a small angiographic catheter (usually 5F) may be left
through or above the stent to maintain access to the biliary tree. The patient is
brought back to the interventional suite the following day to assess stent expansion
and function. If for any reason an additional stent is needed, it is placed at that time.
The small “covering” catheter is removed only after stent adequacy is documented.
Other Transhepatic Percutaneous Biliary Interventions
Percutaneous, transhepatic biliary access may also be used to allow balloon dila-
tion of strictures, removal of intrahepatic stones, and delivery of brachytherapy or
other intraductal therapies.
Fig. 4.3B. Image from a left sided percutaneous biliary drainage shows the 21 gauge
puncture needle in a peripheral lateral segment duct.
Most interventional radiologists and surgeons agree that the best long-term out-
come for treatment of bile duct strictures can be expected from primary repair by an
experienced hepatobiliary surgeon. Surgical success may be more limited in patients
who are poor surgical candidates, have portal hypertension, or who have had 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 can
be expected in cases of short segment, late presentation, low bile duct strictures.
Balloon dilatation is generally performed as a staged procedure after placement
of a percutaneous drainage catheter. Strictures well below the confluence can gener-
ally be treated with one balloon. Strictures at or near the hilus may require two or
more catheters that permit sequential or simultaneous dilation (using “kissing bal-
loons”) at more than one site. After initial dilatation, a 10-12 F drainage catheter is
left across the treated stricture(s) for approximately 4 weeks, at which time the pa-
tient returns for cholangiographic evaluation. If narrowing persists, repeat dilation
may be performed with a larger balloon, followed by another 4-week period with
the drainage catheter across the treated segment. Once the stricture is shown to be
well treated, a catheter is left above rather than across the treated area. This catheter
is then capped, allowing a physiologic trial of the adequacy of dilation to be per-
formed. If this is well tolerated by the patient, the catheter can be removed. Patients
who fail repeated dilation may require long-term catheter drainage or an attempt at
surgical repair or bypass. As mentioned earlier, due to limited long-term patency, we
are hesitant to place metallic stents to treat benign disease. Stents may be placed in
patients with limited life expectancy due to comorbid conditions or in other rare
cases. A proposed etiology for restenosis after metal stent placement is that the metal
Fig. 4.3C. The needle was successfully exchanged for an angiographic catheter,
which was advanced over a steerable wire to the duodenum. This catheter assembly
was then exchanged for the internal-external drainage catheter shown here. The
catheter extends from the lateral segment duct across the common hepatic duct
occlusion and terminates with the distal pigtail in the duodenum. The image nicely
depicts the level of obstruction and shows that this catheter drains both the right
and left hemi-livers.
wire in biliary stents may cause chronic irritation and mucosal hypertrophy. For this
reason, we prefer to use a stent with the least amount of metal in contact with the
duct wall to treat benign disease.
Brachytherapy involves the local delivery of radiation and may be used to treat
intraductal tumor. The radiation source is generally delivered via catheters placed
through recently inserted metal stents. In addition to providing local treatment of
tumor, brachytherapy may prolong the patency of metallic stents by decreasing the
rate of tumor ingrowth.
Percutaneous Abscess Drainage
Percutaneous drainage techniques may be useful in treating patients with abdomi-
nal abscesses, including hepatic abscess. Percutaneous drainage may be necessary to
Fig. 4.3D. Immediately after conversion of the drainage catheter to a Wallstent®.

The catheter has been removed over a guidewire, which extends via the lateral
segment to the distal duodenum. The stent has not yet been opened or shortened to
its stated dimensions and is seen extending from the distal 3rd duodenum to the
left hepatic duct.
treat postoperative abscesses or other collections of fluid such as bile or infected

ascites. Abscess can be diagnosed based on clinical and radiographic findings. Drainage
catheters can be placed under CT, ultrasound, or fluoroscopic guidance.
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 still
present through the stent to allow injection of contrast to assess for stent patency
and location within the biliary tree.
A primary pyogenic liver abscess can also be treated by percutaneous catheter

placement under imaging guidance. Liver abscess may be associated with stone 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. 4.3F. The angiographic catheter has been positioned at the top of the stent, and
contrast has been injected. The stent is perfectly positioned from the confluence of
the right and left hepatic ducts to the duodenum. The intrahepatic ducts are de-
compressed, and contrast flows nicely through the stent.
Abscesses which develop spread from the portal venous system may be associated
with septic pyelophlebitis. Imaging findings of a hepatic mass with portal vein occlu-
sion may mimic those of primary hepatocellular carcinoma. Absence of clinical or
imaging 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 can
be 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 one
aspiration is generally required for complete treatment.
Fig. 4.4A. A biliary obstruction above the bifurcation of the right and left hepatic
ducts was noted. Separate punctures were performed and internal/external biliary
catheters were placed through the obstruction and into the duodenum.
Percutaneous Hepatic Cyst Drainage

Similar interventional techniques may be applied in the treatment of simple
hepatic cysts as well as echinococcal cysts. Simple hepatic cysts are relatively common.
High quality imaging is mandated to prove that all criteria for a simple cyst are met.
Cystadenomas, cystadenocarcinomas, and cystic metastases must not be overlooked.
Asymptomatic simple cysts do not require treatment. Hepatic cysts may become
symptomatic due to their large size which can cause pain or compression of adjacent
structures. Historically, therapy for large hepatic cysts has been surgical, now often
performed laparoscopically. However, percutaneous drainage is a viable alternative
which may obviate the need for surgery in a variety of situations. Catheter place-
ment may be combined with sclerotherapy using absolute alcohol, betadine solu-
tion, or an antibiotic solution.
Fig. 4.4B. Fluroscopy was used to confirm positioning of the biliary catheters.
While percutaneous treatment or even aspiration of hydatid cysts has traditionally

been avoided due to the risk of anaphylaxis, the procedure can be performed safely and
may be combined with injection of hypertonic saline or other scolicidal agents.
Percutaneous Methods for Ablation of Hepatic Neoplasms
While surgery remains the best hope for curative treatment in patients with most
primary and secondary malignancies of the liver, many patients are not candidates
for resection at the time of their presentation. This may be due to the extent or
distribution of disease, underlying liver function or general medical condition of the
patient. For these patients, minimally invasive, percutaneous ablative techniques
represent attractive therapeutic alternatives. Ablative therapies performed by
interventional radiologists include arterial embolization or chemoembolization, and
chemical or thermal ablation.
Embolotherapy
Transarterial 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 is
derived from the hepatic arterial system. This treatment has been used primarily to
Fig. 4.4C. Self-expanding metallic stents were placed. Access to the left system has
been removed, while a guidewire remains within the right ductal system.
treat hypervascular tumors such as hepatocellular carcinoma, neuroendocrine 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 concomitant
intra-arterial administration of chemotherapy and embolic material, including io-
dized oil and particulate matter such as Gelfoam or polyvinyl alcohol particles. At
our 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 complications
associated with chemotherapeutic agents.
Indications
Embolization is performed in an attempt to prolong survival in patients with
hepatocellular carcinoma and non-neuroendocrine, hypervascular liver metastases
Fig. 4.4D. Completion fluoroscopy demonstrates two well-expanded metallic stents

within the right and left ductal system.
who are not surgical candidates. Since neuroendocrine tumors tend to be quite in-
dolent, embolization of neuroendocrine metastases is generally indicated for relief
of symptoms due to hormonal production or tumor bulk. Embolization is occasion-
ally performed to control rapidly enlarging masses.
Contraindications
Embolization should not be performed in the presence of jaundice or hepatic
failure. Better results can be expected for Childs A or Okuda I classified patients.
Any coagulopathy must be corrected and premedication must be given, if necessary,
for contrast allergy. Portal vein thrombosis is a relative contraindication depending
on the distribution of disease, presence of reconstitution, and direction of flow. The
risk of hepatic failure must be considered carefully in this situation. Embolizing very
large tumors carries an increased risk of abscess formation, and size greater than 12
cm is a relative contraindication to embolization.
Technique
Patients are premedicated with prophylactic antibiotics and antiemetics. Patients
with neuroendocrine tumors are given prophylactic octreotide as well. Even nonfunc-
tional neuroendocrine tumors may produce a low level of hormone(s). During or im-
mediately after embolization, massive cell death may result in the release of vasoactive
substances that can cause hemodynamic instability in the absence of premedication.
A right femoral arterial approach is preferred. Arterial anatomy and portal vein
patency is assessed (Fig. 4.5A). The arterial vascular supply to the tumor(s) is then
determined. The embolization technique varies slightly based on the distribution
and type of tumor. Focal cancers are treated as sub-selectively as possible, with the
smallest particles available (currently 50 micron PVA). Sub-selective treatment in-
volves injecting the embolic material suspended in radiographic contrast directly
into the arterial branches supplying the mass via catheters, or microcatheters posi-
tioned under fluoroscopic/angiographic guidance. Patients with multifocal disease
4 are also treated as selectively as possible, but this frequently necessitates emboliza-
tion of an entire hemiliver. Even if disease is widespread and bilateral, only one
hemiliver is treated at a time to minimize the risk of hepatic failure. Embolization is
complete when antegrade flow in the vessel(s) supplying the tumor(s) is no longer
present (Fig. 4.5B). At times it is necessary to use larger particles (100 or 200
micron) as the embolization progresses in order to limit the length of the pro-
cedure and amount of contrast used. It is also occasionally necessary to search
for other nonhepatic arterial branches supplying the tumors, most commonly
those arising from the right phrenic artery.
Most patients will experience some degree of postembolization syndrome (PES)
after the procedure. This consists of pain, nausea and vomiting, and/or fever. All
patients are maintained on antibiotics and antiemetics for 24 hours. Many patients
will require patient-controlled analgesia (PCA) pumps. PES is generally self-limited,
and typically lasts from 24-72 hours.
Percutaneous Ethanol Injection Therapy (PEIT)
Absolute ethanol causes cell dehydration and denaturation as well as small ves-
sel occlusion, presumably due to endothelial cell damage. PEIT has been used to
treat focal HCC. In general, up to three tumors smaller than 5 cm in diameter can
be treated. It is thought that HCC masses are relatively “soft” in the background of
a “hard” cirrhotic liver, promoting distribution of alcohol in the tumors. The converse
situation occurs with most secondary liver tumors, and PEIT is not indicated for
metastases.
Technique
PEIT is most commonly performed using ultrasound guidance but CT guidance
may also be used. Procedures are performed using local anesthesia with conscious seda-
tion. We use a 22 G Westcott type needle to deliver the ethanol, but almost any needle
can be used. The approximate ethanol volume is calculated from the formula V=4/
3p(r+0.5)3. Often it is not possible to inject the entire amount in one session. Even
when the lesion can be well covered in a single treatment, most patients are brought
back the following day for at least a “touch-up”. The platelet count should be checked
daily until treatment is complete as thrombocytopenia may occur after each treatment.
Ideally, we perform PEIT the day after arterial embolization in an attempt to
maximize cytotoxic insult to the tumor, although PEIT certainly may be performed
as a “stand-alone” procedure. We have found that patients are more likely to tolerate
injection of the entire “calculated” ethanol volume when PEIT is performed the day
after embolization then when it is performed alone.
Radiofrequency Ablation (RFA)
RFA involves inserting a probe with an insulated shaft and un-insulated tip into
a tumor. Probes may be straight or may contain multiple wire tines that are de-
ployed from within the shaft of the probe and opened to various diameters. Grounding
pads are placed on the patient to form an electrical circuit. Current is then applied
to the tip(s) of the probe. Ionic agitation causes frictional heating and results in
coagulation necrosis. Current flow decreases as impedance from tissue desiccation
increases. Currently, the largest diameter necrotic lesion that can be created with a 4
single 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 vein
branches, 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 it
impossible to achieve a “treatment margin.” One must also consider potential risk
to adjacent structures such as bowel, gallbladder and diaphragm.
As with PEIT, this ablative treatment is usually performed using local anesthesia
and conscious sedation and may be performed on an outpatient basis.
Figs. 4.5A,B. Arterial emoblization of hepatocellular carcinoma in the right hemiliver.

Fig. 4.5A. Arterial phase image shows a hypervascular mass supplied by branches
of both the anterior and posterior divisions of the right hepatic artery.
Fig. 4.5B. Post-embolization arterial phase image. The branches supplying the tumor
have been sub-selectively embolized. The mass is no longer demonstrated.
Other Percutaneous Ablative Therapies

Cryoablation probes are not yet small enough to be placed percutaneously, and
percutaneous thermal ablative treatments are currently limited to those that cause
necrosis through heating. In addition to RFA, other less popular modalities that
cause coagulative thermal necrosis include interstitial laser photocoagulation, 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 Embolization
Since 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 or
hemiliver with hypertrophy of the untreated portion. This procedure may be useful
for patients who will undergo resection of a large amount of functional hepatic
parenchyma in order to resect a small volume of disease and/or those who will be left
with a very small amount of residual liver after resection. At our institution, we have
begun to perform embolization of the right portal vein prior to right trisegmentectomy
in patients with small left lateral segments and a large volume of uninvolved right-sided
parenchyma.
Technique
A peripheral branch of the portal vein is accessed using a percutaneous transhepatic
approach (Figs. 4.6A-H). We prefer to work ipsilateral to the side of embolization to
avoid inadvertent injury to the liver that will remain postoperatively. Various 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 use
of occlusion balloons and is not visible radiographically making it somewhat more
cumbersome.
Patients generally wait approximately 2-4 weeks after portal vein embolization
before they undergo resection.
4
Transjugular Intrahepatic Portosystemic Shunts (TIPS)
Indications
TIPS is indicated for the treatment of recurrent variceal bleeding which
has not responded to medical and/or endoscopic therapy, or for the control of
refractory ascites.
Contraindications
Absolute contraindications include severe hepatic failure and severe right heart
failure, both of which would be exacerbated by shunt creation. Relative
contraindications include portal vein thrombosis, HCC, hepatic metastases, and
polycystic disease involving the liver.
Technique
The procedure can usually be performed using conscious sedation. Ideally, the
right internal jugular is used, although TIPS can be done using the left internal
jugular vein or the external jugular veins. A catheter is placed through a long sheath
into an hepatic vein (usually the right) where a wedge hepatic venogram is performed.
A long steerable needle is then advanced from the hepatic vein to the portal vein.
Most commonly, the right hepatic and right portal veins are used if possible. A wire
is then advanced to the superior mesenteric or splenic vein and pressures are re-
corded. The shunt tract is then predilated with a balloon, after which a flexible
metal stent, usually 10 or 12 mm, is deployed and dilated. Increasingly, covered
stents are being utilized to prevent thrombosis thought to result from 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 the
portal vein and the IVC of between 6 and 12 mm Hg is achieved.
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 the
central aspect of Segment VIII, adjacent to the right hepatic vein and the inferior
vena cava, and approaching the middle hepatic vein. The patient underwent em-
bolization of the right portal vein in anticipation of right trisegmentectomy and
wedge resection of the lateral segment mass.
Fig. 4.6A. Contrast enhanced CT image demonstrating the mass in Segment VIII
before embolization.
Fig. 4.6B. Contrast enhanced CT image demonstrating the mass in Segment III before
embolization.
Fig. 4.6C. Percutaneous portal venogram prior to embolization. The catheter has
been placed via a right portal venous branch, and the tip of the catheter is within
the main portal vein.
Fig. 4.6D. Percutaneous portal venogram after embolization of the right portal vein.
The catheter is within the main portal vein. Only the left portal venous branches
remain patent. Opacified vessels overlying the right hemiliver are patent Segment
IV branches.
Fig. 4.6E. Contrast enhanced CT image at the level of the Segment VIII lesion, 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.
Fig. 4.6F. Post embolization image from a CT Portogram at the same level. Note the
striking perfusion defect in the right hemi-liver.
Fig. 4.6G. Contrast enhanced CT image at the level of the Segment III lesion, approxi-
mately 2 weeks after embolization of the right portal vein. Note the enlargement of the
lateral segment and the unopacified portal vein branches in the right hemi-liver.
Fig. 4.6H. CT portogram image at the same level as “G.” Note the perfusion defect
in the right hemi-liver.
CHAPTER 5
Perioperative Care and Anesthesia

Techniques
Mary Fischer, Enrico Ferri, Jose A. Melendez
Introduction
The evolution of surgical techniques and anesthetic care is such that the most
challenging procedures have become available for sicker patients. This Chapter
examines the preoperative, intraoperative and postoperative considerations that guide
the anesthetic management of liver surgery.
Preoperative Evaluation
The preoperative status of the patient is currently the main factor in the determi-
nation of the anesthetic risk for any surgical procedure.
Cardiac Evaluation
Perioperative cardiac morbidity is one of the leading causes of perioperative death.
The incidence of myocardial ischemia occurring in patients with coronary artery
disease (CAD) can reach 74%. Myocardial infarction occurs in 2% of the patients.
The incidence of perioperative ischemic complications is significantly reduced by
β-blocker therapy. Table 5.1 shows other factors associated with increased cardiac
morbidity. A complete history and physical examination, followed by a 12-lead EKG,
are the basic components of the preoperative evaluation. Radio-nucleotide stress
test and echocardiography are used to assess the extent of the ischemic disease.
In men between 30 and 55 years, with a history of alcohol abuse for more than
10 years, cirrhotic cardiomyopathy must be expected. Cardiac dysfunction can 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 Evaluation
Postoperative pneumonia is a major risk for patients with poorly compensated
respiratory disease. Anesthesia reduces the functional residual capacity leading to
alveolar collapse. Emphysema, bronchitis and asthma predispose to airway closure
and respiratory failure can follow. Asthma and bronchospasm must be treated prior
to an anesthetic. To establish the extent of disease, and to optimize therapy, patients
may require pulmonary function tests and blood gas analysis. Severe chronic bron-
chitis may require corticosteroids and antibiotics.

Table 5.1. Preoperative factors associated with postoperative life-threatening

complications or fatal cardiac complications
History: Age > 70 yrs
Myocardial infarction in previous 6 months
Physical Examination: S3 gallop or jugular venous distention
Important 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/l
BUN > 50 or creatinine > 3.0 mg/dl
Abnormal SGOT,
5 Signs of chronic liver disease or patient bedridden
Operation: Intraperitoneal, intrathoracic or aortic operation
Emergency operation
*(modified from Goldman (1977), with permission of Massachusetts Medical

Society, Boston)
Hepatic Evaluation
The operative outcome after liver surgery strictly depends on the preoperative
metabolic liver function and the extent of the parenchymal resection. Mild or well-
compensated chronic hepatic disease does not increase risk of death compared to
the general population. Liver function must be estimated from the Child’s classifica-
tion, as aminopyrine breath test and indocyanine green clearance are not readily
available for clinical use. Routine evaluation should include CBC, clotting factors,
serum electrolytes, serum albumin, bilirubin and liver enzymes.
Intraoperative Management
Surgical stimulation and manipulation of the liver dramatically increases the
hepatic oxygen extraction ratio. At the same time, there is a 16% drop in hepatic
blood flow associated with anesthesia and mechanical ventilation and a 40% decrease
with splanchnic surgery. This may be due to a direct effect on the hepatic venous
bed mediated through the hepatic sympathetic innervation. Further impairment on
hepatic blood flow results from decreases in cardiac output from intraperitoneal
insufflation and a head-up tilt. The anesthesiologist should optimize the oxygen
delivery-oxygen extraction ratio, and avoid inducing hypotension, hypovolemia and
anesthetic overdoses which cause reductions of cardiac output and systemic pressure
resulting in decreases in hepatic blood flow.
Low Central Venous Pressure Anesthesia
Fluid load is commonly practiced prior to the resection in order to prevent
hypotension during episodes of uncontrolled bleeding. This procedure results in
vena caval distension which may interfere with surgical dissection. Low central venous
pressure anesthesia (LCVP), below 5 mm Hg, eliminates vena caval distension and
eases mobilization of the liver to permit dissection of the retrohepatic vena cava, and
Perioperative Care and Anesthesia Techniques 75
major hepatic veins. LCVP is usually performed in combination with inflow and
outflow control.
Investigators have demonstrated a relationship between extent of intraoperative
blood loss and morbidity and mortality. The blood loss resulting from a vascular
injury is directly proportional to both the pressure gradient across the vessel wall and
the fourth power of the radius of the injury. Lowering CVP lessens the pressure com-
ponent of the equation and minimizes the radial component of flow by reducing vessel
distension, thereby reducing hepatic venous bleeding during parenchymal transection.
Strict fluid restriction is practiced until the liver resection is completed, although
small fluid boluses may be given to maintain hemodynamic stability. Intravascular
hypovolemia is counteracted with 15˚ head-down tilt. This improves venous return
and preserves renal function. The technique requires appropriate cannulation and
transfusion equipment to face emergency fluid resuscitation. A high level of vigi- 5
lance is obligatory.
Anesthesia is maintained with a combination of isoflurane in O2 and fentanyl
which provides minimal hemodynamic changes. The combination of fluid restriction
and minimal vasodilation from narcotics is usually sufficient to achieve the desired
conditions. In some cases, further peripheral dilation may be achieved by first using
morphine. Only a very small number of patients require intravenous nitroglycerin.
LCVP-anesthesia increases the risk of intraoperative air emboli. Restriction of
nitrous oxide in the gas mixture helps by preventing the enlargement of circulating air
pockets. It is crucial to have rapid occlusion of open venous channels; this results in a
very low incidence (0.4%) of clinically significant air emboli. Monitoring is performed
with end-tidal CO2. Transesophageal echocardiography has proven to be sensitive.
Anesthesia for Vascular Isolation
Hepatic vascular isolation is an alternative surgical approach for liver resection.
It induces a decrease in venous return with a resulting decrease in cardiac index and
increase in systemic vascular resistance. Anesthetic management requires the increase
in CVP to improve cardiac filling and maintain cardiac output. Vasopressors may be
required during the vascular isolation phase. Metabolic acidosis and hyperkalemia
may occur after prolonged vascular isolation. Appropriate therapy is mandatory. In
some cases, the procedure needs to be abandoned due to persistent hypotension
and/or low cardiac index. This technique is more complex, conveys higher blood
loss and transfusion rates, and does not show better results than portal triad clamp-
ing with extrahepatic control of the hepatic veins (Table 5.2).
Obstructive Jaundice
Acute biliary obstruction is associated with an increase in liver blood flow, which
is decreased with chronic obstruction, possibly secondary to increased portal resis-
tance. Decompression of chronic biliary obstruction may result in hemodynamic
impairment and shock. Biliary sepsis may exacerbate this state. Aggressive hemody-
namic monitoring is required to reduce mortality.
Table 5.2. Comparison of operative parameters between hepatic vascular

isolation (HVI) and LCVP-aided hepatectomy (LCVP)
Author Technique Total Major Blood Transfusions
Cases Resections* loss (cc) (units
or cc)**
Mean** Median
Delva et al, HVI 35 35 – – 8.0 ± 8.3

1989†
Emre et al, HVI 16 13 1866 ± 1683 1325 –
1993
Hannoun et al, HVI 15 15 – – 5.8 ± 4.7
1993
5 Habib et al, HVI 56 33 1651 ± 1748 1200 930 ± 750
1994
Emond et al, HVI 48 44 1255 ± 1291 – 1.9 ± 2.6
1995
Belghiti et al, HVI 24 24 1195 ± 1105 – 2.5 ± 3.4
1996
Melendez 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.
Postoperative Care
Immediate Postoperative Concerns
Immediate postoperative concerns common to all major intra-abdominal proce-
dures are bleeding, intravascular volume, renal function, and oxygenation. There
are also some unique issues in patients undergoing hepatobiliary surgery. Liver
regeneration following partial hepatectomy involves rapid cell division (as early as
24-72 hours) and may be critically dependent on cellular ATP stores. 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 with
altered drug pharmacodynamics and pharmacokinetics and attention must be paid
to anesthetic elimination and postoperative pain management. Routine parenteral
administration of vitamin K commonly corrects the coagulation abnormalities within
48 hours. More rapid correction may be accomplished by fresh frozen plasma.
Nonimmediate Complications
Jaundice
A bile duct injury at the time of surgery should be suspected when postoperative
extrahepatic obstructive jaundice occurs. Other more common causes of elevated
unconjugated hyperbilirubinemia include hematoma reabsorption and hemolysis
of transfused blood (Table 5.3). Hepatocellular injury is another possibility in the
differential diagnosis of postoperative jaundice. Common etiologies are sepsis, low
total hepatic blood flow, and infectious hepatitis. When all other factors are
Table 5.3. Differential diagnosis of postoperative jaundice*
Increased Bilirubin Load Biliary Obstruction Hepatocellular Injury

Blood transfusion Intrahepatic cholestasis Hepatic hypoxemia
Hematoma Drug induced Exacerbated chronic
Hemolytic anemia Infection induced hepatitis
Extracorporeal circulation Extrahepatic cholestasis Acute hepatitis: viral,
Hemolysis Bile duct injury alcoholic
Pancreatitis Gilbert’s disease
Retained gallstones Sepsis
Trauma
Toxins, drugs
*(modified from Brown (1988) and Gelman (1992), with permission of F. A. Davis, 5
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 entertained

if halothane was used. With newer, less controversial volatile anesthetics, it is rarely
seen today.
Ascites
Ascites manifests as a result of:
1) impaired albumin and protein synthesis,
2) increased hydrostatic pressure in hepatic sinusoids and splanchnic
capillaries,
3) over-production, transudation and low reabsorption of lymph into the
peritoneal space,
4) renal sodium retention and,
5) impaired renal water excretion, partially due to increased concentrations
of antidiuretic hormone (ADH). Albumin infusion has no beneficial effect
even in the presence of severe hypoalbuminemia. The treatment of ascites
5 underscores 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 patients
require hemodynamic monitoring. Paracentesis should be attempted in
case ascites persists.
Renal Failure
Following hepatobiliary surgery, rapidly progressive renal failure may occur. The
differential diagnosis includes acute tubular necrosis, prerenal azotemia and
hepatorenal syndrome. Hepatorenal syndrome is the development of otherwise
unexplained renal failure with urine sodium < 10 meq/l, hyperosmolar urine, 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. The
pathophysiology of hepatorenal syndrome is based on the pooling of blood in the
splanchnic bed and the resultant decrease in plasma volume. The kidney perceives a
decreased glomerular filtration rate and causes a vasoconstriction that shunts blood
away from the renal cortex. There is no specific treatment for hepatorenal syndrome.
Dopamine (1-2.5 mcg/kg/min) may help maintain urine output. Although sponta-
neous recovery has been reported, mortality is very high. These patients, generally
cirrhotic, may benefit from liver transplant.
Pulmonary Care
Hepatopulmonary syndrome is defined by liver disease, increased alveolar arte-
rial gradients, and evidence of reduced intrapulmonary vascular resistance. In cir-
rhotic patients, an increased synthesis of nitric oxide has been demonstrated that
may lead to arteriovenous shunts in the lungs. The resulting hypoxemia requires
oxygen supplementation and may progress to respiratory failure.
Glucose Metabolism
We might expect the postoperative patient to be prone to hypoglycemia second-
ary to diminished glycogen reserves, increased insulin levels, and impaired gluco-
neogenesis. Yet, dangerous hypoglycemia is rare. Routine (5%) dextrose solutions
should be infused while monitoring glucose serum levels.
Coagulation
Hypocoagulability derives from thrombocytopenia or reduced synthesis of vita-
min K dependent factors; cholestasis also decreases vitamin K absorption and hepatic
stores. Improvements in coagulation may be achieved with vitamin K 10 mg/day.
Another cause of bleeding is fibrinogen deficiency; this situation may benefit from
fresh frozen plasma transfusion. Decreased serum concentration of protein S, protein
C and antithrombin III result in hypercoagulable states that can lead to disseminated
intravascular coagulation (DIC).
Sepsis
Abdominal sepsis is the most common cause of mortality after hepatic resection.
Preoperative biliary manipulation, infected bile, biliary stones, ascites, and blood
loss may all predispose to abdominal sepsis. Other sources of sepsis include the 5
respiratory and urinary systems. Wound infection and a central line catheter should
also be considered as possible sources of infection.
Gastrointestinal Bleeding
The incidence of GI bleeding is 5%, with a mortality reaching 50%. The bleed-
ing site can usually be identified by endoscopy. Treatment includes transfusions,
antacids and H2 blockers. All postoperative hepatobiliary patients should be treated
prophylactically. About 30% of cirrhotic patients have esophageal varices. The emer-
gent treatment should combine blood product transfusion to correct the coagulopathy,
gastric endoscopy with variceal banding or sclerotherapy, and possibly, octreotide
25-100 mcg/min to control bleeding. Life saving procedures may include compres-
sion of the varices via a Sengstaken-Blakemore tube. As rebleeding occurs in 50% of
patients, a definitive surgical treatment should be pursued.
Encephalopathy
Hepatic encephalopathy may be precipitated by GI bleeding, infection, drugs,
diet or dehydration. It manifests as a sudden change in a patient’s mental status or
the onset of asterixis. The precise pathogenesis remains unknown. The historical
postulate has been the accumulation of endogenous ammonia. Other etiologies have
been suggested, including changes in the blood-brain barrier permeability, abnor-
mal neurotransmitter balance, altered cerebral metabolism, impairment of neuronal
Na+-K+ ATPase activity, and increased endogenous benzodiazepines. Standard therapy
is devised to reduce levels of ammonia and other potentially toxic metabolites.
Flumazenil has been administered with some improvement; however, protein
restriction and lactulose administration are still practiced.
Suggested Reading
1. 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.
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 A
Textbook of Liver Disease. 3rd.edition. Philadelphia: WB Saunders 1998; 605-17.
8. Goldman L, Caldera DL, Nussbaum SR et al. Multifactorial index of cardiac risk
in noncardiac surgical procedures. New Engl J Med 1997; 297:845-50.
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 ischemia
5 exceeding 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 hepatic
resections 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 1
CHAPTER 6
Benign Tumors of the Liver:

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

Cell of origin Tumor
Epithelial
Hepatocellular Focal nodular hyperplasia (FNH)
Hepatocellular adenoma (HA)
Regenerative nodule
Cholangiocellular Biliary adenoma

Biliary cystadenoma
Other Epitheliod leiomyoma
Mesenchymal
Endothelial Hemangioma
6 Hemangioendothelioma
Adult
Infantile
Mesothelial Solitary fibrous tumor
Other names: benign mesothelioma or fibroma
Adipocyte Lipoma
Myelolipoma
Angiomyelipoma
Miscellaneous
Tumors Biliary hamartoma
Pseudotumors Focal fatty infiltration

Adrenal neoplasm
Inflammatory pseudotumor
Chronic abscess
Table 6.2. Incidental solid liver tumors: Diagnostic frequency for various
histologies3
Tumor Relative frequency
Hemangioma 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%
Benign Tumors of the Liver 83
Table 6.3. MSKCC experience in managing 152 patients with benign solid liver
tumors 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 6
(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, cavernous
hemangioma, parenchymal bleed into a hepatocellular adenoma, or polycystic liver
disease, but is not diagnostic. Laboratory tests, including liver function tests, are
invariably normal in asymptomatic patients with liver tumors and are, therefore,
not helpful. In rare instances, serum transaminase levels may be elevated in patients
experiencing an acute hemorrhage, thrombosis, or necrosis of tumor, but it is not
pathognomonic for a particular liver pathology. Elevated serum tumor markers, such
as alpha fetoprotein (AFP), carcinoembryonic antigen (CEA), and CA-19-9, are
rarely elevated in benign liver tumors and should suggest the likelihood of an under-
lying malignancy.
In most instances, radiologic studies can provide a precise diagnosis based on the
characteristic 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 hepatobiliary
imaging 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 most
useful imaging modality with regard to differentiating between “indeterminate” and
6
84
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 indicated
Well-demarcated Isodense on noncontrast scan Isodense on T1 Very sensitive
Increased vascular flow Contrast: Irregular peripheral Hyperdense on T2 Blood pooling of
Central venous pooling enhancement Gadolinium enhanced radionucleotide
Delayed 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 SC
Hyperplasia ?Hyperechoic may be well-demarcated on Early hyperdense Contains bile
(FNH) contrast CT with central scar appearance after ducts and
— often isodense gadolinium Kupffer cells
Nonspecific
Hepatic Nonspecific Nonspecific Nonspecific Nonspecific Generally does
Adenoma ?Hyperechoic Hyperechoic Hyperechoic Not indicated not take up Tc 99
Increased blood flow SC because of the
on duplex scanning lack of bile ducts
Heptobiliary Surgery
and Kupffer cells
Nonspecific
* Tc 99 RBC scan—Technetium–labeled red blood cell scan; HIDA—Hepatic aminodiacetic acid scan; Tc 99 SC—Technetium sulfur colloid
scan
malignant tumors. Although many liver tumors have a characteristic angiographic

appearance, the information it provides can currently be obtained by noninvasive
imaging modalities in most situations. Laparoscopy can be used as a diagnostic tool
in some patients by allowing the surgeon to obtain a reliable tissue biopsy using
minimally invasive techniques. In rare cases, the surgical management may be car-
ried out laparoscopically as well.
Benign Liver Tumors
Hemangioma
Hemangiomas are the most common benign solid tumors of the liver and occur
in two variants, capillary hemangiomas and cavernous hemangiomas. Capillary he-
mangiomas are the most common, but are clinically insignificant. They are typically
small, hypervascular lesions (< 2 cm) encountered at the time of laparotomy and
may be the source of considerable diagnostic uncertainty. Establishing the diagnosis
and excluding a malignancy is all that is required. 6
Cavernous hemangiomas are clinically more relevant because of the potential for
complications and associated symptoms. Cavernous hemangiomas have been reported
in up to 7% of patients at autopsy and occur more commonly in adults than in
children. The etiology of cavernous hemangiomas remains uncertain; however, they
most likely represent benign congenital hamartomas. Although the incidence of
cavernous hemangioma has been reported as 1.3-6 times higher in women than in
men, the higher incidence of hemangioma in females is likely a reflection of referral
bias rather than a true difference in incidence. Sex hormones have not been linked
etiologically to the development of hemangiomas. Cavernous hemangiomas may
vary in size from less than 1 cm, to “giant hemangiomas” which may be greater than
30-40 cm. The size of a hemangioma correlates with symptoms, as it is usually large
pedunculated tumors that are encountered at surgery. These tumors are often sharply
demarcated from surrounding liver tissue, have a spongy appearance, and may be
partly necrotic or fibrotic. Occasionally, infarct of the hemangioma may cause it to
be completely fibrosed and, in rare cases, calcified. When this occurs, these tumors
can be extremely difficult to distinguish from other benign and malignant tumors.
The acute nature of some symptoms related to hemangioma may, in fact, not be
related to increase in size, but rather thrombosis and infarct that lead to focal fibrosis
and obliteration of vascular channels in part or whole.
Clinical Presentation
Symptoms from hemangiomas of the liver are generally attributed to rapid
expansion in the size of the lesion or to thrombosis and infarct that lead to stretch-
ing or inflammation of Glisson’s capsule. Occasionally, a large hemangioma may
present as a nontender mass in the right upper quadrant, but more often the physi-
cal examination reveals only vague upper abdominal tenderness with no mass. It
may be possible to auscultate a bruit over a large hemangioma, but this is not pathog-
nomonic. Rarely, a hemangioma may rupture resulting in a hemoperitoneum and
shock requiring emergency surgical care.
Severe thrombocytopenia and the development of a consumptive coagulopathy
have been associated with cavernous hemangiomas of the liver. Although the
Kasabach–Merritt syndrome was initially used to describe thrombocytopenia and

afibrinogenemia associated with hemangiomas of the skin and spleen in infants, this
term is often used to describe similar coagulopathies in children and adults (rare)
with hemangiomas of the liver.
Pathology
Historically, hemangiomas are typically well demarcated and distinct from the
surrounding hepatic parenchyma. The sharp interface between hemangioma and
normal liver parenchyma permits surgical enucleation in most cases. However, not
all hemangiomas are enucleable, and the histologic features of the tumor-liver 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 been
described. A “fibrolamellar interface”, characterized by a capsule-like fibrous ring of
variable 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 well
6 defined. A second variant, the “interdigiting” pattern, is marked by the lack of a
fibrous lamella surrounding the hemangioma which is replaced by an ill-defined
plane between normal liver tissue and the vascular channels of the hemangioma.
These tumors can be quite hazardous to remove without a formal resection. Two
additional histologic variants have been identified, including a “compression” inter-
face, in which the periphery of the tumor is well demarcated in the absence of a
fibrous lamella and an “irregular or spongy” variant which appears to intercalate
into the surrounding liver parenchyma making complete excision hazardous and
unnecessary. Note, despite the invasive appearance of this histologic variant,
hemangiomas are not premalignant lesions and do not invade or metastasize.
The diagnosis of a cavernous hemangioma is generally clear-cut on both macro-
scopic and microscopic examination. In rare instances, an atypical hemangioma
may be confused for other liver conditions including peliosis hepatis, hemorrhagic
telangiectasia (Osler–Rendu–Weber), hemangioendothelioma and other malignant
vascular tumors. As a rule, percutaneous biopsy of a suspected hemangioma should
be avoided as this may result in unnecessary and uncontrollable hemorrhage. Symp-
tomatic lesions, large lesions, or indeterminate lesions should be managed surgically.
Radiologic Evaluation
The initial radiologic evaluation of a suspected hemangioma is often dictated by
the clinical presentation. In most instances, hemangiomas are discovered inciden-
tally on a study performed for other reasons and the degree of diagnostic certainty
provided by this study may obviate the need for additional imaging. If a patient
presents with dull, nonspecific right upper quadrant complaints, ultrasonography is
typically the first study performed. On ultrasound (US), a hemangioma appears as a
hyperechoic mass well demarcated from the surrounding liver. The number and
location of the lesion(s) can be precisely defined on B-mode ultrasound, and the
addition of duplex ultrasonography can provide information with regard to peripheral
blood flow and central pooling of venous blood. On a noncontrast CT scan,
hemangiomas appear as a hypodense mass which exhibits a characteristic pattern of
irregular peripheral nodular enhancement after initial injection of contrast material.
Delayed CT scanning, several minutes after contrast injection, demonstrates central
6
Fig. 6.1A, B. Cavernous hemangioma. A, The gross appearance of a cavernous
hemangioma on cut section is shown. B, A sponge-like architecture with venous
lakes is characteristic of these lesions .
filling of the hypoechoic lesion which persists for some time and is felt to be diag-
nostic of hemangioma (Figs. 6.2 and 6.3). MRI is the most sensitive and specific
means to detect hepatic hemangiomas. The T-2 weighted image demonstrates a
characteristic hyperechoic pattern. The administration of gadolinium results in similar
peripheral enhancement with delayed central filling as was described with CT scan-
ning. Although a technetium-99 labeled red blood cell scintigram (Tc99 RBC scan)
has historically been considered the “gold standard” diagnostic evaluation for
hemangiomas (Fig. 6.4). Technologic advances in axial imaging diagnostic tech-
niques, such as MRI and CT, combined with the additional staging information
these studies provide, have led to less reliance upon RBC scintigrams. Selective hepatic
angiography demonstrates a characteristic neovascularity to these lesions often
described as “corkscrewing.” Rapid filling of the central portion of hemangiomas
from the neovascular periphery yields a “cottonwool” appearance to these lesions.
Despite this characteristic finding, the diagnostic yield of less invasive studies
is such that arteriography is unnecessary in the evaluation of most patients. As
a rule, biopsies, by whatever means, are unnecessary unless a histologic diagnosis
will alter planned therapy.
Treatment
Observation is the most appropriate treatment for nearly all asymptomatic
hemangiomas. To date, there are no documented instances in which a hemangioma
has spontaneously ruptured while being observed. Trastek et al followed 36 patients
with a cavernous hemangioma for up to 15 years (mean 5.5). Among this group
were two infants who were treated with steroids; one child responded. One adult
patient was also treated with external beam radiation and showed marked reduction
in the size of the lesion. The other 33 patients were observed with no other treat-
ment. There were no spontaneous ruptures and, most importantly, no changes in
6
88
Fig. 6.2. Cavernous hemangioma. An MRI with gadolinium is shown below. (A) The precontrast study demonstrates multiple
hypodense lesions within Segments 4, and 6 of the liver. (B) One minute after gadolinium administration early peripheral
enhancement of the lesion is seen. (C) Three minutes after gadolinium is provided, contrast material is seen to fill the lesion from
the periphery. (D) Five minutes after gadolinium administration the center of the hemangioma retains the contrast material.
Fig. 6.3. Sagittal view of a large cavernous hemangioma as visualized on T1 and

