The Management of Gallstone Disease: A Practical and Evidence-Based Approach 9783319638843, 331963884X

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Michael R. Cox Guy D. Eslick Robert Padbury Editors

The Management of Gallstone Disease A Practical and Evidence-Based Approach

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The Management of Gallstone Disease

Michael R. Cox  •  Guy D. Eslick Robert Padbury Editors

The Management of Gallstone Disease A Practical and Evidence-Based Approach

Editors Michael R. Cox Professor of Surgery Nepean Clinical School University of Sydney Sydney, New South Wales Australia

Guy D. Eslick Discipline of Surgery The Whiteley-Martin Research Centre University of Sydney Sydney, New South Wales Australia

Robert Padbury Divisional Director of Surgery Flinders Medical Centre Adelaide, South Australia Australia

ISBN 978-3-319-63882-9    ISBN 978-3-319-63884-3 (eBook) https://doi.org/10.1007/978-3-319-63884-3 Library of Congress Control Number: 2017960804 © Springer International Publishing AG, part of Springer Nature 2018, corrected publication 2018 This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed. The use of general descriptive names, registered names, trademarks, service marks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use. The publisher, the authors and the editors are safe to assume that the advice and information in this book are believed to be true and accurate at the date of publication. Neither the publisher nor the authors or the editors give a warranty, express or implied, with respect to the material contained herein or for any errors or omissions that may have been made. The publisher remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Printed on acid-free paper This Springer imprint is published by the registered company Springer International Publishing AG part of Springer Nature The registered company address is: Gewerbestrasse 11, 6330 Cham, Switzerland

The concept of this textbook was to clearly describe the current management of gallstone disease based on the best evidence available. My involvement is dedicated to two important sources of inspiration and support:    1. My beloved wife Joy and our three children: James, Kathryn and Rebecca. Their love, support and encouragement throughout my career have been invaluable.    2. My late friend and colleague, Associate Professor Patrick Cregan, for his encouragement and ever-­ present quest to improve surgical outcomes by the application of an evidence-based approach and in doing so a reduction in variance. Professor Michael Robert Cox _____________ I would like to dedicate this work to my mother ‘Kathleen’, my brother ‘Richard’ and my late sister ‘Kristine’ who all suffered many years from gallstone disease that was diagnosed but left untreated until they all had a cholecystectomy. My sister’s gallbladder contained 33 white triangular cholesterol stones each approximately 1–2 cm in diameter. Our research has highlighted the benefits associated with gallbladder removal on the index presentation rather than taking a waitand-see approach to patients with gallstone disease. This should be the standard practice to reduce the morbidity and mortality associated with gallstone disease. Professor Guy D. Eslick _____________ I joined this project because of the enthusiasm of Michael and Guy to produce a comprehensive guide to the management of gallstone related problems. I am very pleased with the outcome and would like to dedicate the book to surgical trainees, general and specialist HPB surgeons. I hope the contents of the book will provide a pathway to improvements in consistent evidence based care of the patients we serve. Professor Robert Padbury _____________

Foreword

Book Foreword I It is both unusual and pleasing to read a contemporary book dedicated to the pathophysiology and management of gallstone disease in such detail. It is pleasing because it is a disease which has both fascinated and challenged me for all of my surgical career. It is unusual as the focus of many monographs on this subject is often quite narrow, tending to focus on a particular aspect of cholelithiasis and ignore the fascinating and interesting total complexity of gallstone disease. General surgeons should be fully familiar with this topic as gallstone disease is one of the most common conditions managed by them. This book is also timely. Although the pathophysiology has not greatly changed, the practice options have undergone significant change over the past 15 or so years, stemming from the management shift from open to laparoscopic surgery. Laparoscopy has been a major benefit to patients but has developed its own level of complexity that was not around in the open era. Management of bile duct stones is a good example. It initially appeared that ERCP was to be the preferred method of common duct clearance. This was because a laparoscopic approach from a technical perspective seemed overly complex to many due to lack of equipment and experience. This is now changing and well discussed in this book. The editors have brought together a group of authors who are recognised leaders in their field. The chapter authors have provided an excellent overview with definitive direction in their topic but have provided a good evidence base for these recommendations. Controversial areas have been acknowledged and appropriately debated. The initial chapters are devoted to the pathophysiology and epidemiology of gallstone disease. There follows an excellent description of the clinical presentation as well as an evidence-based approach to the ‘silent gallstone’. A well-structured discussion on acalculous gallbladder disease, both acute and chronic, and the management of gallbladder polyps and gallbladder malignancy clearly outlines the management of these conditions. Aspects of bile duct stone disease are discussed in great depth and breadth. I found the chapter on the early management of gallstone pancreatitis by John Windsor particularly informative as he dispels many myths based on an astute review of the current literature. Complex and challenging problems of gallstones in