T2 weighted images.
symptoms over the course of follow up. In four patients the size of the hemangioma
increased and in three patients the size decreased. Foster followed 44 patients with
hemangiomas for a period ranging from 2 months to 12 years. There were no reports
of rupture, death, or change in clinical symptoms in their series. In the absence of
clinical symptoms, the careful observation of all asymptomatic hemangiomas is the
recommendation of most experienced liver surgeons.
Hepatic resection for a hepatic hemangioma should be approached no differently
than surgery for other tumors of the liver. The surgeon should have extensive knowl-
edge of the anatomy and vascular supply of the liver. The extent of the liver resection
required for removal is directly related to the anatomic location of the lesion and its
proximity to major blood vessels. In patients with symptomatic hemangiomas, some
form of treatment is often necessary. Patients with disabling pain, pressure symptoms,
or acute symptoms related to the hemangioma should undergo surgical resection. The
location of the hemangioma is critical to planning surgical resection. Large central
lesions that abut the portal vein, hepatic outflow tract, or inferior vena cava over a long
distance may pose a prohibitive surgical risk even in experienced hands. In these 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 margin
of normal tissue with the tumor. As such, the most appropriate treatment for most
hemangiomas is enucleation. In some cases, however, it may be safer and more rational
to perform formal lobectomy or extended resection.
The effectiveness of hepatic artery ligation as a treatment for hemangioma has
been described anecdotally; however, its benefit is likely transient. Hepatic arterial
Fig. 6.4. Cavernous hemangioma. A techntium-99 red blood cell scan is shown.
The heart (top center) and spleen are bright on radionucleotide scanning. The liver
retains some contrast but is significantly less intense than the spleen and heart. A
cavernous hemangioma is seen arising from the left lobe of the liver.
ligation or embolization does play a pivotal role in temporarily controlling hemorrhage

from a hemangioma to permit transfer of a patient to an institution where experi-
enced surgical help is available. Radiotherapy has been used successfully to treat
symptoms and induce involution of hemangiomas in some situations, but the rarity
of this occurrence makes the results difficult to interpret. On the whole, data justi-
fying the use of radiotherapy in hemangiomas is scant. However, if surgical therapy

is not possible, radiotherapy seems a reasonable alternative approach to the treat-
ment of symptomatic hemangiomas.
Special Issues: Hemangiomas in Children
Hepatic hemangiomas of infancy and childhood are different lesions from those
seen in adults. These lesions are typically large, and if so, their symptoms are rarely
subtle. The vast venous lakes within these lesions can function as tremendous siphons
for a large amount of the total cardiac output leading to severe congestive heart
failure and death. In children who develop high output cardiac failure, the initial
treatment usually consists of digitalis, diuretics, oxygen, corticosteroids and hepatic
artery ligation. Radiation treatment is often employed and may result in improved
cardiac performance. In contrast to adults, the risk of spontaneous rupture of hepatic
hemangiomas that occur in infancy is great. Similarly, Kasabach-Merritt syndrome
in association with life-threatening thrombocytopenia and afibrinogenemia, occurs
more frequently and may result in death in a high proportion of affected infants. As
6
opposed to the conservative approach to treatment of hemangiomas recommended
for 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 Hyperplasia
Focal nodular hyperplasia (FNH) is the second most common benign tumor of
the liver. Up to 90% of both FNH and hepatic adenomas occur in women of men-
strual age. FNH tumors are almost always asymptomatic lesions discovered
incidentally during a radiological work-up for other reasons. In rare instances, they
may present as a palpable abdominal mass on physical examination. Although a rare
tumor prior to the 1960s, the incidence of FNH has increased markedly in the last
three decades. Notably, the increased incidence in FNH has occurred concurrent
with the introduction and widespread use of ultrasound and CT scanning in clinical
practice, as well as the development and acceptance of the oral estrogen contraceptive
pill (OCP). Whether the increased reporting of FNH tumors represents a true change
in incidence or merely reflects the proficiency of scanning in identifying these lesions
is unclear, but the latter is probably the case. Klatskin and Vana et al reported 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 hepatic
adenoma. However, numerous reports of FNH prior to the 1960s, and its frequent
occurrence in individuals who have never used OCP, cast significant doubt on the
existence of any etiologic association between OCP use and FNH. The potential
effect of pregnancy on FNH (as well as hepatic adenomas) remains poorly under-
stood. Scott et al have reported a single case of a female who had used OCPs for 11
years prior to developing an FNH. After stopping the OCP, the tumor regressed; it
subsequently increased in size during a later pregnancy. Although their report is
provocative, data linking pregnancy and changes in the size or symptoms of an
FNH tumor are scant. As opposed to hepatic adenoma, there are no reports of
spontaneous rupture of FNH during pregnancy. Importantly, although it may be
impossible (without surgical resection) to distinguish an FNH from a well differen-
6 Fig. 6.5. Focal nodular hyperplasia (FNH). A, On cross-section this FNH appears as
yellow-tan lesion that is sharply demarcated from the normal liver in the absence of a
true capsule. The gross and microscopic architecture of these lesions, B, suggests a
regenerative rather than a neoplastic process. Bile duct hyperplasia and Kuppfer cells
are prominent.
tiated primary hepatocellular carcinoma (HCC), FNH tumors do not undergo

malignant transformation.
Pathology
Macroscopically, FNH appear as pale firm lesions distinct from the surrounding
liver (Fig. 6.5). Histologically, FNH tumors are sharply demarcated from the 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 distinguish
from regenerating nodules associated with cirrhosis. Bile duct hyperplasia, and Kupffer
cells are generally prominent in FNH, and often allow differentiation from other
lesions by radionucleotide scanning. Radiographically, FNH are described as having
a “central scar”; however, the core of these lesions is neither necrotic nor fibrotic.
Rather, the central portion of an FNH is composed of a round cell infiltrate and
prominent thick-walled blood vessels divided by fibrous septae.
Most 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 red
to brown, firm nodules with prominent blood vessels on the surface. Larger lesions
can be particularly difficult to distinguish from well-differentiated hepatocellular
carcinoma (HCC). Nearly all FNH tumors are asymptomatic, and unlike other
benign liver tumors, spontaneous rupture is extremely rare. In our experience in
managing 33 patients with FNH tumors, there were no spontaneous ruptures, and
the most common indication for surgical resection was the inability to exclude a
potential hepatic malignancy.
Evaluation
As with other benign liver tumors, laboratory tests, including liver function tests,
are typically normal. An elevation in the serum CEA or AFP level should arouse the
suspicion of a malignancy rather than an FNH. Most radiologic studies of FNH are
nonspecific. FNH are visible by ultrasound but exhibit no characteristic features.
Technicium-99 labeled sulfur colloid scintigraphy may be helpful in demonstrating
the presence of Kupffer cells within a hepatic tumor, but a positive result is not
specific since both hepatic adenoma and HCC can contain Kupffer cells (Fig. 6.6).
Helical contrast CT scanning may demonstrate a well-demarcated lesion with the
appearance of a central scar during the portal venous phase, but these lesions are
often isodense and undetectable. MRI may demonstrate a hypodense lesion with a
central scar, but these findings are not pathognomonic for FNH (Fig. 6.7). The use
of reticuloendothelial agents such as Ferridex, which are taken up selectively by
Kupffer cells, can increase the specificity of both CT and MRI; however, the results
are not specific to FNH. Angiography typically demonstrates a hypervascular mass 6
with enlarged peripheral vessels and a single central feeding artery.
Treatment
In many instances, diagnostic uncertainty will require an open or excisional biopsy.
At the time of surgery, if the lesion is definitively shown to be an FNH, enucleation
of the tumor is sufficient treatment. More often, a firm histologic diagnosis is
unavailable on frozen section, and a formal resection (with a rim of normal tissue) is
required in the unfortunate event that the final pathology demonstrates a malignant
lesion. In situations in which the tumor is truly felt to be an FNH based on 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, number
or symptoms of the lesion(s) should prompt reconsideration of surgical resection.
Even in the absence of strong evidentiary data, discontinuation of OCP use in all
patients with resected or unresected FNH seems prudent.
Hepatic Adenoma
Hepatic adenomas are generally small (< 5 cm), soft, solitary lesions, but may be
multiple in up to 30% of cases. As with FNH, the incidence of hepatic adenomas
has increased alarmingly since the late 1960s. Unlike FNH however, a persuasive
body of literature has emerged demonstrating an etiologic link between OCP usage
and the development of a hepatic adenoma. The risk of developing a hepatic adenoma
is commensurate with length of OCP usage and age over 30. Ninety percent of
patients who develop a hepatic adenoma have used OCPs and the incidence among
those who have used the OCP for more than 2 years is 3-4 per 100,000. Interest-
ingly, the risk of developing a hepatic adenoma while taking OCP may be related to
the amount of estrogen in OCP preparation, and if so, current low estrogen OCP
preparations should decrease the incidence of hepatic adenomas in the future. Re-
gression of hepatic adenoma upon cessation of OCP use has been well documented;
however, progression can occur. There is no convincing evidence linking pregnancy
to the development of hepatic adenoma, but it may increase the incidence of com-
plications associated with hepatic adenomas. In addition to estrogens, several other
hormone therapies, including androgens, clomiphene, danazol and human growth
6 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).
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 increased
incidence of hepatic adenomas.
Pathology
Grossly hepatic adenomas appear pale yellow on cut surface, and may contain a
variegated appearance secondary to internal hemorrhage (Fig. 6.8). Microscopically,
hepatic adenomas are composed of monotonous sheets of hepatocytes, often con-
taining considerable glycogen. Unlike FNH, portal triads and bile ducts are absent
and the existing blood vessels are thin-walled. In contrast to FNH, hepatic adenomas
appear expansive and neoplastic. Bile ducts are distinctly absent from hepatic ad-
enomas. Whether hepatic adenomas undergo malignant transformation remains
unresolved. Several authors have reported instances in which hepatocellular carci-
noma was found adjacent to or within a hepatic adenoma. Further complicating
this for the surgeon is the fact that histologic differentiation between a hepatic
adenoma and a well-differentiated HCC can be very difficult. Differentiation is made
even harder in patients with fibrolamellar HCC since this tumor, like hepatic
adenoma, occurs most commonly in menstrual-aged females.
Up 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 function
tests) are invariably normal. Tumor markers, such as CEA, α-fetoprotein and CA-
19-9), are not elevated.
Benign Tumors of the Liver
Fig. 6.7. Focal nodular hyperplasia (FNH). Pre- and postgadolinium MRI images of a FNH. A, A noncontrast T1-weighted image shows an
isodense lesion in Segment 4B. Portal venous tributaries re nondisplaced and are seen to course through the lesion. B and C, On T2-weighted
image of the same lesion, no mass is visible. D, E, and F, Postgadolinium T1-weighted images demonstrates an early hyperdense appearance,
D, with rapid clearing and an isodense appearance on delayed imaging E and F.
95
6
6
Fig. 6.8. Hepatic adenoma. A, On gross appearance hepatic adenomas appear as
soft, tan lesions. B, Microscopically, hepatic adenomas are composed of monoto-
nous sheets of hepatocytes containing considerable glycogen. Portal triads and
bile ducts are absent and the existing blood vessels are thin-walled. Venous lakes
and zones of necrotic ghost are characteristic.
Radiographic Evaluation
Findings on radiographic evaluation are typically nonspecific. Ultrasound dem-
onstrates a tumor with mixed echogenicity and an overall heterogeneous appear-
ance. CT scan can yield a wide spectrum of disparate findings, but typically
demonstrates a hypodense lesion on noncontrast imaging with a variegated appear-
ance following contrast administration. MRI findings are similar to those on CT
and are nonspecific (Fig. 6.9). A Tc99 sulfur colloid scan may be useful in differen-
tiating between a hepatic adenoma and an FNH, as hepatic adenomas usually lack
bile ducts and appear as a “cold nodule.” Angiographically, hepatic adenomas are
hypervascular lesions with areas of necrosis and hemorrhage.
Treatment
All hepatic adenomas should be resected and considered to harbor dysplastic
changes or frank cancer until pathologic review of the entire tumor (and not a lim-
ited biopsy) proves otherwise. Similarly, control of bleeding from ruptured hepatic
adenomas in unstable patients is best done surgically. However, if surgical exploration
is not feasible, angiographic embolization can be a life saving, temporary maneuver
until transfer to a center with surgical capability is possible. Intraoperatively, hepatic
artery ligation of the right, left, or main vessel can similarly be a life-saving proce-
dure if hepatic resection is contraindicated. All women diagnosed with a hepatic
adenoma should be advised to stop OCP use for life. Yearly follow-up with imaging
is advised for all patients and is mandatory in those patients whose hepatic adenoma
is not causally linked to OCP use. There is little information available relating to the
safety of pregnancy in the setting of a hepatic adenoma. Although it appears that
pregnancy is safe after resection of a hepatic adenoma, women with a hepatic adenoma
that has not been treated should be advised to avoid becoming pregnant.
Fig. 6.9. Hepatic adenoma. T1 and T2-weighted MRI appearance
Additional Liver Tumors

Epithelial Tumor
Biliary Hamartomas
Bile duct adenomas, or hamartomas, are common tumors. They are noteworthy
as they are often mistakenly interpreted as metastatic tumor by the operating sur-
geon. (Note: Biopsy and confirmation of a malignancy for all hepatic lesions is
mandatory. This is most important in situations in which the presence of a meta-
static liver tumor will alter the proceedings of the operation.) Biliary hamartomas
appear as small gray-white nodules that lie beneath the capsule of the liver and are
frequently multiple. Microscopically, they are composed of mature bile ducts sur-
rounded by fibrous tissue.
Mesenchymal Tumors
Solitary Fibrous Tumor
Other names include benign mesothelioma or fibroma.
Solitary fibrous tumors (SFT) are rare mesenchymal tumors that can often be
mistaken for metastatic lesions because of their radiographic and intraoperative
appearance (Fig. 6.10). SFTs can exhibit either a benign or malignant phenotype.
Most tumors are large and symptomatic; often they are palpable on physical exam.
Grossly, they may vary in size from 2 to more than 20 cm in greatest dimension and
are firm, white-to-gray, lesions that may be well or ill-defined. Histologically, most
have a bland appearance with a classic short storiform (so-called patternless) pattern
and absence of cellular atypia, mitoses and/or necrosis; however, in malignant can-
6 cer there may be marked cellular atypia and a high mitotic rate. Immuno-
histochemically, all the SFTs show a strong positive reaction against antibodies for
CD-34 and vimentin. The diagnosis of either a benign or malignant solitary fibrous
tumors is impossible without definitive histologic review, and surgical resection is
indicated in all circumstances.
Lipoma, Myelolipoma, or Angiomyelipoma

Fatty tumors of the liver are extraordinarily rare. Although several reports of
primary lipomas have appeared, there are no reports of a primary hepatic 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 including
myelolipoma, angiolipoma, and angiomyolipoma have been described. The term
“pseudolipoma” has been given to an extracapsular fatty tumor with involutional
changes. This lesion probably results when a free-floating piece of fat, e.g., an appendix
epiploica, becomes trapped between diaphragm and liver surface. Definitive diag-
nosis requires surgical resection to exclude malignancy.
Mesenchymal Hamartomas
Mesenchymal hamartomas represent extremely rare congenital liver tumors that
occur most commonly in infants less than 1 year of age. Unlike biliary hamartomas
that are clinically insignificant, mesenchymal hamartomas can reach enormous size
resulting in significant impairment of hepatic function. Microscopically, hamarto-
mas display a myxoid background of highly cellular embryonal mesenchyme with
random groupings of hepatic cells, bile ducts and cysts. The cystic component is
generally the most prominent feature resulting in a “honeycomb” appearance.
Although benign tumors, mesenchymal hamartomas can result in death due to mass
effect and/or hepatic insufficiency. All mesenchymal hamartomas should be com-
pletely excised if feasible. If complete surgical excision is not possible or prohibitive
for other reasons, surgical debulking may be sufficient since there have been no
reports of recurrence after an incomplete surgical resection.
Fig. 6.10. Solitary fibrous tumors. T1 and T2-weighted MRI appearance.
Myxoma
To date, only three reports of primary hepatic myxomas exist in the literature.
Two hepatic myxomas were resected from children, one of which proved to be inva-
sive. Both children remained disease-free at time of report. Only a single adult case
of hepatic myxoma has appeared. This involved a 58-year-old male with a left lobe
myxoma that ruptured. Definitive diagnosis was not made until four months later
at autopsy. Similar to other rare hepatic tumors, surgical resection is generally indi-
cated to exclude malignancy.
Teratoma
At least seven benign teratomas have been reported. Most occur in children.
They may be cystic and usually are encapsulated and easily resected. Surgical resec-
tion is indicated to exclude malignancy.
Conclusions
An accurate histologic diagnosis and knowledge of their natural history is key to
the management of patients with benign liver tumors. While radiology has made
great strides in identifying and characterizing the features of both benign and malig-
nant liver tumors, the final burden of responsibility for diagnosis and therapy remains
on the surgeon’s shoulders. Increasing experience, improved surgical techniques,
and better perioperative care, currently permits hepatic resection to be performed
with a high level of safety. However, as we learn more about the prognosis and
natural history of most benign tumors, a conservative approach consisting of obser-
vations and serial imaging seems appropriate for most asymptomatic patients in
which a malignancy is not suspected.
Symptomatic patients, without medical or anatomic contraindication to a major

hepatic resection, and those patients in whom a malignancy cannot be excluded,
should undergo abdominal exploration and resection. Preoperative needle biopsy in
these circumstances is often dangerous and inconclusive. Careful examination of
the liver will determine tumor size and location and may provide clues to the diag-
nosis. Adequate wedge incision biopsy of large lesions, and excisional biopsy of small
and peripheral lesions, should allow the pathologist to make an accurate frozen-
section diagnosis and exclude a malignancy. If doubt remains, a formal hepatic
resection is indicated.
Selected Readings
1. 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.
6 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 infants
and children. Arch Dis Child 1960; 35:22–28.
5. Edmundson HA. Tumors of the liver and intrahepatic bile ducts. Atlas of tumor
pathology. Section VII Fasicle 25. Armed Forces Institute of Pathology. 1958.
6. Vana J, Murphy GP, Aronoff BL, Baker HW. Survey of primary liver tumors and
oral contraceptive use. J Tox Environ Health 1979; 5:255–273.
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 1
CHAPTER 7
Hepatocellular Carcinoma
Bryan Clary
Introduction
Although uncommon in the United States, primary cancer of the liver (hepato-
cellular carcinoma) is the fourth leading cause of cancer death worldwide, accounting
for 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 developing
countries. The areas of highest incidence are Western and Central Africa, Eastern
and Southeast Asia, and Melanesia. The incidence in these locations ranges from 30
to nearly 100 cases per 100,000 individuals per year. In contrast, the incidence in
Western countries including the United States, Great Britain, and South America, is
low (2-3 per 100,000). This variation is mostly due to a higher incidence of chronic
viral hepatitis and liver injury. As the proportion of noncirrhotics is greater in the
West and the underlying causes of liver injury differ, the treatment options are some-
what different from those of Eastern patients as well. This Chapter will summarize
the basic characteristics of this disease and discuss the alternative treatments.
Etiology
Underlying chronic liver disease is present in the majority of patients presenting
with hepatocellular carcinoma (HCC). In general, any chronic injury to the liver
can result in HCC, although the most established and important association has
been with viral hepatitis. In the Far East, approximately 85% of patients with HCC
have underlying cirrhosis, most commonly resulting from hepatitis B infection.
Individuals who are seropositive for Hepatitis B surface antigen have at least a 100-fold
increased risk of developing HCC compared to the general seronegative population.
Although the carrier rate for HbsAg in the general Taiwanese population is 10%,
80% of Taiwanese patients with HCC are HbsAg positive. Even in areas where
Hepatitis B infection is not endemic, there remains a strong association between
HCC and Hepatitis B infection. For example in the United States, 25% of patients
with HCC test seropositive for Hepatitis B, a figure which is approximately 6 times
that of the general population. When HCC develops in association with cirrhosis in
Western patients, it is more commonly a result of Hepatitis C. Approximately 70%
of cirrhotic patients with HCC in Japan and Southern Europe are seropositive for
Hepatitis C, whereas in the United States, this figure is approximately 40-50%. It is
thought that cirrhosis arising in the setting of Hepatitis C carries a greater risk of
developing HCC. For patients with cirrhosis from Hepatitis B, the estimated risk is
0.5% per year. In contrast, the risk of developing HCC over a 10-year period in
patients with Hepatitis C has been reported to be nearly 50%. In Western series,

cirrhosis secondary to alcoholic liver disease is seen in 10-30% of patients with

HCC. This is a very uncommon etiology in the Far East experience. HCC is
uncommon in patients with cirrhosis arising from primary biliary cirrhosis; hemo-
chromatosis-induced cirrhosis is associated with a high incidence of HCC. Many
other causes of chronic liver insufficiency have also been associated with HCC. The
radioactive contrast agent thorotrast, now obsolete, has been associated with the
development of HCC (as well as peripheral cholangiocarcinoma and hepatic
angiosarcoma) after delays of 20-30 years. Methyl testosterone and other anabolic
steroids may induce HCC; however, the link between oral contraceptive use and
HCC is not well accepted. Individuals with HCC, in the absence of cirrhosis, tend
to be younger and have an equal male to female ratio in contrast to patients with
cirrhosis where the male to female ratio varies from 3:1 to 8:1.
Diagnosis and Pretreatment Planning
Presentation
Patients with HCC commonly present with advanced lesions given the silent
7 nature of this disease. The most common symptoms among patients with advanced
disease include abdominal pain, weight loss, fatigue, early satiety, and abdominal
distention. It is possible, although infrequent, for HCC to spontaneously rupture
and bleed. A dramatic increase in pain and tenderness in a patient with a known
HCC should lead the physician to suspect this potentially catastrophic event. Tumor
rupture is much frequent in the Far East series and has been reported to be the mode
of presentation in up to 10-15% of patients. Jaundice, if present, may be secondary
to hepatocellular dysfunction, portal vein obstruction, or ductal obstruction in the
presence of locally advanced lesions. Small lesions are usually asymptomatic and
found either during an evaluation prompted by abnormal liver function tests, inci-
dentally on abdominal imaging performed for other reasons. Although screening
patients with hepatitis and cirrhosis for HCC has been shown to result in detection
at earlier stages, the survival benefit of such programs is not clear.
Laboratory Evaluation
Laboratory evaluation is performed to both confirm the diagnosis and estimate
the degree of underlying liver impairment. The laboratory evaluation of a patient
suspected of having HCC should include liver function tests, complete blood counts,
serum electrolytes and creatinine, coagulation parameters, serological tests for hepa-
titis, and α-fetoprotein (AFP). Although a number of sophisticated tests have been
described 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 type
of laboratory and clinical studies influence the treatment strategy. Hypercalcemia
and erythrocytosis are potential paraneoplastic manifestations of HCC and a biopsy
is not necessary. AFP levels are elevated in 75-90% of patients. A level higher than
500 ng/dl in a patient with a liver mass is diagnostic of HCC. An AFP level greater
than 2,000 ng/dl is often indicative of disseminated disease.
Hepatocellular Carcinoma 103
Table 7.1. Child-Pugh classification of liver dysfunction in patients with cirrhosis

Points
1 2 3
Serum Bilirubin (mg/dl) <2.0 2.0-3.0 >3.0
Serum Albumin (g/dl) >3.5 2.8-3.5 <2.8
Protime Elevation (sec) 1-3 4-6 >6
Ascites None Slight Moderate
Encephalopathy (grade) None 1-2 3-4
Grade A 5-6 points

B 7-9 points
C 10-15 points
Imaging
The goals of imaging are multiple and include:
1. identification of lesions,
2. as an aid in determining whether a lesion is cancerous, 7
3. to assess potential resectability,
4. as a guide in planning the extent of resection, and
5. to aid in the planning of nonsurgical approaches in the patients who are
candidates for surgical resection. Ultrasound (US), which is readily avail-
able and inexpensive, is commonly employed in the screening of high risk
patients.
On ultrasound, HCC is commonly isoechoic, with normal liver limiting the
assessment of the extent and number of lesions. In cirrhotic patients, regenerative
nodules are difficult to distinguish from HCC. Despite its limitations, US can be
very useful in delineating the presence and extent of portal venous and biliary ductal
involvement and remains an important component in the preoperative evaluation.
Computerized tomography (CT), which is widely available, is technology rather
than operator dependent (as opposed to US) and remains the most widely utilized
imaging test in these patients. On CT, HCC is isodense with the surrounding liver
parenchyma following contrast injection and, thus, it is important to review both
noncontrast and contrast-enhanced images. Assessment of the portal and hepatic
veins is dependent upon the timing of contrast injection, and as such, if performed
incorrectly, is often inadequate to fully assess these structures. Doppler ultrasound
or magnetic resonance imaging (MRI) should be routinely done to complement CT
evaluation of HCC. At our institution (Memorial Sloan-Kettering Cancer Center),
MRI is felt to be the single best imaging test for treatment planning. MRI with
gadolinium enhancement allows for the identification, quantification and 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 Doppler
ultrasound or MRI readily demonstrates these vascular structures. Preoperative an-
giography with embolization has been recommended by some authors, although we
do not routinely recommend this, except in those patients awaiting total hepatec-
tomy/transplantation since the wait for an available cadaveric donor may be months.
Biopsy
The role of percutaneous biopsy in the assessment of patients with suspected
HCC is controversial. Risks include bleeding, pneumothorax, injury to adjacent
organs, and tumor dissemination. Imaging studies in combination with the labora-
tory evaluation and clinical scenario generally provide sufficient information to make
an accurate preoperative diagnosis. A resectable lesion suspicious for HCC, in a
patient with no contraindication to surgery, does not require biopsy. In addition,
needle biopsy is also not indicated in a patient with an unresectable liver mass and
an AFP level greater than 500 ng/dl. Percutaneous needle biopsy is useful if diagnos-
tic doubt exists in a patient with an unresectable lesion or in patients with an
indeterminant lesion outside the field of the intended resection that would render
them unresectable.
Treatment
The 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 of
7 advanced liver lesions (biliary tract infection, liver failure) than from the less direct
effects of metastatic disease. The variability of outcomes in patients with what appear
to be similar stages of disease makes it difficult to draw firm conclusions about many
of the proposed modes of therapy. Randomized trials comparing no treatment to
surgery, or ablative therapies, have not been conducted and will likely never be
performed. Likewise, randomized trials comparing surgery to ablative forms of therapy
have also not been performed. Patients with small HCC (< 3 cm) who are not
treated have been shown to have survival rates of up to 88% at one year and 55% at
two years. The natural history of patients with HCC is affected not only by the stage
of the malignancy (Tables 7.2, 7.3) but also the degree of underlying liver dysfunc-
tion. In patients not undergoing ablation or resection, the median survival for early
stage disease (Okuda stage I) appears to be 9-12 months. In advanced disease, this is
significantly shortened. In most series addressing patients who are deemed
unresectable either because of advanced tumor characteristics or because of advanced
liver dysfunction from underlying cirrhosis, a significant proportion die from liver
failure and/or the consequences of portal hypertension (hemorrhage). Surgical
resection remains the only potentially curative option in the treatment of HCC. In
addition to being technically feasible, resectability is also determined by
1. the general medical condition of the patient,
2. the absence of extrahepatic disease, and
3. the ability to leave adequate residual liver parenchyma.
The latter may be achieved through orthotopic liver transplantation following
complete or total hepatectomy. An algorithm followed by the author’s institution
for the treatment of patients with HCC is presented in Figure 7.1.
Surgical Resection (Partial Hepatectomy)
Partial hepatectomy is feasible because of the phenomenon of liver regeneration.
Immediately following partial hepatectomy, an incompletely understood process
occurs resulting in the growth of all cellular elements within the remnant. Within
2-3 weeks, the remnant has assumed a size close to that of the original liver and
Table 7.2. TNM staging of hepatocellular carcinoma

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

Stage 1 T1 N0 M0
Stage 2 T2 N0 M0
Stage 3 T3 N0 M0 7
T1-3 N1 M0
Stage 4A T4 N0-1 M0
Stage 4B T-Any N-Any M1
Table 7.3. Okuda staging of hepatocellular cancer

Adverse Factor
Tumor Size >50% hepatic involvement

Ascites Present
Serum Albumin <3gm/dl
Serum Bilirubin >3mg/dl
Stage I No adverse factors

Stage II 1-2 adverse factors
Stage III 3-4 adverse factors
within 6 weeks complete functional capacity is restored. The liver’s capacity for
regeneration is so great that up to 90% of a healthy liver can be resected. In the
noncirrhotic patient, liver resection can be performed at most major medical centers
with an operative mortality rate of less than 5%. In the cirrhotic patient, operative
mortality is closer to 10% in these same centers, emphasizing the fact that the major
determinant of outcome is preoperative liver functional status. As a rule, partial
hepatectomy should be considered in all noncirrhotic patients and in those cirrhotics
with Childs A liver function. Highly selected patients in the Childs B category may
also be candidates. Other contraindications to partial resection include widespread
disease within the liver, extrahepatic disease, significant medical comorbidities, and
tumor thrombus within the main portal vein. In patients without cirrhosis, curative
partial hepatectomy is associated with a 5-year survival of 40-50%, whereas in patients
with cirrhosis most recent large studies report a 5-year survival of 20-40%. As
Fig. 7.1. Treatment algorithm for patients with hepatocellular carcinoma based upon
7 resectability and liver function.
demonstrated in a large series recently published by the Memorial Sloan-Kettering

group, curative resection often involves major hepatectomy. In this contemporary
Western series (1992-1998), 75% of resected patients had a primary tumor size of
greater than 5 cm and required a formal lobectomy or greater 66% of the time.
Prognostic factors of outcome following resection included margin status, the pre-
operative AFP level, tumor size, and the presence of vascular invasion. Neither the
presence of cirrhosis nor the etiology of the underlying cirrhosis (present in 65%)
were significant predictors of a poor outcome. Although the mortality following
resection was less than 5% overall, the postoperative morbidity rate was 45%.
Transplantation (Total Hepatectomy)
Total hepatectomy with liver transplantation is a theoretically attractive option
for the patient with cirrhosis and cancer as it offers the potential benefits of tumor
excision and replacement of dysfunctional liver parenchyma. The outcome follow-
ing OLT for HCC is clearly dependent upon the extent of liver involvement at the
time of treatment. The best results are recorded in patients who had HCC discov-
ered incidentally during transplantation performed for liver insufficiency. Patients
with tumors smaller than 5 cm have a median survival that exceeds 5 years, whereas
in patients with a tumor size greater than 5 cm, it is approximately 2 years. Although
controversy exists over the role of total hepatectomy with OLT in the treatment of
HCC, the lack of donor livers continues to limit the possible implications of this
debate. According to UNOS (United Network for Organ Sharing) figures, 4,413
cadaveric liver transplants were performed in 1998. Of these, only 87 (2.1%) were
given to recipients with malignant neoplasms. UNOS survival data on transplants
performed from 1989 through 1998 demonstrate a 5-year survival of 41% for patients
with a primary malignant neoplasm of the liver compared to an overall survival of
74% for all patients undergoing cadaveric liver transplant. The median waiting time
for a cadaveric liver was 1.4 years in 1998. As total hepatectomy with OLT represents
the only potentially curative option in patients with Childs B or C categories, and
the wait time for a patient with Childs A would be excessively long, many centers
have begun to explore the use of living-related donors as a source of grafts. The
author is, in general, opposed to the use of living donors given the significant mor-
bidity (30-40%) and mortality (2-5%) risks to the donor and the high rate of tumor
recurrence in the recipients. Tumor recurs in the majority of patients following OLT
and is the main reason for the significantly reduced post-OLT survival compared to
patients transplanted for benign diagnoses.
For these considerations, the author’s recommendation is that partial 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 cadaveric
OLT as should patients with well compensated cirrhosis and a small lesion that is
situated such that a large amount of functional hepatic tissue would be sacrificed in
the resection. Consideration of a living-related liver donor should be limited to very
extraordinary situations.
Chemotherapy 7
Chemotherapy, whether given systemically or via intra-arterial means, appears
to have a minimal impact on the clinical course of patients with HCC. Agents that
have been utilized include doxorubicin, 5-fluorouracil (5-FU), and cisplatin. Although
a response rate of up to 20% has been reported, there are no long-term survivors
among this group of patients. Intra-arterial chemotherapy delivered through an
implantable pump has also been tried. Despite an apparent increase in the response
rate, the morbidity and potential mortality associated with general anesthesia, and
the laparotomy required for implantation, limit this approach in patients with
advanced liver dysfunction.
Cryoablation and Radiofrequency Ablation
Cryoablation has been demonstrated to be a safe palliative mode of therapy. In
order to safely perform this procedure, laparotomy is generally performed, although
a laparoscopic approach may be reasonable in certain instances. This is performed
by inserting an insulated cryoprobe through the liver substance into the center of
the mass. Multiple freeze-thaw cycles are performed using super-cooled liquid nitro-
gen. Intraoperative monitoring with ultrasound delineates the growing iceball
ensuring 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 which
was reported by Zhou and colleagues from China. In this series, patients with lesions
smaller than 5 cm (unresectable secondary to concurrent cirrhosis), had a 5-year
survival of 49% versus a 5-year survival of 22% for the entire group. The author
utilizes cryoablation in patients who are unresectable at the time of laparotomy
where the morbidity of a general anesthetic and laparotomy has already been incurred.
Larger tumors and those near major vascular structures are relative contraindications
as the efficacy is diminished in these situations. More recently, interest has been
shifted to thermal ablation by radiofrequency (RFA). Although this may be used
intraoperatively at the time of laparotomy, it can also be administered via a percuta-
neous approach in lesions buried deeply within the liver. Surface lesions, lesions
high in the dome of the liver, and those immediately adjacent to other intraabdominal
organs require an open approach (or possibly laparoscopic). Curley and colleagues
at MD Anderson Cancer Center have presently presented a large series of RFA (done
via laparotomy) in the treatment of various hepatic neoplasms. This treatment appears
safe, yet the long term results are not known at this time. Thermal ablation with
microwave and laser technology have also been described with similar safety profiles
in comparison to RFA. Although the three methods of thermal ablation appear
effective in patients with small tumors, they are generally not appropriate for larger
tumors or those adjacent to the major vessels and bile ducts. We currently utilize
this form of therapy (percutaneous) in Childs B and C patients with small lesions
situated in anatomically accessible sites. We are beginning to explore the use of this
modality intraoperatively as an alternative to cryotherapy.
Arterial Interruption
HCC are known to be very vascular tumors as evidenced by their appearance on
imaging studies and the abundant vascular structures on histologic examination.
Hepatic arterial ligation was at one time the treatment of choice for HCC when
7 lesions were found to be unresectable at the time of laparotomy. In patients with
portal hypertension, nonselective ligation of the main hepatic arteries carries a 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 angiographic
techniques, selective blockade of the hepatic artery branches supplying the tumors
can be performed through embolization. Selective embolization is safe and widely
reported in the literature. In many centers, embolization is conducted with the con-
comitant intra-arterial infusion of chemotherapeutic agents (chemoembolization).
Complications following embolization or chemoembolization can occur and the
reported mortality is as high as 5-10%. Postembolization syndrome (fever, 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 much
less 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 B
cirrhotics, 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. Portal
venous occlusion in the absence of adequate portal venous collaterals also represents
a 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 therapy
appears to offer benefit when compared to best supportive care. Long-term survival
is achieved in a minority of patients although no randomized trial has demonstrated
a benefit when compared to observation. The addition of chemotherapy to embo-
lization (chemoembolization) although theoretically attractive, does not appear to
offer 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
patients with mild liver dysfunction who are clearly not candidates for hepatic resec-
tion.
Preoperative embolization may be appropriate in patients with only mild liver
dysfunction who are awaiting total hepatectomy for HCC given the relatively long
waiting times for cadaveric grafts. Embolization should not be utilized in patients
awaiting partial hepatectomy since it is unlikely to improve the resectability and
may be associated with complications.
Ethanol Injection
Percutaneous ethanol injection (PEI), under either ultrasonographic or CT guid-
ance, is utilized as an ablative form of therapy in many centers for patients with
small tumors. As practiced, this form of therapy is limited to patients whose tumors
are smaller than 4 cm in size. PEI can be performed intraoperatively upon the find-
ing of unresectability, yet its main advantages is that it can be done in a nonoperative
setting. Long-term follow-up by a number of groups has demonstrated long term
survival in a significant minority of patients. Livraghi and colleagues from Italy have
published one of the largest studies documenting the outcome of patients following
PEI. In their series (1995), the five year survival rates for solitary/< 3 cm, solitary/3- 7
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 natural
history 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 liver
dysfunction who are unresectable, PEI has been combined with embolization as a
means of treating moderately sized (3-8 cm) and often multiple lesions (< 5). A
randomized trial by Bartolozzi and colleagues demonstrated a better than 3-year
survival in patients undergoing this combined treatment approach (52%) compared
to embolization alone (30%). It is the author’s practice to combine PEI with embo-
lization in patients with small lesions (< 4-5 cm) even when multiple (less than 5).
Radiation
External beam radiation appears to have limited value in the treatment of HCC
in part because of the relative intolerance of normal liver to therapeutic doses. Whole-
liver radiation with doses of more than 4000 cGy are associated with a greater than
50% risk of radiation hepatitis and liver failure. Recent advances in the technique of
conformal radiation, with three dimensional treatment planning, have increased the
applicability of external beam radiotherapy. The use of radiation sensitizing agents
including 5-FU, the fluoropyrimidines, and gemcitabine has also led to an increased
interest in radiation therapy. In general, external beam radiation therapy is utilized
in patients with large, unilateral, symptomatic tumors that are unresectable.
Radioembolization of liver tumors with Yttrium-90 microspheres has recently
been described as a means of delivering a therapeutic radiopharmaceutical. These
spheres have a mean tissue penetrance of 2.5 mm, with a maximum of 10 mm. Only
a few preliminary reports exist detailing the experience with this technique and
suggest that this modality is quite safe. Clinical trials examining efficacy are in progress.
Conclusion
The treatment of hepatocellular carcinoma should be directed at complete tumor
extirpation whenever possible. The treatment approach is individualized according
to resectability and the presence of underlying liver dysfunction. In patients without
cirrhosis, or only mild liver dysfunction, partial hepatectomy is the best therapeutic
option. For patients with severe liver dysfunction, total hepatectomy with orthoto-
pic liver transplantation should be considered for T1 and T2 lesions. If, during the
course of an operative exploration a tumor is found to be unresectable, we recom-
mend ablation (cryoablation or RFA) as a palliative measure when possible. Patients
with Childs A or Childs B liver dysfunction who are clearly unresectable on the
basis of preoperative imaging can be approached with transcutaneous embolization
with or without concomitant PEI depending on the size, number, and expertise at
one’s respective institution. Ablation should be considered in patients on the wait-
ing list for orthotopic liver transplantation (percutaneous RFA, embolization, PEI)
as a temporary treatment. Patients with Childs C cirrhosis may be candidates for
PEI and potentially percutaneous RFA although these should be performed only in
patients who are still reasonably functional. Patients with symptomatic large lesions
7 not amenable to ablation may be candidates for external beam radiotherapy as a
palliative treatment.
The algorithm presented by the author is based upon the available data within
the existing literature. Much of this data is flawed and primarily retrospective. 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 proper
treatment of this malignancy.
Selected Reading
1. 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 in
746 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 1
CHAPTER 8
Periampullary Cancer
and Distal Pancreatic Cancer
Richard D. Schulick
Introduction
The first successful treatment of a periampullary carcinoma occurred over a cen-
tury ago. In 1899, William S. Halsted of The Johns Hopkins Hospital described a
transduodenal local ampullary resection with reanastomosis of the pancreatic and
bile ducts to the duodenum in a patient presenting with obstructive jaundice. The
patient subsequently developed obstructive jaundice three months after the initial
operation and required a second operation in which a cholecystoduodenostomy was
performed to decompress the biliary tree. The patient died six months later and an
autopsy revealed recurrent ampullary carcinoma invading into the head of the pan-
creas and duodenum.
The first en bloc resection of the head of the pancreas and duodenum for
periampullary carcinoma is credited to Codivilla, who performed the procedure at
the beginning of the 20th century; unfortunately the patient did not survive the
postoperative period. In 1912, Kausch, a German surgeon, performed the first suc-
cessful partial pancreaticoduodenectomy in two stages.
In 1935, Allen Oldfather Whipple (Fig. 8.1) reported his experience in treating
three patients with ampullary cancer using a two-stage formal pancreaticoduodenectomy
at the annual American Surgical Association meeting. He subsequently reported on
a total of 37 pancreaticoduodenectomies during his career, with the operation evolving
from a two-stage to a one-stage procedure by the early 1940s. His one-stage opera-
tion involved reconstruction with an end-to-end choledochojejunostomy, an end-
to-side pancreaticojejunostomy and an end-to side gastrojejunostomy. These
anastomoses were performed to the proximal jejunum, which was constructed in a
retrocolic fashion.
In 1937, Brunschwig, from the University of Chicago and later from Memorial
Sloan-Kettering Cancer Center, extended the indication for pancreaticoduodenectomy
to include cancer of the head of the pancreas. During the 1940s and 1950s,
pancreaticoduodenectomy was performed in limited numbers with variable results.
At that time, the operation carried a hospital mortality that approached 25% in
some series, leading some authorities to abandon the procedure. In the last several
decades, improved hospital morbidity, mortality, and survival after
pancreaticoduodenectomy have been reported. Many centers now report operative
mortalities of less than 4%.

Fig. 8.1. Allen O. Whipple.
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 technical
details of this operation.
Pancreaticoduodenectomy for Periampullary Cancer
Exposure 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 enhanced
with the use of a mechanical retracting device.
Periampullary Cancer and Distal Pancreatic Cancer 113
The first portion of the Whipple procedure is devoted to assessing the extent of
disease and resectability. There is debate as to the benefits of a staging laparoscopy
versus open staging in anticipation of surgical resection or palliation. Proponents of
laparoscopy employ minimally invasive techniques to evaluate for the presence of
metastatic disease in the peritoneal cavity or liver, and some advocate the use of
laparoscopic ultrasonography to assess for local disease involvement. If metastatic or
locally unresectable disease is discovered, the procedure is terminated, and patients
with obstructive jaundice are referred for placement of a percutaneous transhepatic
expandable metallic bile duct stent. Laparotomy is performed only if they develop
gastric outlet obstruction. Opponents of laparoscopy prefer to perform palliative
biliary and gastric bypasses, as well as chemical splanchnicectomy, in patients who
are found to be unresectable. The incidence of gastric outlet obstruction due to a
mass in the head of the pancreas approaches 20% in some series.
At open exploration, the entire liver is assessed for the presence of metastases not
seen by preoperative imaging studies. The celiac axis is inspected for lymph node
involvement. Tumor-bearing nodes within the resection zone do not contraindicate
resection because long-term survival is sometimes achieved with peripancreatic nodal
involvement. The parietal and visceral peritoneal surfaces, the omentum, the liga-
ment of Treitz, and the entire small and intra-abdominal large intestine are carefully
examined for the presence of metastatic disease. An extensive Kocher maneuver is 8
performed by elevating the duodenum and head of the pancreas out of the
retroperitoneum and into the midline, allowing visualization of the superior mesen-
teric artery at its origin with the aorta. The porta hepatis is assessed by mobilizing
the gallbladder out of the gallbladder fossa, and dissecting the cystic duct down to
the junction of the common hepatic and common bile duct. The common hepatic
artery and proper hepatic artery should also be assessed to determine that they are
free of tumor involvement.
If the intraoperative assessment reveals localized disease without tumor encroach-
ment upon resection margins, the resection is performed in relatively standard fash-
ion. If assessment reveals evidence of local tumor extension implying potential
unresectability, the normal sequence for performing the pancreaticoduodenectomy
should be modified. The easiest and safest portions of the resection should be per-
formed first. Many tumors that initially appear unresectable can be successfully
resected by patiently beginning the operation where it is easiest and finishing harder
portions later.
The distal common hepatic duct is divided close to the level of the cystic duct entry
site early during the operation. This allows caudal retraction of the common bile duct
and nicely opens the dissection plane on the anterior surface of the portal vein. During
these maneuvers, the portal structures should be assessed for a replaced right hepatic
artery originating from the superior mesenteric artery. If found, this vessel should be
dissected and protected from damage. The gastroduodenal artery is next identified and
clamped atraumatically. This maneuver confirms its identity as well as confirming that
the hepatic artery is not being supplied solely by retrograde flow through superior
mesenteric artery collaterals (in the setting of celiac axis occlusion).
For a classic Whipple procedure, a 30-40% distal gastrectomy is performed by
dividing the right gastric and right gastroepiploic arteries. The antrectomy is then
completed using a linear stapling device. For a pylorus-preserving
pancreaticoduodenectomy, the proximal GI tract is divided 2-3 cm distal to the

pylorus with a linear stapling device. The right gastric artery can often be spared but
may be taken if it allows better mobilization of the duodenum. The gastrointestinal
tract is divided distally at a point of mobile jejunum, typically 10-20 cm distal to the
ligament of Treitz. The mesenteric vessels to this initial portion of the jejunum are
carefully divided over clamps and tied to avoid bleeding. Once the proximal jejunum
is separated from its mesentery, it can be delivered dorsal to the superior mesenteric
vessels from the left to the right side.
Performing a more extensive Kocher maneuver can identify the superior 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 frequently
surrounded by adipose tissue as it receives tributaries from the uncinate process and
neck of the pancreas, the greater curve of the stomach, and from the transverse
mesocolon. In this location, the superior mesenteric vein is identified by dissecting
the fatty tissue of the transverse mesocolon away from the uncinate process of the
pancreas. Division of the branches emptying into the anterior surface of the supe-
rior mesenteric vein allows continued cephalad dissection. The plane anterior to the
superior mesenteric vein is developed under direct vision, avoiding branches and
tumor involvement. Care is taken to protect the splenic vein as it joins the superior
8 mesenteric vein posterior to the neck of the pancreas. After the plane anterior to the
portal vein and superior mesenteric vein is complete, a Penrose drain is looped under
the neck of the pancreas.
Stay sutures are placed superiorly and inferiorly on the pancreatic remnant to
reduce bleeding from the longitudinal segmental pancreatic arteries. The pancreatic
neck is then divided using the electrocautery after confirming a free plane anterior
to the portal and superior mesenteric veins. The Penrose drain, previously placed
behind the neck of the pancreas, is used to elevate the pancreatic tissue to be divided
and protect the underlying major veins. The site of the main pancreatic duct should
be noted so it can be incorporated into the subsequent reconstruction.
The specimen now remains connected by the head and uncinate process of the
pancreas. These structures are separated from the portal vein, superior mesenteric
vein and superior mesenteric artery. This is performed by serially clamping, dividing
and tying the smaller branches off the portal and superior mesenteric vessels. Dis-
section should be performed flush to these structures to remove all pancreatic and
nodal tissue in these areas. Great care is taken not only to avoid injury to the supe-
rior mesenteric artery and vein at this level, but also to ensure complete removal of
all pancreatic tissue and lymph nodes near these vascular structures. With these
areas dissected, the specimen is removed and the pancreatic neck margin, uncinate
margin and common hepatic duct margins are marked for the pathologists. To speed
up analysis of these frozen section margins, the common hepatic duct margin and
the pancreatic neck margin may be sampled earlier and sent to pathology while the
main specimen is still being removed.
There are multiple options for reconstruction after pancreaticoduodenectomy.
Most commonly, the reconstruction first involves the pancreas, followed by the bile
duct, and then the duodenum. The issues and controversies surrounding the pan-
creatic and biliary reconstruction are outlined by multiple papers specifically
addressing these issues. In brief, the pancreatic anastomosis can be performed to the
jejunum or to the stomach. If the jejunum is used for reconstruction, some groups
favor a separate Roux-en-Y reconstruction for the pancreas or even a double Roux-
en-Y reconstruction for the pancreas and the bile duct. Controversy continues
regarding the best type of pancreaticojejunostomy, the importance of duct-to-mucosa
sutures, and the use of pancreatic duct stents. At the Johns Hopkins Hospital, the
pancreatic reconstruction is typically performed with an end-to-end or end-to-side
pancreaticojejunostomy to the proximal jejunum brought through a defect in the
mesocolon to the right of the middle colic artery. The pancreatic remnant should be
circumferentially cleared and mobilized for 2-3 cm to allow for an optimal 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 of
the pancreas and the seromuscular layers of the jejunum. The inner layer consists of
a running absorbable suture (or interrupted absorbable sutures) that incorporates
the capsule and a portion of the cut edge of the pancreas and the full thickness of the
jejunum. If possible, the inner layer incorporates the pancreatic duct to splay it
open. When completed, this anastomosis nicely invaginates the cut surface of the
pancreatic neck into the jejunal lumen.
The biliary anastomosis is typically performed with an end-to-side
hepaticojejunostomy approximately 10-15 cm down the jejunal limb from the
pancreaticojejunostomy (Fig. 8.3). This anastomosis is typically performed with a 8
single layer of interrupted absorbable sutures. In general, T-tubes are not used for
this anastomosis. If the patient has a percutaneous biliary stent then this is left in
place, traversing the anastomosis.
The third anastomosis performed is the duodenojejunostomy in cases of pylorus
preservation or the gastrojejunostomy in patients who have undergone classic
pancreaticoduodenectomy with distal gastrectomy. This anastomosis is typically per-
formed 10-15 cm downstream from the hepaticojejunostomy, proximal to the jejunum
traversing the defect in the mesocolon (Fig. 8.4). Alternatively, if a Roux-en-Y limb is
utilized, a fourth anastomosis between the jejunum and the jejunum is necessary.
After the reconstruction is completed, closed suction drains are left in place to
drain the biliary and pancreatic anastomoses. Some groups prefer not to place closed
suction drains, accepting that if a fluid collection becomes clinically evident postop-
eratively, percutaneous drainage by interventional radiology may be required.
Distal Pancreatectomy for Distal Pancreatic Cancer
Staging with laparoscopy is often of benefit in patients with distal pancreatic
cancers. If metastatic disease is found, distal pancreatectomy and splenectomy are
unlikely to help in the palliation of the patient. Exposure for a distal pancreatec-
tomy and splenectomy can be obtained through a vertical midline incision from the
xiphoid 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 mechanical
retracting device. Folded sheets placed behind the patient underlying the spleen can
also enhance exposure, especially in patients with a deep body habitus.
The lesser sac should be entered by elevating the greater omentum off the trans-
verse colon. The splenic flexure of the colon should also be mobilized caudally and
away from the spleen by dividing the lienocolic ligament. The spleen can technically
be preserved for benign disease; however, for cancer, most groups prefer to remove
Fig. 8.2. Pancreaticojejunostomy in two layers. Insert at bottom demonstrates how

the cut of the pancreas is intussuscepted within the jejunum using this technique.
the spleen en bloc to gain a wider margin and incorporate the lymph nodes in the
splenic hilum. The spleen is mobilized towards the midline by dividing the lienorenal
ligament with an electrocautery device. The short gastric vessels in the lienogastric
ligament should be also be isolated and ligated. A plane is then developed behind
the pancreatic tail and body, also mobilizing the splenic artery and vein. This dissec-
tion is continued several centimeters beyond the tumor. The splenic artery and vein
are isolated at this level out of the pancreas and are suture ligated. A row of overlapping
Fig. 8.3. Choledochojejunostomy.
“U” stitches of absorbable suture should then be placed. The electrocautery device is
then used to transect the pancreatic parenchyma distal to this suture line (Fig. 8.6).
A frozen section should be performed on the pancreatic margin to confirm clearance of
the lesion. The pancreatic remnant is then overseen to complete the resection. The
pancreatic remnant is then oversewn to complete the resection.
Fig. 8.4. Duodenojejunostomy. A two-layered hand-sewn anastomosis is completed

in this example of a pylorus-preserving pancreaticoduodenectomy.
Fig. 8.5. Roux-en-Y reconstruction after pancreaticoduodenectomy.
Suggested Reading
1. 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. 8.6. Distal pancreatectomy and splenectomy. This figure illustrates transections of
the pancreatic parenchyma using the electrocautery. The spleen is removed en bloc.
10. Trede M, Schwall G, Saeger H-D. Survival after pancreaticoduodenectomy: 118

consecutive 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, Ann
Surg 1997; 226:248-260.
12. Yeo CJ, Cameron JL, Maher MM et al. A prospective randomized trial of
pancreaticogastrostomy 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 1
CHAPTER 9
Hepatic Resection for Colorectal Liver

Metastases: Surgical Indications
and Outcomes
Introduction
The liver is a common site of metastasis for colorectal adenocarcinoma. Radical
surgical extirpation is the most effective therapy for colorectal hepatic metastases
and offers the only chance of cure. Recent improvements in radiologic imaging,
understanding of hepatic anatomy, surgical techniques, and perioperative care have
made liver resection safe. Consequently, the indications for hepatectomy have broad-
ened. Up to 85% of the liver may be resected because hepatic regeneration quickly
ensues and the liver regains its functional capacity. However, it is becoming increas-
ingly obvious that multimodality therapy must be utilized to improve upon the
current surgical results. Effective chemotherapy, either systemic or hepatic arterial,
and biologic or molecular therapy are needed to treat occult microscopic disease
that remains following complete gross tumor removal. This review encompasses the
epidemiology, preoperative evaluation, surgical indications, and surgical results for
patients with hepatic colorectal metastases.
Epidemiology
There are approximately 150,000 cases of primary colorectal cancer in the United
States each year. Hepatic metastases from colorectal cancer are common. About
25% of patients with colorectal carcinoma have liver metastases at the time of initial
presentation and an additional 25% will develop liver metastases, usually within the
first three years. Unlike liver metastases from other gastrointestinal neoplasms, those
from colorectal cancer may occur as a single metastasis or as a few tumors located in
a limited distribution. In the absence of systemic disease, these patients are ame-
nable to resection. Unfortunately, despite those favorable peculiarities, only about
5-10% of patients with liver metastases are resectable for cure.
History
The details of the primary colorectal cancer should be sought. It is important to
determine the location of the tumor, its nodal status, the operation performed, and
postoperative complications. It is customary to review the original pathology slides.
The type and duration of chemotherapy should be ascertained if it was administered.
Most patients with liver metastases from colorectal cancer are asymptomatic, although
large tumors may produce pain. Jaundice is uncommon but may be due to biliary
compression from either involved portal lymph nodes or a centrally placed tumor.
The patient should be questioned about alcohol use or previous hepatitis infection
either of which may impair liver regeneration following hepatectomy. The duration
since the patient’s last colonoscopy should be determined and, if indicated,
colonoscopy should be performed prior to hepatic resection.
Physical Examination
The examination of a patient with colorectal liver metastasis focuses primarily
on the general health of the patient. The cardiovascular status is of particular impor-
tance. Typically, only large or inferior masses are palpable on abdominal examina-
tion. Previous incisions should be noted, especially if laparoscopy or the placement
of a hepatic artery pump is intended. Rectal examination with stool guaiac should
always be performed.
Laboratory Tests
Standard liver function tests are often normal despite the presence of multiple
hepatic metastases. The serum carcinoembryonic antigen (CEA) level is a valuable
marker in those with recurrent colorectal cancer. However, there has been consider-
able debate as to whether vigilant surveillance of patients with resected primary
colorectal cancer impacts upon their survival. In fact, most studies have not shown
9 a survival advantage. However, relatively few patients have been studied and the
benefit in individual cases cannot be excluded. Therefore, the patient’s past CEA
levels, if any, should be determined and a new level drawn. Once patients develop
hepatic metastases, the CEA level is a useful marker of therapeutic response and is a
harbinger of further recurrence. It must be remembered that about 25% of tumors
do not secrete CEA.
Imaging
Radiologic imaging is a critical component of the preoperative investigation of a
patient with colorectal liver metastasis. In fact, it is often used to determine whether
the patient should be considered further for resection. There are now numerous
tests in the armamentarium of the radiologist for the characterization of hepatic
metastases (see Chapter 2). Helical computed tomography (CT) is currently the test
of choice. It is widely available and can rapidly acquire information regarding the
number, size, and location of intrahepatic tumors. The relationship to vascular and
biliary structures is depicted. Newer CT techniques utilize reconstructions to pro-
vide detailed information regarding hepatic artery and portal vein anatomy. CT also
surveys the presence of extrahepatic disease.
A variety of other radiologic tests have also proven useful in the assessment of
patients with colorectal metastasis to the liver. In the hands of a skilled
ultrasonographer, duplex ultrasound can detect small lesions, distinguish cysts from
solid lesions, and demonstrate the involvement or proximity to vascular and biliary
structures. Intraoperative ultrasound is routinely used to search for occult 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
Hepatic Resection for Colorectal Liver Metastases 123
differentiate benign tumors (especially hemangiomas) from malignant lesions. His-

torically, CT portography has been the gold standard for detecting colorectal
metastases. However, it is invasive and expensive and probably does not offer much
advantage over other imaging techniques. Arteriography is still used to define hepatic
arterial anatomy in preparation for hepatic artery pump placement but is likely to
be replaced by CT or MR angiography soon.
Positron emission tomography (PET) using 18F-fluorodeoxyglucose (18-FDG),
which is trapped in glucose avid tumor cells, is currently being studied in patients
with recurrent colorectal cancer. It probably has limited value for detecting occult
intrahepatic metastases but may prove useful in identifying extrahepatic disease
including nodal metastasis and pelvic recurrence. Exploratory laparoscopy is useful
to detect occult intrahepatic lesions, extrahepatic disease such as peritoneal dissemi-
nation, and unsuspected liver cirrhosis. It identifies unresectable disease in about
three-quarters of patients who cannot undergo liver resection. However, with the
increased use of intrahepatic pump chemotherapy and ablative techniques for
unresectable disease, it spares laparotomy in only about 10% of patients.
Preoperative biopsy of liver tumors in patients with a history of colorectal cancer
is rarely necessary. In the setting of a new liver mass or an elevation in the CEA level,
biopsy is not warranted since it carries the risk of tumor dissemination. Biopsy is
generally reserved for those patients with unresectable disease in order to confirm
the diagnosis.
Surgical Indications 9
A 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 cardiovascular
status of the patient should be investigated preoperatively, particularly in elderly
patients. However, age alone is not a contraindication for resection as it has been
shown that hepatectomy may be accomplished with similar morbidity, perioperative
mortality, and survival in patients greater than 70 years old.
Next, the primary colorectal cancer must be resected (or resectable) and the pres-
ence of other extrahepatic disease must be excluded. Extrahepatic disease signifies
unfavorable tumor biology and is associated with a poor outcome. The one excep-
tion is that selected patients with lung metastases from colorectal cancer may benefit
from both lung and liver resection. Preoperative workup should include a recent
colonoscopy, chest x-ray and chest CT. Bone scan and head CT are reserved for
patients with symptoms that suggest involvement of these sites. PET is an investiga-
tional test although many patients that are now referred to tertiary centers have
already undergone PET scanning.
Lastly, the intrahepatic disease and its relation to the major biliary and vascular
structures must allow for complete tumor clearance and preservation of an adequate
liver remnant. What exactly constitutes an adequate margin of resection has been
debated and there are conflicting data. Certainly, negative microscopic margins should
be emphasized. Whether a minimum margin of normal tissue is necessary is not
clear and it may not be attainable in many large and ill-placed tumors. Considerable
effort is now being focused on increasing resectability in patients with multiple,
diffuse tumors or an inadequate amount of uninvolved liver. Preoperative portal
vein embolization has been used recently to induce hypertrophy of the uninvolved
parenchyma in order to reduce the likelihood of postoperative liver failure in patients
who require sacrifice of a large proportion of functional liver. For instance, in patients
who require an extended right hepatectomy for a small tumor that is situated between
the middle and right hepatic veins, a percutaneous embolization of the right portal
vein (and possibly also the Segment IV branches) will induce hypertrophy of the left
lateral segment within a few weeks time. This may make the resection safer. Alterna-
tively, staged hepatectomies are also being performed in patients with multifocal
disease to provide tumor clearance in patients who do not have an adequate amount
of normal liver to undergo a single procedure. As more effective systemic 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 tumors
may benefit from a period of observation after the primary tumor is controlled to
allow for the development of additional liver metastases or to reveal unfavorable
biology that would render liver resection less effective. Patients with larger tumors
may be treated with simultaneous resection. However, patients requiring an extended
resection (especially an extended left hepatectomy) that entails removal of a large
proportion of functional liver parenchyma are generally treated with staged colorectal
and liver resections. Furthermore, when a low anterior resection or an abdomino-
9 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 liver
disease at the time of laparotomy for the primary colorectal tumors are probably
best served by avoiding wedge resections. Biopsy of the lesion is also usually unnec-
essary when the diagnosis is obvious. Patients should be staged postoperatively and
then undergo anatomic based-resection at a later date. Anatomic resection provides
better tumor clearance since the rate of positive margins is 2% versus up to 30% for
wedge resection. It also minimizes blood loss, reduces operative time, and preserves
normal tissue. In patients with metachronous liver colorectal metastases, similar
debate exists regarding the timing of operative intervention. Generally, patients with
small tumors, multifocal small tumors, and short disease-free intervals are observed
for a few months to better select those who will benefit from hepatectomy.
Surgical Results
Complications
Successful outcome in hepatic surgery depends largely upon minimizing 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 median
blood loss was 645 ml. Only 25% of patients required allogeneic transfusion of
packed red blood cells within the first day. Excessive blood loss is not only associated
with increased perioperative morbidity but also with a shorter time to recurrence
and decreased survival after resection of colorectal liver metastases.
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 overall
morbidity and mortality to that of lesser resections. Hemorrhage and liver failure
are the most serious complications after partial hepatectomy. Hemorrhage may occur
during the operation due to technical reasons or in the early postoperative course as
a result of coagulopathy or bleeding from the raw surface of the liver. Late postop-
erative bleeding may originate from the gastrointestinal tract in the setting of hepatic
dysfunction. Hepatic failure is often a sequela of bleeding or infection and may be
life-threatening. It occurs in just a few percent of patients. Cardiovascular events,
including myocardial infarction and pulmonary embolism, may be minimized
through careful preoperative evaluation, intraoperative deep venous thrombosis 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 is
also a concern, especially in patients who undergo resection of a large proportion of
their functioning parenchyma. Significant intra-abdominal fluid collections develop
postoperatively in about 15% of patients and manifest as a fever or leukocytosis.
Most collections contain serosanguinous fluid (or some bile) and usually can be 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 fistulas
are 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-
9
tion of colorectal liver metastases. This is in sharp contrast to the operative mortality
rates of up to 20% for hepatectomy just a few decades ago. The overall operative
mortality for the last 1,001 patients who underwent resection of colorectal metastases
at MSKCC was 2.8%. The decline in perioperative mortality is due to several fac-
tors. First, the surgical anatomy of the liver is now more precisely defined. Next, vast
improvements have been made in surgical techniques such as extrahepatic control of
the hepatic veins and segmental resections. Anesthetic techniques have also contrib-
uted greatly to reduce intraoperative blood loss through the use of low central venous
pressure during hepatectomy. Consequently, the retrohepatic inferior venal caval
dissection and parenchymal transection are accompanied by less blood loss. Impor-
tantly, low central venous pressure is not significantly associated with the develop-
ment of renal failure.
Survival
The results of surgical resection must be interpreted in the context of the natural
history of untreated colorectal metastases to the liver. Scheele reported a median
survival of 30 months in resected patients compared to 14.2 months in resectable
patients who did undergo hepatectomy and 6.9 months in unresectable patients. Of
the 983 patients who did not undergo resection, there were no 5-year survivors.
Others have reported similar findings with rare 5-year survivors in the absence of
surgical resection. In contrast, surgical resection of hepatic colorectal metastases has
been shown in recent series to result in 5-year survival rates of 25-37% (Table 9.1).
Median survival in our experience is 42 months. These results have been widely
reproduced and are consistent. Some cures are achieved as 10-year survival is about
Table 9.1. Results of resection for colorectal liver metastases

Operative Survival
Author N Mortality 1 yr 3 yr 5 yr
(%)
Foster JH
1978* 168 5 – – 20
Hughes KS
1986* 607 – – – 33
Rosen CB
1992 280 4 84 47 25
Gayowski TJ
1994 204 0 91 43 32
Scheele J
1995 434 4 85 45 33
Fong Y
1999 1,001 3 89 57 37
*multi-institutional series
20% and 20-year survival is 15%. In an analysis of 96 actual 5-year survivors at

MSKCC, the actuarial 10-year survival rate was 78%. No other treatment modality
has been shown to provide comparable results.
9 Nevertheless, despite convincing retrospective evidence, the value of hepatec-
tomy in prolonging survival and curing some patients has not been universally
accepted. Certainly, the patients who undergo resection have been selected because
of their favorable tumor biology, but resection appears to be of benefit even under
those circumstances. A prospective randomized trial has not been performed and
will likely never be done given the overwhelming evidence that has accumulated in
favor of hepatectomy.
Prognostic Variables
Several prognostic factors have been reported to predict survival after hepatic
resection of colorectal metastases. A multivariate analysis of the MSKCC data 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-free
interval from the primary to the first liver metastasis of less than 1 year, preoperative
CEA greater than 200 ng/ml, more than one liver tumor, and size of the largest
tumor greater than 5 cm. Patients with 0, 3, or 5 of these factors had 5-year survival
rates of 60, 20, and 14%, respectively.
The other two variables are the presence of extrahepatic disease or a positive
microscopic margin. The rate of positive hepatoduodenal lymph nodes has been
reported to be as high as 28% and is associated with poor survival. Although radical
portal lymphadenectomy is not routinely performed during liver resection for
colorectal metastasis, its addition must be considered. As noted previously, the
exception to extrahepatic disease is the presence of resectable lung metastases. A
group of 81 selected patients at our institution who had both liver and lung resection
(most had a single lung metastasis) for colorectal metastases actually had similar
survival as those who just had liver metastases alone.
The utility of these prognostic factors in the clinical management of an indi-
vidual patient is somewhat limited, however, although they may be used to avoid
surgery in a patient with compromised general medical health. Otherwise, only the
presence of extrahepatic disease and the inability to achieve complete tumor clear-
ance are absolute contraindications to resection. Patients who undergo palliative
resection or who have positive resection margins have been shown to have similar
survival as unresectable patients. Several authors have also stressed the need to obtain
a 1 cm margin noting a 45% 5-year survival with a 1 cm margin versus a 23% 5-year
survival with less than 1 cm. However, we have found that the presence of a negative
margin is most important and have found no difference between margins of less
than or greater than 1 cm.
Recurrent Hepatic Metastases
Partial hepatectomy for colorectal liver metastases only occasionally results in
cure since 80-90% of patients recur and most eventually die from their cancer. In
about a third of the patients who recur, the disease is isolated to the liver. Scheele
reported that on multivariate analysis, recurrence was predicted by satellite metastases,
size greater than 5 cm, nonanatomic liver resections, positive nodes in the primary
tumor, and synchronous colorectal and liver disease. In a recent MSKCC study, a
reduction in intrahepatic recurrence following partial hepatectomy for colorectal
metastasis from 40% to 10% at 2 years has been demonstrated with the addition of 9
adjuvant 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 received
pump and systemic therapy versus 72% for patients given intravenous chemotherapy
alone.
Subsets of the patients with isolated recurrence in the liver are candidates for
repeat hepatectomy that offers the only meaningful chance of prolonged survival.
The experience with repeat partial hepatectomy is scant because such resections
comprise less than 5% of all hepatectomies for colorectal metastasis (Table 9.2).
However, with the increasing safety of hepatic surgery, more reoperations for intra-
hepatic recurrence are now being performed. Although repeat hepatectomy is tech-
nically more challenging due to the presence of adhesions, the change in morphology
of the liver, and the altered position of the vasculature, the perioperative morbidity
and mortality are comparable to that of initial resections. Repeat hepatectomy results
in a 5-year survival as high as 42% in selected patients. Subsequent recurrence is
common and in our own experience, 20 of 25 patients recurred with a median
disease free interval of 9 months although median survival was 30 months. How-
ever, in the absence of any other effective therapy, patients with isolated liver recur-
rence should be considered for repeat hepatectomy.
Conclusion
Partial hepatectomy for hepatic colorectal metastases has become a safe and
effective therapy over the last two decades. Approximately one-third of patients will
achieve long-term survival, although only a small fraction will actually be cured.
Consequently, all patients should be evaluated for resection in the absence of
Table 9.2. Results of repeat resection for recurrent colorectal liver metastases
Operative Survival
Author N Mortality Morbidity 1 yr 3 yr 5 yr
(%)
Elias D
1993 28 4 32 85 35 –
Nordlinger B
1994* 116 1 25 78 33 –
Fong Y
1994 25 0 28 90 30 30
Fernandez-Trigo V
1994* 170 – 19 86 45 32
Adam R
1997 64 0 20 87 60 42
Yamamoto J
1999 90 48 31
*multi-institutional series
nonpulmonary extrahepatic disease. Patients who are borderline candidates for re-
section due to their distribution of disease, or limited amount of uninvolved paren-
9 chyma, may benefit from preoperative chemotherapy or portal vein embolization.
For recurrence after resection, repeat hepatectomy provides a survival benefit for
some patients. It is clear that further improvements in survival following hepatec-
tomy for colorectal metastases will depend on the development of more effective
adjuvant therapies. Adjuvant hepatic arterial chemotherapy appears to be one such
emerging approach.
Suggested Reading
1. Fong Y, Fortner J, Sun RL et al. Clinical score for predicting recurrence after hepatic
resection for metastatic colorectal cancer: Analysis of 1001 consecutive cases. Ann
Surg 1999; 230:309-318.
2. Kemeny N, Huang Y, Cohen AM et al. Hepatic arterial infusion of chemotherapy
after resection of hepatic metastases from colorectal cancer. N Engl J Med 1999;
341:2039-2048.
3. Scheele J, Stangl R, Altendorf-Hofmann A. Hepatic metastases from colorectal
carcinoma: impact of surgical resection on the natural history. Br J Surg 1990;
77:1241-1246.
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 colorectal
metastasis. Repeat Hepatic Metastases Registry. Surgery 1995; 117:296-304.
CHAPTER 1
CHAPTER 10
The Surgical Approach to Non-Colorectal

Liver Metastases: Patient Evaluation,
Selection and Results
Jonathan B. Koea
Introduction
Liver resection for metastatic cancer has been reported for over a century. How-
ever, it was not until 1977 when Foster and Berman published a report of liver
resection for a variety of several metastatic cancers that the concept gained general
acceptance. Subsequent investigators have demonstrated that hepatic resection for
metastatic colorectal cancer can be routinely undertaken with a perioperative mor-
tality of less than 5%, and a 5 year disease free survival of at least 30%. This is
significantly better than nonsurgical treatment with either chemotherapy or radia-
tion in terms of patient survival, treatment related complications, and mortality.
The role of hepatic resection and cytoablative techniques in the management of
non-colorectal metastases is less well defined, although for metastatic neuroendo-
crine tumors, hepatic resection appears to offer long-term palliation and a chance of
cure. 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 interest
in the resection of liver metastases from a variety of non-colorectal cancers. While in
many centers these patients are still considered to be incurable and are managed
solely based upon symptoms, there is a growing body of literature suggesting that
aggressive treatment of selected patients results in an improved quality of life, pro-
longed survival and possible cure (Fig. 10.1).
This Chapter reviews the methods of investigation, patient selection, and results
for resection and cytoreductive techniques in the management of non-colorectal
liver metastases. It must be emphasized that little is currently known of the natural
history of resected metastases in many conditions, and as such, only carefully se-
lected patients should be considered for aggressive management as part of prospec-
tive clinical series and trials.
Patient Selection
Tumor Biology
Hepatic resection of colorectal and liver metastases has yielded a 30%, five-year
disease-free survival in most series. A variety of tumor and patient prognostic vari-
ables have been put forth to aid in the selection of patients for hepatic resection.
Fig. 10.1. Comparison of survival in 96 patients undergoing liver resection for

noncolorectal, nonneuroendocrine metastases with 577 patients undergoing liver
resection for colorectal metastases. Reprinted with permission from Harrison LH,
Brennan MF, Newman E et al. Surgery 121:625-633, 1997.
Disease Free Interval

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

In most solid tumors, the presence of untreated extrahepatic disease significantly
limits the prospect of patient cure. Great effort is typically made during preopera-
tive staging examinations to detect occult disease within the chest and peritoneal
cavities and thus limit unnecessary surgical explorations. If hepatic resection is to be
undertaken, complete resection of all intra-abdominal tumor deposits is mandatory,
and in nearly all instances, noncurative resection offers no survival alternatives beyond
supportive therapy (Fig. 10.3). The exceptions to this rule are:
1. nonfunctioning neuroendocrine tumors, since the growth rate of this 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, and
4. ovarian carcinoma, since the benefits of tumor debulking have been docu-
mented and effective adjuvant chemotherapy is available in some instances.
The Surgical Approach to Non-Colorectal Liver Metastases 131
Fig. 10.2. Comparison of survival after liver resection for noncolorectal,

nonneuroendocrine metastases for patients with a disease free interval (DFI) of less
than 36 months with those with a DFI of more than 36 months. * p < 0.05 log rank
test. Reprinted with permission from Harrison LH, Brennan MF, Newman E et al.
Surgery 121:625-633, 1997.
10
Fig. 10.3. Comparison of survival after liver resection for noncolorectal,

nonneuroendocrine metastases for patients with curative intent and those resected
with palliative intent. * p < 0.05 log rank test. Reprinted with permission from
Harrison LH, Brennan MF, Newman E et al. Surgery 121:625-633, 1997.
Patient Performance Status

Adequate patient performance status is an important prerequisite for hepatic
resections of any type and can be quantified using the Karnofsky Performance Score
(KPS) (Table 10.1). An adequate level of preoperative functioning is necessary to

not only survive surgical intervention, but also to permit patient ambulation and
efforts in the rehabilitation process. Poor patient functional status (KPS < 50) usu-
ally indicates significant comorbidities that render resection unsafe, or significant
occult metastatic disease that would render resection unwise. In particular, hepatic
resection in patients with cirrhosis is associated with a mortality of 5-15% and mor-
bidity rates of 30-50%. Patients with Childs B or C cirrhosis are not candidates for
hepatic resection (Table 10.2).
Preoperative Staging
History and Physical Examination
A thorough medical history and physical examination represent a critical part of
the staging process. The history should concentrate on clarifying presentation and
treatment of the primary lesion. It is important to obtain copies of the original
operative records and the pathology. If there is doubt over the tissue diagnosis, patho-
logical slides should be reviewed. It is often useful to have a preoperative discussion
with the surgeon who operated on the primary lesion. The patient’s prior medical
history should be elicited with particular reference to the presence and severity of
comorbid conditions and KPS. It is also important to investigate the patient’s family
history with respect to familial cancer syndromes and elucidate the patient’s social
situation in terms of support and caregivers who will be available to assist with
rehabilitation.
The physical examination should be thorough while concentrating on excluding
10 sites of extrahepatic disease (lymphadenopathy, pleural effusions, ascites and cuta-
neous metastases), identifying significant comorbid conditions and detecting signs
of liver disease or decompensation (spider nevi, tremor, ascites, abnormal collateral
vessels).
An important part of this interview is simply to get to know the patient. Most
patients with metastatic disease will be patients for life and while some have unreal-
istic expectations of treatment goals, most simply want an honest assessment of
their condition and sound advice about their therapeutic options. Time spent in
defining the patient’s goals and expectations in this initial phase will facilitate the
remainder of the preoperative and postoperative management.
Optimal staging investigations will be partially dictated by the findings on the
history and physical examination, with any unexplained symptoms such as weak-
ness or bone pain mandating specific investigation. However, even in asymptomatic
patients, 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 Profile
The 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 a
hemoglobin of 10 g/dl, is necessary for safe elective hepatic surgery.
Table 10.1. Karnofsky Performance Status

Score
90-100 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 Points
1 2 3
Albumin (g/dl) >3.5 2.8-3.5 <2.8
Bilirubin (mmol/l) <25 25-40 >40
Prothrombin time <4x normal 4-6x normal >6x normal
Ascites None Mild Moderate
Encephalopathy None Mild Moderate
Childs A = 5-6 points; Childs B = 7-9 points; Childs C = 9-15 points.
10
Serum Electrolytes and Liver Function Tests
Serum electrolyte determinations are undertaken to define asymptomatic renal
dysfunction and unexpected electrolyte abnormalities. Serum creatinine does not
rise significantly until renal function is reduced by a factor of 50%. The prevalence
of 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 limited
information 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.
Electrocardiogram
Electrocardiography is useful to detect evidence of previous myocardial infarc-
tion or asymptomatic rhythm disturbance. It is mandatory in any patient with a
history of cardiopulmonary disease or age > 40 years. In patients with a history of
significant cardiac disease, an echocardiogram and an assessment of cardiac perfu-
sion is usually indicated.
Chest Radiograph
Postero-anterior and lateral radiographs of the chest should be obtained preop-
eratively. The most commonly detected abnormality is cardiac enlargement or chronic
obstructive pulmonary disease. The frequency of these abnormalities is related to
patient age. In patients less than 5 years of age, abnormalities were found in 7.5% of
chest radiographs, while in 5% of patients over 40 years of age.
Bone Scans
Whole body radionuclide bone scanning should be undertaken in patients with
bony symptomatology to define osteolytic metastases. Plain radiographs of the area
should also be performed. There is little evidence that whole body bone scans are of
benefit in asymptomatic patients.
Computed Tomography
Computed tomographic (CT) scans of the brain are indicated in patients with
new or unexplained neurological symptoms; however, this examination has no value
as a screening examination in asymptomatic patients.
Although we have shown that CT of the chest is not useful in selecting colorectal
cancer patients for hepatic resection, we feel that CT scans of the chest, abdomen and
pelvis should be carried out in all patients with noncolorectal hepatic metastases. Both
bone and lung windows should be constructed for chest scans to define occult meta-
static disease. Noncontrast and contrast enhanced scans of the abdominal cavity and
pelvis should be performed with particular attention to demonstrating the intra-ab-
dominal lymph node basins. CT portography should also be considered, as this is often
the most effective means to demonstrate hepatic metastases. In addition it will provide
valuable information regarding the relationship of lesions to vascular structures.
Positron Emission Tomography
Positron 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 undergoes
10 phophorylation by hexokinases to FDG-6-phosphate, and is selectively retained
within tumor cells. The sensitivity of PET scanning for most tumors is currently
unknown. However, Fong et al have recently assessed the use of PET scanning in
patients with metastatic colorectal cancer. These investigators found that PET scans
altered clinical management in 23% of cases of metastatic colorectal carcinoma by
identifying unsuspected extra-hepatic disease. In addition, 17% of patients with
positive PET findings directed surgical biopsy that proved unresectable extra hepatic
disease. PET scanning was not as sensitive at defining small (< 1 cm in diameter)
peritoneal deposits and additional intrahepatic lesions. These results imply that PET
may be a useful investigational modality for defining extrahepatic disease in patients
with metastatic colorectal carcinoma. Although its effectiveness in preoperative clinical
staging of other solid tumors is unknown, PET scanning should be considered in all
patients with non-colorectal non-neuroendocrine metastases prior to hepatic
resection.
Magnetic Resonance Imaging
MRI of the liver is useful in defining unsuspected intrahepatic disease not visu-
alized on CT or CT portography. In addition, MR cholangiography and MR
angiography represent noninvasive investigations that define abnormalities in the
biliary and hepatic arterial systems.
Diagnostic Laparoscopy, Laparoscopic Ultrasound,

and Peritoneal Cytology
The increased availability and sensitivity of MR and CT scanning has led to
increased reliance on these imaging modalities. Diagnostic laparoscopy has proven
useful in the staging of upper gastrointestinal malignancies, particularly gastric and
pancreatic carcinoma. Its use in primary and secondary hepatobiliary cancers was
recently assessed by Jarnagin et al. These investigators demonstrated that laparoscopy
identified 26 of 39 patients with unresectable disease in a heterogeneous group of
primary and secondary hepatobiliary cancers. In patients who underwent only stag-
ing laparoscopy rather than exploratory laparotomy, laparoscopic staging resulted in
a reduced length of hospital stay (2.2 versus 8.6 days) and hospital charges in compari-
son to laparotomy. Laparoscopy was most useful in detecting unexpected peritoneal
metastases (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 anatomical
relationship of metastatic lesions to intrahepatic vasculature and locating small intrahe-
patic lesions that were not defined on preoperative radiological investigation. Whether
this technique should be performed routinely is at present unclear.
The use of peritoneal cytology to define occult peritoneal metastatic disease
has gained increased attention with regard to pancreatic cancer and gastric cancer,
two diseases in which potential recurrence is common. Whatever the particular
cytology, the routine use of peritoneal cytology as a potential staging tool requires
further investigation.
Preoperative Preparation 10
Staging
All patients with non-colorectal metastases should be subjected to extensive pre-
operative clinical and radiological staging. Asymptomatic patients with extrahepatic
disease are not considered for surgical resection. Patients with symptomatic hepatic
metastases can be candidates for either nonoperative treatment, such as transarterial
embolization, radiofrequency ablation, alcohol injection, or in rare instances, palliative
hepatic resection.
Informed consent should be obtained from all patients. This should include a
full description of the nature of the procedure, anticipated benefits, possible com-
plications and treatment alternatives. For many tumors (i.e., metastatic ovarian,
testicular and neuroendocrine), effective adjuvant chemotherapy is available and
coordinated discussions between the treating medical oncologists, radiation
oncologists, interventional radiologists and others, is a vital part of the preoperative
evaluation. Ideally, discussions relating to the care of these complex patients should
occur at combined medical/surgical management conferences.
Operative Technique
Laparoscopy
Although laparoscopy can be performed under local anesthesia, staging
laparoscopic examinations should be performed using general anesthesia to allow
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 not
performed or thorough examination of the bowel or lesser sac was omitted.
With the patient supine, a 12 mm Hasson cannula is inserted into the abdomi-
nal cavity under direct vision using an open technique. In the Hepatobiliary Service
at Memorial Sloan-Kettering Cancer Center (MSKCC), the trocar is placed in the
right or left upper quadrant along the line of the planned bilateral subcostal inci-
sion. Intra-abdominal examination is carried out using a 30 degree angled scope. A
10 mm port can be placed in the contralateral upper quadrant for the purposes of
peritoneal lavage and biopsy. If laparoscopic ultrasound is available this can directed
toward the liver. A 5 or 10 mm port can be added in the left upper quadrant for
retraction and biopsy. Before undertaking formal staging, any ascitic fluid should be
aspirated and sent for cytology. At our own institution, 200 ml of normal saline is
then instilled and specimens for cytology study purposes are aspirated from the
pelvis and both subphrenic spaces. If present, peritoneal adhesions should be di-
vided and a thorough, systematic examination of the peritoneal cavity carried out.
The parietal peritoneum over the hemi-diaphragms, anterior abdominal wall and
pelvis should be examined for metastatic disease and carefully inspected. With the
patient in 30˚ of reverse Trendelenburg and 10˚ of left lateral tilt, the anterior and
posterior surfaces of the left lobe can be directly seen. It may be possible to perform
bimanual palpation of the liver using a grasping forceps inserted via a 5 mm port.
Identification of deeply placed hepatic lesions can be undertaken with laparoscopic
ultrasound using a 7.5 MHz probe inserted through the right upper quadrant port.
10 The transverse colon should then be elevated and the inferior surface of the
transverse mesocolon inspected. An assessment of nodal disease along root of the
mesentery and the ligament of Treitz is then carried out. The small intestine and its
mesentery should be inspected for metastases. Peritoneal or liver biopsies should be
taken at this point and sent for frozen section examination. An assessment should be
made of the mobility of the stomach and direct extension of disease to liver, spleen,
colon or duodenum. Entry into the lesser sac by incising the gastrohepatic ligament
permits evaluation of the caudate lobe and lymph nodes in the porta hepatitis and
celiac areas.
At completion of the procedure, a 10 mm port site should be closed and 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 surgery
under the same general anesthetic.
Techniques of Resection
A detailed description of the techniques for liver resection is provided in Chap-
ter 16. In brief, all liver resections are performed under controlled central venous
pressure (CVP) maintained at less than 5 mmHg. This permits easy control of blood
loss if a major hepatic vein or the interior vena cava is entered. Dissection is per-
formed with the patient in a 15˚ Trendelenburg. A bilateral subcostal incision is
made and a midline vertical extension is used if required for adequate exposure. The
segment of liver to be resected is mobilized by detaching all ligamentous attach-
ments. Alternatively, a right subcostal incision with midline extension is adequate

for most resections. The falciform ligament is dissected close to the liver to expose
the suprahepatic IVC and the hepatic veins above the liver. Hilar structures are
controlled by extrahepatic dissection of the porta hepatitis. Intraoperative ultra-
sonography is performed to assess the liver for additional lesions and to confirm the
hepatic vascular anatomy in relation to the tumor.
Prior to transection of the right hepatic vein, the portal and hepatic arterial in
flow are divided using the techniques discussed in more detail in Chapter 16.
For right-sided resections, the hepatic veins are divided sequentially from the
lower border of the liver progressing upward until the right hepatic vein is isolated.
The right hepatic vein is either stapled or cross-clamped, divided and oversewn. For
left-sided resections, the left and middle hepatic veins are isolated by dissection at
the upper border of the ligamentum venosum and similarly divided after control of
the left hepatic inflow.
Transection of the parenchyma is performed using a tissue crushing technique to
permit identification of small vessels and biliary radicals which are controlled by
hemoclips. Large intrahepatic veins are suture ligated. Parenchymal division is per-
formed using intermittent inflow occlusion (Pringle maneuver) which is released
every 5-10 minutes to relieve portal venous congestion and permit hepatic perfu-
sion. As alluded to above, hepatic outflow control is obtained prior to parenchymal
division in most cases.
Tumor debulking and enucleation techniques can be utilized in the manage-
ment of patients with metastatic neuroendocrine disease. Tumor debulking is car-
ried out with inflow occlusion and can be undertaken by parenchymal division at
the margin of the lesion. There is often an avascular plane which, once entered, 10
allows removal of metastatic neuroendocrine disease with a narrow surrounding
margin of normal parenchyma. This often provides long term symptomatic relief
for these patients. In addition, cryotherapy assisted resection is also useful in the
management of metastatic lesions. This technique utilizes initial cryotherapy of the
lesion, followed by wedge resection of the iceball and a margin of hepatic tissue,
using parenchymal division with intermittent in flow occlusion (Fig. 10.3). For a
more detailed description see Chapter 18.
Nonoperative Techniques
There are currently three techniques of nonresectional therapy widely in use.
Transarterial particle embolization has been in continuous clinical use for the last 25
years. Advances in percutaneous arterial puncture technique and flexible catheter
technology have enabled interventional radiologists to cannulate intrahepatic arte-
rial branches using a femoral artery approach, and to selectively occlude these branches
using inert particles of latex or Ivalon sponge to reduce ischemic tumor infarction.
This technique is well-established and results in complete tumor necrosis in
approximately 70% of patients with hepatocellular carcinomas (HCC) or neuroen-
docrine tumors. The reported mortality rate is <1% with a morbidity rate of 5%.
Percutaneous ethanol injection techniques, typically performed for HCC, make use
of either CT or ultrasound to guide needle placement into the tumor. It may result
in complete tumor necrosis in 60% of HCC with a low morbidity rate (~5%).
Radiofrequency thermal ablation (RFA) represents a new technique for the treatment
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 lesion
using ultrasound guidance. Heating of the electrode tip, when placed within a tu-
mor, results in tumor ablation. Initial experience with this technique indicates that
complete tumor necrosis can be achieved in over 90% of patients with low mortality
(<1%) and morbidity (10%). Whether radiofrequency thermal ablation of a tumor
translates 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 related
concerns or significant comorbidities should be referred for some type of
nonresectional therapy preferably within a clinical trial. At present, there are no
guidelines to assess the relative merits of these various techniques. However, each
technique does not only offer the opportunity to ablate metastatic disease, but may
also be useful to relieve tumor-related symptoms with low rates of complication.
Results
Neuroendocrine Metastases
The surgical management of hepatic metastases from neuroendocrine carcinoma
is currently in evolution. These tumors are rare and significant numbers are seen
only in a few centers which focus on treating hepatobiliary malignancies. Neuroen-
docrine tumors generally follow an indolent course with a mean survival of 8 years
reported in untreated patients with advanced metastatic disease. This long natural
history makes defining the effectiveness of therapeutic intervention difficult and has
engendered a conservative attitude toward radical treatment. However, three quar-
10 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 interest
in aggressive management have emerged. Recent experience has demonstrated that
complete surgical resection can produce significant symptom relief and a cure rate
of 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 37
patients treated with hepatic resection. Curative resection was undertaken in 17
patients and palliative resection in 20; 11 were disease free at a median follow up of
19 months. Palliative resection resulted in complete relief of symptoms in 60%,
incomplete relief in 35%, and one postoperative death. An additional 74 patients
have 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 operative
mortality in this series was 2.7%.
The long natural history of these lesions has also made it acceptable to treat large
tumor deposits with enucleation rather than formal hepatic lobectomy as this will
often result in long-term disease control. Soreide et al have presented the results of
repetitive debulking in 75 patients. Only half of these patients had liver-directed
surgery and only four hepatic resections were performed. Despite seven postopera-
tive deaths, this therapy resulted in a 3-fold increase in median survival (216 months
in treated patients vs 48 months in untreated patients).
There is currently controversy regarding the importance of resection of the primary
tumor in patients with neuroendocrine carcinoma metastatic to the liver. Chamberlain
et al have recently reviewed the experience at MSKCC with this condition. These
The Surgical Approach to Non-Colorectal Liver Metastases
Table 10.3. Summary of significant reported series of hepatic resection for neuroendocrine metastases
Reference N Histology Curative Palliative Operative Relief of Survival
Mortality 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 months

median
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)
139
10
investigators compared outcomes in patients who had concomitant resection of the

primary lesion at the time of the hepatic resection with those who had the primary
tumor 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 be
removed. Similarly, palliative surgical resection should be considered for symptom
control if at least 90% of tumor volume can be removed. Palliative resection in the
absence of symptoms should also be considered in patients with tumors located
adjacent to or threatening vital structures. Paradoxically, these patients should come
for early resection as continued growth of strategically placed tumors often renders
them 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 demonstrated
a 96% response rate for both hormonal and pressure related symptoms following
embolization. The procedure related mortality was 6% in this series. However, it is
unclear whether embolization results in improved survival in these patients.
Orthotropic liver transplantation has been undertaken in patients with metastatic
neuroendocrine carcinoma, but the results have been disappointing with approxi-
mately 90% of patients dying as a result of recurrent disease within 12 months of
transplantation.
10 Non-colorectal, Non-Neuroendocrine Metastases

The results of major clinical series reporting curative hepatic resections for non-
colorectal, non-neuroendocrine metastases are summarized in Table 10.4. Because
of the limited experience with this type of hepatic resection, most clinical series are
small and report results collectively rather than by tumor types. Few series specify
the total numbers of cases operated upon and concentrate on discussing long-term
survivors. It is therefore difficult to clarify the total number of patients who are
eligible for hepatic resection or the effectiveness of surgical treatment.
Head and Neck
The 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 Harrison
and Schwartz report survivors following resection of metastatic parotid and thyroid
carcinomas indicating that these tumors may have a more indolent biology and
resection may be considered in selected cases.
Lung
The results of hepatic resection for metastatic carcinoma of the lung are poor.
Schwartz reported on five patients with metastatic lung cancer who underwent liver
resection. There were no long-term survivors. Lindell reported the only long-term
survivor (185 months), a patient who underwent resection of bronchial carcinoma
metastatic to the liver.
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 of
Curative Survivors Survivors Survivors
Resections 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 11
24-26
Sarcoma* 3,21,22,27 63 15 6
18,19,25
Periampullary 20,21, 22 2 3
25,27
Melanoma 3,19-22, 36 4 3 10
25,27 10
Renal/Wilms 21,25 3, 41 12 12
18-20,22
Uterine 3,19-22, 15 3 1
25,27
Ovarian 3,19-22,27 10 1 2
Testicular 3,18 25 1
Adreno- 3,19,21, 14 1 1 5
cortical 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 cases

from Memorial Sloan-Kettering Cancer Center.
Esophagogastric
Ochiai 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 and
gastrectomy were performed in 21 patients. The median interval between gastric
and hepatic resection in the remaining 8 patients was 21 months. Four patients (4/
29%) survived more than five years following gastric resection. Among patients
undergoing synchronous resection, the presence of serosal invasion was the single
prognostic factor that could be assessed during surgery. Among patients undergoing
metachronous resection, the authors found that if lymphatic and venous invasion
by the primary tumor was present, hepatic resection was unlikely to be of benefit.
These investigators emphasized that metastatic disease restricted to the liver is rare
in gastric cancer in the absence of significant lymph node involvement and perito-
neal disease. Miyazaki et al also emphasized the importance of an adequate surgical
margin and number of lesions in the resection of gastric metastases. The majority of
patients (69%) in their series who developed recurrent hepatic disease had multiple
lesions that were resected with margins of < 10 mm. Bines et al demonstrated that en
bloc resection of large gastric tumors which directly invade the liver may result in
long-term survival. Two of three patients in their series survived 10 years. These
authors argued strongly against hepatic resection for synchronous or discontinuous
metastases under any circumstance.
Pancreas/Periampullary
Hepatic resection of metastatic adenocarcinoma of the pancreas has not resulted
in any documented long-term survivors. In comparison, Berney has reported two
10 survivors following hepatic resection for metastatic ampullary cancer and cystad-
enocarcinoma of the pancreas at 70 and 84 months, respectively. Malt and Elias
have emphasized that in patients who present with hepatic metastases of unknown
primary, the majority will harbor a primary tumor in the pancreas or colon.
Renal Carcinoma/Wilms Tumor
A number of investigators have demonstrated that long term survival is possible
following hepatic resection for both renal cell carcinoma and Wilms tumor. Schwartz
reported that four patients out of a total of 13 who underwent hepatic resection for
metastatic renal cell cancer survived longer than 5 years. In 20 patients with Wilms
tumor, seven were alive and free of disease 5 years after hepatic resection. Foster has
also 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 resection
for metastatic renal cell carcinoma and Wilms tumor are very similar to those for
metastatic colorectal carcinoma. Consequently, hepatic resection for solitary meta-
static lesions from primary renal carcinoma and Wilms tumor should be strongly
considered 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 no
outcome data available for this technique.
Melanoma
The results for hepatic resection of metastatic melanoma are poor. However,
Harrison has reported two 5 year survivors following hepatic resection. In contrast,
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 localized
disease. 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 adjuvant
immunotherapy.
Sarcoma
The most common sarcoma to metastasize to the liver is a gastrointestinal stro-
mal tumor. If localized to the liver, resection appears worthwhile. Harrison reported
27 patients with metastatic sarcoma, the majority being gastrointestinal stromal tu-
mors, with a median survival of 31 months with one 5-year survivor.
Ovarian
Hepatic resection for metastatic genitourinary tumors is generally associated with
a favorable outcome. In the series reported by Harrison et al, hepatic resection was
performed in 34 patients with metastatic genitourinary tumors and was associated
with 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 to
emphasize that most ovarian carcinomas are actually extrahepatic lesions which grow
into the liver, and in these patients, the primary aim of surgery is operative debulking
to enhance the effects of postoperative chemotherapy. 10
Adrenocortical
Resection of metastatic adrenocortical carcinoma is associated with a 20-30%
long term survivorship. Harrison et al reported seven resections with two long-term
survivors. Schwartz reported two long-term survivors (131 and 132 months,
respectively) out of eight patients undergoing resection.
Breast
Systemic chemotherapy remains the mainstay of therapy for patients with local-
ized and advanced breast cancer. Hepatic resection has been undertaken in highly
selected patients with solitary breast metastases. Nineteen patients with metastatic
breast carcinoma have been considered for hepatic resection at MSKCC with a median
of 46 months from resection of the primary to hepatic resection. Laparoscopy revealed
extrahepatic 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 hepatic
lesions (> 2) and the presence of positive resection margins were adverse prognostic
factors. Elias et al point out that metastases should be isolated and chemosensitive if
resection is to be considered, while also noting that up to 30% of patients will also
have involved hilar lymph nodes.
Conclusions
Although there is no prospective data or published randomized trials, there are
sufficient retrospective studies to demonstrate that hepatic resection for metastatic
Fig. 10.4. Comparison of survival after liver resection for genitourinary cancers, soft
tissue tumors (including melanoma) and gastrointestinal tumors. * p < 0.05 log rank
test. Reprinted with permission from Harrison LH, Brennan MF, Newman E et al.
cancer is safe and can be undertaken with acceptable morbidity and mortality. Little
is currently known about the natural history of treated metastases since, historically,
10 patients with metastatic disease were regarded as incurable and managed symptom-
atically. However, it is clear that aggressive resection does, in some cases, result in
significant survival advantage. Overall, the survival rates for melanoma and stomach
primaries are close to 30% at three years although less than 20% at five years. For
carcinoma of the testis, renal cell carcinoma, Wilms tumor, gynecological tumors,
and gastrointestinal stromal tumors, survival is close to 50% at three years. The
indications for hepatic resection should be cautiously expanded to include patients
with these tumors. Careful patient selection should be undertaken with preopera-
tive staging investigations prior to resection. All patients should become part of
prospective clinical protocols. In addition, every attempt should be made to treat
patients postoperatively with any available adjuvant therapies to optimize their chance
of disease-free survival.
Selected Reading
1. 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 consecutive
cases. Ann Surg 1999; 230:309-321.
3. Harrison LE, Brennan MF, Newman E et al. Hepatic resection for noncolorectal
nonneuroendocrine 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 emission
tomography scanning on selection of patients for resection of hepatic colorectal
metastases. Am J Surg 1999; 178:282-287.
5. Jarnagin WR, Bodniewicz J, Dougherty E et al. Prospective analysis of staging

laparoscopy in patients with primary and secondary hepatobiliary malignancies. J
Gastrointestinal Surg 2000; 4:34-44.
6. Billingsley KG, Jarnagin WR, Fong Y et al. Segment-orientated hepatic resection
in 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 assist
hepatic resection. J Am Coll Surg 1995; 180:171-176.
8. Norton JA, Doherty GM, Fraker DL et al. Surgical treatment of localized gastrinoma
within the liver: A prospective study. Surgery 1998; 124:1145-1152.
9. McEntee GP, Nagorney DM, Kvols LK et al. Cytoreductive hepatic surgery for
neuroendocrine 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 patients
with 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 for
control 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 carcinoid
tumors. World J Surg 1990; 14:377-385.
16. Doussett B, Saint-Marc O, Pitre J et al. Metastatic endocrine tumors: medical
treatment, surgical resections or liver transplantation. World J Surg 1996;
20:908-915.
10
17. Chen H, Hardcare JM, Uzar A et al. Isolated liver metastases from neuroendocrine
tumors: 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 liver
metastases from a noncolorectal primary: Indications and results based on 147
monocentric 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 J
Surg 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 Surg
1988; 208:421-434.
23. Ochiai T, Sasako S, Mizuno S et al. Hepatic resection for metastatic tumors from
gastric 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 from
gastric 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 multiple
hepatic resections of liver tumors originating from primary gastric tumors. Surgery
1993; 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 Open

Cholecystectomy
Introduction
Gallstones are extremely common throughout the Western world and are found
in approximately 10% of the adult population. Gallstones occur twice as commonly
in 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 Pima
Indians have a reported incidence of gallstones that may approach or surpass 50% of
the adult population.
The majority of gallstones remain asymptomatic and silent throughout the life
of an affected individual and it is estimated that only 20-30% of all patients ever
develop symptoms. The risk of a patient with asymptomatic gallstones developing
biliary-related symptoms is estimated at 1-2% per year, with a risk of 0.1% per year
of developing severe complications such as gallbladder perforation or empyema.
In nearly all cases, cholecystectomy is the treatment of choice for symptomatic
gallstones. At present, cholecystectomy is the most common elective operation per-
formed worldwide, with approximately 500,000 cholecystectomies performed
annually (1990 figures). It seems reasonable to surmise that this number has increased
with the advent and widespread application of laparoscopic cholecystectomy tech-
niques. The indications for cholecystectomy are variable. In most series, 70-80% of
patients undergo elective cholecystectomy for chronic cholecystitis or biliary colic
in conjunction with ultrasonographic evidence of gallstones. Only 10-30% of patients
undergo cholecystectomy due to complications of acute cholecystitis.
The 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 result
of inflammation due to cystic duct obstruction by a gallstone impacting in Hartmann’s
pouch. Interestingly, although bile remains stagnant within the gallbladder over long
periods of time, bacterial contamination of the gallbladder is not routine. Indeed, at
the time of operative cholecystectomy, 60-70% of gallbladder cultures are sterile. If
organisms 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 acute
gallbladder inflammatory changes were due to coincident bacterial infection is prob-
ably false. Indeed, the current consensus is that the initial cascade of events leading

Surgical Techniques of Open Cholecystectomy 147
to acute biliary colic and acute cholecystitis is mucosal damage due to trauma from
an impacted gallstone that sets off an inflammatory cascade and resultant symp-
toms. Classically, biliary colic is characterized by the acute onset of right upper
quadrant pain, with or without radiation to the back or right scapular area. Clinical
interview can frequently elicit a history of less severe episodes of similar pain often
preceded by nausea and vomiting. In the case of acute cholecystitis, patients are
often febrile and may demonstrate some degree of abdominal rigidity and a Murphy’s
sign indicating an underlying peritoneal irritation from the distended and inflamed
gallbladder. Jaundice is rare in the setting of both acute and chronic cholecystitis
and, when present, should suggest the presence of choledocholithiasis, secondary
cholangitis, or partial obstruction of the common duct by either edema or a stone
(Mirizzi’s syndrome). Physical exam may demonstrate right upper quadrant pain
and at times abdominal rigidity. A palpable gallbladder or mass in the right upper
quadrant is present in up to 25% of cases. In general, making the diagnosis of acute
cholecystitis is not difficult with the differential generally limited to peptic ulcer
disease, gastroenteritis, acute pancreatitis, retrocecal appendicitis, or right-sided
diverticulitis. Laboratory evaluation is generally nonspecific and demonstrates only
a leukocytosis. In the setting of choledocholithiasis or cholangitis, elevation of the
serum bilirubin and alkaline phosphatemia are present. An elevated amylase level is
present in the setting of gallstone pancreatitis and may help exclude other diagnoses.
Chronic cholelithiasis typically presents with severe pain characteristic of biliary
tract 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 pain
arising from chronic cholecystitis, or “biliary colic,” is manifested by right upper
quadrant abdominal pain occurring in association with eating a fatty meal. As with
acute cholecystitis, pain often radiates to the scapular area and is associated with
nausea and occasional vomiting. However, these symptoms are not specific and the 11
differential diagnosis is broad and includes peptic ulcer disease, gastroesophageal
reflux, 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 Studies
The 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, and
in the setting of complicated acute cholecystitis, evidence of emphysematous chole-
cystitis with air in the gallbladder wall may also be appreciated. Pneumobilia, or air
in the biliary tree, normally indicates the presence of a cholecystoenteric fistula and
if appropriate, the diagnosis of gallstones ileus may be entertained.
Ultrasonography should be the initial study performed if the diagnosis of either
acute or chronic cholecystitis is considered. Ultrasound is quick, noninvasive and
easily obtainable. Characteristic ultrasound findings of acute cholecystitis include a
thickened gallbladder wall with the presence of posterior acoustical shadowing from
stones contained within the gallbladder. Occasionally, no stones are seen and mate-
rial described as biliary sludge or mucosal sloughing may be noted. These findings
are common in the setting of acalculous cholecystitis. Air in the gallbladder wall,
gallbladder wall thickening, and pericholecystic fluid are also common with severe
disease. Calcifications of the entire gallbladder wall, the so-called “porcelain
gallbladder,” or the presence of gallbladder polyps, should raise a concern of a
possible malignancy.
Gallbladder scintigraphy is commonly used to confirm the diagnosis of acute
cholecystitis. In this setting, aminodiacetic acid derivatives (HIDA) are used to dem-
onstrate a functioning or nonfunctioning gallbladder. This test has a sensitivity and
specificity in the range of 97% and 87%, and is regarded by many as most accurate
test. The absence of isotope uptake within the gallbladder is generally regarded as an
indication of cystic duct obstruction (Fig. 11.1). The presence of isotope in the
pericholecystic area outside the gallbladder is a valuable secondary benefit of an
HIDA scan and often correlates with the presence of gangrenous cholecystitis or
gallbladder perforation. Note the results of an HIDA scan may be inaccurate in the
setting of significant hyperbilirubinemia (>5 mg/dl), in which case cholecystitis limits
biliary flow.
Additional imaging modalities that may be useful in select circumstances include
computed tomography scans, intravenous cholangiography, and oral cholecystogra-
phy. Currently, these studies are utilized when the diagnosis is in doubt and have
only limited indications.
11
Fig. 11.1. showing nonfilling of an acutely inflamed gallbladder.