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Foreword

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pregnancy, post-cholecystectomy syndromes and gallbladder disease in cirrhotic patients are well discussed with clear evidence-­based direction given. The remainder of the book is devoted to technical aspects of gallstone management. The detail here is exceptional. Not only are the technical aspects well discussed, there are multiple ‘tips and tricks’ on how to avoid trouble and how to get out of it. The chapters on cholecystectomy and transcystic stent insertion by Michael Cox provide exceptional advice to both the novice and expert. The chapter on duct clearance by Les Nathenson is incredibly detailed and informative. This book is well conceived, well written and well illustrated. It is a definitive work that is well referenced. This book should appeal to the surgical trainee and would undoubtedly provide all the information required to become competent in gallstone management. It will also appeal to the practicing surgeon, particularly in its technical aspects. Unlike many conditions, complex gallstone disease can ‘ambush’ even the most experienced surgeon requiring difficult intraoperative decisions. This book provides an inventory of experience that would be invaluable to the practicing surgeon. In particular it gives clear direction for those who are still a little reluctant to explore bile ducts laparoscopically. This book will interest all surgeons who manage gallstone disease from the novice to the expert. Phil Truskett, AM, FRACS, FACS, FASGBI, FRCSEd Prince of Wales Hospital, Sydney, Australia

Foreword

Book Foreword II It has been 135 years since the first open cholecystectomy was performed and just over 30 years since the first reports of laparoscopic cholecystectomy. Given this history, one might think that there would not be a lot of new information on gallstone disease to pass along today. Certainly, one would think that new developments could be covered in a single comprehensive review article. But here we are entering a thick book with 23 chapters, all focused on gallstone disease and the surgeon’s role in managing gallstone disease and its complications. So here is my observation: Despite a 30-year career studying and reporting on the management of biliary tract disease, I discovered unique observations in each chapter. The level of detail and the comprehensive approach to each chapter provide ‘in-depth’ knowledge necessary to REALLY understand all aspects of gallstone disease and its proper management. For the student, wishing to ‘know it all’ to impress the professor, there are details to delight. Each chapter is rich in anatomy, physiology, pathology, imaging and evidence, sufficient to provide complete learning for the novice and ‘pearls’ for the professor who has lived and breathed gallbladder disease for 30 years. That would be me. Certainly, it is possible to be a competent gallbladder surgeon without mastering the entire contents of this book. Most general surgeons might refer a patient for transcystic stenting or post-operative ERCP. Most surgeons might see one or two patients in a career with Mirizzi’s syndrome, and half that many patients with gallstone ileus. And don’t we already know everything we need to know about how to do a laparoscopic cholecystectomy? The answers to these statements is clear. We might be able to get by with less knowledge and understanding, but there is nothing as enjoyable and as critical to quality care as learning more about a common disease. This book accomplishes this task. It is well written, authoritative and comprehensive. Dig in! Portland, OR, USA