Perioperative Management
As 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. A
second-generation cephalosporin is usually sufficient aerobic coverage, although in
the 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 to
keep the patient comfortable, as peritoneal irritation from acute cholecystitis can be
significant. The patient should be kept fasted to reduce cholecystokinin release and
both gallbladder and bile duct stimulation.
Timing of Surgery
The timing of surgery is generally dictated by the severity of the symptoms.
Indications for emergency or urgent cholecystectomy include deterioration of the
patient’s clinical condition or physical signs of generalized peritonitis with an
inflammatory abdominal mass, gas in the gallbladder lumen or biliary tree, and the
onset of intestinal obstruction. Note, despite the fact that several of these signs or
symptoms may be present, if comorbidities exist that would otherwise make an
operation prohibitive, a percutaneous tube cholecystostomy is often the initial 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 a
laparoscopic 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 of 11
diagnosis), 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 least
six controlled prospective trials of treatment have all shown a clear benefit for early
cholecystectomy, a delayed approach is still frequently practiced. It is our experience
that the edema which develops during an episode of acute cholecystitis permits an
easier operation, both open and laparoscopically, if performed within the first 24-48
hours of diagnosis.
Operative Technique for Cholycystectomy
Precise knowledge of normal and variant anatomy of the biliary tree is para-
mount to performing a safe and successful cholycystectomy. Inadvertent iatrogenic
injury to the biliary tree is associated with tremendous morbidity and mortality, and
the importance of proper visualization, exposure, and identification of all structures
prior to ligation cannot be overemphasized.
A Brief Review of Biliary Anatomy
Chapter 1 reviews normal liver and biliary anatomy in depth. However, frequent
re-review of this information is a useful exercise for both the novice and experienced
biliary surgeon.
The gallbladder is normally adherent to the undersurface of Segment V of the

liver. The gallbladder runs transversely from beneath the free edge of Segment V
medially and inferiorly towards the hepatoduodenal ligament. Peritoneal folds that
also cover the major structures within the hepatoduodenal ligament envelop the
neck of the gallbladder and cystic duct. The junction of the cystic duct with the
common bile duct forms one of the angles of the so-called Calot’s triangle. In sum,
Calot’s triangle is framed by the position of the common hepatic duct, cystic duct
11
Fig. 11.2. Cystic duct and gallbladder anomolies. A, Bilobed gallbladder; B, septum of
the gallbladder; C, diverticulum of the gallbladder; D, variation in the ductal
anatomy. Represented with permission from LH Blumgart. Surgery of the Liver and
Biliary Tract, 3rd ed. LH Blumgart, V. Fong et al. ©2000 W.B. Saunders.
Fig. 11.3 Calot’s triangle. The common hepatic duct, cystic duct and cystic artery
define the anatomic boundary referred to as Calot’s triangle.
and cystic artery (Fig. 11.1). Exposure and identification of these anatomic 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, the
anatomy of the gallbladder itself is typically constant. Note however, agenesis of the
gallbladder, left-sided gallbladders (attached to the undersurface of Segment II, III,
or IV), double gallbladders and other abnormalities have been described. 11
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, or
aberrant entry of a right or left sided hepatic duct, are the sources of nearly all biliary
injuries. Figure 11.2 depicts the more common means by which the cystic duct
enters the common bile duct. Normally, the cystic ducts takes a fairly serpigenous
course prior to entry into the mid to distal common bile duct. However, cystic duct
length is variable and may be quite short or even absent. At other times, the cystic
duct may be long and enter the common bile duct on the left side by coursing either
above or beneath it. Finally, though separate from the common bile duct, the cystic
duct may share a fibrous septum with the duct making it appear short and predis-
posing to potential injury.
In our experience, failure to recognize an abnormal confluence of the hepatic
ducts is the single most common surgical error leading to biliary injury. These
abnormalities may occur in 30-45% of patients, so adherence to surgical technique
and vigilance in properly recognizing these anomalies cannot be stressed enough.
The more common anomalies encountered are discussed in Chapter 1 (Fig. 1.9 A
and B). The most common abnormalities typically involve aberrant or low entry of
one or both right-sided sectoral ducts; however, abnormalities involving the cystic
duct are not infrequent. In our experience, injury to a right posterior sectoral duct
inserting low on the common bile duct and mistaken for the cystic duct is the most
common biliary injury.
Surgical Technique
With the advent of laparoscopic cholycystectomy (Chapter 12), experience in
performing open cholecystectomy is rapidly vanishing. The view obtained
laparoscopically is different than the view at open operation. Moreover, the perfor-
mance of an open cholecystectomy is today typically performed only as an en passant
operation (where too little attention to technique may occur), or when laparoscopic
operation is deemed unsafe, in which case difficult anatomy and dangerous 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 performed
necessitates proper supervision.
Incision
Open cholycystectomy has traditionally been performed through a right subcos-
tal or Kocher incision, and this is the incision we recommend. However, a midline
incision also provides good access to the right upper quadrant, and may be preferred
if cholecystectomy is to be performed as part of another operation. The advent of
minimally invasive surgery has led some surgeons to describe “keyhole” cholecystec-
tomy during which 2-3 cm incisions are utilized to improve postoperative cosmesis
and 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-abdominal
organs that need proper evaluation.
Exposure
11 Upon initial entry into the peritoneal cavity, careful assessment of all intra-
abdominal organs should be completed whenever possible. Although special care
should certainly be made to carefully examine the liver, gallbladder, bile duct and
pancreas, palpation of all intra-abdominal organs frequently identifies additional
pathology or resolves clinical questions that arose on preoperative imaging studies.
When examining the gallbladder, palpation should not be overly vigorous to avoid
pushing stones down into the common bile duct. Often, a dense fibro-inflamma-
tory reaction limits identification of the gallbladder, and an extensive effort may be
required to carefully dissect the omentum, stomach, duodenum, small bowel, and
colon off the gall bladder. Dense adherence of the colon or duodenum to the 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. In
cases of chronic cholecystitis or biliary colic, the gallbladder may be difficult to
identify due to scarring or an intrahepatic location. In this scenario, the supraduodenal
bile duct should be exposed with recognition of the cystic duct followed by an
antegrade cholecystectomy.
Decompression of the Gall Bladder
In most instances, a distended gallbladder is a useful finding because it facilitates
the subsequent dissection of the gallbladder from the undersurface of the liver.
However, not too infrequently a grossly distended gallbladder obscures the surgeon’s
ability to adequately identify the structures in Calot’s triangle. In this setting, de-
compression of the gallbladder is necessary. The technique utilized to decompress
the gallbladder is generally dependent upon available instruments but need not be
complex. We typically place a purse-string suture in the fundus of the gallbladder,
after which we make a cholecystotomy with a trocar or scissors. Bile and stones are
aspirated, cultures obtained (mandatory in the setting of cholecystitis and cholangi-
tis), and the suture tied to avoid the annoying leak of bile which typically follows.
Choice of Retractor and Exposure
As an initial maneuver, a hand is carefully introduced into the space between the
undersurface of the ribs/diaphragm and the anterior surface of the right liver. This
maneuver allows air to enter that space and permits mobilization of the right liver
out of the right upper quadrant. Two rolled up laparotomy sponges may be placed
above the liver to further mobilize it down into the operative field. Regardless of
which incision is utilized, a body wall retractor is placed in the right upper quadrant
to aid exposure for the operating surgeon. Although this has historically been the
role of the medical student, junior housestaff or surgical assistant, we favor the 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 this
purpose. An operative towel or sponge is placed over the right colon and small
bowel that is used to pack the viscera inferiorly within the abdominal cavity. The
first assistant’s left hand is then used to provide gentle but constant caudal retraction
on the hepatoduodenal ligament. Once initial mobilization of the gallbladder has
begun, a second hand-held retractor is frequently placed over the free edge of the
liver to provide exposure to the cystic duct-common bile duct junction.
Antegrade Technique 11
We favor performance of an antegrade cholecystectomy whenever possible. Careful
attention to surgical technique when performing this operation significantly limits
the potential for biliary injury. The fundus of the gallbladder is typically grasped
with a long Kelly clamp and retracted inferiorly. Scissors or the electrocautery are
used to incise the gallbladder serosa 5 mm from the liver edge. Using sharp dissec-
tion, a plane is developed on both the anterior and posterior surfaces of the gallbladder
allowing it to become separated from the liver. When the gallbladder is not acutely
inflamed this can be accomplished readily using the Metzenbaum scissors; however,
when acute inflammation is encountered, electrocautery is preferred. Small surgical
clips can be used to ligate rare arterial branches or small bile ducts that run directly
from the liver to the gallbladder. At the level of the gallbladder infundibulum, the
cystic artery is identified as it enters the gallbladder, typically on the anterior serosal
surface. This should be carefully dissected circumferentially in order to visualize the
terminal arterial branches entering the gallbladder prior to ligation. This maneuver
is the best means to avoid inadvertent division of an aberrant right hepatic artery.
The gallbladder infundibulum is traced down to the level of the cystic duct. Care
should be directed to avoid significant manipulation of the gallbladder to prevent
the migration of stones into the cystic duct or common bile duct. If stones are felt
within the cystic duct, an attempt should be made to “milk” the stones back into the
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 there
is any question that a biliary anomaly exists. Chapters 2 and 3 provide a detailed
discussion on the role of endoscopic retrograde cholangiopancreatography (ERCP)
as well as the interpretation of cholangiographic findings. Therefore the discussion
here will be limited to operative technique alone.
Once the infundibulum-cystic duct junction is identified, a clamp or ligature is
secured proximally to prevent bile and stones from leaking out of the gallbladder. A
second ligature is placed more distally around the cystic duct, but not secured. A
small 2-3 mm transverse incision is made at the level of the infundibulum—cystic
duct junction. A variety of cholangiogram catheters are currently in use; the author
prefers the Ponsky cholangiogram catheter that has a 1 cc balloon that can be inflated
to hold the catheter in position. If the surgeon encounters difficulty introducing the
cholangiogram catheter, this is typically due to the presence of a stone, a valve or the
tortuous course of the cystic duct. Manual palpation can usually exclude the pres-
ence of a stone, after which a fine tipped clamp can be carefully inserted into the
cystic duct to permit gentle dilatation. Once the catheter is positioned, the distal
suture is tied snug to hold the catheter in place. All retractors are removed and the
patient is rotated slightly to the right for better exposure. For similar reasons as
discussed in Chapter 12 it is our current practice to perform all cholangiograms
using C-arm fluoroscopy. If contrast passes rapidly into the duodenum (which often
occurs after ERCP and papillotomy), and obscures exposure of the intrahepatic bile
ducts, a vessel loop can be placed about the hepatoduodenal ligament preventing
distal flow. Once the cholangiogram is performed, the catheter is removed and the
cystic duct is divided between the ties.
11 The gallbladder should always be opened and inspected in the operating room
for the presence of tumors and aberrant biliary anatomy. Any doubt as to the biliary
anatomy should prompt a cholangiogram if one has not already be obtained.
Mild to moderate hemorrhage from the gallbladder fossa is a common and 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 has
occurred, Surgicel or Gelfoam may be required and in very rare instances, direct
parenchymal suturing is required.
Debate continues as to whether one should routinely drain an open cholecystec-
tomy. The experience gained with laparoscopic cholecystectomy, in which drains are
rarely placed, would suggest a drain is unnecessary in most cases. However, as noted
previously, today open cholecystectomies are typically performed for laparoscopic
failures in which case the same “rules” may not apply. Simply stated, the surgeon
must exercise his or her best judgment based on experience and prior teaching. If
one is more comfortable leaving a drain, one should do so. The drain is typically
removed the next day if drainage is less than 50 cc, but should remain if drainage is
excessive or bile stained.
Retrograde Technique
Much of the technique described for antegrade cholecystectomy is applicable to
performing a retrograde cholecystectomy. Careful exposure and identification of
anatomic structures is once again the key. The technique of retrograde cholecystec-
tomy, historically performed less often, has now become commonplace in the era of
laparoscopic cholecystectomy (which is performed retrograde). A large Kelly clamp
is initially placed on the fundus and/or body of the gallbladder to provide superior
and lateral retraction. The thin layer of peritoneum covering the hepatoduodenal
ligament is incised at the level of the infundibulum of the gallbladder anteriorly
towards the cystic plate (and the base of the quadrate lobe (Segment IV)), and 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 Kitner
or peanut) exposes the cystic duct and allows development of Calot’s triangle. The
cystic duct can be encircled at this point to prevent stones from migrating further,
but it should not be divided. The cystic artery typically lies superior and medial to
the cystic duct and is usually readily identified. Once again, this artery should be
followed to its terminal branches on the gallbladder prior to ligation. At this point
the infundibulum-cystic duct junction is typically well exposed, and the cystic duct
can be doubly ligated and divided. If a cholangiogram is to be performed, the same
technique as described above should be used.
After the cystic duct and cystic artery are divided, superior and lateral retraction
on the gallbladder is applied, and the serosa of the gallbladder is excised in a retro-
grade fashion. Occasionally, a posterior cystic artery lying behind and medial to the
main cystic artery may be encountered. This should be carefully inspected to see
that its terminal branches end in the gallbladder (and not the right lobe of the liver)
prior to ligation. Small terminal arterial branches and bile ducts may arise directly
from the liver and enter the gallbladder. As when performing a laparoscopic
cholycystectomy, these are typically easily handled with the use of the electrocau-
tery. Upon removal of the gallbladder, the surgeon is reminded once again to inspect
it carefully for tumors and normal anatomy. Issues relating to whether a drain should 11
be left have been discussed previously.
Closure
If a midline incision was utilized, the abdomen is closed in the standard fashion
using either a running or interrupted suture technique. We favor the use of a perma-
nent or semi-permanent suture, and typically close with a #1 double loop PDS
suture. If a right subcostal incision is used, the question always arises as to whether
one should close the anterior and posterior rectus sheaths in two layers or in one.
In reality, this probably makes little difference, and surgical decision should be
guided by judgment and experience. This author favors a two-layer closure using
two #1 double looped PDS sutures. The skin can be closed with skin staples or a
subcuticular suture.
CHAPTER 12
Laparoscopic Cholecystectomy
and the Laparoscopic Management
of Common Bile Duct Stones
Fredrick Brody
Introduction
In less than a decade, laparoscopy has significantly effected general surgical 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 is
an increased rate of biliary duct injuries. This devastating injury is avoided by adher-
ing to a systematic approach to laparoscopic cholecystectomy regardless of patient
or disease acuity.
Indications
Patients with cholecystitis present with a broad range of symptoms depending
on the severity of their disease. The majority of patients present with right upper
quadrant or epigastric abdominal pain with radiation to the right flank associated
with right upper quadrant tenderness on physical examination. Ultrasound findings
of gallbladder wall thickness greater than 4 mm, echogenic gallbladder contents,
and pericholecystic fluid collections are consistent with acute cholecystitis. After
confirming the diagnosis, the patient is kept NPO and started on intravenous fluids
and a second generation Cephalosporin. Though somewhat controversial, early
operative intervention is generally indicated within the first 24-72 hours of 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 relative
contraindications.
Laparoscopic Cholecystectomy
After inducing general anesthesia, each patient is placed supine with arms tucked
to the side and an orogastric tube is placed. A Foley catheter is not required if the
patient voids prior to induction. Abdominal access is performed through the umbi-
licus. An open technique with a Hasson trocar as opposed to a closed technique
with a Veress needle decreases major complications while enabling high flow rates
immediately after insertion. Three subsequent ports are placed after exposing the
gallbladder. The epigastric port is placed 2 cm below the xiphoid process correlating

Laparoscopic Cholecystectomy 157
with the level of the cystic duct and gallbladder infundibular junction. The patient
is then placed at 40˚ of reverse Trendelenburg and rotated 15˚ to the left. This allows
the colon and small intestine to fall into the pelvis while elevating and rotating the
plane of dissection perpendicular to the surgeon (Fig. 12.1).
The final two ports are placed in the midclavicular and anterior axillary lines
respectively. These ports should be at least 2 cm below the costal margin. If these
ports are misplaced, they should err laterally and inferiorly. Medially displaced trocars
interfere with laparoscopic visualization while superiorly displaced trocars inhibit
lateral and inferior retraction of the gallbladder infundibulum.
An inline grasper (Karl Storz, Charlton, MA) is introduced through the anterior
axillary trocar and the gallbladder fundus is grasped and elevated over the liver edge.
Blunt stripping of multiple adhesions extending from the colon, duodenum, or
pyloric region may be required. Cautery is never used to release these adhesions as
current can easily conduct to these structures. Delayed duodenal perforations two
to three days postoperatively are well documented in the literature following ill advised
cautery at this juncture of this procedure. Another inline grasper is introduced through
the midclavicular port and the gallbladder infundibulum is grasped and retracted
laterally and posteriorly towards the spine. This simple maneuver places the cystic
duct at right angles to the common bile duct and ensures that the cystic duct is out
of alignment with the common bile duct (Fig. 12.2).
Prior to dissecting Calot’s triangle, a preliminary examination through the 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 and
first assistant. Identification by both surgeons at this stage enables critical commu-
nication throughout the entire procedure. By identifying Calot’s node and the
infundibular-cystic duct junction, the inferior aspect of the biliary dissection is
ascertained. A safe dissection revolves around the infundibular-cystic duct junction
at the level of Calot’s node.
Dissection begins with a Maryland dissector (Karl Storz, Charlton, MA) along
the lateral aspect of the gallbladder infundibulum. The peritoneum overlying this 12
region is stripped in a downward fashion along the course of the cystic duct. As this
peritoneum is gradually stripped, the infundibular-cystic duct junction becomes
apparent. The dissection proceeds medially along the anterior surface of the cystic
duct. Calot’s node is gently pushed medially exposing the entire anterior surface of
the cystic duct. Minimal manipulation of Calot’s node avoids persistent and annoy-
ing bleeding.
The posterior cystic duct surface is exposed by retracting the gallbladder
infundibulum across its longitudinal access towards Segment IV of the liver using
the midclavicular inline grasper. This maneuver exposes the posterior peritoneum
overlying the cystic duct and gallbladder infundibulum. Using a Maryland dissec-
tor or hook cautery, the posterior peritoneum is carefully stripped. This dissection
exposes the posterior surface of the cystic duct and gradually “lengthens” the duct
by several millimeters. The infundibulum is then returned to its original lateral
and posterior position.
The concave surface of the Maryland dissector is then positioned along the medial
aspect of the cystic duct. The tips of the instrument should now point towards
Segment VIII of the liver. The infundibulum is again retracted across its longitudi-
12
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 are
clearly identified through the posterior peritoneum, the instrument is gradually
nuzzled through this thin layer of tissue. If the tips are not readily identified, the
anterior and posterior peritoneal dissection is repeated until the intervening tissue is
adequately attenuated. This critical step may require blunt dissection with a Kittner or
hydrostatic dissection with the suction-irrigator during an acute inflammatory process.
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.
After 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 hook
cautery. This is performed in a cephalad direction on top of the cystic duct towards
12
the infundibular-cystic duct junction. The peritoneum along the lateral portion of
the cystic artery is released simultaneously during this maneuver. By dissecting the
peritoneal elbow of the cystic artery, the artery is released and straightened facilitat-
ing clip application (Fig. 12.3). The crotch of the infundibular-cyst duct junction is
developed by gently sliding the hook cautery beneath each peritoneal layer and 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 placed
against the medial side of the cystic duct without current. Gentle pressure with the
heel against the duct opens the anterior-posterior window and helps expose the
remaining peritoneal layers in the crotch of the infundibular-cystic duct junction.
These remaining peritoneal bands are subsequently divided.
With the infundibular cystic duct junction adequately exposed, the cystic artery
dissection is completed with the hook cautery and Maryland dissector. The dissection
remains at or above the level of Calot’s node. The peritoneum overlying the cystic
artery is divided and the Maryland dissector is used to gently encircle the cystic
artery. The nuzzling technique with the dissector tips is utilized again. When the
Fig. 12.3. The peritoneum overlying the cystic artery “elbow” is released. This
maneuver straightens the cystic artery facilitating clip application.
cystic artery is approached at or above the level of Calot’s node, posterior branches
of the cystic artery may not be apparent. It is safer to assume that posterior branches
of the cystic artery are present until completing further dissection.
12 The cystic duct and artery are now separated by a clear window without any
intervening tissue (Fig. 12.4). This window was previously described by Soper and
Strasberg as the “critical view.” With the critical view completed, one clip is placed
across the cystic duct-infundibular junction. A 3 mm ductotomy is made 4 mm
from this clip. The cystic duct is milked proximally with a Maryland dissector to
extrude any stones or debris through the ductotomy. The inline grasper is then
removed from the midclavicular port and reinserted through the epigastric port.
The infundibulum is regrasped and retracted laterally so the cystic duct is aligned
with the shaft of the midclavicular trocar.
An Olsen clamp with a Ponsky cholangiocatheter is introduced through the
midclavicular port. The clamp and infundibulum are aligned to ensure easy passage
of the cholangiocatheter through the ductotomy. Utilizing dynamic fluoroscopy, a
scout film is obtained localizing the tip of the cholangiocatheter. Initially, only 2-3 cc
of contrast dye are injected identifying the cystic duct common bile duct junction.
This also establishes the actual length of the cystic duct. The fluoroscopy unit is
shifted caudally a few centimeters and the course of the distal common bile duct is
identified by injecting another 5 cc of contrast. Contrast should flow easily through
the distal common bile duct with imaging of the duodenum. The fluoroscopy arm
Fig. 12. 4. The critical view is completed by dissecting the intervening tissue between
the cystic artery and duct.
is shifted cephalad and another 5 cc of contrast is injected to visualize the common

hepatic duct and the proximal hepatic radicals. Filling of the proximal radicals is
enhanced by placing the laparoscope on top of the second portion of the duodenum
and applying gentle pressure towards the spine while injecting contrast. This ma-
neuver compresses the distal common bile duct and forces contrast proximal into
the hepatic radicals. It is critical to image the hepatic radicals of Segments V and VI
to ensure the absence of any accessory ducts communicating with the gallbladder. If
the gallbladder is demonstrated during fluoroscopy, a clip is needed for the duct drain-
12
ing directly into the gallbladder. If the cholangiogram is within normal limits, the
clamp and catheter are removed and two clips are placed just distal to the ductotomy.
The cystic artery is then secured with two clips and both structures are divided.
The hook cautery is then used to release the lateral and medial peritoneum along
the gallbladder and liver confluence. The infundibulum is lifted towards the ante-
rior abdominal wall creating tension on the peritoneal bands within the gallbladder
fossa. These bands are isolated individually with the hook cautery as opposed to the
spatula. Continuous cautery in a horizontal motion with the spatula risks injury to
a torturous right hepatic duct or right hepatic artery. Individual dissection of these
peritoneal bands with a hook cautery may prolong the operative procedure, but it
helps avoid inadvertent injury to these particular structures. Similarly, delicate dis-
section with the hook identifies any posterior cystic artery branches requiring
hemoclips. The gallbladder is removed through the umbilicus and the three ports
are removed under direct vision to verify hemostasis. It is our practice to first place
the gallbladder in a specimen bag within the abdomen prior to removal.
Laparoscopic Common Bile Duct Exploration

If the cholangiogram identifies gallstones greater than 3 mm in diameter, their
location determines the next step. If the stones are located in the common hepatic
duct or above the cystic duct-common bile duct junction, a choledochotomy is
performed. Another 5 mm port is placed in the right upper quadrant to complete
this dissection. The cystic duct is traced down to its junction with the common bile
duct. The anterior surface of the common bile duct is dissected while avoiding injury
to the 3 and 9 o’clock vessels. Using microscissors, a 1 cm longitudinal
choledochotomy is made 1 cm below the junction of the cystic duct and common
bile duct. After applying a thin layer of mineral oil along a 3.3 mm choledochoscope,
it is gently introduced through the choledochotomy and guided cephalad towards
the stone. Continuous normal saline irrigation for the choledochoscope and a sec-
ond video system are required. With the stone in view, a wire basket is advanced
beyond the stone (Fig. 12.5). The basket is opened and slowly withdrawn towards
the stone. When the stone eventually falls between the wires of the basket, the wires
are closed and the entire choledochoscope is removed keeping the stone under di-
rect vision at all times. This procedure is repeated until the duct is cleared of all
stones and debris greater than 3 mm. A cholangiogram is obtained by injecting
contrast through the working channel of the choledochoscope to ensure complete
stone extraction. The choledochoscope is removed and a 14F T-tube catheter is
placed through the choledochotomy. Ideally, the draining arm of the T-tube exits
through the cystic duct making closure of the choledochotomy easier. Interrupted
4-0 vicryl sutures are used to close the ductotomy. A completion cholangiogram is
obtained through the T-tube to verify stone extraction and a water tight closure of
the ductotomy. Finally, a 10 mm Jackson Pratt drain is placed.
If the initial cholangiogram identifies stones within the cystic duct or below the
junction of the cystic duct and common bile duct, a transcystic exploration is per-
formed (Fig. 12.6). Approximately 90% of choledocholithiasis are found below the
cystic duct junction in the distal common bile duct. The cystic duct may need dila-
12 tation with sequential Fogarty catheters to accommodate the choledochoscope. A
well lubricated 3.3 mm choledochoscope is introduced through the cystic duct and
advanced to the offending stone. Baskets are used for retrieval and a completion
cholangiogram is performed. A T-tube is not needed for transcystic explorations;
however, a 10 mm Jackson Pratt drain is left next to the cystic duct stump.
Postoperatively, patients undergoing a routine laparoscopic cholecystectomy are
discharged from the recovery room. Patients undergoing duct explorations are
admitted and advanced to a regular diet. Patients with T-tube catheters undergo a
cholangiogram on postoperative day 21. If the cholangiogram is normal the T-tube
is removed. Following a transcystic exploration, the Jackson Pratt 10 mm drain is
removed on postoperative day 1 if the patient is tolerating regular food and there is
no bile in the suction bulb of the Jackson Pratt drain.
12
Fig. 12.5. The choledochoscope is introduced through a longitudinal ductomy below

the cystic duct junction. Wire baskets are used to extract the stones.
Selected Reading
1. 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.
12
Fig. 12.6. The choledochoscope is introduced distally through the cystic duct and
baskets are passed for stone extraction.
4. Strasberg S, Hertl M, Soper NJ. An analysis of the problem of biliary injury during
laparoscopic cholecystectomy. J Am Coll Surg 1995; 180:101-124.
5. Trus TL, Hunter JG. Laparoscopic bile duct techniques. 1995; 2 (2):118-127.
CHAPTER 1
CHAPTER 13
Surgical Techniques for Completion

of a Bilioenteric Bypass
Pierre F. Saldinger, Leslie H. Blumgart
Scope of the Problem
Surgical relief of obstructive jaundice is indicated in benign as well as malignant
strictures of the bile ducts and less frequently for stone disease. Benign strictures are
most commonly seen after injury to the common hepatic duct during 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 has
to perform a hepaticojejunostomy to one or several intrahepatic bile ducts which
can present a technical challenge. A biliodigestive bypass to an intrahepatic bile duct
will provide excellent biliary decompression and palliation in the case of an
unresectable bile duct cancer. Lastly, a biliodigestive anastomosis can be of use in
complex stone disease.
This chapter will outline the anatomical aspects, technical details, and general
considerations with respect to performing a biliodigestive anastomosis.
Anatomy
It is essential to be cognizant of the anatomical details and variants of the extra-
and intrahepatic biliary tree as well as adjacent hepatic arterial and portal venous
structures. The normal biliary and vascular anatomy is depicted in Figures 13.1 and
13.2. The important ductal anomalies are nearly all related to the manner of
confluence of the right and left hepatic ducts and of the cystic duct. In addition,
anomalies occur with such a high frequency that the surgeon must be acquainted
with their range and should always expect the unusual.
The most common variation is an abnormal junction between the cystic duct
and the main extrahepatic biliary channel. The cystic duct may join the common
hepatic duct high, almost at the hilus of the liver (Fig. 13.3). The right hepatic duct
as such may be absent and the major ducts draining the anterior and posterior sec-
tors of the right liver may join the left hepatic duct separately to form the common
hepatic duct. In some cases, the right anterior or right posterior sectoral duct may
run a long extrahepatic course to join the common duct, and the cystic duct may
drain directly into such a duct. However, while these variations are common, there
is almost always a consistent anatomy to the left hepatic duct and its branches.
The right hepatic duct has a short extrahepatic portion, but the left hepatic duct
always has an extrahepatic course (Fig. 13.4), the length of which reflects the width

Fig. 13.1. Normal extra- and intrahepatic segmental biliary anatomy. Reprinted
with permission from: Surgery of the Liver and Biliary Tract (3rd Edition), Blumgart LH,
13
Fig. 13.2. Normal hepatic segmental vascular anatomy. Reprinted with permission
from: Surgery of the Liver and Biliary Tract (3rd Edition), Blumgart LH, Fong Y and WH
Jarnigan (Eds.) W.B. Saunders, London, UK (2000).
Surgical Techniques for Completion of a Bilioenteric Bypass 167
13
Fig. 13.3. Cystic duct and gallbladder anomolies. A, Bilobed gallbladder; B, septum of
the gallbladder; C, diverticulum of the gall bladder; D, variation in the ductal anatomy.
Blumgart LH, Fong Y and WH Jarnigan (Eds.) W.B. Saunders, London, UK (2000).
of the quadrate lobe at the base of the liver. If the quadrate lobe has a broad long
base, then the left hepatic duct has a longer rather transverse course, whereas if the
quadrate lobe has a narrower more pyramidal base, the left hepatic duct has a shorter
somewhat more oblique course. The duct traverses to the left together with the left
branch of the portal vein within a peritoneal reflection of the gastrohepatic ligament,
fused with Glisson’s capsule on the undersurface of the quadrate lobe (Fig. 13.5).
Fig. 13.4. Relation of right and left hepatic ducts. Reprinted with permission from:
Surgery of the Liver and Biliary Tract (3rd Edition), Blumgart LH, Fong Y and WH
The left duct and left branch of the portal vein are joined by the left branch of
the hepatic artery, enter the umbilical fissure of the liver within which division of
vessels to and confluence of ducts from the left lobe (Segments II and III) and the
13 quadrate lobe (Segment IV) occur. The left hepatic duct receives major tributaries
from each of these segments which converge in the umbilical fissure dorsocranial to
the left portal vein. Hepatic ductal tributaries from the quadrate lobe (Segment IV)
and hepatic arterial and portal venous branches supplying it re-curve to Segments
IVA and IVB (Fig. 13.6).
The ligamentum teres, in the lower edge of the falciform ligament, traverses the
umbilical fissure of the liver which is usually, but not always, bridged in its 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 anteriorly
and caudally, giving off branches to Segments II and III of the left lobe and to
Segment IV (Fig. 13.6).
The most common vascular anomaly is an accessory or replaced right hepatic
artery originating from the superior mesenteric artery. This anomaly is present in
about 20-25% of patients. The right hepatic artery runs posterolateral to the right
of the common bile duct in close proximity to the cystic duct. The artery is prone to
injury during cholecystectomy particularly if injury to the common bile duct occurs.
Fig. 13.5. Extrahepatic course of the left hepatic duct within Glisson’s capsule.
Its presence has to be ascertained prior to any isolation of the common bile duct in
13
order 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, major
right or left hepatic duct, or to the Segment III duct of the left lobe.
It is generally not necessary to proceed with biliary drainage prior to proceeding
with a bilioenteric anastomosis in cases of obstructive jaundice. In fact, it is often
easier to perform an anastomosis on a bile duct that is dilated secondary to obstruc-
tion. However, preoperative biliary drainage is advised in patients with sepsis from
cholangitis in order to stabilize the patient prior to surgery.
It is of utmost importance to obtain as much information as possible on both the
level and etiology of biliary obstruction prior to surgery. With the advent of high
quality magnetic resonance cholangiopancreatography (MRCP), there is limited need
for preoperative percutaneous or endoscopic cholangiography to determine the level
Fig. 13.6. Branching of portal pedicles within the umbilical fissure. A, left portal vein;
13 B, left hepatic duct; C, Segment III sytem, note the duct (black) lies adjacent to the
portal venous branch; D, ligamentum teres. Reprinted with permission from: Surgery
of the Liver and Biliary Tract (3rd Edition), Blumgart LH, Fong Y and WH Jarnigan (Eds.)
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 liver
resection.
Fig. 13.7. An MRCP image demonstrating a cholangiocarcinoma. A large tumor is seen

at the confluence of the right and left hepatic ducts. The gallbladder is distended which
suggests origin or spread to the mid-bile duct causing cystic duct occulusion.
Incisions
Adequate exposure allowing full visualization is necessary for good biliary-enteric
anastomosis. 13
A midline incision allows access to the mid-common bile duct and can be adequate
for a common duct exploration, choledochoduodenostomy, or a low
hepaticojejunostomy. While being less morbid than a bilateral subcostal incision, it
does not allow appropriate access to the hilus and should not be used if a hilar
dissection is anticipated.
If in doubt, a right subcostal incision is a better choice as it can be extended
upwards to the xyphoid or across the midline as a bilateral subcostal incision, which
allows excellent exposure of the extrahepatic bile duct and liver. If a bilateral subcos-
tal incision is employed, the use of a broad-bladed retractor fixed to an overhead
support elevating the costal margin is valuable.
In cases of right lobar atrophy with posterior rotation of the hilar structures, it
might be necessary to extend a bilateral subcostal incision into the right chest to
provide safe access to the hilus.
Abdominal Exploration
Upon opening the abdomen, it is important to fully expose the liver and the
supracolic compartment of the abdomen. An important early step is division of the
ligamentum teres and freeing of the falciform ligament from the abdominal wall
back to the diaphragm. If previous surgery has been carried out, adhesions are 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 be
found adherent to the base of the liver; the colon may be densely adherent to the
scar of the gallbladder fossa. At this point, one proceeds with the planned operation,
resection in the case of a malignant stricture, or bypass in the case of benign or
unresectable malignant strictures
There are three critically important fundamentals in biliary-enteric anastomoses:
1. Identification of healthy, tumor-free bile duct mucosa proximal to the
site of obstruction.
2. The preparation of a segment of the gastrointestinal tract, usually a 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 make
its blind end subcutaneous (Fig. 13.8). If this technique is selected, the Roux loop
must be made long enough to allow the blind end of the jejunum to reach the
abdominal wall without tension. This technique will allow percutaneous access to
the loop which may be necessary for adjuvant biliary tree intervention. When this is
done, a silastic tube is left across the anastomosis and brought out through the loop
in order to provide initial access. It should be emphasized, however, that in the usual
circumstance, where an anastomosis is obtained between the mucosa of the bile
duct and the jejunum, there is usually no need for transanastomotic tubes and no
evidence that intubation assists long-term patency. The authors now advocate a simple
sutured anastomosis in the average case. Indeed, transanastomotic stents carry their
own complications and these are thus avoided.
13
Basic Anastomotic Technique
It is valuable to have an established routine for biliary-enteric anastomosis. Al-
though some anastomoses are low and easily performed, a regular technique that
facilitates 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 of
jejunum 70 cm in length is prepared and brought up (preferably in a retrocolic
fashion) for completion of an end-to-side anastomosis. The end-to-side anastomosis
is then performed using the technique described by Blumgart and Kelley
(Figs. 13.9-13.13).
The anterior layer of sutures is placed first and prior to any attempt to place the
posterior row. If more than one ductal orifice is visible at the hilus, these are best
approximated with a row of sutures so that they can be treated as a single duct for
anastomotic purposes (Fig. 13.9). If this cannot be done, then the entire anterior
row to all exposed ducts is inserted first so that the separated orifices can be treated
Fig. 13.8. Blind-end Roux-en-Y. Hepatocojejunostomy to the Segment III branch. The
Roux-en-Y limb is brought out to the skin to provide subcutaneous access. The
anastomosis is stented with a transjejunal tube which permits access for interventional
diagnostic and therapeutic maneuver.
as if single. Attempts to complete one anastomosis and then another are difficult,
and sometimes impossible. These sutures are serially introduced starting from the
left and working to the right (Fig. 13.10). We recommend using a mono- or
polyfilament absorbable suture of 4/0 size or smaller if necessary.
This first step not only permits precise placement of the anterior row of sutures,
which may be very difficult if the posterior layer is inserted first and tied, but also
facilitates precise placement of the posterior layer (Fig. 13.11), which is likewise 13
placed serially from left to right. The posterior layer of sutures is now tied (Fig. 13.12).
The previously placed anterior row of sutures is now completed.
Alternative Anastomotic Techniques
In some cases, where the bile duct is large and easily exposed, a simpler 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 is
anastomosed just proximal to the duodenum such as after a Whipple
pancreaticoduodenectomy.
Choledochojejunostomy or Hepaticojejunostomy
This operation is usually performed in an end-to-side fashion; however, a side-
to-side hepaticojejunostomy can be performed using techniques similar to those
described for choledochoduodenostomy (see below).
Fig. 13.9. Placement of the posterior row for hepaticojejunostomy. Reprinted with
permission from: Surgery of the Liver and Biliary Tract (3rd Edition), Blumgart LH, Fong
Y and WH Jarnigan (Eds.) W.B. Saunders, London, UK (2000).
Technique
13 The gallbladder, if present, is removed in a retrograde fashion. A tie is left in the
cystic duct as an aid in manipulating the common bile duct. The common bile duct
is dissected well above the obstruction, and care is taken to avoid an accessory or
replaced right hepatic artery, if present. The duct is divided and the lower end of the
common bile duct is closed with a running suture. The exposed common bile duct
is now sutured into the jejunum using either technique described above.
Approaches to the Left Duct
Approaches to the left duct are useful in cases of high strictures where there is
not enough bile duct proximally to perform an anastomosis. This can be the case
secondary to a benign stricture after bile duct injury or due to a tumor.
The left ductal system can be approached in two different ways:
1. Display the left hepatic ducts by opening the umbilical fissure, elevating
the base of the quadrate lobe and lowering the left hepatic ductal system
from the undersurface of the quadrate lobe (Hepp – Couinaud approach).
Fig. 13.10. Placement of the posterior row for hepaticojejunostomy. Reprinted with
permission from: Surgery of the Liver and Biliary Tract (3rd Edition), Blumgart LH, Fong 13
Y and WH Jarnigan (Eds.) W.B. Saunders, London, UK (2000).
2. Expose the left hepatic ducts by dissection at the base of the ligamentum
teres (ligamentum teres or Segment III approach).
Hepp–Couinaud Approach
This technique allows performance of an anastomosis to the extrahepatic left
bile duct in cases of high benign strictures, provided there is an intact communica-
tion between the right and the left liver.
The ligamentum teres is transected and a firm tie is placed so that it may be
elevated and used as a retractor. The liver is elevated to display its undersurface. The
bridge of tissue (if present), connecting the left lobe of the liver to the quadrate lobe,
is divided with diathermy (Fig. 13.12).
The hilar plate is now lowered. This consists of dissecting between Glisson’s
capsule at the base of the quadrate lobe and the peritoneal reflection encasing the
Figs. 13.11A, 13.11B. Placement of anterior row for hepaticojejunostomy. Reprinted

13
Fig. 13.12. Cutting of the bridge of tissue connecting the left lobe of the liver to the
quadrate lobe. Reprinted with permission from: Surgery of the Liver and Biliary Tract
(3rd Edition), Blumgart LH, Fong Y and WH Jarnigan (Eds.) W.B. Saunders, London,
UK (2000).
13
Fig. 13.13A. Lowering of the hilar plate. A, The initial line of incision is shown. The
hilar plate is lowered and the left hepatic duct is exposed. Reprinted with permis-
sion from: Surgery of the Liver and Biliary Tract (3rd Edition), Blumgart LH, Fong Y and
WH Jarnigan (Eds.) W.B. Saunders, London, UK (2000).
left portal triad (Figs. 13.13A, 13.13B). This maneuver allows exposure of the 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 then
performed by the technique illustrated previously.
Ligamentum Teres (Round Ligament) Segment III Approach
While the vast majority of high benign strictures can be approached and dealt
with as described above, it is occasionally difficult to expose the left hepatic duct
beneath the quadrate lobe. This may be due to dense adhesions, bleeding, or a large
13 Fig. 13.13B. Lowering of the hilar plate. Reprinted with permission from: Surgery of
the Liver and Biliary Tract (3rd Edition), Blumgart LH, Fong Y and WH Jarnigan (Eds.)
and overhanging quadrate lobe. On occasion, the extrahepatic length of the left
hepatic duct may be relatively short and oblique, making the approach difficult. In
the setting of a carcinoma of the bile duct, a tumor extending into the left duct from
the confluence area may preclude the use of the main left duct. In any event, 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 the
umbilical fissure.
It is important to note that unilateral drainage of the left hepatic duct, in the
presence of a tumor which completely excludes the right liver and right hepatic
ducts from the anastomosis, is effective in the relief of jaundice provided the left
lobe of the liver is not atrophic.
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). The
liver to the left of the ligamentum teres is split and a small segment of liver tissue is
removed thus exposing the duct to Segment III (Fig. 13.14). A side-to-side anasto-
mosis to a loop of jejunum is then carried out by the techniques described above
Choledochoduodenostomy
A choledochoduodenostomy is infrequently used for the relief of biliary tract
obstruction in malignant disease, and much more frequently for the patient with
biliary obstruction due to gallstones. In the latter case, side-to-side
choledochoduodenostomy is preferable.
A choledochoduodenostomy is usually performed at the conclusion of a com-
mon bile duct exploration in lieu of T-tube placement.
13
Fig. 13.14. Exposure of Segment III. The ligamentation teres is retracted internally
and the peritoneum on the left side is incised carefully to expose the Segment III
duct. This process is tedious and should be done carefully to avoid bleeding. Re-
printed 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).
Indications
The single most important condition allowing the performance of a
choledochoduodenostomy is an enlarged common bile duct. A duct measuring less
than 12 mm in diameter is an absolute contraindication. The following are situa-
tions which are amenable to a choledochoduodenostomy. Contraindications include
duodenal ulcer and acute pancreatitis.
1. Retained or recurrent stones in the common bile duct
2. Cholangitis
3. Ampullary stenosis
4. Primary common duct stones calculi or stasis bile
5. Tubular stricture of the transpancreatic portion of the choledochus usu-
ally due to chronic pancreatitis
6. A combination of these above
7. Low iatrogenic stricture
8. Malignant obstruction in the periampullary area
Technique
Two technical criteria are essential for a proper choledochoduodenostomy: a
common duct of 1.4 cm in diameter at the minimum and a stoma size of 2.5 cm.
The degree of satisfaction with the procedure will depend upon the develop-
ment of a standard technique for the rapid construction of a stoma that allows free
entry and egress from the common bile duct.
While attempts are made to remove stones and particulate matter from the com-
mon bile duct, impacted stones at the distal common bile duct that are not easily
retrieved, and stones in the hepatic duct are not pursued vigorously prior to the
anastomosis.
The duodenum is fully mobilized by a Kocher maneuver and thus approximated
toward the common bile duct. A duodenotomy is performed perpendicular to the
choledochotomy. The anastomosis is performed either in an interrupted fashion or
as a continuous suture. The interrupted technique is illustrated (Figs. 13.15-13.17).
13
Fig. 13.15. Lines of incision. Choledochoduodenostomy performed using an inter- 13

rupted technique. Reprinted with permission from: Surgery of the Liver and Biliary
Tract (3rd Edition), Blumgart LH, Fong Y and WH Jarnigan (Eds.) W.B. Saunders,
London, UK (2000).
13
Fig. 13.16, top. Fig. 13.17, bottom. Reprinted with permission from: Surgery of the
Liver and Biliary Tract (3rd Edition), Blumgart LH, Fong Y and WH Jarnigan (Eds.) W.B.
Saunders, London, UK (2000).
CHAPTER 1
CHAPTER 14
Hilar Cholangiocarcinoma: Surgical

Approach and Outcome
Ronald S. Chamberlain, Leslie H. Blumgart
Cholangiocarcinoma is an uncommon malignancy with an incidence of
1.2/100,000. This neoplasm accounts for less than 2% of all cancer diagnoses with
equal sex distribution. The incidence of cholangiocarcinoma increases with age, with
two-thirds of all cases occurring in patients over 65. Jaundice is the presenting com-
plaint in 90-98% of patients with cholangiocarcinoma. Additional complaints include
weight loss (29%), abdominal pain (20%), and occasionally fever (9%). Jaundice
may be absent if the tumor is intrahepatic or involves only the right or left hepatic
duct. In these cases, the resultant lobar obstruction leads to ipsilateral hepatic lobar
atrophy whose only manifestation may be an elevated alkaline phosphatase. Despite
a high incidence of bactobilia in patients with both complete and incomplete ob-
struction due to cholangiocarcinoma, cholangitis is a rare presentation. However, a
two-fold increase in postoperative infectious complications has been reported in
association with preoperative instrumentation and stenting.
Cholangiocarcinoma can arise anywhere along the biliary tree from the ampulla
of Vater to the intrahepatic biliary radicals (Fig. 14.1). Upper third or hilar tumors
(56%) are those located proximal to the cystic duct up to and including the bifurca-
tion into right and left hepatic ducts. Middle third tumors (17%) are located from
the upper border of the duodenum and extending to the cystic duct junction. Lower
third or distal bile duct tumors (18-27%) arise between the ampulla of Vater and the
upper border of the duodenum. Intrahepatic cholangiocarcinoma (IHC) are rare
neoplasms accounting for 6-10% of all cholangiocarcinoma and are managed 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 surgical
approach to distal bile duct tumors, namely pancreaticoduodenectomy.
Etiology and Pathology
The etiology of cholangiocarcinoma is unknown; however conditions resulting
in acute or chronic biliary epithelial injury may predispose its development. These
conditions include primary sclerosing cholangitis in which occult cholangiocarcinoma
has been identified in up to 40% of autopsy specimens and 9-36% of liver explants,
and choledochal cysts or Caroli’s disease which demonstrate a 2.5-28% incidence of
malignant transformation. Oriental cholangiohepatitis, a rare form of pyogenic cho-
langitis, also has a 5-12% lifetime incidence of cholangiocarcinoma. Additional risk
factors include biliary tract infection with parasites (e.g., Clonorchis sinensis and

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

percentages.
Opisthorchis viverrin), chronic typhoid carrier states, and exposure to various chemi-
cal carcinogens, including asbestos, digoxin, and nitrosamines.
14 Cholangiocarcinomas are generally well-differentiated slow-growing adenocar-
cinomas which may be mucin producing. Hematogenous spread is rare, but nodal
metastases occur in up to one-third of all cases. Extensive subepithelial tumor spread
beyond the gross margin is common, and may extend 1-2 centimeters in each direc-
tion. Cholangiocarcinoma are classified as papillary, nodular-sclerosing, or diffuse
type based upon its macroscopic appearance. The papillary variant is least common
but carries the most favorable prognosis. Papillary tumors commonly involve the
distal bile duct and grow as intraluminal soft, polypoid tumors. The nodular variant
occurs most commonly in the upper and mid-duct and presents as a fibrotic mass
with intraductal projections. The sclerosing variant is most commonly seen in hilar
tumors, and appears as annular thickening of the duct wall with both longitudinal
and radial tumor infiltration. The diffuse type, which involves the entire extrahe-
patic bile duct, is both rare and universally fatal.
Hilar Cholangiocarcinoma: Surgical Approach and Outcome 185
The preoperative evaluation of a patient with suspected cholangiocarcinoma is
as important as the operative course and is directed toward four primary objectives:
1. Assessment of the extent and level of biliary tract and portal vein
involvement.
2. Assessment of the liver for evidence of lobar atrophy or concomitant liver
pathology.
3. Evaluation for the presence of nodal and/or distant metastases.
4. An assessment of the patients overall fitness for surgery.
Although a variety of complex radiologic and interventional studies have been
utilized in the work-up of these patients, it is our practice to perform a combination
of duplex ultrasonography and magnetic resonance cholangiopancreatography
(MRCP) which we believe provides more comprehensive and relevant information
than any other combination of studies. Duplex ultrasonography is noninvasive and
can identify the site of biliary obstruction and the presence or absence of portal
venous involvement with a high degree of sensitivity and specificity (Fig. 14.2). The
efficacy of MRCP as a noninvasive means of acquiring reliable and precise informa-
tion about the anatomy of both the intra- and extrahepatic biliary tree, and the level
of tumor involvement has been well documented, and has all but replaced the need
for percutaneous and endoscopic cholangiography in our practice (Figs. 14.3A, B).
Preoperative histologic confirmation of cholangiocarcinoma is difficult to obtain.
Percutaneous needle biopsies and endoscopic brush biopsies are reliable only if they
identify a malignancy (sensitivity < 50%), and excessive reliance upon negative results
may miss the opportunity to resect an early lesion. Whereas the vast majority of
extrahepatic strictures are the result of cholangiocarcinoma, histologic diagnosis is
not mandatory prior to exploration. In the absence of clear evidence of unresectability,
all suspected cholangiocarcinoma should be considered for resection (Table 14.1).
Table 14.1. Criteria for unresectability in patients with cholangiocarcinoma

Medical comorbidities limiting the patients ability to undergo major surgery
Significant underlying liver disease prohibiting liver resection necessary for

curative surgery based on preoperative imaging 14
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

14 Fig. 14.2. Ultrasound image demonstrating tumor abutting, but not invading portal
vein. M, mass; RPV, right portal vein; LPV, left portal vein.
Staging
The two most commonly utilized staging systems for cholangiocarcinoma are
the American Joint Committee on Cancer (AJCC) TNM system and the modified
Bismuth-Corlette classification for HCCA (Tables 14.2 and 14.3). A new proposed
T staging which takes into consideration both vascular involvement by local tumor
extension, and the presence or absence of liver atrophy has recently been proposed
(Table 14.4). This T staging system is predictive of resectability, likelihood of nodal
or distant metastases, and overall survival.
Fig. 14.3A. Magnetic resonance cholangiopancreatography imaging delineating

extrahepatic biliary ductal anatomy and a hilar cholangiocarcinoma.
Surgical Resection for Hilar Cholangiocarcinoma

Treatment Results
Irrespective of the anatomic location, complete surgical resection with a negative
histologic margin is the only therapy with curative potential for cholangiocarcinoma,
and all efforts should be made to achieve negative margins when feasible.
Distal Bile Duct Tumors
Tumors of the distal bile duct require either a pancreaticoduodenectomy, or less
commonly, a local bile duct excision. Technical details related to these tumors are
addressed in Chapter 8. Very few surgical series of distal bile cancers have been 14
reported. Zerbi et al reported on 27 patients with distal bile duct cancer who under-
went pancreaticoduodenectomy. Operative mortality was 3.7%, and morbidity was
44%. All patients had negative histologic margins. The vast majority of patients
were stage IVA (81.5%, N = 22) due to pancreatic invasion, and 48% of patients
had lymph node metastases. Only 7.4% (N = 2) of patients had tumors limited to
the bile duct without either nodal, lymphatic or neural invasion identified. Despite
the addition of adjuvant therapy in 48% of patients, the authors report a mean
survival of 22 months and actuarial 3- and 5-year survival of 20 and 13% respec-
tively. Fong et al reported on 104 patients with distal bile duct cancer of which 45
patients were resected (43%). Thirty-nine patients underwent a
pancreaticoduodenectomy, and six patients had a common bile duct excision only.
A negative histologic margin was obtained in 86% of cases. Mean survival for the
Fig. 14.3B. Percutaneous transhepatic cholangiogram of the same tumor dem-

onstrating hilar obstruction and delineation of the intrahepatic anatomy and
extrahepatic anatomy.
resected patients was 33 months, with a 3- and 5-year survival of 46% and 27%.
These results are consistent with other series of distal bile duct cancer patients and
are generally indistinguishable from reports on survival following resection for pan-
14 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 liver
resection for HCCA in 50-100% of cases. Using this approach, a negative histologic
margin was achieved in more than 56% of cases and at a minimum was associated
with a trend towards increased survival in all studies. The operative mortality rate in
these aggressive series are zero to 14%. Madariaga et al performed liver resection in
100% of HCCA cases and reported the highest operative mortality rate of 14%.
These authors pursued an extremely radical approach to the management of HCCA,
in which 9 of 27 patients underwent vascular reconstruction of the portal vein,
hepatic artery or both in an attempt to get tumor clearance. All four operative deaths
Table 14.2. AJCC staging systems for cholangiocarcinoma

Stage 0 Tis N0 M0
Stage I T1 N0 M0
Stage II T2 N0 M0
Stage III T1,2 N1,2 M0
Stage IVA T3 Any M0
Stage IVB Any Any M1
Tis - Carcinoma in situ
T1 - Tumor invades subepithelial connective tissue (T1a) or fibromuscular
layer (T1b)
T2 - Tumor invades perifibromuscular connective tissue
T3 - Tumor invades adjacent structures: liver, pancreas, duodenum, stomach,
gallbladder, colon or stomach.
N0– No lymph node metastases
N1 - Metastasis in the cystic duct, pericholedochal and/or hilar lymph nodes
N2 - Metastasis in the peripancreatic (head only), periduodenal, periportal,
celiac, superior mesenteric, and/or posterior pancreaticoduodenal
lymph nodes.
M0 - No distant metastases
M1 - Distant Metastases
Table 14.3. Modified Bismuth–Corlette classification for hilar

cholangiocarcinoma
Type I Below the confluence
Type II Confined to confluence
Type IIIa Extension into right hepatic duct
IIIb Extension into left hepatic duct
Type IV Extension into right and left hepatic ducts
Other modifications of the Bismuth-Corlette classification system have been

suggested, but have not been widely accepted.
Table 14.4. Proposed modified T stage criteria for hilar cholangiocarcinoma

14
T1 Tumor confined to the confluence and/or right or left hepatic duct
without portal vein involvement or liver atrophy
T2 Tumor confined to the confluence and/or right or left hepatic duct with
ipsilateral liver atrophy. No portal vein involvement demonstrated.
T3 Tumor confined to the confluence and/or right or left hepatic duct with
ipsilateral portal vein branch involvement with/without associated
ipsilateral lobar liver atrophy. No main portal vein involvement
(occlusion, invasion, or encasement)
T4 Any of the following:
i) Tumor involving both right and left hepatic ducts up to secondary
biliary radicals bilaterally
ii) Main portal vein encasement
14
190
Table 14.5. Collective series of surgical resection for hilar cholangiocarcinoma reported since 1990
Author Study Resected Liver Histologic 3-year Operative
years N= resection margin survival mortality
% status (%) (%) (after liver
positive Negative Margin + Margin - resection)
Hadjis, 8 27 60% 44% 56% 17.5 mo* 22 mo* 7.4%

1990
Bismuth, 30 23 57% 61% 39% 12% 50% 0%
1992
Baer, 1992 4 21 43% 33% 67% 21 mo * 40 mo* 5%
Suigura 18 85 100% 43% 57% 11% 41% 8.4%
1994
Pichlmayr, 18 125 76% 27% 73% 12.2% 40.1% 10.5%
1996
Nakeeb, 23 109 7% 74% 26% 9%** 19%** 6.7%
1996
Madariaga, 14 28 100% 50% 50% 18% 40% 14%
1998
Figueras, 8 16 50% 37% 63% N/A 43% 0%
1998
Nagino, 19 138 90% 22% 78% N/A 42.7% 5.6%
1998
Miyasaki, 14 76 86% 25% 75% 8% 40% 4.6%
1998
Burke, 1998 6 30 73% 17% 83% 0%** 56%** 6%
* Figures reflect median survival

** Figures reflect 5-year survival rates
occurred in the nine patients requiring vascular reconstruction. In sum, whereas

curative resection depends on negative margins, we believe a surgical strategy that
includes partial hepatectomy in most cases of HCCA is both necessary and justified.
Liver Transplantation
The role of orthotopic liver transplantation (OLT) for cholangiocarcinoma
remains very controversial. Although OLT has been performed for both resectable
and unresectable HCCA, the high incidence of lymph node metastases associated
with this disease has limited adoption of this approach. Pichlmayr et al have reported
a series of 249 patients with HCCA in which 125 patients underwent resection, and
25 patients underwent OLT. Resectional therapy yielded equivalent or superior overall
5-year survival (27.1% versus 17.1%) at all stages of disease. Klempnauer et al have
subsequently reported on four (12.5%) 5-year survivors out of a total of 32 patients
that underwent OLT for HCCA. During this same time period 151 HCCA patients
were resected with curative intent, and 28 patients (18.5%) survived 5 years or
more. These results led the authors to conclude that radical resection offers the best
possibility of prolonged survival with a good quality of life. Although additional
reports of OLT for HCCA have appeared, OLT should not be considered a standard
form of therapy for patients with HCCA.
Palliative and Adjuvant Treatment for Cholangiocarcinoma
In the setting of advanced local disease or obvious nodal or distant metastases,
therapeutic intervention should be directed towards the relief of biliary obstruction
and its associated symptoms. Biliary decompression for jaundice in the absence of
symptoms is not justified. Biliary decompression is indicated for relief of symptoms,
facilitation of biliary access for investigational palliative therapies, and as a means to
allow recovery of hepatic parenchymal function in patients who might be candi-
dates for chemotherapeutic protocols. Percutaneous or endoscopic biliary stent place-
ment is the preferred method of decompression if unresectability is determined prior
to surgery. If unresectability or the presence of metastatic disease is identified at
laparotomy, palliative options include postoperative placement of transhepatic or
endoscopic stents, surgically placed transhepatic stents, or a surgical bilioenteric
bypass. When deciding among these options, the general physical condition and age
of the patient, in addition to projected short life expectancy must be considered.
Procedure related morbidity, including the need for prolonged or frequent hospital 14
or physician visits, limits the quality of remaining life and consumes valuable time.
In expert hands, percutaneous biliary drainage can be placed in almost all patients
and circumstances. In many instances multiple stents may be required. We prefer
metallic wall stents to plastic stents for long-term palliative relief of malignant bil-
iary obstruction. These stents are completely internal, require no catheter care, and
have a longer duration of patency than plastic stents (6-8 months). In the absence of
infectious symptomatology, the entire liver need not be drained, as it is has been
shown that only 30% of the functioning hepatic mass needs to be decompressed for
relief of jaundice.
Intrahepatic Surgical Bilioenteric Bypass
If patients are identified at laparotomy to be unresectable, we favor performing
an intrahepatic bilioenteric bypass to the Segment III hepatic duct. This procedure
provides excellent palliation, eliminates the need for frequent hospital visits for stent
change, and can be performed with low operative morbidity and mortality. In a
recent series of 20 patients undergoing Segment III bilioenteric bypass there was no
operative mortality, and a one-year patency rate of 80% was observed.
Surgical Techniques
Careful attention to the technical aspects required to perform a resection for
hilar cholangiocarcinoma is extremely important. In general there are two approaches:
1. Local resection: This entails en bloc removal of the entire supraduodenal
common bile duct (CBD), cystic duct, gallbladder, together with clear-
ance of the supraduodenal tissues of the hepatoduodenal ligament
including the related lymph nodes. A hepaticojejunostomy (Roux-en-Y)
to the remaining hepatic duct elements is required in all cases.
2. En bloc resection and reconstruction as described in (1) combined with a
right, left or extended hepatectomy: A liver resection is mandatory when
the tumor extends unilaterally either into the right or left liver, but leaves
the contralateral portion of the liver free of tumor with an intact biliary
drainage and blood supply.
A detailed description of the operative technique for resection of a hilar
cholangiocarcinoma follows. The technique for liver resection will not be described
since it is addressed in detail in Chapter 16.
Laparoscopy
It is our current practice to perform a diagnostic laparoscopy prior to a laparo-
tomy for hilar cholangiocarcinoma. In our experience, laparoscopy has identified
unsuspected intra- or extrahepatic disease altering the surgical decision to proceed
to laparotomy in 25% of cases. We begin by marking our proposed laparotomy
incision on the anterior abdominal wall with a felt pen. In general, we utilize a
bilateral subcostal (Chevron) incision that can be extended in the midline for
additional exposure if a concomitant liver resection is to be performed. Other 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 subcostal
location along the lateral edge of the proposed incision. A 30˚ camera is used to
enable complete visualization over the dome of the right and left liver. A second
14 10-mm trocar is introduced in the left subcostal location through which additional
instruments for retraction or biopsy are inserted. All segments of the liver are evalu-
ated carefully. Exposure of the caudate lobe is difficult, but can be facilitated by
placing the patient in a step reverse Trendelenberg position with slight rotation to
the left. The lesser omentum is incised and the caudate lobe inspected. Any suspi-
cious hepatic lesions should be biopsied. The hepatoduodenal ligament is carefully
inspected, and suspicious nodes unlikely to be encompassed in the resection are
excised or biopsied. All peritoneal surfaces should be carefully inspected similarly.
The greater omentum, lesser omentum, and gastrocolic omentum should also be
inspected If no contraindications to laparotomy are identified, an initial right sub-
costal incision is made. This limited incision permits bimanual palpation of the
liver, a more complete abdominal evaluation, and the performance of an intraoperative
hepatic ultrasound. The ultrasound should focus primarily on identifying unsuspected
intrahepatic metastases. Unilobar metastases that would be encompassed with an

ipsilateral hepatectomy are not a contraindication to surgical resection. All suspected
liver lesions should be biopsied with histologic confirmation of malignancy. If no
contraindications are encountered, a Chevron incision or right subcostal incision
with midline extension is completed.
Exposure and Retraction
Upon initial entry into the peritoneal cavity, exposure of the region of the
hepatoduodenal ligament is of primary importance. Although manual retraction
with handheld retractors has historically been the role of the medical student, junior
house staff, or surgical assistant, we favor the placement of a retractor that can be
fixed to the operating table to provide steady constant retraction. A Buckwalder,
Thompson, or Goligher retractor is suitable for this purpose. If there are no signifi-
cant adhesions, an operative towel or sponge may be placed over the right colon and
small bowel that can be used to pack the viscera inferiorly within the abdominal
cavity. Usually, division of the hepatocolic ligament and mobilization of the hepatic
flexure is required to aid exposure.
Once the right colon and abdominal viscera are retracted inferiorly, the first
assistant’s left hand is used to provide gentle but constant caudal retraction on the
hepatoduodenal ligament. The falciform ligament is divided between Kelly clamps,
and a tie is left on the proximal end permitting it to be used as a retractor for the
liver. In order to facilitate access to the biliary confluence and related vessels, the
CBD is transected below the cystic duct and above the duodenum. This maneuver
is mandatory, as it is impossible to differentiate vascular invasion by tumor from a
dense fibroblastic response unless the bile duct is reflected upward to reveal these
structures. Dividing the thin layer of peritoneal tissue which envelopes the
hepatoduodenal ligament usually allows easy identification of the CBD. If there is
any question, aspiration of bile with a 25 G needle provides positive confirmation.
Once encircled, the CBD is divided with a knife or electrocautery. The distal end of
the CBD is oversewn, and a suture is left in the proximal duct to permit retraction
on the CBD as it is traced upwards towards the hilum (Fig. 14.4).
The hilus of the liver is dissected according to one or a combination of 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 by 14
dividing the tongue of liver tissue bridging the base of the quadrate lobe (Segment
IV) to the left lobe (Fig. 14.5).
Alternatively, or in combination with the above technique, the liver may be split
in the Glissonian plane with division of the substance of the parenchyma down to
the hilus. Pursuance of these techniques results in mobilization of the quadrate lobe
that can then be retracted upwards. In our experience this is rarely indicated, but in
some instances it may be the only way to expose the hilum adequately.
The hepatic artery and its branches should be carefully exposed and skeletonized.
All surrounding lymphatic tissue should remain attached to the CBD and resected
en bloc. The common bile duct is carefully swept upward off the underlying portal
vein. The lymphatic tissue, which always lies lateral to the portal vein (and in some
Fig. 14.4. Resection of a hilar cholangiocarcinoma. Initial approach to a hilar

cholangiocarcinoma is made through the distal common bile duct and access to
the hilum. Reprinted with permission from: Surgery of the Liver and Biliary Tract
(3rd Edition), Blumgart LH, Fong Y and WH Jarnigan (Eds.) W.B. Saunders, London,
UK (2000).
14 cases contains a replaced right hepatic artery), should similarly remain attached to
the mobilized CBD.
A retrograde cholecystectomy, as described in Chapter 12, is performed next.
The cystic artery is identified and ligated; however, the cystic duct is traced to its
insertion in the CBD and left attached. Elevation of the common bile duct, together
with the gallbladder and related connective tissue exposes the vessels, allowing
dissection in a plane posterior to the tumor and anterior to the portal vein and
hepatic artery (Fig. 14.6). It is now, only after performing this extensive dissection,
that differentiation between vascular involvement by tumor as opposed to merely a
dense fibroblastic response, can be accomplished. Ipsilateral vascular involvement
would necessitate a hepatic resection for cure. Contralateral vascular involvement
would render the tumor unresectable, or require vascular resection and reconstruction.
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. Reprinted
Though practiced infrequently by the authors, the utility of vascular resection for hilar 14
cholangiocarcinoma is very controversial and will not be addressed in this chapter.
When local resection is to be performed, exposure of the left hepatic duct is
pursued. Once identified, it is marked with stay sutures and transected (Fig. 14.7).
A thin rim of tissue is taken for histological examination in order to establish tumor
clearance. The proximal end of the left hepatic duct is reflected to the right together
with the tumor, the mobilized common hepatic channel, and the gallbladder. This
allows continuation of the dissection towards the right hepatic duct which is always
shorter. This right hepatic duct is now cleared, marked with sutures and similarly
transected. The specimen is now removed. Once again, a thin rim of tissue is taken
for histological examination in order to establish tumor clearance. If a liver resection
is to be performed, this is completed prior to division of the right hepatic duct, and
the liver and biliary complex are removed together.
Fig. 14.6. Resection of a hilarcholangiocarcinoma. The gall bladder is removed

and the common bile duct is divided to assess vascular involvement. Reprinted
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 sectoral
ducts and the caudate lobe ducts at the confluence. Hopefully, such variations may
have been indicated on preoperative cholangiography. After removal of the tumor
there may be two, but more frequently three, four, or even five ducts exposed. Adja-
cent ducts are sutured together using # 4-0 Vicryl suture. It is usually possible to
create situations in which there are no more than three separate orifices to be anas-
tomosed. A suitable Roux-en-Y loop of jejunum is now prepared by dividing the
jejunum 10-15 cm distal to the ligament of Treitz with a GIA stapler. The Roux
limb is usually brought up in a retrocolic fashion through the bare area in the trans-
verse mesocolon. The anastomosis is completed in an end-to-side fashion between
the exposed ducts and the side of the jejunal loop (close to the termination) using a
single layer # 3-0 Vicryl interrupted suture employing the technique of Blumgart
Fig. 14.7. Resection of a hilar cholangiocarcinoma. The left bile duct is identified
(tumor-free) and transected. Reprinted with permission from: Surgery of the Liver
and Biliary Tract (3rd Edition), Blumgart LH, Fong Y and WH Jarnigan (Eds.) W.B.
Saunders, London, UK (2000).
and Kelly (Fig. 14.8). This technique is extensively described in Chapter 13. It is 14
important to note that when performing high biliary anastomoses to multiple ducts,
the anastomoses should not be done to a single duct at a time working sequentially;
such an approach is very difficult at best and may be impossible. Rather, the pre-
ferred method is to place the entire anterior sets of sutures to all exposed ducts and
then separately place the entire posterior row of sutures. The jejunum is then rail-
roaded up on the posterior sutures. The posterior layer of sutures to all exposed
ducts are tied first and then individual anterior layers are completed sequentially. A
10 F Jackson Pratt drain is routinely left through a separate stab wound incision.
Palliative Approaches
The majority of patients with hilar cholangiocarcinoma are not suitable for
resection due to the presence of metastatic disease, advanced age and comorbidities.
If unresectability is determined preoperatively, therapeutic options include no
Fig. 14.8. Resection of a hilar cholangiocarcinoma. A Roux-en-Y limb of jejunum is

brought to the edge of the transected right and left bile ducts for primary anastomosis.
treatment at all or percutaneous biliary stenting if indicated for symptoms or to

14 facilitate access to other treatment. If the tumor is found unresectable at laparotomy,
available options are either a biliary-enteric anastomoses (we prefer a Segment III
bypass described in Chapter 13) or transtumoral tube. The technique for a palliative
bypass or intubation may be combined with radiotherapeutic approaches in some
instances, but no prolongation of survival for this technique has been demonstrated. In
rare instances, palliative (incomplete) resection may be combined with intubation.
Assessment of the results of various palliative methods is difficult. In many series,
patients submitted to surgical decompression may have been suitable for a com-
bined biliary and hepatic resection and therefore constitute a better risk group, while
in other instances patients were possibly too ill to tolerate any form of treatment at
all. In many series, histological confirmation of the nature of the stricture is not
available, and in many instances it is not sought. In contradistinction, the wide-
spread availability of percutaneous and endoscopic biliary decompression techniques
and expertise has in some cases led to the application of these palliative approaches
prior to due consideration of resection, or whether biliary-enteric bypass might 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 and
into the intrahepatic ducts exiting through the anterior abdominal wall. The lower
end of the tube is also delivered at the skin. The tube thus traverses the tumor and
allows drainage of bile into the gut. The tube can be readily washed out and can be
replaced by attaching a second tube to one end and pulling it through the estab-
lished sinus track. The procedure may be combined with a Roux-en-Y
hepaticojejunostomy rather than bring the lower end out through the common bile
duct—a technique we prefer. Although there is no doubt U tubes provide palliation,
they do not prolong survival. If U tubes are used, it is paramount that care be taken
to confirm a malignant diagnosis before claims of long term survival after intuba-
tion or indeed any other treatment option can be accepted. In our opinion, recent
advances in the development of percutaneous and endoscopic intubational tech-
niques and endoprostheses have made operative tubal placement rarely necessary.
Adjuvant Therapy
At this time there is no effective adjuvant therapy for cholangiocarcinoma. The
literature contains four small phase II chemotherapeutic trials for cholangiocarcinoma.
A single study reported one complete response with a partial response (PR) rate of
21.4% using a regimen of 5-FU, leucovorin, and carboplatin. In more recent reports
however, minimal response and PR rates far less than 20% are the norm. We have
reported on the management of 12 HCCA patients treated with 2000 cGy delivered
via intraductal brachytherapy catheters afterloaded with Iridium, and followed by
5000 cGy of external beam radiation over 5-6 weeks. Mean survival among the
group was 14.5 months with all patients surviving 6 months. Similar promising results
utilizing external beam radiotherapy alone and neoadjuvant chemoradiotherapy have
been reported; however all approaches are considered investigational and should be
applied selectively if at all.
Photodynamic therapy has recently been applied in the palliative management
of HCCA. Unresectable patients treated intravenously with a hematoporphyin
derivative, followed two days later by intraluminal cholangioscopic photoactivation 14
have shown a precipitous fall in serum bilirubin and a subjective improvement in
quality of life. No procedural related morbidity or mortality was reported. Median
survival was 14.5 months. Although this new modality appears promising, validation
of these results awaits further investigation.
Conclusion
Cholangiocarcinoma is an uncommon malignancy that almost uniformly 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 attainable
only in the minority of patients (< 30%). Distal bile duct cancer is treated by
pancreaticoduodenectomy or local bile duct excision with survival rates similar to those
seen with pancreatic cancer. In regards to the management of HCCA, data now exist
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 prolong
survival. No effective adjuvant therapy can be recommended. In sum, radical surgery
remains the mainstay of therapy for all forms of cholangiocarcinoma. The rarity of
this neoplasm and the expertise required for its management should prompt physi-
cians and patients to seek care at specialized hepatobiliary referral centers.
Selected Readings
1. 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 presurgical
clinical 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 Livingstone
1994:1051-1067.
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 hilar
cholangiocarcinoma. Ann Surg 1992; 215:31-8.
7. Fong Y, Blumgart LH, Lin E et al. Outcome of distal bile duct cancer. Br J Surg
1996; 83:1712-5.
8. Nagorney DM, Donohue JH, Farnell M et al. Outcomes after curative resections
of cholangiocarcinoma. Arch Surg 1993; 128:871-79.
9. Blumgart LH, Benjamin IS, Hadjis NS et al. Surgical approaches to
cholangiocarcinoma at the confluence of hepatic ducts. Lancet 1984; 1:66-70.227:
821-833.
10. Chamberlain RS, Blumgart LH. Hilar cholangiocarcinoma: A review and com-
mentary. Ann Surg Oncol 2000 Jan-Feb; 7(1):55-66.
14
CHAPTER 1
CHAPTER 15
Surgical Management
of Gallbladder Cancer
Introduction
Gallbladder adenocarcinoma is a treacherous entity. It produces symptoms late
in the course of the disease, disseminates rapidly from the primary site, and responds
infrequently to nonsurgical therapy. The overall median survival for all patients is
less than 6 months. The disease is up to five times more common in females. It is
usually associated with gallstones, although few patients with gallstones actually
develop gallbladder cancer. It is the most common biliary tract cancer and is the
fifth leading gastrointestinal malignancy in the United States. Nevertheless, gall-
bladder adenocarcinoma is seldom encountered and, consequently, its diagnostic
evaluation and management are not widely appreciated.
Anatomical Considerations
The management of gallbladder cancer requires a thorough knowledge of the
common variations in the biliary tract and hepatic vasculature and the normal
anatomy of the gallbladder with its relation to surrounding structures. The gallblad-
der is situated in the inferior aspect of the liver at the junction of Segments IVb and
V. It lies in proximity to the major portal structures and often abuts the duodenum
or transverse colon. Terminal branches of the middle hepatic vein are adjacent to the
gallbladder bed. The right anterior portal pedicle lies deeper in the substance of the
liver and branches into the Segment V and VIII pedicles.
A thorough understanding of the patterns of tumor dissemination is essential to
the management of gallbladder cancer. The disease spreads through the lymphatics
via the bloodstream or by direct invasion. The lymphatic drainage of the gallbladder
has been well-defined. The immediate (N1) drainage comprises the cystic duct node
and the pericholedochal nodes. From there, drainage proceeds to the N2 nodes that
include the posterior pancreatic, periduodenal, periportal, superior mesenteric, com-
mon hepatic artery, interaortocaval, and celiac lymph nodes. All other nodes are
considered M1. Hematogenous metastases most commonly occur to the liver and
lung and, less commonly, the brain. Direct spread occurs by local invasion, spread
through the peritoneum, or extension along the wounds. Local invasion of the liver
occurs readily in gallbladder cancer because the normal gallbladder wall is quite thin
and gallbladder cancer is known to disseminate early within the peritoneal cavity.
Consequently, the subserosal plane of gallbladder dissection that is commonly utilized
in routine cholecystectomy should be avoided when a gallbladder cancer is suspected.

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 commonly
accepted is the American Joint Committee on Cancer (AJCC) TNM staging criteria
which is outlined in Table 15.1.
Symptoms
Patients with gallbladder cancer are often initially asymptomatic. Nonspecific
symptoms of abdominal pain and weight loss may mimic the symptoms of benign
gallbladder disease. Jaundice is an ominous sign in patients with gallbladder cancer.
It is the result of direct tumor invasion of the common bile duct, ductal compres-
sion by tumor, or involved lymph nodes. It suggests that the tumor is advanced or
originated in the gallbladder neck or cystic duct and is therefore more likely to
involve the portal vascular structures. It should be remembered that Mirizzi syn-
drome may be associated with a gallbladder cancer.
Diagnostic Evaluation
A 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 the
surgeon review the sonographic images prior to planning biliary surgery, even when
benign biliary disease is suspected. Magnetic resonance cholangiopancreatography
(MRCP) may be used to define ductal anatomy and avoids contamination of the
bile that is associated with direct cholangiography. In a patient without jaundice, a
computerized tomography (CT) of the abdomen and pelvis may be sufficient to
search for intra-abdominal dissemination. If percutaneous transhepatic cholangiog-
raphy (PTC) or endoscopic retrograde cholangiopancreatography (ERCP) is per-
formed, then cytology or brushings should be obtained. It should be emphasized
that a tissue diagnosis is not necessary prior to surgical exploration. Percutaneous
biopsy should be avoided, especially given the chance of tumor spread along the
needle tract or in the peritoneum and should be reserved solely to confirm a malig-
nant diagnosis in unresectable disease.
A few specific radiologic findings should be assessed. In particular, the presence
of liver invasion or liver metastases should be sought. Lymphadenopathy may repre-
sent metastatic disease or local inflammation. A calcified “porcelain” gallbladder
15 may indicate the presence of an underlying gallbladder cancer. The finding of a
mid-common bile duct stricture should always raise the suspicion of a gallbladder
cancer. Gallbladder tumors that arise in the neck of the organ may be difficult to
distinguish from hilar cholangiocarcinoma.
Clinical Presentations
Patients may present to a physician or a referral center with a variety of clinical
scenarios including:
1. A patient may be discovered to have a gallbladder mass preoperatively or
at the time of laparoscopy or laparotomy (Fig. 15.1).
Surgical Management of Gallbladder Cancer 203
Table 15.1. TNM staging criteria for gallbladder cancer

Stage I T1 N0
Stage II T2 N0
Stage III T1-2 N1
T3 N0-1
Stage IVA T4 N0-1
Stage IVB Any N2 or M1
T1 tumor invades lamina propria or muscle
T2 invasion of perimuscular connective
tissue
T3 liver invasion <2 cm or involves 1
adjacent organ
T4 liver invasion >2 cm or involves 2
adjacent organs
The AJCC TNM staging of gallbladder cancer is outlined along with the definition
of tumor (T) stage. Nodal (N) stage is defined in the text.
2. A patient has already undergone a cholecystectomy, either for suspicion

of gallbladder cancer or for presumed benign disease, with the incidental
discovery of a cancer in the pathologic specimen (Fig. 15.2).
Gallbladder Mass Identified Preoperatively
A gallbladder mass identified preoperatively enables referral to a specialty center
if necessary. It allows for a complete discussion with the patient regarding the range
of operations (cholecystectomy to radical resection) that may be performed. Thor-
ough radiologic evaluation is also possible. Unfortunately, a mass may be visible but
overlooked in the presence of gallstones. A gallbladder polyp that is less than 1 cm in
size may be observed with serial imaging. Larger masses should be considered to be
malignant until proved otherwise, although only a fraction of them will actually
contain cancer. A “porcelain” gallbladder should also be resected. To avoid the pos-
sibility of dissemination to port sites or the peritoneum during insufflation at
laparoscopy, 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 be
made to avoid inadvertent entry into the gallbladder and potential tumor spillage. If
the mass is found to penetrate into the liver, the operation should be adjusted accordingly.
15
Gallbladder Cancer Identified Intraoperatively
A gallbladder cancer may be detected at the time of operation. If it is recognized
at exploration during laparoscopy or laparotomy, then the procedure should usually
be aborted if radical resection is required. In this way, the patient can be further
evaluated and appropriately consented. If there is doubt about the diagnosis, then
fine needle aspiration with minimal manipulation of the tumor may be performed.
However, it is paramount not to compromise resectability. Cholecystectomy should
be avoided as a means to make the diagnosis when the surgeon is not prepared to
perform radical resection if the cancer is greater than Stage I.
Fig. 15.1. Treatment algorithm for patients found to have gallbladder carcinoma
before or during exploration.
A gallbladder cancer may also become known immediately after the removal of
the 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 convert
15 to laparotomy only if he is able to carry out a radical resection if one is indicated. If
an open cholecystectomy was performed, and the surgeon is not prepared to per-
form a radical resection, the cystic duct node should be taken and the cystic duct
margin proved to be negative by frozen section.
Gallbladder Cancer with Prior Operation
With the advent of laparoscopic cholecystectomy, a frequent occurrence is the
incidental finding of an occult gallbladder cancer in the pathologic specimen. If
another surgeon operated upon the patient, emphasis should be placed upon gain-
ing as much information as possible about the primary tumor because its location
may dictate the type of operation that is now necessary. Consultation with the primary
Fig. 15.2. Treatment algorithm for patients discovered to have gallbladder can-
cer after previous operation.
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 cystic
duct are also important. The initial tests performed prior to the first operation should
also be reviewed. The presence of a mass may often be found retrospectively, especially
on ultrasound studies.
A re-operation for gallbladder cancer should include excision of all prior surgical
wounds (port sites, drain sites, laparotomy wounds) because of the frequency of
local tumor recurrence. Often, the duodenum or transverse colon is densely 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 a
re-resection is distinguishing tumor from scar tissue that has developed from the
initial procedure. For this reason, many patients will require a bile duct and liver
resection to guarantee adequate clearance. A re-resection should be performed in
patients with Stage II to IV A disease (see below). The patient should be aware of the
possibility that no additional disease may be found in the pathologic specimen even
if a radical operation is undertaken.
15
Surgical Approach
A patient who is medically fit without evidence of metastases and has a normal
chest x-ray, should undergo exploration for resection since it offers the only chance
of cure and long-term survival. The treatment of gallbladder cancer is based on the
stage (radiologic or pathologic) of disease and the prior therapeutic interventions.
Treatment by Tumor Stage
The treatment of a Stage I tumor confined to the mucosa is simple cholecystec-
tomy. If it is discovered intraoperatively, the cystic lymph node should be excised
and the portal nodes should be carefully evaluated although they are unlikely to be
involved. Often, these tumors are discovered incidentally at pathologic examina-

tion. No further therapy is indicated because few of these patients will recur. Patients
with Stage II tumors are the most likely to benefit from radical resection (or
re-resection) that includes an en bloc lymphadenectomy and liver resection with or
without bile duct resection. These patients will have a 50-70% 5-year survival rate
with complete resection. Stage III and IVA patients should have similar treatment
and most of them will require extended hepatic resection. This group of patients can
be expected to have about a 20-40% 5-year survival rate after complete resection.
Stage IVB patients should undergo palliation for symptomatic jaundice. Therapy
should be minimized given their short survival. In most cases, interventional radio-
logic procedures can provide biliary drainage with the use of Wallstents. In patients
who were explored with the presumption of less advanced disease, a Segment III
enteric bypass may be indicated.
Laparoscopy
Laparoscopy is advocated to identify occult peritoneal or hepatic metastases that
would preclude resection and obviate laparotomy. Often, the port sites can be posi-
tioned in the line of the intended laparotomy incision. The finding of gross ascites
should prompt cytological evaluation which, if positive, would make a resection
contraindicated.
Lymphatic Dissection
If 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 to
palpate the retropancreatic lymph nodes. The hepatic artery nodes should also be
inspected. N2 nodal disease is considered inoperable, although some surgical groups
advocate combined pancreaticoduodenectomy and hepatectomy. In the absence of
N2 disease, the incision should be extended to the xiphoid and the retractors posi-
tioned. A Goligher retractor is preferred with blades that retract both costal margins
laterally and upward. Alternatively, a Buchwalter retractor may be used. The lym-
phatic dissection begins with sweeping the superior retropancreatic nodes upward
to the hilus of the liver. The bile duct is identified at the superior border of the
pancreas and is divided and lifted forward to further expose the lymphatic tissue in
the porta and improve the completeness of lymphadenectomy. Some prefer to avoid
bile duct transection (and thus reconstruction) for patients with T2 tumors without
15 previous surgical intervention or those with tumors located in the fundus. The gas-
troduodenal artery is dissected free and usually preserved. The dissection continues
with skeletonization of the hepatic artery and portal vein up to the hilus and then to
the duct that is being preserved (usually the left hepatic duct).
Liver Resection
The extent of hepatectomy necessary in the resection of gallbladder cancer is
somewhat controversial. It depends on the location of the primary tumor and whether
an operation has already been performed. For tumors with minimal (T3) liver inva-
sion, a formal anatomic Segment IVB and V resection is preferred over a wedge
resection to guarantee adequate tumor clearance and minimize bleeding and biliary
leak. The Segment IVB vessels can be controlled just to the right of the umbilical
fissure through a hepatotomy that is performed during a Pringle maneuver. The

Segment V portal triad is identified within the parenchyma with care given to 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 tumor
clearance. Actually, an extended right lobectomy is often necessary inferiorly. Mean-
while, the plane of a right hepatic lobectomy is followed cephalad (which is at some
distance from the tumor), thus sparing Segment IVA. There are rare instances when
an extended left lobectomy may be indicated to remove a gallbladder cancer.
Bile Duct Resection and Reconstruction
Whether every patient with a T2 or greater gallbladder cancer needs resection of
the common bile duct is unclear. In the absence of direct tumor invasion, it is usu-
ally done to facilitate a thorough portal lymphadenectomy. In certain patients, such
as those who are thin or those with tumors of the fundus, biliary resection (with its
increased morbidity) may be avoided. However, it is usually performed for resection
of T2 or greater tumors. When bile duct resection is necessary, a standard
hepaticojejunostomy is created to the common hepatic duct or lobar duct (almost
always the left hepatic duct) using a 60-70 cm Roux-en-Y limb. This is described in
detail in other chapters.
Summary
Gallbladder cancer continues to be a challenging disease. A detailed knowledge
of biliary anatomy and familiarity with the dissemination pattern of gallbladder
cancer prepares the surgeon to perform a variety of operations depending on the
location of the tumor and the patient’s previous treatment.
Suggested Reading
1. 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 carcinoma
of the gallbladder based on the histologic analysis of 48 surgical specimens. Am J
Surg 1992; 163:239-245.
3. Fong Y. Submitted. Ann Surg.
15
CHAPTER 16
Techniques of Hepatic Resection

Sharon Weber, William R. Jarnagin, Leslie H. Blumgart
Introduction
Hepatic resection is the most effective treatment for patients with primary and
selected secondary malignant tumors. It is also indicated for certain benign lesions.
In nearly all instances involving patients with malignant hepatic disease, resection is
the only treatment with curative potential. Over the past 30 years, improvements in
perioperative care and surgical technique have dramatically decreased the morbidity
and mortality of major hepatic resection, thus making it a viable treatment option
for many patients.
The risk of hemorrhage has been the major obstacle to the safety of hepatic
resection. While this remains a concern, blood loss and transfusion requirements
have been markedly reduced as a result of changes in operative technique. Although
portal triad clamping reduces hepatic arterial and portal venous bleeding during
parenchymal transection, this has no effect on bleeding from the hepatic veins which
are usually the major source of blood loss. Inflow and outflow vascular control be-
fore parenchymal transection, low central venous pressure anesthesia, and anatomi-
cally based resections, are all important components of contemporary hepatic resection
and 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 to
lower intraoperative blood loss or transfusion requirements.
Operative Technique
In 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 tumor
was previously considered to be essential, recent studies have shown that a resection
margin of a few millimeters is probably adequate. Regardless, anatomically based
segmental resections are the best means of achieving a negative margin. Wedge re-
sections have a higher incidence of positive margins, are associated with greater
blood loss, and should be avoided except for small peripheral lesions.
Major intraoperative bleeding is generally the result of injury to the hepatic veins
or vena cava. To minimize venous bleeding, early control of the hepatic veins is
performed before dividing the liver, and the venous outflow is divided after control-
ling the inflow blood supply. A low central venous pressure (CVP) of 5 mm Hg or
less minimizes bleeding from disrupted hepatic veins, which may occur during
mobilization or parenchymal transection. Early fluid restriction is maintained to
achieve both low CVP and the minimal volume necessary for renal perfusion, but