John G Hunter, MD, FACS, FRCS Edin

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Contents

1 Operative Anatomy and Surgical Landmarks of the Biliary System����������������������������������������������������������������������    1 Thomas R. O’Rourke 2 Biliary Imaging for Gallstone Disease������������������������������������������   21 Piers Dugdale 3 Epidemiology and Pathogenesis of Gallstones����������������������������   53 Amy M. Cao and Guy D. Eslick 4 What Are Biliary Symptoms?������������������������������������������������������   67 Daniel J. Kilburn and Nicholas A. O’Rourke 5 Asymptomatic Gallstones��������������������������������������������������������������   75 Guy Shingler and Val Usatoff 6 Symptomatic Gallbladder Stone Disease ������������������������������������   87 Michael R. Cox 7 Obstructive Jaundice and Cholangitis�������������������������������������������������� 105 Thomas G. Wilson 8 Early Management of Biliary Pancreatitis����������������������������������  117 Alistair B.J. Escott and John A. Windsor 9 Gallbladder Polyps, Sludge and Adenomyomatosis ������������������  137 Tom Elliott 10 Biliary Pain and a Normal Ultrasound����������������������������������������  147 Amy Cao, Guy D. Eslick, and Michael R. Cox 11 Acute Acalculous Cholecystitis ����������������������������������������������������  155 Bruce Su’a, Andrew G. Hill, and Garth H. Poole 12 Gallstone Disease in Pregnancy����������������������������������������������������  169 Michael R. Cox 13 Rare Problems: Mirizzi Syndrome, Fistula and Gallstone Ileus������������������������������������������������������������������������  181 Matías Czerwonko, Martin de Santibañes, and Eduardo de Santibañes

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14 Incidental Gallbladder Cancer Post Laparoscopic Cholecystectomy����������������������������������������������������������������������������  199 Asma Sultana, Robert Padbury, and John Chen 15 Post Cholecystectomy Symptoms ������������������������������������������������  205 Nicholas A. O’Rourke and Anzel Jansen van Rensburg 16 Laparoscopic Cholecystectomy: Operative Technique��������������  221 Michael R. Cox 17 Intraoperative Cholangiography��������������������������������������������������  249 Elena Rangelova and Robert Padbury 18 Cholecystostomy: Indications and Subsequent Management ����������������������������������������������������������������������������������  263 Christopher B. Nahm, Sandra Nozawa, and Thomas J. Hugh 19 Cholecystectomy in  Cirrhosis ������������������������������������������������������  279 Marcos V. Perini and Michael A. Fink 20 Laparoscopic Bile Duct Exploration��������������������������������������������  291 Leslie Nathanson 21 Transcystic Stenting and Post-­Operative ERCP for CBD Stones at Laparoscopic Cholecystectomy��������������������  307 Michael R. Cox 22 Identification and Management of Bile Leaks Post Cholecystectomy����������������������������������������������������������������������������  327 George Kalogeropoulos and Ian J. Beckingham 23 Identification and Management of Bile Duct Injuries and Post-Operative Strictures������������������������������������������������������  347 Arthur Richardson Erratum��������������������������������������������������������������������������������������������������  E1 Index��������������������������������������������������������������������������������������������������������  371

Contents

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Operative Anatomy and Surgical Landmarks of the Biliary System Thomas R. O’Rourke

Introduction Surgery for gallstones remains one the most common surgical procedures in the developed world. Carl Langenbuch of Berlin performed the first successful cholecystectomy in June 1882. Muhewig performed the first laparoscopic cholecystectomy in 1986. Laparoscopic cholecystectomy is now the most common laparoscopic operation performed by general surgeons. Knowledge of the surgical anatomy is key in performing a safe surgical procedure and preventing unwanted injury to surrounding structures. It has long been recognized that the anatomical variations of the bile ducts and blood vessels in the porta hepatis are associated with accidental injury, especially bile duct injury [1]. Whilst the intricate knowledge of hilar anatomy required to perform surgery for cholangiocarcinoma is reserved for the hepatobiliary specialist, variation from the normal biliary anatomy should be expected in at least 20% of patients and up to 30% will have aberrations in arterial anatomy.

T.R. O’Rourke, M.B.B.S., B.Med.Sc., F.R.A.C.S. HPB and Liver Transplant, Princess Alexandra Hospital, Ipswich Rd, Brisbane, QLD 4102, Australia Greenslopes Private Hospital, Greenslopes, QLD, Australia e-mail: [email protected]

Thus, the surgeon performing cholecystectomy should be equipped with the knowledge to recognize aberrant anatomy when encountered.