Techniques of Hepatic Resection 209
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. If
the patient appears to be resectable, a right subcostal incision is made with extension
of the incision as necessary. Exploration for extrahepatic disease is performed. The
round ligament is divided, leaving a long suture on the hepatic side for traction. The
falciform ligament is divided up toward the hepatic veins, and the right triangular
ligament and the coronary ligament are partially divided with cautery (Fig. 16.1).
Once fully mobilized, the liver is examined with bimanual palpation and intraop-
erative ultrasound (IOUS) both to identify the tumor(s), the presence of additional
disease, and to assess the relationship of the tumor(s) to the major vascular structures.
For right-sided resections, the right liver is detached from its diaphragmatic
attachments by completely dividing the right triangular ligament and exposing the
bare area of the liver. This is facilitated by rotating the table away from the surgeon,
retracting the right lobe of the liver medially and anteriorly, and pulling the dia-
phragm laterally. The peritoneum at the inferior border of the liver is divided lateral
to medial, taking care to avoid injury to the right adrenal gland. Small veins drain-
ing from the liver into the IVC are separated from the caudate process all the way up
to the hepatic venous confluence (Fig. 16.2). During this dissection, a ligamentous
band is encountered which arises from the caudate lobe on the left, passes posterior
to the IVC, and attaches to Segment VII. This ligament may contain small vessels or
hepatic parenchyma and must be divided in order to expose the right hepatic vein.
For left-sided resections, the left liver is mobilized by dividing the left triangular
ligament and left coronary ligament to the lateral margin of the IVC, avoiding injury
to the left hepatic vein. The lesser omentum should be incised and the ligamentum
venosum, which runs along the anterior surface of the caudate lobe to enter the left
hepatic vein, should be ligated and divided.
Right Hepatectomy
Right hepatectomy involves removing all hepatic parenchyma to the right of the
middle hepatic vein (Segments V, VI, VII, and VIII). If necessary, the middle he-
patic vein can be sacrificed during right hepatectomy since the umbilical and left
hepatic veins will provide adequate drainage of the remaining left liver. After full
mobilization, vascular inflow and outflow control should be achieved. Three general
approaches have been described for achieving vascular inflow control: extrahepatic
dissection within the porta hepatis with division of the right hepatic artery and right
portal vein prior to division of the parenchyma (Fig. 16.3); intrahepatic control of
the main right pedicle within the substance of the liver prior to parenchymal transec-
16
tion (pedicle ligation); or intrahepatic control of the pedicle during parenchymal
transection. For the overwhelming majority of resections, we control the inflow
extrahepatically with either a hilar dissection or, if possible, the pedicle ligation tech-
nique. Proceeding with liver resection before inflow control is achieved is not advised.
Extrahepatic vascular control begins with cholecystectomy. If the gallbladder is
involved by the tumor, it should not be removed, but the cystic duct and cystic
artery ligated and divided. The common hepatic artery should then be dissected
16
Fig. 16.1. Initial exposure of the liver. A. Upward retraction of the ribs is achieved with
an overhead retractor. The ligamentum teres is divided. B. The falciform ligament is
divided up toward the hepatic veins to expose the inferior vena cava. The divided end
of the ligamentum teres is used to retract the liver. Reprinted with permission from LH
Blumgart. Liver resection—liver and biliary tumours (with comments by B Launois and
C. Huguet, Hepatic cryosurgery addendum by Y Fong). Surgery of the Liver and Biliary
Tract, 2d Edition. LH Blumgart, ed. 1994. © Churchill Livingstone.
Fig. 16.2. The liver has been fully mobilized and is retracted laterally to the patient’s
right. Multiple small veins draining posteriorly from the liver into the inferior vena
cava are carefully dissected and divided from the caudate process to the hepatic
venous confluence. This allows full mobilization of the right lobe of the liver. 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 Y
Fong). Surgery of the Liver and Biliary Tract, 2nd Edition. LH Blumgart, ed. 1994. ©
Churchill Livingstone.
sufficiently to reveal the right and left branches after which the right branch can be
divided with suture ligatures. The portal vein is then exposed. Again, the right and
left branches should be clearly identified. A small branch from the right portal vein
to the caudate process is a constant finding and should be controlled early in the
dissection. This maneuver facilitates exposure of an additional length of the right
portal vein making it easier to divide. Once adequately dissected, the right portal
vein may then be divided between vascular clamps and oversewn or, as we prefer, 16
divided with a vascular stapler.
Vascular anomalies are not uncommon, and the surgeon should be prepared to
deal with them. The common variations of arterial anatomy are well-described.
However, variant anatomy of the portal vein is also encountered, the most common
of which is a separate origin of the right anterior and posterior branches. For all
major hepatic resections, it is essential to fully define the vascular anatomy in order
to avoid potentially disastrous injury to the contralateral branch.
Fig. 16.3. Extrahepatic dissection within the porta hepatis for a right hepatectomy. A.
The cystic and hilar plates are lowered to expose the right pedicle. B. The peritoneum
overlying the common bile duct is incised. The cystic duct and cystic artery are ligated
and divided. A tie has been left on the cystic duct for retraction. C. The right hepatic
duct is dissected. D. The right hepatic duct has been ligated and divided with absorb-
able suture. The right hepatic artery is dissected, ligated and divided. E. The right portal
vein is dissected, doubly clamped and divided. The branch from the caudate process is
either divided prior to dividing the right portal vein. F. The proximal end of the portal
vein is oversewn with vascular suture. Reprinted with permission from LH Blumgart,
Liver resection—liver and biliary tumours (with comments by B Launois and C. Huguet,
Hepatic cryosurgery addendum by Y Fong). Surgery of the Liver and Biliary Tract, 2d
Edition. LH Blumgart, ed. 1994. © Churchill Livingstone.
When possible, we perform a pedical ligation maneuver to control the partial

structures. This technique has several advantages over hilar dissection. After remov-
ing the gallbladder, two hepatotomy incisions are made medially at the base of the
gallbladder fossa and within the caudate process parallel to the IVC (Fig. 16.4).
With the portal triad occluded (Pringle), a finger or clamp is then passed into the
16 substance of the liver to encircle the main right pedicle (Fig. 16.5), which is encased
in a tough, fibrous sheath (Fig. 16.6). Bleeding from terminal branches of the middle
hepatic vein may occur but is readily controlled. Residual liver tissue is then cleared
away to expose the pedicle and identify the anterior or posterior branches to the
individual segments for segmental resections. Before dissecting the pedicle, it is
essential to divide all posterior venous branches entering the IVC (Fig. 16.2); other-
wise, these veins may be torn and significant hemorrhage will occur. Once the right
pedicle is isolated, it should be occluded temporarily and the portal triad clamp
Fig. 16.4. Approach to pedicle ligation during right hepatectomy. The gallbladder
has been removed and the cystic and hilar plates lowered. Hepatotomy incisions
are made in the caudate process (1) and in the gallbladder fossa (2) to allow control
of the right pedicle. Reprinted with permission from LH Blumgart. Liver 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, 2d
Edition. LH Blumgart ed. 1994. © Churchill Livingstone.
released to reveal the line of demarcation along the principal plane. Performance of
a pedicle ligation eliminates the need for hilar dissection, thereby saving time and
reducing the potential of injury to the bile duct or contralateral vascular structures.
Once again, we stress that this approach is not appropriate for tumors that encroach
on the hilus, since the resection margin will be compromised.
When hilar dissection is used, it is not necessary to attempt to encircle and di-
vide the right hepatic duct after the vascular pedicle is isolated. This maneuver risks
injury to the biliary confluence. Control of the right hepatic duct can be obtained
during parenchymal transection.
With the inflow controlled, outflow control of the right hepatic vein is achieved
next (Fig. 16.7). Although the right hepatic vein is visible after initial mobilization,
complete control requires further dissection of the avascular tissue along the supra- 16
hepatic vena cava, between the right and middle hepatic veins. The right vein can
then be encircled and divided with a vascular stapler (preferably) or divided between
vascular clamps and oversewn. Alternatively, the right vein may also be controlled
and divided within the substance of the liver during parenchymal transection,
although extrahepatic control is our preference.
The line of parenchymal transection may be to the left or right of the middle
hepatic vein, depending on the location of tumor. The surgeon should not hesitate
Fig. 16.5. Intrahepatic control of the right pedicle using finger dissection. After the
hepatotomy incisions are made, finger dissection of the parenchyma is used to
isolate the right pedicle. A curved clamp may also be used. Note the proximity of
the middle hepatic vein. Reprinted with permission from LH Blumgart. Liver 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, 2d
Edition. LH Blumgart ed. 1994. © Churchill Livingstone.
to divide the middle vein if necessary, since the umbilical vein will provide adequate
drainage of Segment IV. Parenchymal division begins by marking the line of transec-
tion with the electrocautery and cutting the capsule with scissors. Stay sutures of 0
chromic catgut are placed on either side of the transection plane and used for trac-
tion as dissection proceeds. A Kelly clamp is used to crush the liver parenchyma, and
exposed vessels are controlled with clips, ligatures or the vascular stapler. Although
the liver can tolerate warm ischemia for up to 60 minutes, intermittent portal triad
clamping during the parenchymal transection phase allows decompression of the
mesenteric veins. After transection is complete, the raw surface of the liver is exam-
ined for hemostasis and bile leaks. The argon beam coagulator is used to control raw
surface oozing. Biliary leaks should be clipped or suture ligated.
The authors do not use closed suction drainage after routine hepatic resection
16 unless concomitant biliary resection and reconstruction have been performed, if a
portion of the diaphragm has been resected and repaired, or if there is obvious bile
leakage that cannot be fully controlled with suture ligation.
Extended Right Hepatectomy (Right Hepatic Lobectomy
or Right Trisegmentectomy)
The additional removal of Segment IV during right hepatectomy (V, VI, VII,
VIII) constitutes an extended right hepatectomy or right trisegmentectomy. The
initial steps are similar to right hepatectomy, with division of the right hepatic vein
Fig. 16.6. Isolation of the portal pedicles. A portion of the liver has been removed
to demonstrate the intrahepatic portion of the main right portal pedicle. Within the
liver, the pedicles are encased within a thick fibrous sheath. Again, note the prox-
imity of the right pedicle to the middle hepatic vein. Reprinted with permission
from LH Blumgart. Liver resection—liver and biliary tumours (with comments by B
Launois and C. Huguet, Hepatic cryosurgery addendum by Y Fong). Surgery of the
Liver and Biliary Tract, 2d Edition. LH Blumgart ed. 1994. © Churchill Livingstone.
and portal pedicle. The bridge of tissue connecting Segments III and IV, which may
be well-developed hepatic parenchyma in some patients, is divided to reveal the
lower part of the umbilical fissure. The ligamentum teres can be seen within the
umbilical fissure, joining the left portal vein.
After the right pedicle is divided, the recurrent vessels from the umbilical
fissure to Segment IV are controlled (Fig. 16.8). This may be achieved within
the umbilical fissure or during parenchymal transection. The right hepatic vein
is divided as described above.
The liver is transected just to the right of the falciform ligament using the stan-
dard parenchymal crushing technique. The middle hepatic vein is encountered as dis- 16
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 the
middle hepatic vein. This is of particular concern for tumors involving Segment IVa.
Left Hepatectomy
Removal of Segments II, III and IV constitutes a left hepatectomy. After full
mobilization of the left triangular ligament, inflow control is achieved outside of the
liver at the base of the umbilical fissure (Fig. 16.9). The bridge of tissue connecting
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 hepatic
vein. 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 hepatic
vein had been divided and the stump oversewn with vascular suture. It is gen-
16 erally not necessary to control the vena cava above and below 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 Y Fong). Surgery of the Liver and Biliary Tract, 2d Edition. LH
Blumgart ed. 1994. © Churchill Livingstone.
Fig. 16.8. Extended right hepatectomy. A. Recurrent vessels from the umbilical fissure
to Segment IV are divided and suture-ligated just to the right of the falciform ligament.
The recurrent vessels may also be divided from within the umbilical fissure, taking care
to avoid injuring the main left pedicle. B.Division of the liver parenchyma proceeds
toward the inferior vena cava to the right of the falciform ligament. Reprinted from LH
C. Huguet, Hepatic cryosurgery addendum by Y Fong). Surgery of the Liver and Biliary
Tract, 2d Edition. LH Blumgart ed. 1994. © Churchill Livingstone.
Segments III and IV on the undersurface of the liver must be divided. The hilar
plate is lowered and the left hepatic artery identified and divided. The portal vein is
identified at the base of the umbilical fissure. If the caudate is to be preserved, then
the portal vein is controlled beyond the origin of the principal caudate branch which
usually arises from the left portal vein. The long extrahepatic course of the left bile
duct can be identified behind the portal vein and divided at the umbilical fissure, or
controlled from within the hepatic parenchyma.
The left and middle hepatic veins are controlled after mobilizing the left lobe
and lifting it anteriorly and to the right (Fig. 16.10). The gastrohepatic ligament is
initially divided exposing the ligamentum venosum, which itself is divided just prior
to entry into the left hepatic vein. Control of the veins is obtained by careful dissec-
tion from above and below the liver; a passage is developed from just to the right of
the middle hepatic vein from above and the superior border of the caudate lobe 16
from below. The middle and left hepatic veins most often enter the IVC as a single
trunk (Fig. 16.10), but may be independent in some cases. The veins are divided
and stay sutures placed along either side of the principal plane, followed by paren-
chymal transection.
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 the
entire left liver including the caudate lobe. B. Division above the caudate branch
will preserve the caudate blood supply and devascularize Segments II, III, and IV.
C. The point of division to divide the Segment II pedicle. D. The point of division to
divide the Segment III pedicle. Note: The pedicles to IVa and IVb branch off the
right side of the left portal triad with the umbilical fissure and can be controlled
here for an extended left lobectomy. Reprinted with permission from LH Blumgart.
Liver resection—liver and biliary tumours (with comments by B Launois and C.
Huguet, Hepatic cryosurgery addendum by Y Fong). Surgery of the Liver and 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 III
and IV, is divided after mobilization. For tumors lying close to the fissure, the pedicles
to Segments II and III can be dissected individually within the umbilical fissure
(Fig. 16.9). An alternate approach for peripheral lesions is splitting the liver
16 anteroposteriorly just to the left of the falciform ligament. The Segment II and III
pedicles can then be divided during parenchymal transection. The left hepatic vein
can be controlled and divided within the liver substance posteriorly, thus obviating
the need for extrahepatic dissection. However, if the tumor approximates the left
hepatic vein, extrahepatic dissection and control are essential.
Extended Left Hepatectomy (Left Trisegmentectomy)
An extended left hepatectomy involves removal of Segments V and VIII (the
anterior sector of the right liver) in addition to a left hepatectomy (Segments II, III
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 just
to the right of the middle hepatic vein from above and the superior border of the
caudate lobe (A to B). The veins are clamped, ligated and divided. IVC = inferior
vena cava; MHV = middle hepatic vein; LHV = left hepatic vein; GB = gallbladder.
Reprinted with permission from LH Blumgart. Liver resection—liver and biliary
tumours (with comments by B Launois and C. Huguet, Hepatic cryosurgery adden-
dum by Y Fong). In: LH Blumgart ed. Surgery of the Liver and Biliary Tract, 2nd
Edition. 1994. Edinburgh UK.
and IV). This is among the most challenging of hepatic resections; the difficulty lies
in defining the plane of transection (Figs. 16.11 and 16.12). Injury to the posterior
sectoral pedicle, or to the right hepatic vein, must be avoided at all cost.
The presence of a large accessory right hepatic vein is a potentially important
finding, especially for tumors encroaching on the main right hepatic vein origin,
and may allow sacrifice of the main right hepatic vein for tumor clearance. Dissec-
tion proceeds as with a left hepatectomy, with the portal triad approached from the 16
left side. If the caudate lobe is to be included in the resection (Fig. 16.11, inset), the
left hepatic artery and portal vein should be ligated close to their origins in order to
disconnect the blood supply to both caudate and Segments II and III (Fig. 16.9). If
the caudate is preserved, the left portal triad is transected at the base of the umbilical
fissure, preserving the blood supply to the caudate (Fig. 16.9). If possible, the 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.
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 is
along the ligamentum venosum, the base of the quadrate lobe and hilus, and along
the right scissura lateral to the gallbladder fossa. If the caudate lobe is to be resected,
the left hepatic artery and left branch of the portal vein are divided close to their
origins (inset). Reprinted with permission from LH Blumgart. Liver resection—liver
and biliary tumours (with comments by B Launois and C. Huguet, Hepatic
cryosurgery addendum by Y Fong). In: LH Blumgart ed. Surgery of the Liver and
Biliary Tract, 2d Edition. 1994. © Churchill Livingstone.
16 Controlling the middle and left hepatic veins extrahepatically is important to reduce
blood loss during parenchymal transection.
The greatest challenge to the procedure is defining the plane of transection,
which is horizontal and anterior and parallel to the right scissura, just lateral to the
gallbladder fossa. If the inflow has been completely divided, the line of transection
will be shown extending from the anterior border of the right hepatic vein to an area
to the right of the gallbladder fossa. If the right anterior sectoral pedicle has not been
controlled, which may not be possible initially because of proximity of the tumor,
the plane of transection is more difficult to conceptualize.
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 (small
arrow) may be taken within the liver substance. Reprinted with permission from LH
C. Huguet, Hepatic cryosurgery addendum by Y Fong). In: LH Blumgart ed. Surgery of
the Liver and Biliary Tract, 2nd Edition. 1994 © Churchill Livingstone.
Using intermittent portal triad occlusion, the parenchyma is divided from the
inferior surface upwards and from right to left in a horizontal plane. In order to
facilitate the dissection, the liver is rotated clockwise to convert the horizontal plane
to a vertical one. The dissection proceeds anterior to the right posterior pedicle;
when the liver is rotated, the dissection will be just medial to the pedicle. The line of
transection is often dictated by the tumor, since tumors close to the posterior pedicle
or the right hepatic vein will limit the resection. 16
Extended left resections can be done safely with mortality rates only slightly
higher than other resections. Postoperative morbidity is significant, however, with
biliary leak and abdominal abscess being the major complications. Because of the
small remnant, significant postoperative liver dysfunction may result and patients
are more likely to develop significant ascites.
Fig. 16.13. Caudate lobe resection. The caudate lobe may be approached from the
right or left, although dissection from both sides is often necessary. The attachment
from the caudate to the IVC has been divided. The inflow to the caudate has been
divided (above) and the caudate veins are now controlled in turn. Note the 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 disease
and for liver and biliary tumors. In: LH Blumgart, Y Fong eds. Surgery of the Liver
and Biliary Tract, 3d Edition. 2000. © W.B. Saunders.
Caudate Lobe Resection (Segment I Resection)

The caudate lobe is most commonly removed en bloc as part of a major hepatic
resection to achieve tumor clearance and, less commonly, as an isolated caudate
resection. Damage to the middle or left hepatic veins is a major risk of isolated
caudate lobectomy (Figs. 16.13 and 16.14). The caudate may be approached from
the right or left, although dissection from both sides is often necessary (Fig. 16.13).
Dissection from the right side is necessary for bulky lesions that prevent access from
the left or when the caudate is excised en bloc with the right liver. After division of
the gastrohepatic omentum and the ligamentous attachments from the caudate to
the IVC, the right liver is mobilized with division of the posteriorly draining veins
along the entire retrohepatic cava. The dissection then proceeds along the anterior
16 surface of the IVC, lateral to medial with control of the caudate veins. Some of these
veins may be more easily controlled from the left side. The branches to Segment I
from the left portal vein and hepatic artery are then dissected close to the base of the
umbilical fissure just before the entry of the left portal triad. The caudate is then
separated from its attachment to the right liver with inflow occlusion.
A principal approach from the left side may be possible with smaller tumors or
when the caudate is to be removed en bloc with the left liver. The left lateral margin
of Segment I is freed by dividing the fibrous attachment posteriorly to the IVC and
Fig. 16.14. An alternative approach to isolated caudate resection. The liver is split
along the principal plane to allow detachment of the right side of the caudate
under direct vision of the middle hepatic vein. This approach may help reduce the
risk of inadvertent injury to the middle vein, which can result in significant hemor-
rhage. Reprinted with permission from LH Blumgart, Liver resection for benign
disease and for liver and biliary tumors. In: LH Blumgart, Y Fong eds. Surgery of the
Liver and Biliary Tract, 3d Edition. 2000. © W.B. Saunders.
diaphragm, exposing the veins draining the caudate into the cava. The approach to 16
the inflow vessels remains the same.
An alternative approach to an isolated Segment I resection involves mobilization
of the caudate as described above, followed by splitting of the hepatic parenchyma
along the principal plane (Fig. 16.14). This approach provides access to the right
border of the caudate, which can be disconnected under direct vision of the middle
hepatic vein and may prevent uncontrolled bleeding.
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 Y
Fong). Surgery of the Liver and Biliary Tract, 2d Edition. LH Blumgart ed. 1994. ©
Churchill Livingstone.
Segmental Resection
Because they are defined by anatomic structures with their own pedicles, each
hepatic segment can be resected individually (Fig. 16.15), or in combination with
other segments as part of a larger resection. This section describes some of the more
commonly performed anatomical sub-lobar hepatic resections.
Right Posterior Sectorectomy (Segments VI and VII)
Removal of Segments VI and VII constitutes a posterior sectorectomy. In this
resection, all hepatic tissue below and lateral to the right hepatic vein is removed.
The right hepatic vein can also be sacrificed, if necessary, since the middle hepatic
vein will provide adequate drainage of Segments V and VIII (anterior sector). Even
if the right hepatic vein is to be preserved, it should be fully dissected and exposed to
16 allow rapid control if injured during parenchymal transection. The right portal pedicle
is exposed and the anterior and posterior branches identified. The posterior pedicle
is clamped and the line of demarcation between the anterior and posterior sectors is
demonstrated. The pedicle may be divided and parenchymal dissection performed.
The line of transection is horizontal and posterior to the right hepatic vein, but may
be extended into the anterior sector with sacrifice of the right hepatic vein, if necessary.
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 completely
exposed. The approach is similar to that used for posterior sectorectomy except that
the anterior pedicle is divided, and the line of transection indicated between the
right and middle hepatic veins. The line of transection can be extended into Seg-
ment IV if necessary for complete tumor clearance.
Segment IV Resection
Segment IV is divided into a posterosuperior portion (IVa) and an anteroinferior
portion (IVb), which can be resected together or separately. The left branches of the
portal vein and hepatic artery supply the inflow to Segment IV. The middle hepatic
vein provides venous drainage via medial branches. The umbilical vein provides
additional drainage and may drain into the middle or left vein. Division of the
bridge of tissue overlying the umbilical fissure is performed and the hilar plate 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 divided
just to the right of the falciform ligament and along the principal plane. Control of
the Segment IV feedback vessels is as described for extended right hepatectomy.
Initial division of these vessels will delineate the extent of the resection. The middle
hepatic vein may be preserved or divided.
Central Resection
Removal of Segments IV, V, and VIII (Segment IV plus an anterior sectorectomy)
constitute a central resection. This seemingly complex procedure is used to maxi-
mize the amount of remnant liver left after resection because both the posterior
sector and the left lateral segment are preserved. The approach to a central resection
is similar to that used for a posterior sectorectomy and left lateral segmentectomy,
except these are preserved rather than removed. The right anterior and posterior
sectoral portal triads are identified and the anterior pedicle clamped. Transection is
performed with intermittent Pringle, carefully preserving the right posterior pedicle
and the right hepatic vein. Segment IV is devascularized and resected as described
for a Segment IV resection. The middle hepatic vein must be divided; a vascular
clamp may be used to occlude the vein during parenchymal transection.
Wedge Resections
Wedge resections are associated with a higher incidence of positive margins and
greater blood loss and should therefore be avoided in most cases. However, they may 16
be appropriate in selected cases. Small, peripheral lesions can be safely excised with
adequate margins using an intermittent Pringle maneuver. After dissection of the
porta hepatis to place an umbilical tape, intraoperative ultrasound is performed to
confirm the lesion, identify other lesions, and define the relationship of the lesion to
major vascular structures. An adequate margin of excision is marked using cautery.
Stay sutures are applied on either side of the lesion and within the area of excision.
Parenchymal dissection is performed in a standard fashion using a crushing technique
to ensure that the normal parenchyma does not fracture around the tumor and that
adequate margins are maintained without “coning” in on the lesion.
Postoperative Care
As discussed above, drains are not necessary for routine hepatic resection with-
out concomitant biliary resection and reconstruction; in fact, drains are associated
with 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 levels
can drop quite low without supplementation. For large-volume liver resections, elec-
trolytes, blood count and coagulation profiles are checked postoperatively and daily
for 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) is
never necessary and only serves to raise the serum glucose levels and induce an
osmotic diuresis. In general, packed red blood cells are administered if the hemoglo-
bin falls to 8 mg/dL or lower and fresh frozen plasma is given if the PT is greater
than 17 sec. An understanding of the decreased clearance of hepatic-metabolized
drugs is important in selecting pain medication as small doses may linger. Unex-
plained fever or rising bilirubin with normalization of other hepatic function
parameters suggests an intra-abdominal bile collection and should be investigated
with a CT scan. Such collections usually resolve within a few days with percutane-
ously placed drains; reoperation is rarely necessary.
Selected Reading
1. 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 resection
is 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 or
removal 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
16 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 1
CHAPTER 17
Technique for Placement of the Hepatic

Arterial Infusion Pump
N. Joseph Espat
Introduction
Colorectal metastases confined to the liver will develop in up one-third of the
140,000 patients per year newly diagnosed with colorectal cancer. Unfortunately,
surgically resectable hepatic disease occurs in only 20-30% of these patients. In
brief, patients with hepatic metastases considered for surgical resection must be free
of extrahepatic disease. Although bilobar hepatic metastases are no longer consid-
ered to be a contraindication to resection, the resection should be anatomic with
preservation of portal vein inflow and hepatic vein outflow to the residual liver. A
more detailed discussion on the concepts relevant to the assessment of these patients
as operative candidates is contained elsewhere in this text.
The relatively limited population of patients who are appropriate for curative
hepatic resection implies that the majority of patients (70-80%) will be treated with
systemic adjuvant chemotherapy. Yet, although systemic chemotherapy is the main-
stay of treatment for patients with metastatic disease, less than one-third of patients
demonstrate a response to this therapy and, historically, the five-year survival for
these patients is less than 3%.
Systemic chemotherapy for the treatment of hepatic disease has evolved into
liver-directed chemotherapy. Hepatic artery infusion pumps (HAIP) using an
implantable, automatic drug delivery mechanism is one approach. 5-flurode (FUDR)
based regimens administered through HAIP have been utilized successfully with
improved median survival in selected patients. However, other drug regimens with
and without FUDR have also shown promise. Chemotherapy delivered via a HAIP
elicits superior clinical response rates and limited toxicity when compared to stan-
dard systemic treatment.
The use of regional hepatic artery chemotherapy delivered via HAIP is based on
three key concepts:
1. Hepatic metastases > 3 mm in size derive their blood supply from the
hepatic artery and not the portal vein
2. A 4-fold increase in concentration of chemotherapy (e.g., FUDR) is
achieved when injected through the hepatic artery as opposed to systemic
infusion.
3. Certain chemotherapeutic agents are almost completely extracted during
the first pass through the liver allowing for large doses to be given with
minimal side effects.
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 with
synchronous colon and hepatic disease, hepatic metastases within 24 months of the
primary tumor, or patients undergoing hepatic resection with minimal free margins
or demonstrated persistent disease.
Nonresectional hepatic ablative therapies (e.g., radiofrequency ablation,
cryoablation), for patients not otherwise candidates for surgical resection, have been
popularized by the early promising results demonstrated in small series. In these
patients, HAIP therapy may be used as a component of their treatment. However,
the long-term outcome for this approach remains to be established.
Preoperative Patient Evaluation
This section will be necessarily brief, as the topic of metastatic work-up for patients
with colorectal cancer is covered elsewhere. Patient eligibility for enrollment into
clinical trial is specifically defined by the study protocol. In general, the following
criteria are common to most HAIP clinical trials:
• History of histologically confirmed colorectal adenocarcinoma metastatic
to the liver with no clinical or radiographic evidence of extrahepatic disease.
• Liver metastases must comprise < 70% of the liver parenchyma.
• WBC >3,500 cells/mm3 and platelet count > 150,000 cells/mm.
• Albumin >2.0 gm%
• Total serum bilirubin < 2.0 mg/dl.
• No active concurrent malignancies.
• No active infection, ascites, or hepatic encephalopathy.
• Prothrombin time within 1.5 seconds of normal.
Furthermore, patients meeting these criteria must have favorable vascular anatomy
for HAIP placement.
HAIP placement requires that a catheter (Fig. 17.1) be introduced into the gas-
troduodenal artery (see following section, technique for placement of HAIP), so
that pump flow is directed necessarily towards the liver via the hepatic artery(s).
17 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
Technique for Placement of the Hepatic Arterial Infusion Pump 229
Fig. 17.1. Visceral angiogram: (gastroduodenal artery, left hepatic artery, right
hepatic artery).
by MRA provide at least equivalent anatomic information (Fig. 17.2), although

their routine use awaits validation.
Our preferred operative technique for HAIP placement in patients with stan-
dard vascular anatomy is presented.
Surgical Technique for the HAIP Placement
Patients should receive prophylactic preoperative gram-positive antibiotic cover-
age and this should be continued for 24 hours following the operation. Operative
draping of the patient for this procedure should extend cranially to the nipple line
and inferiorly to the symphysis. The skin is prepared with a bactericidal such as a
Betadine or Hibiclens solution. The skin is dried with an absorbent sterile towel and
a providone-iodine adhesive drape is placed on the operative field. We prefer the use
of a right subcostal incision extended slightly beyond the midline. This approach
provides ample exposure to the right upper quadrant and spares the left side of the
abdomen for the creation of the pump pocket (Fig. 17.3).
Intra-abdominal adhesions will be present in patients who have previously
undergone colectomy. Some of these adhesions will need to be cleared to prevent
inadvertent injury during retraction, dissection, or when passing the pump catheter
across the abdomen from within the peritoneum. 17
Cholecystectomy is routinely performed to prevent chemical cholecystitis. The
hepatic artery is easily identified in the porta hepatis, both by location and palpable
tell-tale arterial thrill. Favorable anatomy for pump placement has been verified
prior to coming to the operating room by angiogram or MRA.
Fig. 17.2. Visceral MRA: (gastroduodenal artery, left hepatic artery, right hepatic artery.
17
Fig. 17.3. Planned incision for laparotomy (right sub-costal) and pump placement
(left sub-costal).
The gastroduodenal artery (GDA) is located immediately inferior to the proper

hepatic artery coursing inferiorly towards the proximal duodenum (Figs. 17.1 and
17.2). Sharp dissection to isolate the GDA is performed, taking care to ligate or clip
the surrounding lymphatic vessels. The common bile duct (CBD) lies lateral to the
GDA, and injury to the CBD must be avoided during the dissection. Medially and
deep to the GDA lies the portal vein, and again, great care is needed while dissecting
in this area.
After circumferentially dissecting the GDA, a right angle instrument is used to
facilitate the passing of a suture ligature around this vessel. This suture will be used
for traction as arterial branches are cleared off for approximately 1 cm towards the
duodenum and head of the pancreas, 1 cm toward the proximal common hepatic
artery, and 1 cm towards the bifurcation of the hepatic artery (but proximal to the
right and left divisions).
Up to 15% of patients may have an accessory left hepatic artery arising from the
left gastric artery, which should be (but is not always) identified by the preoperative
imaging. In order to maintain drug-only arterial blood flow to the liver, this vessel
must be identified and ligated. Elevation of the left lobe of the liver to assess for the
presence of a nonvisualized left hepatic artery is mandatory. This is best accomplished
by dividing the lesser omentum with ligation of the accessory vessel if it is present.
Once this is accomplished, arterial flow from the GDA should be only towards
the liver via the common hepatic artery and the liver should receive only drugs
containing blood flow.
Considerations for Patients with Variant Anatomy
The technique previously described is applicable only for patients with standard
arterial anatomy. As discussed, it is important to identify any aberrant arterial 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 hepatic
artery 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 a
noncrushing vascular clamp to assess for potential liver ischemia. If no obvious
ischemia is noted, the vessel can be ligated. However, at least one artery to either
lobe of the liver arising from the hepatic artery after the take-off of the GDA must
be preserved. Crosshepatic arterial perfusion to the contralateral lobe of the liver
develops rapidly after ligation of the replaced lobar artery in the patient with a
nontoxic liver. In contrast, if ischemic changes are observed during “trial-clamping”,
then that vessel should be preserved and cannulated separately to maintain adequate
hepatic perfusion.
Replaced Right Hepatic Artery (RRHA)
The most common variant arterial anatomy is a replaced RHA with a standard 17
left hepatic artery (LHA) and GDA. A RRHA is most commonly identified by
palpation as it exits from behind the duodenum, courses lateral to the common bile
duct, and posteriorly within the hepatoduodenal ligament. The RRHA has no side
branches that can be used to insert the catheter; however, arteriotomy or direct
puncture under vascular control can be used for placement of a polyethylene or 22
gauge “angiocatheter” with subsequent connection to the HAIP catheter. Placing

the 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 the
placement of a double-catheter pump where one catheter is placed into the LHA
from the GDA and the second catheter is inserted directly into the RRHA to assure
bilateral perfusion. The latter is the approach we prefer when possible.
Replaced Left Hepatic Artery (RLHA)
A RLHA can be identified coursing within the gastrohepatic ligament along the
inferior edge of the liver. The RLHA arises from the left gastric artery (LGA) and there
is a normal RHA. In this setting, the HAIP catheter can be inserted into the GDA to
perfuse the RHA with ligation of the RLHA. Another technique is the placement of a
double-catheter pump, where one catheter is inserted into the LGA to perfuse the
RLHA and the other catheter is inserted into the GDA to perfuse the RHA.
Trifurcation of the Common Hepatic Artery (CHA)
into RHA, LHA and GDA
Trifurcation of the CHA into a RHA, LHA and GDA is another described ana-
tomic variant that can be managed by inserting the HAIP catheter into the GDA
1 cm proximal to the takeoff of the GDA from the CHA to allow for adequate 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 HAIP
catheter into the splenic artery, advancing it into the CHA with ligation of the GDA
and left and right gastric arteries, will obtain bilateral perfusion. A more complex
approach to deal with this anatomy is to construct a conduit using a short segment
vein graft for catheter insertion into a selected artery with subsequent ligation of the
other vessels. We do not recommend this latter approach.
These variant arterial anatomies underscore the importance of preoperative
assessment of vascular anatomy in order to be prepared at the time of operation.
Failure to appropriately identify and ligate aberrant arteries and arterial branches
may result in malperfusion.
Creation of the Subcutaneous Pump Pocket
The pump pocket is usually created on the left side of the abdominal wall unless
a colostomy is present. The pump is placed well below the left costal margin to
prevent patient discomfort from the hard metal pump abutting against the ribs. The
skin incision is transverse and should measure no more than 1 cm wider than the
width of the actual pump to be placed (Fig. 17.4). The subcutaneous tissues are
divided using electrocautery up to, but not into, the abdominal wall fascia. Continuing
inferiorly along the adipose-fascial interface, the pocket is extended for about 8-10
cm (actual pocket size should be planned based on the size of the actual model of
17 pump to be implanted). Strict attention to hemostasis must be maintained during
the dissection of the subcutaneous pocket to minimize the risk of hematoma and
lessen the risk of subsequent complications.
The automatic mechanism that drives catheter flow is initiated (“primed”)
by filling the pump reservoir with a standard volume of heparinized saline
(volume is specific to the pump model), which is placed in a warm water bath
Fig. 17.4. Abdominal CT with HAIP in the left lower quadrant. Note that the pump
body housing rests directly on the fascia.
at body temperature to activate it. Flow through the catheter is driven by 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 the
solution concentration regulates the amount of drug delivery.
The pocket is tested for fit of the pump body and catheter while maintaining a
“no-contact” technique with the skin. Pump architecture and specifications will vary
according to manufacturer and model; however, all designs will have a catheter with
an internal component that exits through the pump body (Fig. 17.5). This catheter
must be inserted into the abdominal cavity through the anterior abdominal wall
and subsequently placed into the GDA. In performing this maneuver, care should
be taken to avoid injury to vessels coursing through the posterior surface of the
rectus abdominus muscle.
Pumps have anchoring “loops” (Fig. 17.5) fused to the pump body housing to
prevent “flipping” or axial rotation of the pump, within the subcutaneous pocket.
Using a skin retractor, the inferior edge of the pump pocket is elevated towards the
ceiling; interrupted nonabsorbable sutures are placed into the fascia of the anterior
abdominal wall and passed through each anchor loop. The two distal anchors are
sutured first and not tied until the two proximal sutures are placed. Until the sutures 17
are tied, the ends of the cut suture are held in place by individual clamps. The
inferior pump pocket edge is elevated and the distal anchor sutures are tied, pulling
the pump down into the pocket as it is fastened down. Care should be taken to
insure that the pump catheter does not become twisted or damaged during this
maneuver. With the pump in place, the catheter is free within the abdomen.
Fig. 17.5. Hepatic artery infusion pump; the catheter exits the pump body housing
at the 6 o’clock position. Note the four anchor loops located around the body
housing.
The catheter is measured and cut sharply such that the tip has an oblique angle
and only one of the flanged catheter hubs remains. The catheter length should be
long enough to reach the junction of the GDA with the hepatic artery but not
extend beyond it. In this manner, flow-out of the catheter will necessarily go only
towards the liver.
The GDA is ligated in continuity as it enters the duodenum. The position of
this suture will determine the length of artery available for catheter insertion. Once
the catheter is prepared as described above, and the branches off of the GDA and
other arteries have been cleared, proximal and distal control of the hepatic artery is
obtained using pediatric vascular clamps. A #11 scalpel blade is used to incise the
anterior wall of the GDA in a transverse fashion. An arteriotomy introducer is in-
serted into the GDA lumen to facilitate passing of the catheter tip into the vessel
lumen. The catheter is advanced using nontoothed forceps and the previously placed
circumferential traction suture ligature is tied down onto the catheter behind the
flanged hub. Care is needed to insure that the knot is not too tight as to impede or
17 occlude flow through the catheter. We advocate the use of an additional separate
suture to prevent inadvertent arterial dislodgement. We place a 4-0 prolene suture
through the adventitia of the GDA behind the flanged hub of the catheter and
circumferentially encompassing the vessel, again not encroaching on the catheter
lumen. The distal (outflow) vascular clamp is removed, followed by the proximal
(inflow) clamp.
Assessment of Hepatic Perfusion

Intraoperative fluorescein test is generally performed after pump placement to
assure liver-only perfusion. Using the side port of the pump, approximately 3-5 cc
of fluorescein (nondiluted) are injected, followed by illumination with a Wood’s
lamp. If all the arterial branches have been properly ligated or clipped, only the liver
should demonstrate fluorescence. Do not aspirate into the pump when injecting it
as this will result in small clot formation and subsequent pump malfunction. Subse-
quently, the pump is flushed with 10 cc of heparinized saline. The pump pocket is
closed in two layers using absorbable suture material. The abdominal incision is
closed in standard fashion.
Postoperative hepatic perfusion and extravasation (i.e., stomach, duodenum, and
spleen) via HAIP is assessed three days postoperatively by a Technetium-labeled
macroaggregated albumin hepatic scan. This will confirm liver-only pump perfu-
sion and is necessary prior to the initiation of HAIP therapy (Fig. 17.6).
Brief Comments on Technical Complications
Analysis of the technical complications associated with hepatic artery infusion
pump placement, reveals that HAIP complications can be divided into those occur-
ring either early (< 30 days postpump placement), or late (>30 days) (Table 17.1).
Furthermore, complications are divided into arterial, catheter, perfusion or pump
related.
Arterial complications include intimal dissection and thrombosis. Arterial 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. Catheter
dislodgement is a rare occurrence in the early postoperative period; most dislodgement
occurs late. Catheter dislodgement may be accompanied by hemorrhage that can be
life-threatening. Catheter occlusion is a late occurrence and can be salvaged by lytic
therapy.
Malperfusion is defined as the identification of organ perfusion other than the
liver (i.e., stomach, duodenum or spleen). Extrahepatic perfusion can occur with
catheter misplacement or failure to identify and ligate the appropriate arterial branches
off the GDA. If malperfusion is apparent, a patent branch of the common hepatic
arterial system that continues to perfuse the distal stomach or duodenum is often
identified. Once localized, this complication is corrected by laparotomy with liga-
tion of the patent branches of the GDA or CHA. More recently, patent vessel branches
have been embolized at arteriography, obviating the need for re-laparotomy.
Pump infections are more frequent in the late period (> 30 days postoperatively)
and are the pump related complication that most often results in the premature
termination of therapy. However, pump salvage rates of approximately 25% are 17
obtainable for both early and late pump infections.
Complications related to local and regional toxicity of the therapeutic agents are
well characterized elsewhere.1,5
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 is
evident and although the actual pump is not well-visualized, it is located where
the catheter originates.
Table 17.1. Early and late technical complications of HAIP ( n=391)6
Complication Early Terminated Late Terminated

Arterial 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%) 0
Total 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)
17 following pump placement. These data represent a median follow-up interval of
16 months (range 1-110). A total 3% early and 9% late technical failure rates were
observed. The prevention of late arterial thromboses and catheter dislodgement
would prevent the majority of premature treatment terminations related to pump
complications.
Summary
In 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 the
management of these patients is to provide a reliable system for the administration
of regional chemotherapy. The efficacy of hepatic artery infusion pump (HAIP)
chemotherapy for metastatic colorectal cancer confined to the liver is currently the
subject of several national multi-center randomized trials.
Selected Reading
1. Allen Mersh, TG, Earlam S, Fordy C, Abrams K, Houghton J. Quality of life and
survival with continuous hepatic-artery floxuridine infusion for colorectal liver
metastases [see comments]. Lancet 1994; 344:1255-6000.
2. Chang AE, Schneider PD, Sugarbaker PH et al. A prospective randomized trial of
regional versus systemic continuous 5-fluorodeoxyuridine chemotherapy in the
treatment of colorectal liver metastases. Ann Surg 1987; 206:685-933.
3. Ensminger WD, Rosowsky A, Raso V et al. A clinical-pharmacological evaluation
of 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 intravenous
5-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 of
fluorodeoxyuridine in patients with liver metastases from colorectal carcinoma. A
randomized trial. Ann Intern Med 1987; 107:459-655.
6. Dudrick PS, Picon A, Paty PB et al. Technical Complications Associated with
Hepatic Arterial Infusion Pumps for Metastatic Colorectal Cancer. (In Prepara-
tion)
7. Sigurdson ER, Ridge JA, Kemeny N et al. Tumor and liver drug uptake following
hepatic artery and portal vein infusion. J Clin Oncol 1987; 5:1836-400.
8. Wagner J S, Adson MA, Van Heerden JA et al. The natural history of hepatic
metastases from colorectal cancer. A comparison with resective treatment. Ann
Surg 1984; 199:502-588.
9. Weiss GR, Garnick MB, Osteen R et al. Long-term hepatic arterial infusion of
5-fluorodeoxyuridine for liver metastases using an implantable infusion pump. J
Clin Oncol 1983; 1:337-444.
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.
17
CHAPTER 18
Non-Resectional Hepatic Ablative

Techniques:
Cryotherapy and Radiofrequency Ablation
Ronald S. Chamberlain and Ronald Kaleya
Introduction
The liver is a frequent site of both primary and metastatic tumors. Surgical 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 cancer
present 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 of
the liver has been the impetus behind the development of multiple alternative treat-
ment modalities. Tumor histology, stage and site of the primary tumor, extent of
hepatic parenchymal involvement, presence of extrahepatic disease, and the clinical
condition of the patient influence the appropriateness of the various alternative treat-
ments. Available alternatives include hepatic artery chemotherapy (Chapter 17) he-
patic arterial embolization or chemoembolization (Chapter 4), percutaneous ethanol
ablation (Chapter 4), cryotherapy (percutaneous, laparoscopic, or open techniques),
and thermal ablation that includes radiofrequency, microwave, and laser ablation.
Nearly all of these modalities can be performed percutaneously or by using 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, and
the subject of considerable on-going study. Based upon this data, several prospective
and retrospective analyses have demonstrated that liver failure is the primary cause
of death in up to 90% of these patients. Non-resectional hepatic ablative strategies
have been developed in an attempt to alter either the course of the disease and/or
cause of death in patients with unresectable liver tumors.
Indications for Non-Resectional Ablative Therapies
Histology
Primary liver cancer is the most common malignancy in Southeast Asia and
Africa and remains the leading causes of cancer-related deaths world wide. Each year
there are approximately 1.2 million cases of HCC in the world with 1 million deaths.
While relatively rare in the United States (16,000 cases per year), the mortality is