Embryology A basic knowledge of the embryology of the liver and biliary system is helpful to understand the variation in surgical anatomy. Current understanding of some aspects of the developing biliary system remains incomplete whilst other details are debated or disproved [2–4]. The hepatic diverticulum (liver bud) develops from the ventral side of the developing duodenum during the fourth week of gestation. The cranial part of the diverticulum will form the intrahepatic biliary tree while the caudal part will form the extrahepatic biliary tree consisting of the gallbladder, cystic duct, common bile duct, common hepatic duct and distal parts of the right and left hepatic ducts (Fig. 1.1a). The extrahepatic biliary anatomy develops in close contact with the hepatic artery. Thus when aberrant anatomy is experienced, other aberrations should be expected. An earlier theory that the embryological duct system undergoes a solid stage and will later recannalize, failure of which will result in biliary atresia, has been disproved. Similarly, the theory that the extrahepatic biliary systems develop completely independently from the intrahepatic

© Springer International Publishing AG, part of Springer Nature 2018 M.R. Cox et al. (eds.), The Management of Gallstone Disease, https://doi.org/10.1007/978-3-319-63884-3_1

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b­ iliary tree and the systems are initially discontinuous has been contradicted. The current understanding is that the extrahepatic bile ducts and developing intrahepatic bile ducts maintain luminal continuity from the start of organogenesis. It is speculated that there is a rapid proliferation resulting in several channels in the porta hepatis during the fifth week of gestation. Remodelling of these channels might explain some of the variations in configuration of the right and left hepatic ducts and perhaps the presence of subvesicle ducts (ducts of Luschka). Whatever the complete mechanism maybe, a description by Moosman in 1970 [5] is a helpful description for the surgeon. The stylised diagram

a

Fig. 1.1 (a) A stylised diagram of the biliary tree development from the heaptic bud around the fifth week of gestation. From: Moosman DA 1970. The surgical significance of six anomalies of the biliary duct system. Surgery, Gynaecology and Obstetrics 131: 660–665. Two examples of failure of normal biliary development or remodelling (b) A case that displays uncanny resemblence to the theroetical diagram in 1.1a. From: Schorlemmer GR, Wild RE, Maudell V, Newsome JF. Cholecystohepatic Connections in a Case of Extrahepatic Biliary Atresia. JAMA 1984; 252(10): 1319–1320. (c) A case of the intra-hepatic ducts draining diectly into the gallbladder as seen at ERCP with a supporting digram

of the development of the biliary duct system gives some visual reference to a system where failure of regression and remodelling of multiple hepatic ducts might lead to anomalies (Fig. 1.1a). Biliary atresia, choledochal cysts, gallbladder agenesis are all survivable congenital malformations of the biliary system. All are incompletely understood. Although anecdotal, examples of cases where the case for failed remodelling might explain aberrant biliary anatomy are displayed in Figs. 1.1b and 1.1c. The case from Schorlemmer [6] of a 5 year old with multiple ducts draining into the gallbladder has an uncanny resemblance to the diagram from Moosman. This patient was

Multiple hepatic ducts Hepatic diverticulum

Hepatoduodenal duct

Duodenum Ventral pancreas

b

1  Operative Anatomy and Surgical Landmarks of the Biliary System Fig. 1.1 (continued)

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c

ii. There is a process of remodelling of the bile channels connecting the intrahepatic and extrahepatic ducts that leads to a wide range of potential variations in anatomy iii. The hepatic arterial system develops in unison with the biliary tree, so if a variation in arterial anatomy is found, one can expect variation in biliary anatomy, or vice versa.

The Gallbladder

Fig. 1.2  An MRI demonstrating an Intrahepatic gallbladder

thought to have a degree of biliary atresia although the extrahepatic bile duct was present albeit narrow and atrophic. In Fig. 1.1c, the anatomy might suggest a failure of development of the cystic duct, with bile ducts draining into the gallbladder that is incontinuum with the distal bile duct. The example in Fig. 1.2 is a case of intrahepatic gallbladder. The key points for the surgeon to grasp are: i. The intrahepatic and extrahepatic bile ducts develop from separate parts of the liver bud.