Ablative Techniques in the Management of Hepatobiliary Malignancies 239
nevertheless greater than 90%. Among patients with HCC, only 15 to 25% are
operable at presentation and even fewer patients are resectable with curative intent.
Despite this fact, the majority of patients with unresectable disease have tumor 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 only
24% were candidates for hepatic resection; these figures clearly demonstrate the
central role that ablation therapy can play in the treatment of hepatic tumors.
Metastatic Disease
The liver is one of the most common sites of metastatic spread for many cancers,
particularly gastrointestinal malignancies. Unfortunately, most malignancies that
spread to the liver also spread elsewhere making regional ablative therapies 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 a
small proportion of patients with metastases confined to the liver are operable due
to limitations imposed by tumor characteristics and patient co-morbidities. Several
authors have estimated that only 8 to 12% of all patients who develop liver me-
tastases from colorectal primaries are resectable for cure. While the percentage of
patients who may be candidates for non-resectional ablative therapies is unknown,
it is probably in the area of 15-20%.
Non-resectional therapeutic approaches have been applied anecdotally to a vari-
ety of other tumor histologies in addition to colorectal cancer. These include, but
are 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 cannot
be advocated outside of a clinical trial. The only exception to this rule may be the
use of radiofrequency ablation for the treatment of metastatic neuroendocrine tu-
mors for which a considerable body of literature is emerging.
Additional Indications and Contraindications
Absolute indications and contraindications for cryotherapy and RFA remain
undefined. As a general rule, most experienced centers advocate treating not more
than four lesions at a time and limit the total volume of liver treated to < 20- 30%.
Patients with more than 40% of liver volume replaced with tumor are usually not
candidates for ablative therapy alone. Non-resectional ablative strategies are par-
ticularly attractive approaches for the treatment of many patients with HCC who
have limited functional hepatic reserve due to cirrhosis. These techniques permit
pinpoint tumor ablation while maximizing the preservation of normal liver. In some
instances, ablative modalities may be used in conjunction with resective therapy to
treat a “close” or “positive” margin of resection.
Cryotherapy
The Physiology of Cryoinjury: Deep Freeze 18
The mechanism by which subzero temperatures destroy tumors are not tissue
specific. Normal and neoplastic tissues are sensitive to exposure to extreme cold.
The explanations for how cryotherapy results in cell death are multifactorial, and
include both physical and chemical mechanisms depending upon the rate of
cooling. 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 to
the percent of cell death achieved.
When a cryoprobe is inserted into the liver, three overlapping zones of injury
develop within the iceball. The rate of freezing decreases in proportion to the
distance from the probe and creates zones of intermediate and slow cooling. 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 the
cryolesion). The dynamics of the freezing process cause different mechanisms of
injury to occur in these three zones.
Cooling Rates
Cooling rates affect the proportion of cells killed in a single freeze cycle. Maximal
cell death is achieved by using either slow or rapid cooling rates whereas greatest cell
survival is seen with intermediate cooling rates. Cellular dehydration causes the lethal
injuries when slow cooling rates are used, while rapidly cooled cells are destroyed by the
mechanical action of ice crystallization.
Intra- and extracellular fluids are complex solutions containing varying amounts of
protein, macromolecules and electrolytes. The presence of these solutes depresses the
freezing point of water and allows it to supra-cool rather than crystallize below 0˚C.
Because of differences in the composition of the intra- and extracellular compartments,
the extracellular fluid freezes before the intracellular fluid. As ice forms within the
extracellular space, solutes are excluded leaving a hyperosmotic extracellular environ-
ment. Cellular dehydration occurs as the unfrozen intracellular water flows out of a cell
along the osmotic gradient. As a consequence of cellular dehydration, the intracellular
pH and ion concentrations are altered, proteins denature and membrane bound 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 cryolesion
thaws, the extracellular fluid thaws first creating a relatively hypotonic environment.
Water flows into the hyperosmolar and hypertonic cells causing them to burst. This
type of injury predominates in the slowly cooled zone at the periphery of the cryolesion.
In contrast, rapidly frozen tissue is destroyed by an altogether different mecha-
nism. Cooling rates on the order of 50˚C per minute cause intracellular fluid to
freeze 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 cell
death. This type of cooling is present only in close proximity to the cryoprobe.
With intermediate cooling rates (1-10˚C per minute), the cells dehydrate and the
extracellular fluid turns to ice. However, the temperature falls fast enough to freeze the
intracellular water before cellular dehydration reaches a critical level. Intracellular ice
formation excludes solute, thereby increasing intracellular osmotic concentration, equal-
izing the osmotic gradient, and preventing further cellular dehydration. In this setting,
18 the critical level of dehydration allowing influx of solute is not reached, thus protecting
the cell from the lethal injury caused by water influx during the thaw cycle. Cells in the
zones of intermediate cooling therefore have improved survival, and several freeze-
thaw cycles are necessary to effect complete cell death.
Hypothermia and the Thawing Process

The sensitivity of different tissues to hypothermia varies considerably. Most nor-
mal hepatocytes exposed to temperatures below –15 to -20˚C die, whereas nearly all
hepatocytes cooled to -10˚C survive. Bile ducts, connective tissue and vascular struc-
tures tolerate lower temperatures than hepatocytes. Unfortunately, liver tumors are
even 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 less
than -40˚C is sought. In practice, assuring that all tumor cells reach this temperature
requires the iceball to extend at least 1 cm beyond the temporal edge of the tumor.
Additional tissue damage occurs during the thawing from the process of
recrystalization. In brief, as the tissue warms ice crystals reform, coalesce and 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 ablated
in one freeze/thaw cycle, multiple cycles are necessary to ensure that tumor cells at
the periphery reach the depth of hyperthermia required for reliable cell kill.
Technical Aspects of Cryotherapy

Hepatic cryotherapy can be performed through a variety of approaches, includ-
ing the percutaneous, laparoscopic and open method. The open approach allows
the 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 Preparation
Precise radiologic evaluation of the volume, location, and proximity of the liver
tumors(s) to the hepatic vasculature and biliary structures is the key to performance
of successful cryotherapy and RFA. Patients with more than 40% of the liver 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 employed
prior to either cryotherapy or RFA. This is most important in those rare instances
during which a conversion to resection is necessary due to unexpected resectability
or intraoperative complications. A unique, but rare, complication of cryotherapy
that must be anticipated is “cryoshock.” This complication is typically manifested
by profound systemic hypotension, pulmonary failure, renal failure, and
coagulopathies. Renal failure can be minimized by aggressive intraoperative hydration.
Hypothermia can be alleviated using heated fluid, airway circuits and a Bair Hugger™
warming system, and any signs of excessive bleeding should be aggressively treated
with appropriate blood products.
Operative (Open) Approach

The abdomen may be approached through a subcostal, bilateral subcostal (Chev-
ron-type), or mid-line incision. The peritoneal cavity is carefully inspected for any
evidence of extrahepatic metastases. Enlarged lymph nodes, particularly those in the
hepatoduodenal ligament, should be evaluated by frozen section. The falciform liga- 18
ment is divided up to the level of the hepatic veins to permit careful bimanual
palpation. A 5 MHz intraoperative ultrasound transducer is used to evaluate each seg-
ment of the liver systematically to determine the extent of disease and its relationship
to the vascular and biliary structures. All lesions seen on preoperative studies should
be confirmed by intraoperative ultrasound and/or biopsy.
Once an intraoperative strategy is defined, a Penrose drain or vessel loop is placed
around the porta hepatis should inflow occlusion be required later. The cryoprobe is
introduced into the center of each lesion under ultrasound guidance. The 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 through
the 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 spillage
and 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 the
probe 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 deep
intraparenchymal and poorly palpable tumors. After identification of the tumor by
intraoperative ultrasound, an echogenic needle is passed into the center of the lesion
and is subsequently exchanged for a J-wire. Once the J-wire is in place, the tract is
dilated with a coaxial dilator and peel away sheath. The dilator is withdrawn after
proper position is established and the cryoprobe is inserted through the sheath into
the center of the tumor. The correct positioning of the cryoprobe should be re-
evaluated in two or three different axes. Ideally the probe is placed through the
tumor with the tip near the opposite margin.
The size and location of the tumor governs the type of cryoprobe used. The
surgeon must be familiar with the physiology of cryotherapy in order to determine
which shape of probe is most suitable for the situation. The most commonly used
cryo-system employs vacuum insulated probes and supra-cooled liquid nitrogen 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 an
8 mm trocar probe creates a freeze zone up to 6 cm. Probes may be used in tandem
to create larger lesions. Flat-faced probes which form a “half-moon” lesion may be
applied directly to the surface of the liver to form lesions 3 to 4 cm in size.
Once the cryoprobe is positioned, great care must be taken to insulate the sur-
rounding tissue. Laparotomy sponges are usually sufficient for this purpose. The
freezing process then commences. At -100˚C, the cryoprobe becomes stuck in the
hepatic parenchyma, and additional probes may be safely placed. When one is just
beginning to perform cryotherapy we recommend using one probe at a time in
order to ensure adequate monitoring of the cryoablation and reduce the risk of
intraoperative hypothermia. The freeze front appears as a hyperechoic rim with 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 process
usually takes 8 to 15 minutes to complete depending upon the efficiency of the
cryosystem and the size of the tumor.
Following completion of the first freeze cycle, the tissue is thawed passively. Com-
18 plete thawing may take up to 20 to 30 minutes. Since cryotherapy failure usually
occurs at the periphery of the ice ball, we recommend thawing only the most periph-
eral centimeter before initiating the second freeze cycle. This technique reduces opera-
Fig. 18.1. Variety of different size and shapes depending upon the clinical scenario.
tive time without compromising clinical efficacy. Additional freeze-thaw cycles are
accomplished in a similar fashion.
Following completion of the second freeze-thaw cycle, the probe is actively re-
warmed allowing it to disengage before the tumor completely thaws. The probe
tract is packed with Surgicel™ or a similar hemostatic material and gentle pressure
is applied to the liver to prevent delayed hemorrhage. The thawing ice ball should be
handled gently to prevent a cleavage plane from developing between of the iceball
and the normal liver parenchyma that can result in massive bleeding. Bleeding in
the probe site is common but generally stops promptly as the coagulation cascade
activates at body temperature.
Postoperative Care
Drains are not typically used and the abdomen is closed in the standard fashion.
Postoperative care is usually unremarkable and the patients can eat on the second
postoperative day. A transient elevation of liver enzymes, leukocytosis, drop in the
platelet count, and high fever are common in the early postoperative period. The
rise in the liver transaminases is directly related to the volume of liver treated and
usually resolves within one week. Platelet count typically bottomout in the first few
days and then stabilize and returns to normal or supranormal levels in 7 to 10 days.
Less commonly, the coagulation profile deteriorates with increased partial thrombo-
plastin and prothrombin times; however the development of clinically disseminated
intravascular coagulopathy is rare.
18
Fig. 18.2. Real time ultrasound of cryotherapy. Probe is outlined by black bars. A
hyperechoic (white) freeze front marks the edges of the iceball. The loccation of
the tumor is indicated.
Radiofrequency Ablation
The Physiology of Thermal Injury
The theory that it may be possible to use heat to induce tissue injury is not new.
The Edwin Smith papyrus (1700 BC) contains the first written mention of the use
of heat in a therapeutic fashion to treat tumors. Throughout the last century, both
whole-body and local hyperthermia have been extensively evaluated for their 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, no
reproducible clinical results have been generated and there is no current medical
indication for systemic hyperthermia treatment. Local hyperthermia, which refers
18 to 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 in
providing both symptom relief and restoration of function for tumors that block the
bronchus, esophagus, colon or rectum. Unfortunately, techniques, which are useful

to recannulate hollow viscus organs or parts of the respiratory tree, have no clinical
use for most solid organ metastases. Recent technologic advances, however, have
now made it feasible to induce thermal injury in precise anatomic locations while
avoiding injury to surrounding tissue. Radiofrequency, microwave, and laser abla-
tion are three such modalities that may have both curative and palliative roles in the
treatment of solid tumors. This chapter will focus on RFA.
Radiofrequency Thermal Ablation (RFA)
d’ Arsonval (1886) performed the initial experiments using radiofrequency (RF)
thermal ablation and demonstrated that alternating electrical current (>10 kHz)
could pass through living tissue without resulting in neuromuscular excitation. This
discovery provided the framework for the development of medical diathermy and
the application of the electrocautery in surgery. The clinical utility of RF ablative
techniques to induce controlled lesions with anatomic precision has already been
exploited in the fields of cardiology and neurology where it has been used to treat
cardiac arrhythmias, seizures, and movement disorders. The application of this tech-
nology in the treatment of hepatic tumors did not occur until 1990. These initial
reports detailed the use of ultrasound guided RF ablation to induce deep thermal
injury in hepatic tissue while sparing normal parenchyma. Since that time RF 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, clinical
reports 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. These
studies include reports detailing the superiority of bipolar versus monopolar elec-
trodes, pronged versus straight electrodes, and new cooled-tip electrodes. A detailed
analysis of these new approaches is beyond the scope of this chapter.
The Physiology of RFA: Energy Transfer
RF ablation refers to the induction of thermal injury due to frictional heat gen-
erated by the ionic agitation of particles within tissue following the application of
alternating current in the radiofrequency range (200-1200 mHZ). The frictional
heat that occurs desiccates the surrounding tissue leading to the evaporation of in-
tercellular water and coagulation necrosis. In point of fact, radiofrequency waves
play no role in the induction of tissue injury during RF ablation. The agitation of
ions within the tissue occurs only around the needle or electrode through which the
alternating current is applied. Unlike other forms of local hyperthermia, the elec-
trode does not become hot. The anatomic precision of the zone of injury varies
based on the size, position, and shape of the electrode used. Heat (i.e., ionic agita-
tion), which concentrates around the tip of the electrode, is rapidly dissipated with
further 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 required
for coagulation of hepatic tissue to occur. Although the degree of injury around the 18
needle increases with both rising temperature and length of time over which the
heat is applied, temperatures above 110˚C result in tissue charring and vaporization
which limits the amount of heat deposition which occurs by increasing electrical
impedance. At present, this remains a major limitation on the size of lesion that can
be treated with this modality.
Technical RFA Issues: Generators and Electrodes
Three RF generators are commercially available for clinical or experimental use
in the Unites States. All three units provide alternating current within the
radiofrequency range and function based upon the same principles. They differ 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 frequency
supplied by a 50 RF watt power output (Fig. 18.3). The electrode is a 15-guage
stainless needle insulated by thick plastic, with a 1.0 cm active tip and four to eight
nickel-titanium retractable hooks. The maximum deployment diameter for the hooks
is currently 7 cm, and each hook is equipped with an individual thermistor to 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-
18
Fig. 18.3. RITA Medical Systems RFA Generator.

Fig. 18.4. Cartoon demonstrating insertion of radiofrequency needle with deploy-

ment of prongs. Central area represents tumor, with surrounding halozone area
representing normal rim of tissue ablated outside the tumor.
ing of the inner chamber of the electrode with cooled saline is believed to increase
the zone of thermal injury via two distinct mechanisms. Cooling the tip of the
electrode potentially prevents charring of adjacent tissues (keeping resistance low),
and thereby increasing the zone of thermal injury. The continuous perfusion of the
surrounding tissue with saline via the side ports in the electrode theoretically in-
creases the number of ions in the target tissue resulting in more ionic agitation and
thermal injury. Unlike the RITA device, the length of the active tip is variable, between
1 and 3 cm, and can be changed based on the size of the lesion being treated. The RF
device manufactured by Radiotherapeutics is a 90 W alternating current generator
with a multiple array electrode with 10 curved prongs which deploy from the end of
the electrode. The large number of prongs is thought to provide a more spherical injury
than the straight probe (Radionics). Unlike the RITA electrode, the Radiotherapeutics
electrode does not have individual thermistors at the end of each prong. Comparison
data between these three devices is currently not available.
18
Indications and Contraindications
At present, there are no clear indications for RF thermal ablation, and both the
curative and palliative potential of this modality remains unproven. (Table 18.1) We
recommend that RFA use be limited solely to those patients who are not candidates for
surgical resection. Although significant research is currently underway to optimize
RF thermal ablation technology, only tumors up to 5 cm in diameter can be effec-
tively treated by a single ablation. Although multiple adjacent ablations can be per-
formed to encompass larger lesions, overlapping of ablation fields increases tissue
charring and impedance thereby limiting effectiveness. A 7 cm ablative probe from
RITA is due to come to market shortly.
As with cryotherapy, the complication rate increases, and the likelihood of
achieving a therapeutic benefit decreases as the number and size of the treated
lesions increase. Although there are no absolute contraindications to RF thermal
ablation, most authors advocate limiting treatment to those patients with less than
four lesions. Patients with obvious extrahepatic disease, and those with limited life
expectancies (< 6 months), are similarly unlikely to benefit from ablative therapies
and should not be treated.
Table 1. Indications and contraindications for hepatic ablative therapy
Indications
Patients with four or fewer, small (< 5 cm) primary hepatocellular or
metastatic colorectal tumors who are not candidates for surgical resection
due to:
• Poor general health
• Cirrhosis or hepatic insufficiency
• Tumor location or distribution prohibiting surgical consideration
• Recurrent hepatic disease (relative)
• Patient refusal
• Patients with small (< 5 cm) hepatocellular carcinomas awaiting orthotopic
liver transplantation
• As adjuvant at the time of hepatic resection to treat tumors
which are not amenable to surgical removal
• Patients with four or fewer, small (< 5 cm) non-colorectal hepatic me-
tastases. Tumor biology and the natural history of the malignant tumor
should be considered carefully before treatment for non-colorectal
metastases 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
18 • Pregnancy
• Severe pulmonary disease
• Active infection
• Refractory coagulopathy
Technique
RF thermal ablation can be performed percutaneously, laparoscopically, or at the
time of laparotomy. Technically, the performance of RF thermal ablation is the same
regardless of which method is utilized. However, hepatic exposure, access to tumor
locations, as well as patient monitoring are different depending upon the approach.
Significant controversy currently exists as to the optimal way to perform RFA. The
lowest risk of recurrence (or persistence) is associated with open laparotomy, but
acceptable recurrence rates (though higher) have also been reported with the
laparoscopic approach. Percutaneous RF thermal ablation represents another viable
option. However, prior to referral to an interventional radiologist for treatment, all
patients with liver metastases should be discussed at a multidisciplinary tumor board
meeting to optimize treatment. For the sake of consistency we shall describe the
open technique.
Operative Technique
The abdomen is opened using a subcostal, bilateral subcostal (Chevron) or mid-
line incision. A careful exploration for extrahepatic disease is carried out, and after
complete mobilization, bimanual and ultrasound examination of the liver is per-
formed. Once the decision is made to proceed with RFA, the needle is introduced
into the selected area of the tumor using sonographic guidance. We utilize the RITA
device at our institution. Using this device, the tip of the needle is positioned at the
deepest part of the tumor prior to deploying the electrodes. The prongs are initially
deployed approximately two-thirds of their maximum length, and the ablation is
started at a power setting of 25 W and increased to 50 W over the next 30 seconds.
Once the temperature at the tip of the prongs exceeds 90˚C, the prongs are de-
ployed fully. The temperature is kept at 90–110˚C for 6 minutes to complete the
ablation process. Overlapping ablations are completed to encompass the entire 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 to
encompass the entire tumor with a satisfactory margin of normal tissue. As with
surgical resection of hepatic tumors, a margin of 1 cm is ideal, but often not attain-
able. At the completion of the ablation process, the prongs are retracted and the
needle tract is cauterized as it is removed (Fig. 18.5).
Results
Cryotherapy
Cryotherapy of primary liver cancer has been reported in approximately 250
patients to date (Table 18.2). These numbers include patients who have undergone
cryotherapy alone or in combination with resection, percutaneous alcohol injection
(PEI), chemotherapy, or hepatic arterial ligation. Among patients treated with cryo-
therapy alone, the five-year survival rate was 28%, and as expected this correlated
well with the size of the primary tumor treated. Five-year actuarial survivals of 40% 18
were observed in tumors less than 5 cm, but were only 25% for tumors >5 cm. The
pattern of recurrence (or persistence) was predominantly hepatic.
Fig. 18.5. A, Pre-op contrast-enhanced CT scan demonstrating a metastatic tumor

in the left lateral segment of the liver. B, Post-op contrast-enhancing CT scan dem-
onstrated a hypodense area in the left lateral segment, and a second in the right
lobe (not seen in A).
18
Table 18.2. Published series of cryotherapy for hepatic tumors
Author (Year) Histology Patients (N = ) Results

Zhou (1996) HCC 167 Combined series of cryo
alone plus cryo combined
with other treatment 32%
5-year actuarial survival
Haddad (1998) CRM 31 Combined series 7 mo

PLC median disease free
Other survival
Seifert & Morris (1998) CRM 116 Combined series 13%

5-year survival 26 mo
median survival
Yeh (1997) CRM 24 Combined series 85%
31 mo median survival
Adam (1997) HCC 34 Combined series 52%

CRM 5-year survival
Korpan (1997) CRM 63 Combined series 4%

Shafir (1996) CRM 39 Cryo alone 65%

HCC 3-year actuarial survival
Other
Crews (1997) CRM 40 Cryo alone 30%

HCC 5-year actuarial survival
Other
Weaver (1995) CRM 140 Combined series

Other 62% 2-year actuarial
survival 22 mo median
survival
Wrens (1997) HCC 12 Cryo alone 19 mo

median 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% NED

Other at 11 months
McKinnon (1996) CRM 11 Combined series 73%

PLC alive at 18 months
Heniford (1998) CRM 12 Cryo alone 83% alive 18

Other at 11 months
Dale (1998) CRM 6 Combined series 100%

alive at 17 months
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 will
replace PEI as first line therapy for unresectable HCC.
Liver Metastasis
Currently, long-term studies of patients treated with cryotherapy are inadequate
as few provide follow-up beyond 2 years. More concerning, cryotherapy has typi-
cally been utilized as a salvage procedure or in combination with other treatment
modalities which limits any ability to draw conclusions about its efficacy. Ravikumar
et al have reported the best results with overall and disease free actuarial survivals of
78% and 39%, respectively, among 18 patients undergoing an R0 cryoablation of
liver metastasis. Although encouraging, these results have not been duplicated in
more recent studies in which survival rates remain highly variable. Note, however,
despite the wide variation in outcome following cryotherapy, approximately 20% of
patients in nearly all published studies have achieved a durable survival.
We believe that current data support the ongoing use of cryosurgery in clinical
trials only. Cryotherapy should not be used in cases of resectable disease. As with
other regional therapies, survival appears closely related to the size of the lesions
treated and the volume of liver replaced by tumor.
If performed properly, local disease control should be in the range of 60 to 90%.
Yet despite this control, the pattern of recurrences remain primarily hepatic, with or
without extrahepatic disease, and underscores the need for multi-modality approaches.
Radiofrequency Ablation
Hepatocellular Carcinoma and Liver Metastases
To date there are nine published studies detailing the outcome of radiofrequency
ablation for a variety of primary malignant hepatic tumors (Table 18.3). Rossi et el
(1996) reported their initial series of 50 patients with either small HCC (N = 9) or
metastatic tumors (N=11). The histology of the metastatic tumors was varied and
included six colorectal metastases, one breast tumor, one gastric tumor, one gastrinoma
and one thymoma. Tumor size was 3.5 cm in less than all but one case. The 1-, 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 patients
recurred. Among the 16 patients that recurred, only two recurred in a previously
treated area. The outcome in patients with metastatic disease was less favorable with
50% of patients recurring within the first year and only two patients remaining
disease free at 11 months on follow-up. There were no procedure-related complica-
tions. Rossi et al (1998) has subsequently reported an additional 37 patients treated
with RFA. In this group there were 26 patients with HCC and 14 patients with
hepatic metastasis, all tumors were less than 3.5 cm. In the HCC patient group
100% tumor ablation was achieved when assessed by CT scan. Seventy-one percent
of patients remain tumor free at a follow-up of 10 months. These results are compa-
18 rable to those reported for both surgical resection and percutaneous ethanol injec-
tion for small hepatocellular cancers. Among the 14 patients with metastatic disease
the results were less encouraging. Although 93% showed evidence of complete tumor
ablation at post-procedural CT scan, 82% of patients developed recurrent disease

by 14 months of follow-up.
Solbiati et al (1997) reported on 16 patients with a variety of metastatic liver
tumors who underwent RFA. All tumors treated were between 1.5 and 4.5 cm.
Two-thirds (67%) of all tumors remained unchanged or regressed with a mean 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 a
separate study, Solbiati et al (1997) reported on the treatment of an additional 29
patients. Ninety-four percent of patients were alive at one year and 50% of patients
remained disease free. There were no serious complications in either study.
Livraghi et al (1997) treated 15 patients harboring 25% separate metastatic liver
tumors with RFA. Seventy-four percent (N=11) of patients had colorectal metastases,
with the remaining having a variety of other tumor histologies. A complete radio-
logic response was obtained in 52% of patients at six months; however, only one
complete response occurred in tumors greater than 3 cm in size. Allgaiere et al (1991)
reported on 12 patients with HCC treated with RFA. All patients had compensated
liver cirrhosis with Child-Pugh A or B classification. Exclusion criteria were tumors
greater than 5 cm, portal vein thrombosis, refractory ascites or dilated bowel ducts.
Eleven patients had solitary tumors and one patient had two tumors. Eighty-three
percent had complete necrosis by CT assessment; however, only 52% had no evi-
dence of viable tumor on CT six months later. Curley et al (1999) have reported on
125 patients with metastatic liver disease managed with open RFA and have 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.
Summary
Minimally invasive ablative treatments for inoperable hepatic metastasis are a
promising technique that can be performed with low morbidity. Recent advances in
the technology have made it possible to treat more and larger lesions using these
approaches. Given the simplicity of RFA, we prefer it to cryotherapy, though com-
parison studies are lacking. However, the absence of strong data supporting the
efficacy of either approach in prolonging overall survival, informed consent and
judicious patient selection are paramount. Neither RFA nor cryotherapy should be
used as an alternative to curative resection. Hepatocellular cancer, colorectal me-
tastases, and hepatic neuroendocrine metastases remain the only histology for which
substantial data exist to support the use of either approach outside of a clinical trial.
Suffice it to say that when possible even these patients should be treated on protocol.
In short, RFA and cryotherapy represent promising technologies with the po-
tential to impact on a large percentage of patients with liver only tumors for whom
current treatments offer no hope. Future trials will demonstrate whether our hopes
are to be confirmed, or remain in vain.
18
Table 18.3. Clinical results of radiofrequency thermal ablation (RFA) for hepatic
tumor
Author (Year) Histology Patients (N = ) Results

Rossi (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 hepatic
recurrence. No treatment
related complications.
Mets 11 50% recurrend @ < 12 mo
2/11 NED (mean F/U 11
months)
Solbiati (1997) Mets 16 67% of tumors table (mean
18.1 mo) 67% 1-yr tumor-
free survival One minimal IP
bleed
Solbiati (1997) HCC (N=19) 29 26/28 HCC completely
ablated on CT
Mets (N=10) 19/23 tumor-free by CT 3/3
liver explants had viable of
tumor at ablation margin
One serious IP bleed
Rossi (1998) HCC Mets 23 36/37 had CR on CT No
14 major complications
Allgaier (1999) HCC 12 10/12 complete ablation
on CT. All patients tumor-free
(mean F/U 5 mos.) No major
complications
Lencioni (1998) HCC 80 Randomized to RFA or PEI
CR by CT—91% RFA
85% PEI
Recurrence rates
RFA-2% PEI-13%
Rhim (1999) HCC Mets 25 69% complete ablation on
CT
13% recurrence
17 Four complications
2 IP bleeds
1 needle track seeding
1 diaphargm injury
Siperstein (1999) NET Mets 66 88% demonstrated shrinkage
after ablation
12% recurrence (N = 22)
Bauer (1999) Mets 20 92% experience > 50%
increase in pre-op CEA No
complications
Abbreviations: IP, intraperitoneal. CR, complete response, CT%, computed

tomography scan
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CHAPTER 1
CHAPTER 19
Surgical Techniques in the Management

of Hepatic Trauma or Emergencies
H. Leon Pachter, Amber A. Guth
Introduction
The liver is the most frequently injured intraperitoneal organ, at risk by virtue of
its location and size for both penetrating and blunt thoracoabdominal trauma. While
complex hepatic injuries carry a 20% mortality rate, the routine use of high-speed
computed tomographic (CT) scanning in the evaluation of bluntly-injured trauma
patients has resulted in the detection of minor, asymptomatic injuries that would
not have been diagnosed in the past. The frequent recognition of these lesser hepatic
injuries has prompted the adoption of nonoperative management of liver trauma
over the last decade. In this Chapter, the indications for operative and nonoperative
management, surgical techniques, and outcomes of hepatic injuries are reviewed.
History
Modern surgical treatment of hepatic injuries dates back to 1870, with Bruns’
description of the first successful operative debridement of a gunshot wound to the
liver. The next major surgical advance was Pringle’s report in 1908 of his technique
to occlude hepatic blood flow by compressing the porta hepatis, allowing repair of
hepatic injuries before death from exsanguination.
During World War I, the reported mortality from liver injuries was 66%. By
World War II, with improvements in anesthesia and patient support, this had dropped
to 27%. In the decade following the war, liver stitches placed through the wound to
approximate the injured liver and provide hemostasis by compression was described;
however, the technique of packing massive hepatic injuries was condemned. By the
time of the Korean War in the early 1950s, mortality dropped further to 14%.
During the 1970s, many of the current techniques used to manage hepatic inju-
ries were popularized including direct control of hemorrhage by ligation of bleeding
vessels rather than anatomic resection or the use of large liver stitches to compress
the site of bleeding. By the 1980s, the techniques of finger-fracture exposure of
vascular injuries, the selective use of perihepatic packing, and improvements in criti-
cal care support of the severely injured patient had become routine components of
trauma management.
First published in 1989 (and subsequently revised in 1994), the Liver Injury
Scale developed by the American Association for the Surgery of Trauma (AAST) has
become the standard describing hepatic injuries (Table 19.1).

Table 19.1. American Association for the Surgery of Trauma Liver Injury Scale;
1994 Revision*
Grade Injury Description
I Hematoma
Subcapsular, nonexpanding, < 10 cm surface
area
Laceration Capsular tear, nonbleeding, < 1 cm parenchy-

mal depth
II Hematoma Subcapsular, nonexpanding, 10-50% surface

area: intraparenchymal nonexpanding
< 10 cm diameter
Laceration Capsular tear, active bleeding; 1-3 cm

parenchymal depth, < 10 cm length
III Hematoma Subcapsular, > 50% surface area or expand-

ing; ruptured subcapsular hematoma with
active bleeding; intraparenchymal hematoma
> 10 cm or expanding
Laceration > 3 cm parenchymal depth
IV Hematoma Ruptured intraparenchymal hematoma with

active bleeding
Laceration Parenchymal disruption involving 25-75% of

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

hepatic lobe or > 3 Couinaud’s segments
within a single lobe
Vascular Juxtahepatic venous injuries
VI Vascular Hepatic avulsion
*J Trauma 1995; 38:323
Diagnosis of Blunt Hepatic Trauma

Motor vehicle accidents (MVAs) account for the majority of blunt hepatic inju-
ries, with unrestrained drivers and passengers at greatest risk, and pedestrians struck
by vehicles, falls and assaults accounting for the remaining injuries.
Advances in prehospital care, such as intubation and fluid resuscitation in the
field coupled with rapid transport times, have resulted in increasingly critically in-
jured patients reaching the hospital alive. Hemodynamically unstable patients with
obvious hemoperitoneum should be quickly resuscitated and immediately trans-
19 ferred to the operating room as further work-up only delays definitive treatment
and results in death from exsanguination (Fig. 19.1).
Surgical Techniques in the Management of Hepatic Trauma 259
Fig. 19.1. Triage of blunt hepatic trauma in the Emergency Department
The hemodynamically stable patient can undergo further diagnostic studies and
subspecialty consultation as needed. However, the trauma surgeon must recognize
the limits of physical exam in detecting intra-abdominal injuries. Data from the
1970s demonstrated that up to 43% of patients thought to have a normal abdomi-
nal exam at initial presentation were subsequently found at laparotomy to have
significant intra-abdominal injuries. Particularly treacherous, are patients with
deacceleration injuries, who may present without obvious changes in vital signs or
on physical exam but, due to unrecognized ongoing bleeding, can suddenly collapse
hemodynamically. This scenario is particularly dangerous when the patient is un-
dergoing radiologic evaluation such as CT and is relatively inaccessible to the trauma
team. Thus, the trauma surgeon must be in continuous attendance of the patient,
despite hemodynamic stability, until the evaluation is complete and the presence or
absence of injuries definitively established.
Diagnostic Tests
Four major diagnostic modalities are currently used to detect intra-abdominal
injuries:
1. diagnostic peritoneal lavage (DPL),
2. CT scanning,
3. ultrasound, and
4. laparoscopy (Table 19.2).
19
Table 19.2. Diagnosis of hepatic injury

Technique Pros Cons
Diagnostic Peritoneal Bedside procedure Does not distinguish

Lavage Rapid serious from trivial
Extremely low injuries
false-negative rate Procedural
complications
CT Scan Complete evaluation Expensive

of intra-abdominal Removes patient from
organs monitored setting
Ultrasound Rapid bedside Less specific information

procedure regarding individual
organ injuries than CT
scan
Laparoscopy Accurately detects Role of comprehensive

peritoneal intra-abdominal
penetration evaluation not
established
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 bedside
utilizing local anesthesia. A small opening is surgically created in the anterior
abdominal wall just below the umbilicus (supraumbilical in patients with pelvic
fractures) and if no free blood is noted, the peritoneal cavity lavaged with a liter of
lactated Ringers, and the effluent examined for RBC and WBC counts, amylase,
and particulate matter. Diagnostic peritoneal lavage reliably detects intraperitoneal
blood (98% accurate), and has been particularly useful in patients with altered 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 insignificant
intraperitoneal blood, and
2. inability to detect retroperitoneal and diaphragmatic injuries.
Its use has largely been supplanted by CT and trauma ultrasound.
Computed Tomographic Scanning (CT)
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 still
not very sensitive for diaphragmatic injuries. With increased use of CT in hepatic
injuries, it became clear that small amounts of free blood in the peritoneum was not
19 associated with significant injuries, and thus, numerous patients have been spared
nontherapeutic exploratory surgery which would have been performed based on the
presence of RBCs in the DPL fluid.
However, CT scanning has its own drawbacks, and is contraindicated in the
hemodynamically unstable patient.
Ultrasonography (US)
First popularized in Europe, bedside US has become a powerful tool in the evalu-
ation of blunt abdominal trauma. Within minutes of arrival in the Emergency
Department (ED), the presence of free blood can be detected during a rapid bedside
scan of the hepatorenal space, left subdiaphragmatic space, and pelvis. This has
proved especially useful in the hemodynamically unstable, multiply injured patient
in whom the site of bleeding is not immediately evident.
The technique is operator-dependent, but the radiologic skills can be acquired
by trauma surgeons. It is currently used to detect free blood, but experience with
scanning the liver parenchyma is accumulating, and this technique may reduce de-
pendence on costly CT scanning in the future.
Laparoscopy
In an effort to minimize the performance of nontherapeutic trauma laparoto-
mies, diagnostic laparoscopy for stable penetrating abdominal trauma has been used
with increasing frequency. There are scattered reports of hepatic injuries diagnosed
and managed with laparoscopic techniques such as intracorporeal suturing and ap-
plication of hemostatic agents. However, its reliability in detecting hollow viscus
injuries has not been established, and the ability of laparoscopy to establish the
presence or absence of peritoneal violation from penetrating abdominal trauma
remains undefined.
Nonoperative Management of Hepatic Injuries
In the latter part of the 20th century, the ability to detect blunt hepatic injuries,
initially utilizing DPL and subsequently CT scanning, raised a new set of questions
about what is appropriate management of these injuries. The sensitivity of these
techniques resulted in a significant increase in diagnosis and laparotomy for trivial,
nonbleeding hepatic injuries. The recognition that up to 67% of celiotomies per-
formed for blunt abdominal trauma were nontherapeutic, and that up to 86% of all
blunt hepatic injuries had stopped bleeding by the time surgery was performed,
prompted a re-evaluation of the indications for surgical management of the stable
patient with blunt hepatic injury, especially in light of the success of nonoperative
management in pediatric patients. Early concerns about the inability of hepatic in-
juries to stop bleeding spontaneously, and missed concomitant intra-abdominal in-
juries, have proven to be unfounded.
Blunt Hepatic Injuries
As per Figure 19.1, hemodynamic stability is the crucial factor in selecting pa-
tients for nonoperative management. Additional qualifying criteria include absence
of peritoneal signs on physical exam, delineation and American Association for the
Surgery of Trauma (AAST) grading of hepatic injury by CT scan, and lack of asso-
ciated abdominal injuries that require surgical management. At present, at least 50% 19
(and possibly up to 80%) of patients with blunt hepatic injury are candidates for
nonoperative management. Initially, nonoperative therapy was considered appro-

priate only for AAST grade I to III injuries. With experience, it now appears that
hemodynamic stability supersedes injury grade, and approximately 21-38% of selected
patients with grade IV or V injuries can be safely managed nonoperatively. How-
ever, in a recent multi-institutional study authored by Pachter, only 14% of grade
IV or V injuries were managed nonoperatively, and this group accounted for 67% of
all patients who failed and required surgical control of bleeding. Thus, while 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 the
understanding that they are at greater risk for failure, and must be monitored closely
in a critical care setting with immediate availability of the operating room.
The current approach to nonoperative therapy relies heavily on CT imaging to
both define the extent of hepatic injury, as well as evaluate the rest of the abdomen
for associated injuries. While early reports highlighted missed hollow viscus injuries
(the true incidence ranges from 0.22-3.5%), these injuries should be detected by
clinical monitoring of the patient, even if they are not demonstrated on initial
abdominal CT evaluation.
While initial CT grading of hepatic injuries does not always correlate with intra-
operative findings or outcome, certain findings mandate immediate intervention. A
contrast “blush”, or pooling of contrast within the liver parenchyma, represents free
arterial bleeding, leaving the patient at risk for sudden hemodynamic 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 injuries
utilizing 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, allowing
for rapid intraoperative identification and management of the lacerated artery.
Outcome of Nonoperative Management
The overall success rate for nonoperative management is 96%. The mean trans-
fusion rate is 1.9 units, half the operative requirement in matched patients. Late
hemorrhagic complications occur infrequently, and the overall rate of hepatic-related
deaths in adult patients appears to be approximately 0.3%.
The complications of bile leaks and abscesses are uncommon, with frequencies
of 3 and 0.7% respectively. In the septic, jaundiced patient, these collections can be
initially approached by radiologic-guided percutaneous drainage, with the caveat
that prompt improvement should result. If not, CT imaging should be performed.
If the drainage catheter is in the proper location, but the septic state is not improv-
ing, immediate surgery should be undertaken for drainage and debridement. An
alternative approach to bilomas is endoscopic sphincterotomy and stenting of the
common bile duct. By facilitating outflow at the ampulla of Vater, bile flows prefer-
entially into the duodenum rather than through the peripheral, higher resistance
duct injury.
Follow-up CT scanning is not necessary after an uncomplicated course of
nonoperative management for grades I-III injuries, and its role is still being evalu-
ated for complex grade IV and V injuries.
19
Penetrating Hepatic Trauma

The role of nonoperative management of penetrating hepatic injuries in the
hemodynamically stable patient has not been established, although its success in
selected cases of penetrating splenic injury suggests a possible role in liver injuries as
well. This is a scenario where one can foresee laparoscopic evaluation defining the
extent of hepatic injury in addition to its current role in the mere detection of peri-
toneal violation.
Surgical Management of Complex Hepatic Injuries
While the majority of blunt injuries to the liver are now managed nonoperatively,
the complex grade IV to V injuries (which account for 10-20% of hepatic injuries)
usually present with hemodynamic instability due to extensive destruction of the
liver parenchyma. These injuries present a formidable challenge to the trauma sur-
geon. The algorithm outlined in Figure 19.2 summarizes the techniques needed to
successfully manage these potentially lethal injuries.
Profuse hemorrhage results in hypothermia, acidosis and coagulopathy, a deadly
combination. Intraoperative management by both the anesthesia and surgical staffs
must be directed at correcting these parameters; otherwise death is imminent. If
normothermia, correction of acid-base status and coagulopathy cannot be achieved,
the operation must be aborted and “damage control” employed. Prior to 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-flow
fluid 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 and
bimanual compression of the liver performed to control bleeding and allow ongoing
resuscitation by anesthesia.
Operative Management of the Injured Liver
Portal Triad Occlusion (Pringle Maneuver)
The first step in controlling massive hemorrhage (Table 19.3) is portal triad
occlusion, accomplished by placing a nontraumatic vascular clamp across the hepatic
artery, portal vein and common bile duct at the level of the foramen of Winslow.
Hepatic vein bleeding is not controlled by this maneuver and other techniques must
be employed (see below).
How long can the human liver tolerate normothermic ischemia? While 20 min-
utes is the commonly accepted time period, data from elective hepatic resections for
malignancy implies that the liver can tolerate inflow occlusion for up to 90 minutes.
However, this observation cannot be extrapolated to the injured liver for a number
of reasons. Collateral blood supply is common in large tumors; additionally, these
resections are performed under controlled conditions with optimization of the
patient’s hemodynamics, both preoperatively and intraoperatively, unlike the trauma
patient whose medical history may not be known, and whose liver is often exposed
to significant periods of hyperprofusion before reaching the operating room. Thus,
at Bellevue Hospital, there has been a long interest in manipulating the local hepatic
environment to provide hepatocyte protection and minimize the risk of ischemic 19
Table 19.3. Principles of initial intraoperative management of complex hepatic

injuries
A. Bimanual compression of liver and anesthesia resuscitation
B. Portal triad occlusion (Pringle maneuver)
C. Finger fracture hepatotomy to expose lacerated blood vessels and bile ducts
for repair
D. Debridement of nonviable hepatic tissue
E. Vascularized omental pedicle pack of injury site
F. Closed suction drainage
Fig. 19.2. Surgical management of complex hepatic injuries
injury to the liver. While the use of high-dose steroids (previously considered to play
a role in hepatocyte protection) has recently been shown in an animal model to be of
no benefit, cooling the liver to 32˚C, while maintaining systemic normothermia by
the techniques outlined above, may provide cryoprotection. While some authors
advocate reperfusion of the liver after 15-20 minutes by releasing the cross-clamp
for 5 minutes, data from Pachter et al detailed 81 consecutive patients who under-
went cross-clamping with hepatocyte protection for a mean period of 32 minutes
(up to 75 minutes) without adverse sequelae.
19
Additional Techniques of Vascular Control

Juxtahepatic 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 approaches
have been described including insertion of atriocaval shunts, sequential total vascu-
lar isolation of the liver with or without venous bypass, direct exposure of the injury
by the finger-fracture technique, “damage-control” tamponade of the injury by pack-
ing the liver with laparotomy pads, and subsequent re-exploration of the liver once
the patient has stabilized. Isolated case reports describe emergent hepatectomy and
transplantation for the shattered nonsalvagable liver.
Hepatic Hemostasis
Once bleeding has been minimized by the Pringle maneuver, the injury is explored
and local hemostasis achieved.
Deep Liver Stitches

This technique is mentioned only to be condemned. Large simple absorbable
liver sutures on a blunt-tipped needle are passed through normal liver parenchyma
surrounding the injury and tied snugly to provide compressive hemostasis. 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 liver
parenchyma can also result in hepatic necrosis.
Finger Fracture Hepatotomy

This technique addresses the shortcomings of deep liver stitches, allowing expo-
sure of the injured vascular and biliary system, and precise repair or ligation of these
structures. After portal triad occlusion, the liver is mobilized by division of the coro-
nary and triangular ligaments. The mobilized liver is brought forward into the wound
and stabilized by the first assistant’s left hand. Next, the injury is opened by dividing
the hepatic parenchyma in a nonanatomic fashion following the direction of the
injury. A suction catheter or clamp is used to gently divide the liver, and fine sutures
or clips to divide the bridging blood vessels and bile ducts. Care must be taken not
to inadvertently injure the main right and left hepatic ducts, or to extend the area of
the hepatotomy so widely that the blood supply to the surrounding liver is divided,
rendering the injury site ischemic and at increased risk for necrosis and abscess for-
mation.
Debridement
Removal of all devascularized hepatic parenchyma is necessary to prevent devel-
opment of postoperative septic complications. Although counterintuitive, the injury
site must be debrided back to well-vascularized bleeding tissue, recognizing that an
intact Glisson’s capsule may hide an extensive zone of deeper devitalized liver.
Omental Pack
Next, a vascularized pedicle of greater omentum, based on either the right or left
gastroepiploic vessels, is mobilized and placed within the injury site. The liver edges 19
are then brought gently together over the omentum using 0 or 00 chromic liver
sutures. Besides eliminating dead space and providing mild compressive hemostasis,
the omentum may play a role in combatting sepsis through fixed tissue macrophages
and immunoglobulins.
Drains
Routine drainage of hepatic injuries remains controversial. While open drainage
using passive Penrose drains is clearly associated with increased rates of perihepatic
postoperative sepsis, the evidence regarding closed suction drainage is debatable.
Recent studies have implicated independent factors such as hypotension, blood trans-
fusions, and the presence of additional intra-abdominal injuries (all indicators of
the severity of injury), rather than the mere presence of closed suction drains.
Additional Techniques of Hepatic Hemostasis
Hepatic Resection
Formal hepatic resection is associated with a prohibitively high mortality (up to
43%) and is rarely indicated except in occasional cases where the extent of injury
requires lobectomy.
Mesh Hepatorrhaphy
Experience with absorbable mesh wrapping of the injured spleen in the late 1980s
lead to the application of this technique to liver injuries. It is useful in cases of wide
decapsularization with bleeding which is difficult to control with the techniques
described above. However, the major mechanism of hemostasis is by local tampon-
ade of the liver, unlike hepatic packing with laparotomy pads which, by displace-
ment and compression, can result in an “abdominal compartment syndrome”, and
which requires reoperation for lap pad removal and definitive management of inju-
ries. The major technical pitfall of this procedure is possible compromise of blood
flow through the porta hepatis and vena cava.
Perihepatic Packing and “Damage-Control” Laparotomy

Extensive 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 established
the role of perihepatic packing in this setting, with recent reports citing a 67-77%
survival rate when employed in a timely fashion. To be successful, the trauma sur-
geon must recognize the futility of proceeding with surgery early in the course of the
operation, quickly packing the liver closing the laparotomy incision with towel clips,
and transferring the patient to a critical care area for resuscitation and correction of
hemodynamic and hematologic parameters. When the decision to abort surgery
and pack the abdomen is delayed and the technique applied as a last desperate 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 between
the liver and lap pads. Other injuries that require immediate attention are quickly
addressed (for example, hollow viscus injuries stapled closed and vascular injuries
19 shunted), and the abdomen closed with towel clips. Jackson-Pratt drains are placed
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 majority
of injuries can be managed with the techniques described above. Liver packing ap-
pears to be especially efficacious in juxtahepatic injuries, whereas other approaches
such 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 vena
caval shunting should be made, but rather the operation terminated and the patient
fully resuscitated. It is not unusual for the bleeding to have ceased at the time of
re-exploration and pack removal. If there is bleeding from a juxtahepatic injury at
the time of reoperation, the patient is stable and appropriate surgical staff are 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 in
the “abdominal compartment syndrome,” Increased peak inspiratory pressure,
abdominal distention, and oliguria due to intra-abdominal venous occlusion results.
The intra-abdominal pressure can be measured by a manometer attached to the
Foley catheter which measures pressure within the bladder and reflects the intra-
abdominal pressure. If abdominal hypertension is present, it must be released by
opening the abdominal incision and utilizing prosthetic material (sterile urology
irrigation bags, Gortex) to bridge the gap between the skin edges.
Return to the operating room is predicated upon reversal of the patient’s hypo-
thermia, acidosis and coagulopathy, which can usually be accomplished within 24-36
hours. Leaving the abdomen packed for greater than 72 hours is associated with
perihepatic sepsis rates of up to 83%.
Selective Hepatic Artery Ligation

Since the previously described techniques are usually adequate to provide 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 artery
injuries, when ligation results in a 42% survival compared to 14% for primary arte-
rial repair.
Complications of Surgical Management
Recurrent Bleeding
This is uncommon, with an incidence of 2-7%. In stable patients, angiography
and selective embolization is the preferred initial approach. The unstable patient
must return immediately to the operating room, with intraoperative resuscitation
occurring simultaneously with re-exploration of the injury, identification and con-
trol of the source of bleeding.
Hemobilia
Iatrogenic injuries from percutaneous liver biopsy and transhepatic stents are the
most common etiologies. Only 30% of patients present with the classic triad of
right upper quadrant pain, gastrointestinal bleeding, and jaundice. Since the bleed-
ing is often intermittent, endoscopy may not be diagnostic as there may not be
active bleeding noted at the ampulla of Vater at the time of endoscopic evaluation. 19
Angiography is both diagnostic and therapeutic, identifying the traumatic hepatic
artery aneurysm, as well as providing access for selective embolization of the injured
vessel. Surgical management is rarely needed, except in cases with a very large 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 before
opening the aneurysm, as exsanguinating hemorrhage can result before the internal
surface of the aneurysm can be oversewn.
Intra-abdominal Abscess
While hemorrhage is responsible for early mortalities following complex hepatic
trauma, perihepatic sepsis, and associated ARDS and multiple organ system failure,
are the cause of late morbidity and death. In a review of eight publications describ-
ing 3663 cases of hepatic trauma from the late 1980s, the overall abscess rate was
9.7% and abscess-associated mortality was 41%. More recent reports place the 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 open
passive drains. Thus, the rate of perihepatic sepsis and its high attendant mortality
can be minimized by careful surgical technique including debridement of nonviable
tissue, meticulous hemostasis, and avoidance of passive drains.
Most abscesses are diagnosed by CT imaging of the liver. If a well-defined collec-
tion is present, percutaneous drainage can be attempted under radiologic guidance
with a caveat that failure of the patient to improve within 24-48 hours mandates
re-exploration.
Bile Fistulae
While not uncommon, bile leaks usually resolve spontaneously and rarely pose a
management problem. If the drainage persists at 50 mL/day for greater than two
weeks, a biliary fistula is present. The incidence ranges from 7-10%. With adequate
external drainage (to prevent biloma formation) and free flow of bile through the
ampulla of Vater into the duodenum, the fistula should close spontaneously.
High output fistulae of 300 mL/day or greater must be managed more 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 of
the lacerated bile duct is a useful temporizing intervention, particularly in the mul-
tiply injured critically ill patient. Sometimes the ductal injury will heal over the
stent, eliminating the need for surgical repair.
Recently, the use of self-expanding endoprosthesis stents has also been described
in the management of major bile duct injuries.
ERCP is another useful tool in the diagnosis and management of major bile duct
leaks. Sphincterotomy, stent placement, and nasobiliary stent insertion all increase
the rate of bile flow through the ampulla of Vater, decreasing pressure in the 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 Fistulae
19 These are rare lesions, usually diagnosed after penetrating trauma. Angiography
establishes the diagnosis and can prove therapeutic in cases amenable to selective
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. For
large fistulae, or those located in the portal triad, embolization has a 42% success
rate. Surgical approaches include ligation, primary repair, or bypass grafting. Some-
times the aneurysmal sac must be approached directly by opening it and oversewing
the orifices of all entering vessels, a situation where complete vascular control can be
difficult to obtain, and in which use of a cell-saver can be life saving.
Outcome of Hepatic Trauma
In summary, the majority of hepatic injuries are minor grade I and II injuries
diagnosed by CT imaging of the abdomen in the hemodynamically stable bluntly
injured patient, and can be safely managed nonoperatively with an expected 96%
success rate.
The overall mortality rate for hepatic injuries is 10%. Complex hepatic injuries
(grades III-V) represent 10-20% of all hepatic trauma and account for the vast
majority of hepatic-related deaths. The mortality rate from complex hepatic inju-
ries has decreased from 50-20% over the last decade, due in part to the widespread
application of nonoperative management, and the use of damage-control laparo-
tomy and ERCP. In addition, the interventional radiologist, with the ability to per-
form selective angiography and embolization, percutaneously drain abscesses and
bilomas, and stent biliary tract injuries, has become a crucial member of the team
caring for the patient with complex hepatic injuries.
Selected Reading
1. 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 Trauma
1996; 40:31.
3. Pachter HL, Hofstetter SR. The current status of nonoperative management of
blunt hepatic injuries. Am J Surg 1995; 169:442.
4. Morris JA, Eddy VA, Blinman TA et al. The staged celiotomy for trauma: issues in
unpacking 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. J
Trauma 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.
19
CHAPTER 20
Liver Transplantation
Patricia A. Sheiner, Rosemarie Gagliardi, D. Sukru Emre
In 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 antirejection
medications and organ preservation solutions, survival rates began to improve, and
orthotopic liver transplant (OLT) became an accepted therapy for advanced liver dis-
ease. In 1983, a National Institutes of Health (NIH) consensus conference concluded
that OLT for end-stage liver disease “deserves broad application.” Presently, 1-year
patient survival rates of 85-90% and 5-year patient survival rates of 70% are very
common.
Indications
Patients must have acute or chronic end-stage liver disease with complications that
make long-term survival unlikely (Tables 20.1 and 20.2).
Possible Contraindications to Liver Transplantation
Human Immunodeficiency Virus
Until recently, human immunodeficiency virus (HIV) was an absolute contrain-
dication to liver transplant. With multidrug therapy permitting long-term survival
in HIV patients, the issue is being readdressed. A few programs have already trans-
planted patients under strict protocols. These individuals are HIV antibody positive
but 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 Sepsis
Extrahepatic sepsis remains an absolute contraindication. With immunosuppres-
sion after transplant, uncontrolled infection becomes deadly.
Patients with small hepatocellular carcinoma (HCC) (<5 cm), without evidence
of portal vein thrombosis, have long-term results after liver transplant equal to those
achievable in transplant recipients without tumors. Patients with larger tumors have
a high incidence of recurrence. We have found that tumor size >8 cm or major
venous invasion is associated with rapid recurrence and unacceptable patient and
graft survival after transplantation. At our center, patients with tumors between 5-8
cm undergo transplantation under a multimodality protocol that includes
pretransplant chemoembolization and intra- and postoperative systemic chemotherapy

Liver Transplantation 271
Table 20.1. Etiologies of end-stage liver disease
Adult Diseases 20
• Hepatitis C virus (HCV) - Leading indication for liver transplant in USA (20%).
• Hepatitis B virus (HBV) - Leading indication for liver transplant in Orient.
• Autoimmune hepatitis - Usually affects young women. Transplant indicated for
minority of patients who fail immunosuppressive therapy.
• Cryptogenic cirrhosis - Diagnosis of exclusion; may involve unidentified virus
or autoimmune disease.
• Alcoholic cirrhosis
• Cholestatic diseases primary biliary cirrhosis (PBC) - Usually affects middle-age
women, who develop jaundice and fatigue. Associated with antimitochondrial
autoantibody. Transplant appropriate with bilirubin >10 mg/dl or upon
development of portal hypertension.
• Primary sclerosing cholangitis (PSC) - Usually affects men. Associated with
inflammatory bowel disease. Patients develop recurrent cholangitis and are at
risk for developing cholangiocarcinoma.
• Fulminant hepatic failure - Encephalopathy within 2 months of onset of
jaundice. Involves massive necrosis in previously healthy liver.
Causes include HBV, HAV, drug toxicity (e.g., from acetaminophen or
isoniazid), Wilson’s disease, autoimmune hepatitis. Multiorgan failure
develops. Before availability of transplant, mortality from cerebral edema or
sepsis was 80%. Decision to transplant emergently is based on predictors of
spontaneous recovery, including Factor V level, etiology, age, and interval
from jaundice to encephalopathy >1 week. Some die on waiting list.
• Budd chiari syndrome - Caused by hepatic vein obstruction, most often
associated with myeloproliferative disease. Transplant indicated for hepatic
failure.
• Biliary atresia - Leading indication for pediatric transplantation (55%).
Portoenterostomy (Kasai procedure) is treatment of choice before 2-3 months,
but 2/3 eventually fail. Transplant required if Kasai wasn’t done by 3 months,
and for failed Kasai.
• Inborn errors of metabolism - Some cause liver destruction (e.g., Wilson’s
disease, antitrypsin deficiency). Others do not (e.g., hemophilia, oxalosis) and
may indicate auxiliary segmental orthotopic or heterotopic transplant.
• Postnecrotic cirrhosis and fulminant hepatic failure
• Hepatoblastoma - Better results than for hepatoma.
Table 20.2. Complications of end-stage liver disease

• Spontaneous bacterial peritonitis
• Difficult to control ascites
• Encephalopathy
• Worsening synthetic function
• Hepatorenal syndrome
• Hepatocellular carcinoma less than 5 cm, confined to liver with no extra
hepatic metastases
• Failure to thrive (pediatric especially)
• Fulminant hepatic failure
• Disease-specific—PBC—increasing bilirubin,
PSC-episodes of cholangitis, inborn errors of metabolism
with adriamycin. Results of this protocol are still being evaluated. An important
concern is how to manage patients with small tumors while they wait for transplant.
20 In the current United Network for Organ Sharing (UNOS) allocation system, the
presence of a tumor gives a patient relative priority. Because wait times may be long,
however, a patient who is initially a good transplant candidate may become 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 3
months. If the tumor grows or if other small lesions develop, we attempt to control
tumor growth with alcohol injection, radiofrequency ablation (for tumors <5 cm),
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 to
tumor patients while their tumors are relatively small.
Cholangiocarcinoma
Cholangiocarcinoma (CCA), a complication of long-standing primary scleros-
ing cholangitis (PSC), is a contraindication to transplant at many centers because of
historically high recurrence rates, even with small and in situ carcinomas discovered
incidentally. In a patient with PSC, a new dominant stricture, an acute rise in 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 have
achieved 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 Tumors
In most cases, the presence of metastatic tumors (e.g., colorectal, breast, GI tract,
etc.) is an absolute contraindication to liver transplant. Such tumors recur rapidly
after transplant and there are no known long-term survivors. Patients with certain
slow-growing tumors such as metastatic neuroendocrine tumors and carefully se-
lected patients with leiomyosarcomas confined to the liver have undergone trans-
plantation with good 5-year survival.
Pulmonary Hypertension
The association of pulmonary hypertension and end-stage liver disease is well
described, with reported incidences ranging from 2-4%. The etiology of pulmonary
hypertension in end-stage liver disease is unclear, but one frequently proposed hy-
pothesis is that in patients with portal hypertension, the pulmonary vasculature
may be exposed to vasoactive mediators normally metabolized by the liver. When
these patients undergo major surgery, anesthetics, hypoxemia, and acidosis may 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. This
effect will in turn exacerbate the problems of acidemia and hypoxemia, leading to acute
right heart failure and an inability to maintain perfusion pressures to the left heart.
Advanced Age
Given the scarcity of organs, some programs have an age limit for recipients. At
our center, we are more concerned with older recipients general health than with
their age. A 70-year-old patient in the ICU with renal failure is not likely to survive
long-term after transplant. On the other hand, 70-year-old patients in relatively
good health except for liver disease may do very well, with survival rates similar to
younger patients. The shortage of organs has made waiting times very long, and
patients deteriorate while they wait for transplant. This fact has affected the eligibil- 20
ity of older patients. Now, because living-related transplants allow US to bypass the
waiting list and schedule transplants electively, we are able to transplant older pa-
tients successfully.
Psychosocial Contraindications
Active drug or alcohol use is an absolute contraindication to transplant. Although
rules regarding drug or alcohol abstinence vary, most transplant programs require a
6-month abstinence period as well as participation in a rehabilitation program. 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 may
not be able to manage his/her medications and frequent hospital visits, thus risking
the success of the transplant and possibly wasting the organ.
Organ Allocation
Currently, organ allocation in the United States is determined by both medical
urgency and time on the waiting list, within 11 geographic regions. The waiting list
is dynamic, in that a patient’s status can change over time. Within each region, and
then within a given blood group, patients are prioritized first by medical urgency.
Then, for all patients with the same medical urgency status, priority is given to the
person with the most time accrued on the waiting list.
Medical Urgency
Under the current UNOS system, there are four medical urgency statuses for
each blood group. Each patients status is determined mainly on the basis of the
Child-Turcotte-Pugh (CTP) score (Table 20.3). The advantage of the CTP score is
that it is objective; it provides a uniform standard for programs at all centers. The
disadvantage is that it does not permit subjective evaluation by the physician of an
individual patients degree of illness. In order of increasing urgency, the four levels are
status 3, status 2B, status 2A and status 1. To meet waiting list criteria, a patient must
have at least 7 points on the CPT score. Point requirements are shown in Table 20.4.
Timing of Transplantation
The benefits and risks of liver transplantation are great. For each patient, the
risk:benefit ratio changes as the course of illness proceeds. The goal is to perform
transplantation when the patient’s likelihood of surviving without a new liver is low,
but before the patient is too ill to survive the procedure. Toward this end, the role of
the hepatologist is to optimize patient’s medical conditions on the waiting list and
to identify life-threatening complications that afford higher priority on the list. 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 become
liver transplant candidates. For example, an elderly bed-bound patient with low
albumin and no muscle mass is unlikely to survive a transplant. Early involvement
of nutritionists and physical therapists is becoming increasingly important.
Table 20.3. Child-Turcotte-Pugh (CTP) scoring system to assess severity of liver

20 disease
Points 1 2 3
Encephalopathy None 1-2 3-4
Ascites Absent Slight At least

moderate
(or controlled
despite diuretic
treatment by
diuretics)
Bilirubin (mg/dl) <2 2-3 >3
Albumin (g/dl) 2.8-3.5 <2.8
Prothrombin time <4 4-6

(secs. prolonged) >6 or (INR)
<1.7
1.7-2.3
>2.3
For primary biliary cirrhosis, primary sclerosing cholangitis, or other cholestatic

liver diseases:
Bilirubin (mg/dl)* <4 4-10 >10
Preoperative Planning
Liver Volume
Although 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 woman
with an 800 cc liver volume, and a liver from a small child will not support an adult
with an 1800 cc liver. (Occasionally, the presence of massive ascites can allow a
larger liver to be put into a smaller person.) In living-donor liver transplants, it is
particularly 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 volume
required 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 Electrolytes
End-stage cirrhotics, especially those with massive ascites and renal insufficiency
who are taking diuretics, may have low sodium levels. Postoperatively, approximately
1% of liver recipients exhibit clinical findings ranging from mental status changes to
stupor to death. These findings have been ascribed to the presence of central pontine
myelinolysis (CPM), a known complication after liver transplant. While the etiol-
ogy may be multifactorial, a known risk factor is rapid change in serum sodium
level. Rapid transfusion of blood products and fluid, common during transplant, 20
may lead to swift correction of serum sodium and posttransplant CPM. In the OR,
judicious fluid administration is particularly important. Every effort should be made
to correct sodium levels preoperatively, using continuous veno-veno hemofiltration
(CVVH) or even dialysis if necessary to remove excess fluid slowly.
Correction of Platelet or Clotting Abnormalities
Patients with end-stage liver disease often have low platelet counts (due to hy-
persplenism) and elevated prothrombin times. Preoperative correction or partial cor-
rection with fresh frozen plasma and platelets is important to diminish the risk of
bleeding during the placement of large-bore central venous catheters as well as dur-
ing the hepatectomy itself.
Antibiotics; Spontaneous Bacterial Peritonitis
All patients receive antibiotics preoperatively, usually for three doses only. In
some cases, a longer course of antibiotics may be needed. For example, a patient
with spontaneous bacterial peritonitis (SBP) who has received 3 days of therapy and
has a normal tap may undergo transplant, but the full course of antibiotics should
be completed. Patients who have received long-term antibiotic therapy pretransplant
are at higher risk for fungal infection, and use of an oral antifungal agent (e.g.,
fluconazole) during the first 2 weeks posttransplant should be considered.
Tumors
When patients with large HCC (>5 cm) are taken to the OR for transplant,
exploration is done first, to rule out extrahepatic spread. Often, lymph nodes from
the porta hepatis are biopsied. A back-up recipient is usually waiting, in case the
tumor patient is no longer a candidate for transplant.There are a variety of protocols
for larger HCCs. One consists of intraoperative infusion of adriamycin during the
anhepatic phase to prevent spread of tumor during mobilization of the liver. Postop-
eratively, if the pathology report indicates vascular invasion by the tumor, a course
of adjuvant chemotherapy may be indicated.
Hepatitis B
Patients with hepatitis B, especially DNA-positive patients, were once consid-
ered poor transplant candidates due to high rates of severe recurrence and death, but
use of long-term passive immunization with hepatitis B immune globulin (HBIg)
has improved their outcomes. Prophylaxis consists of approximately 45 million U
HBIg intraoperatively, followed by 25 million U on postoperative days 1, 2, and 3
and monthly thereafter. Because the hepatitis B virus can develop resistance, many
programs also add a second agent, lamivudine, to the regimen.
Donor Selection
Identification of good donor livers is key to successful outcomes. Today, there
are few absolute contraindications to liver donation. These include active intrave-
nous drug abuse, infection with the human immunodeficiency virus, increasingly
abnormal liver function tests, alcoholic hepatitis on biopsy, >40% macrovesicular
fat on biopsy, or active hepatitis. Formerly, it was believed that age >60, pressor use,
and prolonged hospital stay were contraindications to donation. These strict criteria
20 have been broadened at many centers. We now know that the quality of the donor
liver is based on many factors that must be considered together. The presence of
antibody to hepatitis C virus in donor serum is not necessarily a contraindication.
We now know that hepatitis C virus commonly recurs after transplant, even when
the donor is hepatitis C negative. Furthermore, the outcome and severity of recur-
rence in hepatitis C patients who receive grafts from hepatitis C positive donors is
no different from that in patients who receive hepatitis C negative livers. Livers
from hepatitis C positive donors are biopsied, however, and organs with chronic
active hepatitis are discarded. Use of hepatitis B core antibody (HBcAb) positive
livers for hepatitis B recipients with hepatitis B immune globulin (HBIg) prophy-
laxis is also accepted.
Intraoperative Considerations: Monitoring, Patient
Positioning
During the transplant, central venous or pulmonary artery monitoring is neces-
sary for monitoring pressures and cardiac output. A Swan-Ganz catheter may help
detect previously undiagnosed pulmonary hypertension. An arterial line is essential
for monitoring of blood pressure, and adequate venous access is mandatory in case
massive transfusions are needed. The patient is placed supine on the OR table and
prepped with the left arm extended, in case bypass is needed. The right arm may be
left by the patients side.
Selection of Operation and Cadaveric Donor Operations
The liver is normally brown, smooth, and sharp-edged and producing viscous,
golden bile. Steatotic livers are large and yellow, with round edges. The presence and
severity of steatosis is best confirmed with frozen section biopsy. Livers that are firm
and edematous in the absence of high CVP and with poor intraoperative bile 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 stable
donors, dissection is traditionally performed before the organs are flushed of blood.
A rapid-flush technique, used in unstable donors, involves perfusion before most of
the dissection. In either case, the hepatic arterial supply must be carefully delin-
eated. The portal vein is cannulated via the inferior mesenteric vein. The distal aorta
is cannulated after systemic heparinization. When all teams are ready, the supraceliac
aorta is cross-clamped, cold preservation solution is flushed through the portal and
arterial systems, and crushed ice is placed in the abdomen. Exsanguination and
perfusate venting are accomplished via the vena cava. The common bile duct (CBD)
is divided close to the duodenum, the hepatic artery is dissected down to the aorta
and divided with an aortic patch. The portal vein is dissected to the confluence and
divided. The diaphragm, supra/infrahepatic IVC and remaining peritoneal attach-
ments are divided. The liver is removed and preserved in UW solution. Iliac artery
and vein grafts are harvested as well.
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- 20
sion is made. In many patients with portal hypertension, large blood vessels can be
encountered even in the muscle and fascial layers. The abdomen is opened, and
ascites, if present, is drained. The falciform ligament is divided. The left triangular
ligament is divided. Control of the hepatoduodenal ligament is obtained by opening
the gastrohepatic ligament. The hepatic arteries are carefully dissected and divided.
The common bile duct is divided. The portal vein is cleared of remaining tissue in
the hepatoduodenal ligament. The right side of the liver is mobilized. The infrahepatic
vena cava is exposed circumferentially. The right adrenal vein is divided and the bare
area dissected off the retroperitoneum. The caudate lobe is freed from the
retroperitoneum. The suprahepatic cava is cleared circumferentially. When the liver
is attached by only three structures—the portal vein, infrahepatic cava, and 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 the
warm ischemic time. There are variations in the recipient operation, but the follow-
ing is a standard approach.
Vascular Anastomoses
Caval Anastomosis
The native suprahepatic caval cuff is fashioned and the end-to-end anastomosis
is performed with heavy running suture. The infrahepatic caval cuffs are fashioned
and similarly anastomosed.
Portal Vein Anastomosis and Reperfusion
The portal vein cuffs are fashioned and anastomosed end-to-end with fine su-
ture. Running technique is usually used, and the sutures tied with so-called growth
factor (an air knot), to avoid purse stringing and stricturing this delicate anastomo-
sis. The graft is then reperfused with portal blood. Approximately 500 cc of blood is
vented from the cava before removing the caval clamps in order to rinse out cold
hyperkalemic preservation solution, acidotic blood, and air. Hemostasis is secured.
In cases of complete portal vein thrombosis an interposition graft from the spleno-
mesenteric confluence is employed, using donor iliac vein. Another alternative is a
jump graft from the SMV that is tunneled through the mesocolon and lesser sac.
Hepatic Artery Anastomosis
The recipient common hepatic artery is anastomosed end-to-end to the
donor celiac axis with fine suture using delicate technique. If hepatic artery
inflow is inadequate, as occurs when there is an intimal dissection or hepatic artery
thrombosis, a jump graft of donor iliac or carotid artery from the infrarenal aorta,
end-to-side, is tunneled to the hilum either retropancreatic or through the lesser sac.
Grafting from the supraceliac aorta is an alternative.
Bile Duct Anastomosis

The donor and recipient common bile ducts are anastomosed end-to-end using
20 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 months
later, after a normal cholangiogram has been obtained. Many surgeons no longer
use T-tubes routinely. If there is a major size discrepancy between the donor and
recipient ducts, or if the recipient bile duct is diseased (as in PSC) or too small (as
in pediatric cases), a choledochojejunostomy is performed. The duct is anasto-
mosed to a Roux-en-Y limb of jejunum using a stented end-to-side technique.
Piggyback Technique
In case of caval size discrepancy or when using reduced-size grafts without a
cava, the piggyback technique can be used. The liver is dissected off the cava, the
short hepatic veins are ligated, and the hepatic veins are identified. The right hepatic
vein is clamped and divided and oversewn with 5-0 prolene. The left and middle
hepatic veins are clamped and the liver removed. The left and middle hepatic veins
are opened to make one cuff. Performing a piggyback maintains venous return to
the heart but does not affect portal hypertension. The donor suprahepatic cava is
anastomosed to the left and middle hepatic veins using 4-0 Prolene running sutures.
The portal vein and artery anastomoses are performed as with a standard bypass.
Before reperfusion, a chest tube is placed in the donor infrahepatic cava (either with
a purse string suture or with clamps that will prevent bleeding around the tubes).
The portal clamp is opened and 500 cc of blood is bled out of the chest tube. The
caval clamp is removed and the donor infrahepatic cava is ligated with 2-0 silk ties.
Bypass
Veno-venous bypass (VVB) was originally introduced in an attempt to modify
the hemodynamic changes that occur during the anhepatic phase of liver transplan-
tation. During this period, venous flow through the portal vein and inferior vena
cava is interrupted and may cause major hemodynamic changes.The standard tech-
nique involves cannulation of the transected portal vein, the axillary vein, and the
femoral vein, which is cannulated via the saphenous vein. This system diverts blood
from the lower extremities and the splanchnic bed into the suprahepatic systemic
circulation. Modifications of the VVB technique have been described and may be
considered as alternatives to the standard technique. Recently, cannulation of the
inferior mesenteric vein, rather than the portal vein, has been described for use with
VVB. This method offers the advantage of early decompression of the portal system
before dissection of the hepatoduodenal ligament and may significantly reduce early
blood loss, particularly in patients with a history of previous upper abdominal sur-
gery. On the other hand, there are disadvantages associated with this procedure. It
prolongs operative time, air and thrombotic emboli have been reported, and flows
must be maintained at 1000 ml/min or greater. At lower flow rates, clots and plate-
let aggregation are more likely. The heparinless VVB system cannot use a heat
exchanger. Such heat loss from the bypass circuit contributes to the hypothermia
and subsequent coagulopathy. The routine use of VVB is now controversial. When
the Mount Sinai Medical Center began its liver transplant program in 1988, VVB
was used routinely. As the program grew and we gained anesthetic and surgical
20
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. Reprinted
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 history
of recent variceal bleed, in whom clamping of the portal vein can cause acute variceal
bleeding in the OR.
Split Livers
The increasing gap between supply and demand has resulted in higher mortality
among candidates on the waiting list. In attempts to narrow this gap, besides 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 single
donor liver. The liver can be split through the falciform ligament, creating left lateral
segment and extended right lobe grafts, or splitting can be done through the main
scissura, to create left lobe and right lobe grafts (Figure 20.1). Donor selection for
split transplant is extremely important. Fifty years is the upper age limit for donors
for split liver transplant. Donors should have perfect liver function, with no steatosis.
The final decision of whether a liver is suitable for splitting should be made only
20
Fig. 20.2. Left lateral segment split graft specimen. Reprinted with permission from:
Surgery of the Liver and Biliary Tract (3rd Edition), Blumgart LH, Fong Y and WH
after evaluation by an experienced surgeon. The liver partition can be done on the
back table after standard liver procurement (ex situ splitting) or during the 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 has
many advantages over ex situ splitting, including better control on the cut surface
bleeding upon reperfusion, shorter ischemia time, and better overall evaluation of
both sides of the grafts.
Living Donors
Living donor liver transplantation is another innovative technique. Hepatic grafts
from living donors were first used for pediatric recipients. More recently, with excel-
lent results in children and with established donor safety, living donor liver transplants
have been performed for adult recipients as well. In pediatric recipients younger
than age 5, an adult’s left lateral segment usually provides adequate liver volume. For
teenage recipients, a left lobe should be used. For adults, right lobe grafts are neces-
sary to ensure enough liver volume for recipient. Because this procedure subjects a
healthy individual (donor) to major surgery, donor safety is essential, and informed
consent is crucial. The risks and benefits of the living donor operation must be
explained to the donor, the recipient, and their immediate families. In addition, 20
donors should be thoroughly evaluated by an unbiased physician. The examinations
should include a history and physical, chest x-ray, EKG, blood work (including liver
functions and viral serologies), and MRI with calculation of liver volume. In our
experience with pediatric and adult living donor liver transplants, the donor opera-
tion has been asssociated with low rates of morbidity and mortality. The procedure
provides many advantages to the recipient. The transplant operation can be sched-
uled electively (without having to wait for a cadaveric organ), before the recipient
develops serious complications of end-stage liver disease. Furthermore, since the
donor is healthy and the ischemia time is short, graft quality is better than with
cadaveric liver allografts. The recipient and donor operations are performed 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 decreased
dramatically with increasing experience in technique and recipient selection.
Recipient Operation for Split and Living Donor Grafts
The operation to implant a right lobe split graft is similar to orthotopic whole
liver transplantation (see above). In the case of left or left lateral segment split grafts
and all living donor liver grafts, the allograft does not have the vena cava, and 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 the
right or left portal vein) and the recipient portal vein using 6/0 prolene continuous
suture. The hepatic artery anastomosis is performed between the allograft hepatic
artery (either right or left) and the recipient right or left hepatic artery using 8/0
prolene interrupted sutures. For anastomoses in pediatric recipients, an operating
microscope is necessary. When the entire length of the recipient portal vein and
hepatic artery are dissected into the hilum, extension grafts are rarely needed. In the
majority of the cases, bile duct anastomosis is done by Roux-Y hepatico-jejunos-
tomy using interrupted 6/0 PDS sutures.
Results
With improvement in pretransplant patient care, evolution of surgical techniques,
better preservation fluids, modern immunosuppressive medications, and state-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 have
helped 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 remains
incomplete. 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-
lems early after transplantation. Long-term studies are needed to determine the ef-
fects of recurrence of these diseases on outcome.
20 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 rates
of 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 of
the favorable indications for liver transplantation, with 1-year disease-free survival
reaching 90%.
Index 283
2-(18F)-fluoro-2-deoxyglucose (FDG) Carcinoembryonic antigen (CEA) 83,

123, 134, 144 93, 94, 122, 123, 126, 254
5-fluorouracil (5-FU) 107, 109, 127, Caudate lobe 2-5, 7, 8, 14, 16, 136,
199, 237 192, 196, 209, 217-219,
5-flurode (FUDR) 127, 227 221-223, 277
Caudate lobe resection 222, 223
A
Index
Celiac artery 6
Central resection 225
Acute pancreatitis 35, 40, 147, 180 Charcot’s triad 39
Adrenal gland 2, 209 Child’s classification 63, 74, 102, 105,
Adrenocortical 143 107-110, 132, 253, 273, 275
Alpha fetoprotein (AFP) 44, 83, 93, Child-Turcotte-Pugh scoring system
102, 104, 106 (CTP) 273, 275
American Association for the Surgery Cholangiocarcinoma (Klatskin tumor)
of Trauma Liver Injury Scale 259 14, 31, 33, 102, 170, 183-188,
Aminopyrine breath test 74 190-192, 194-197, 199, 200,
Angiomyelipoma 83, 98 202, 270, 272
Antacids 79 Cholecystectomy 17, 34, 40, 49, 146,
Antithrombin III 79 149, 152-156, 162, 163, 165,
Arterial-Portal Venous Fistulae 268 168, 194, 201, 203-205, 207,
Ascites 44, 52, 57, 67, 78, 79, 102, 209, 229
104, 125, 132, 206, 221, 228, Choledochoduodenostomy 171, 173,
253, 269, 270, 274, 275, 277 179-181
Choledocholithiasis 34, 147
B Choledochoscope 162, 164
Bile Fistulae 268 Cholelithiasis 22
Biliary calculi 28 Cirrhosis 21, 44, 59, 92, 101, 102,
Biliary endoprosthesis 37 104-108, 110, 123, 132, 133,
Biliary hamartomas 97, 98 135, 239, 249, 253, 256, 270,
Bilioenteric Bypass 165, 191 275
Bilioenteric bypass 10, 14, 191, 192 Cisplatin 107
Biloma 58, 268 Colorectal adenocarcinoma 121, 228
Biopsy 28, 42, 44, 53, 81, 85, 86, 96, Colorectal cancer 121, 122, 123, 129,
97, 100, 102, 104, 123, 124, 134, 227, 228, 237-239
134, 136, 192, 202, 242, 267, Colorectal liver metastases 124, 125,
275, 276 127, 128, 129
Bismuth 186, 188, 190 Common bile duct 6-8, 10-12, 23,
Blunt hepatic trauma 258, 260 30, 34, 35, 37, 39, 40, 49, 113,
Bone scan 123 150-153, 157, 158, 160-162,
Brachytherapy 54, 56, 199 168, 169, 171, 174, 179, 180,
Breast cancer 143 187, 192-195, 197, 199, 202,
Breast carcinoma 143 207, 213, 231, 262, 263, 276,
Buckwalder retractor 153, 193 277
Computed tomography (CT) 20-25,
C 28, 33, 38, 44, 46, 52, 55, 57,
64, 68-72, 83, 84, 86, 87, 91,
CA-19-9 83, 94 93, 96, 103, 109, 122, 123, 134,
Calot’s triangle 150, 153, 155, 157, 135, 137, 148, 202, 226, 232,
159, 160 251, 253, 254, 257, 259-262,
268, 269, 274
Coronary artery disease (CAD) 73 218, 220, 221

Couinaud’s classification 174 Extended right hepatectomy 124, 214,
Cryoablation 66, 107, 110, 228, 242, 225
252 External beam radiation 87, 109, 199
Cryoinjury 239
Cryoprobe 107, 240, 241, 242 F
Index
CT arterial portography 46
Cystic artery 6, 14, 15, 150, 151, 153, Feridex 22
155, 160, 161, 194, 209, 213 Fibrinogen deficiency 79
Cystic duct 10-14, 18, 52, 113, 146, Fine needle aspiration (FNA) 42, 203
148, 150-155, 157-160, 162, Finger fracture hepatotomy 265
164, 166, 170, 183, 188, Fluoropyrimidines 109
192-194, 201, 202, 204, 205, Focal nodular hyperplasia 23, 28, 43,
209, 213 81, 83, 91, 93-95
D G
Deep liver stitches 265 Gallbladder adenocarcinoma 201
Diagnostic peritoneal lavage (DPL) Gallbladder fossa 2, 3, 113, 154, 161,
259-261 172, 212, 220, 221
Diaphragm 1, 3, 65, 98, 153, 172, Gallbladder scintigraphy 148
209, 214, 223, 249, 276 Gastroduodenal 6, 8, 15, 108, 113,
Disseminated intravascular coagulation 206, 228, 231
(DIC) 79 Gelfoam 62, 154
Distal pancreatectomy 112, 115, 120 Gemcitabine 109
Dopamine 78 Genitourinary cancers 145
Dormia basket 35 Glisson’s capsule 11, 12, 85, 167, 168,
Doxorubicin 107 175, 193, 265
Drain 7, 9, 10, 14, 52, 53, 114, 115, Goligher retractor 153, 193, 206
154, 155, 162, 165, 197, 202,
205, 225, 242, 268, 269
H
Duodenojejunostomy 115, 119 H2 blockers 79
HbsAg 101
E Hemangiomas 23, 24, 43, 81, 85-87,
Electrohydraulic lithotripsy (EHL) 37 89, 90-92, 123
Embolization 38, 52, 61-71, 90, 96, Hemobilia 267
103, 108-110, 123, 124, 128, Hepatic adenomas 23, 81, 91, 93, 94,
135, 137, 140, 238, 262, 96, 97
267-269 Hepatic artery infusion pumps (HAIP)
Embolotherapy 61 227-229, 232, 235, 237
End-stage liver disease 270, 272, 275, Hepatic artery ligation 89, 91, 267
281 Hepatic encephalopathy 79, 228
Endoscopic retrograde Hepatic veins 2-7, 75, 103, 124, 125,
cholangiopancreatography 137, 208, 209, 211, 213, 217,
(ERCP) 34, 38-41, 154, 202, 218, 220, 222, 225, 241, 265,
268, 269, 272 278
Endoscopic sphincterotomy (ERS) Hepaticojejunostomy 115, 165, 171,
34-36, 38-40, 262 173-175, 177, 192, 199, 207
Extended left hepatectomy 6, 124, Hepatitis B 44, 101, 275, 276, 282
Index 285
Hepatitis C 101, 270, 276, 281 Liver abscess 58, 108

Hepatocellular carcinoma 23, 42, 44, Living donor liver transplantation 280
59, 62, 64, 83, 92, 94, 101, 104, Low central venous pressure anesthesia
107, 110, 270 (LCVP) 74, 75, 77, 80, 208
Hepatorenal syndrome 78 Lung cancer 140
Hepp-Couinaud approach 174, 175
M
Index
HIDA scan 148
Hilar plate 3, 11, 12, 14, 175, 176,
179, 193, 194, 217, 225 Magnetic resonance imaging (MRI)
20-23, 26-28, 30, 33, 43, 44, 46,
I 83, 84, 87, 89, 93, 95, 96, 98,
103, 134, 281
Indocyanine green clearance 74 Main hepatic scissura 6
Inferior mesenteric vein 9, 10 Maryland dissector 157-160
Intra-abdominal abscess 268 Mechanical lithotripsy 36
Melanoma 62, 141-145, 239
J Mesenchymal hamartomas 98
Mesh hepatorrhaphy 266
Jackson Pratt drain 162, 197 Metastases 28, 55, 60, 62-64, 67, 113,
Jaundice 39, 40, 52, 63, 76, 102, 108, 121-132, 134-136, 138-145,
111, 113, 122, 147, 165, 169, 184-188, 191, 193, 201, 202,
178, 183, 191, 199, 200, 202, 205, 206, 226-228, 237, 239,
206, 267, 270 241, 245, 249, 252, 253, 255,
256, 270
K Methyl testosterone 102
Karnofsky Performance Status 132 Myelolipoma 83, 98
Klatskin tumor Myxoma 99
see Cholangiocarcinoma
Kocher maneuver 113, 114, 180, 206
N
Kupffer cells 84, 92-94 Na+-K+ ATPase 79
Neuroendocrine carcinoma 138, 140
L
Laparoscopic cholecystectomy 17, 34,
O
40, 146, 149, 154, 155, 156, Obstructive jaundice 52, 76, 111,
159, 162, 204 113, 165, 169, 199
Laser lithotripsy 36, 37 Okuda staging 104
Left gastric vein 10 Olsen clamp 160
Left hepatectomy 6, 16, 17, 124, 215, Omental pack 265
218-221 Ovarian carcinoma 130
Left hepatic duct 11, 14, 16, 17, 56,
165, 167-169, 171, 176-178, P
183, 188, 193, 195, 206, 207
Left lateral segmentectomy 218, 225 Pancreatic cancer 115, 135, 199
Left lobectomy 207, 219 Pancreatic imaging 23, 28
Left trisegmentectomy 218 Pancreaticoduodenectomy 111-115,
Lienorenal ligament 116 118, 119, 173, 183, 187, 199,
Ligamentum teres 2, 168, 171, 172, 206
175, 179, 211, 215 Pancreaticojejunostomy 111, 115,
Lipoma 83, 98 117, 120
Percutaneous abscess drainage 56 Recurrent Bleeding 267

Percutaneous cholangiography 38 Renal failure 78, 125, 241, 272, 281
Percutaneous cholecystostomy (PC) Rendezvous technique 37
39, 49, 52 Replaced right hepatic artery (RRHA)
Percutaneous ethanol injection therapy 231, 232
(PEIT)/percutaneous ethanol Right gastric artery 6, 114
Index
injection (PEI) 64, 65, 109, Right hepatectomy 124, 209,

110, 137, 252-254 212-214, 217, 225
Percutaneous hepatic cyst drainage 60 Right hepatic duct 11, 14, 18, 161,
Percutaneous portal venogram 68, 71 165, 188, 195, 213
Percutaneous transhepatic cholangiog- Right hepatic lobectomy 207
raphy (PTC) 46, 47, 49, 52, Right scissura 5, 220, 221
202 Right trisegmentectomy 14, 66, 69,
Periampullary cancer 111, 112 214
Perihepatic Packing 266 RITA Medical Systems, Inc. 246
Perihepatic packing 257, 266 Round ligament 177, 209
Photodynamic therapy 199 Roux-en-Y 115, 118, 165, 172, 177,
Ponsky cholangiocatheter 160 192, 196, 199
Portal triad occlusion (Pringle Roux-en-Y reconstruction 115, 118
maneuver) 137, 207, 221, 225,
263, 265
Portal vein 3, 6-11, 14, 16, 46, 52, 59, S
61, 63-69, 71, 89, 102, 105,
113, 114, 122-124, 128, 167, Sarcoma 141, 143, 239
168, 171, 184, 185, 187, 188, Segment I resection 222, 223
193, 194, 206, 209, 211, 213, Sengstaken-Blakemore tube 79
215, 217, 219, 221, 222, 225, Sepsis 37-40, 46, 52, 53, 75, 76, 79,
227, 231, 249, 253, 263, 265, 209, 266, 267, 268, 270
270, 272, 276-279, 281 Solitary fibrous tumors (SFT) 98
Portal vein embolization 67, 69, 123, Splenectomy 115, 120
128 Splenic artery 46, 116, 232
Positron emission tomography (PET) Split-liver transplantation 279
123, 134 Squamous cell carcinoma 140
Protein C 79 Steatosis 276, 279
Protein S 79 Superior mesenteric vein 8, 10, 114
Pulmonary function tests 73 Surface anatomy 2
Pulmonary hypertension 272, 276 Surgicel 154, 243
Q T
Quadrate lobe 167, 168, 174, 175, Teratoma 99
177-179, 193, 221 Thompson retractor 153, 193
Thorotrast 102
R Thrombocytopenia 44, 64, 79, 85,
86, 91, 132
Radioembolization 109 Transjugular intrahepatic
Radiofrequency ablation 135, 228, portosystemic shunts (TIPS) 67
239, 252, 272 Triangular ligaments 1, 2, 265
Radionics 247
Radiotherapeutics 247
Index 287
U
Ultrasonography (US) 20-23, 28, 83,
86, 103, 113, 137, 147, 256,
261, 273
Umbilical fissure 2, 3, 7, 11, 14, 16,
Index
46, 48, 168, 171, 174, 206, 215,
217, 218, 219, 222, 225
Umbilical vein 2, 6, 7, 214, 225
V
Vena cava 2-4, 7, 10, 65, 69, 74, 76,
89, 136, 208, 210, 211, 213,
217, 218, 266, 276-278, 281
Vitamin K 76, 79
W
Wallstent® 55, 56
Wedge resections 124, 208, 225
Whipple procedure 112, 113
LANDES LANDES
BIOSCIENCE V ad e me c u m BIOSCIENCE V ad e me c u m
Table of contents (excerpt)
Hepatobiliary
1. Essential Hepatic and Biliary 9. Hepatic Resection for Colorectal
Anatomy for the Surgeon
2. Imaging of the Liver, Bile
Liver Metastases: Surgical
Indications and Outcomes Surgery
Ducts and Pancreas 10. The Surgical Approach to Non-
3. Endoscopic and Percutaneous Colorectal Liver Metastases:
Management of Gallstones Patient Evaluation, Selection
and Results
4. Interventional Radiology
in Hepatobiliary Surgery 11. Surgical Techniques of Open
Cholecystectomy
5. Perioperative Care and
Anesthesia Techniques 12. Laparoscopic Cholecystectomy
and the Laparoscopic
6. Benign Tumors of the Liver: Management of Common Bile
A Surgical Perspective Duct Stones
7. Hepatocellular Carcinoma 13. Surgical Techniques for
Completion of a Bilioenteric
8. Periampullary Cancer and
Bypass
Distal Pancreatic Cancer
The Vademecum series includes subjects generally not covered in other handbook
series, especially many technology-driven topics that reflect the increasing
influence of technology in clinical medicine.
The name chosen for this comprehensive medical handbook series is
Vademecum, a Latin word that roughly means “to carry along”. In the Middle
Ages, traveling clerics carried pocket-sized books, excerpts of the carefully
transcribed canons, known as Vademecum. In the 19th century a medical publisher
in Germany, Samuel Karger, called a series of portable medical books
Vademecum.
The Landes Bioscience Vademecum books are intended to be used both in the
training of physicians and the care of patients, by medical students, medical house
staff and practicing physicians. We hope you will find them a valuable resource.
All titles available at

I SBN 1- 57059- 630- 1 Ronald S. Chamberlain
www.landesbioscience.com
Leslie H. Blumgart
9 781570 596308

Hepatobiliary Surgery Blumgart

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LANDES LANDES

All titles available at

Ronald S. Chamberlain, MD, MPA, FACS

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

Copyright ©2003 Landes Bioscience

Please address all inquiries to the Publisher:

Library of Congress Cataloging-in-Publication Data

The surgical care of patients is a full commitment. As most of

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

Lynn A. Brody Sukru Emre

Karen T. Brown N. Joseph Espat

Bryan Clary Enrico Ferri

Douglas R. DeCorato Mary Fischer

William R. Jarnagin Patricia A. Sheiner

Ronald N. Kaleya Richard D. Schulick

Jonathan B. Koea Lawrence H. Schwartz

Essential Hepatic and Biliary Anatomy

Hepatobiliary Surgery, edited by Ronald S. Chamberlain and Leslie H. Blumgart.

Aberrant segmental anatomy of the liver is uncommon. The presence of a di-

the common hepatic duct retroduodenal or retropancreatic and anomalous entry

Biliary drainage of the caudate lobe is less predictable. Conceptually, the

Imaging of the Liver, Bile Ducts

Hepatobiliary Surgery, edited by Ronald S. Chamberlain and Leslie H. Blumgart.

displaying anatomic information. Certain MR contrast agents, such as gadolinium

Table 2.1. Comparison of imaging modalities

Table 2.2. Contraindications for MR imaging*

Table 2.3. Test selection based on body part

Ranking is in order of preference (1 being the most preferred). When two

Fig. 2.2A. Hepatic hemangioma: Ultrasound examination demonstrates a

Fig. 2.3C. Contrast enhanced T1-weighted MRI demonstrates heterogeneous

enhancement, HCC typically demonstrate a pseudocapsule of compressed paren-

Fig. 2.4A. Hepatocellular cancer. Arterial dominant phase CT demonstrates a

Fig. 2.5A. Hilar cholangiocarcinoma (Klatskin tumor): Ultrasound examination

Fig. 2.6. Pancreatic mass: Ultrasound examination demonstrates a normal appearing

Fig. 2.7A. Microcystic adenoma: A CT examination demonstrates a mass in the

Endoscopic and Percutaneous Management

Large Bile Duct Stones

3 Acute Gallstone Pancreatitis

Interventional Radiology in Hepatobiliary

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

a diagnosis of a hepatic adenoma. Needle biopsy is rarely requested to diagnose

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

functional information is needed. At our institution, this is done most commonly to

Therapeutic and Palliative Procedures

Figs. 4.3A-F. Percutaneous biliary drainage catheter placement and subsequent

Fig. 4.3D. Immediately after conversion of the drainage catheter to a Wallstent®.

treat postoperative abscesses or other collections of fluid such as bile or infected

A primary pyogenic liver abscess can also be treated by percutaneous catheter

Percutaneous Hepatic Cyst Drainage

While percutaneous treatment or even aspiration of hydatid cysts has traditionally

treat hypervascular tumors such as hepatocellular carcinoma, neuroendocrine me-

Fig. 4.4D. Completion fluoroscopy demonstrates two well-expanded metallic stents

Figs. 4.5A,B. Arterial emoblization of hepatocellular carcinoma in the right hemiliver.

Other Percutaneous Ablative Therapies

Perioperative Care and Anesthesia

Hepatobiliary Surgery, edited by Ronald S. Chamberlain and Leslie H. Blumgart.

Table 5.1. Preoperative factors associated with postoperative life-threatening

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

Table 5.2. Comparison of operative parameters between hepatic vascular

Delva et al, HVI 35 35 – – 8.0 ± 8.3

*Major resections include all lobectomies and extended lobectomies.

Table 5.3. Differential diagnosis of postoperative jaundice*

Increased Bilirubin Load Biliary Obstruction Hepatocellular Injury

eliminated, the diagnosis of anesthetic related hepatotoxicity might be entertained