The gallbladder is a sac shaped organ with a bulbous fundus, body and tapered neck. It sits on the ventral surface of the liver in the gallbladder fossa. Importantly this marks the principle plane of the liver between segments 4b and 5. The fundus of the gallbladder usually projects a little beyond the sharp edge of the liver and touches the parietal peritoneum of the abdominal wall. The fundus may be palpable or tender to ­palpation in a diseased gallbladder at the lateral edge of the right rectus muscle at the costal margin. The peritoneum covering the liver passes smoothly over the gallbladder. Occasionally the gallbladder can have a narrow mesentery and this will predispose it to volvulus (Fig. 1.3).

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a

Fig. 1.3  A gallbladder torsion in a 72 year old woman that presented with a clinical diagnosis of acute cholecystitis. The ultrasound revealed sludge, a thickened gallbladder wall and peri-cholecystic fluid. A laparoscopy there was a long mesentry attaching the gallbladder to the liver

Occasionally the gallbladder is deeply embedded within the liver. The gallbladder is separated from the hepatic parenchyma by the cystic plate, which is a connective tissue prolongation of the hilar plate. The fundus is usually the most adherent to the cystic plate. The neck of the gallbladder is not attached to the cystic plate nor tightly bound by peritoneum. The cystic duct is commonly adherent to gallbladder at the neck making an angle and the appearance of a diverticulum known as the infundibulum or Hartmann’s pouch. Hartmann’s pouch is a morphologic rather than anatomic entity (Fig. 1.4) [7]. The gallbladder functions to store and concentrate bile. The liver will produce between 500 and 1000 ml of bile per day. The gallbladder will typically store 30–50 ml of bile but can distend to accommodate up to 300 ml. The most important regulator of gallbladder filling is the sphincter of Oddi tone and resistance with retrograde filling of the gallbladder. After endoscopic sphincterotomy gallbladder filling is frequently absent. Within the gallbladder sodium chloride channels

b

over a small area with a complete torsion of the gallbladder. The twist was at the jucntion of the neck and cystic duct (a) with the sucker behind the gallbladder after dissection off the liver. (b) the sucker is against the CBD

Fig. 1.4  Hartmann’s pouch is a morphological entity due to adhesion of the proximal cystic duct to the neck of the gallbladder. From: Van Eijck FC, van veen RN, Kleinrensink GJ, Lange JF. Hartmann’s gallbladder pouch revisited 60 years later. Surg Endosc 2007; 21: 1122–1125

1  Operative Anatomy and Surgical Landmarks of the Biliary System Fig. 1.5 (a) An operative specimen of a duplicated gallbladder. Note there is a single cystic duct. (b) Variations of duplicated gallbladder with both a single cystic duct or 2 seperate cystic ducts

a

b

in the epithelium concentrate bile. Mucous secreting cells are mainly found near the neck of the gallbladder. After ingestion of food, CCK released by the duodenum and parasympathetics from the Vagus nerve influence gallbladder contraction and release of bile. The gallbladder is usually ~7 cm in size. The size varies widely and is influenced by pathology such as obstruction or chronic fibrosis. In rare cases the gallbladder can be duplicated with either a single or double cystic duct (Fig. 1.5). The commonest phenotypic abnormality of the gallbladder is the folding of the fundus in the manner of a Phrygian cap (Fig. 1.6). The incidence is 4% and can be mistaken for a mass in the gallbladder on imaging. Gallbladder adenomyomatosis is

Fig. 1.6  A Phrygian cap on routine ultrasound

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a benign entity of the gallbladder fundus that is diagnosed in 2–8% of all cholecystectomies with a higher prevalence in elderly females. This occurs due to hyperplasia of the gallbladder epithelium and is benign. It is often mistaken as gallbladder cancer and if unrecognized may lead to unnecessary radical surgery (Fig. 1.7) (Chap. 9) [8, 9]. A left sided gallbladder is rare with a reported incidence of 0.2–1.1%. It will sit on segment 3 to the left side of the falciform ligament (Fig. 1.8).

The gallbladder body may be in direct contact with the round ligament. It represents a developmental anomaly most likely due to persistence of the right umbilical vein to become part of the portal system and a failure of segment 4 to develop. It is always associated with biliary and vascular anomalies and is associated with a high rate of bile duct injuries at cholecystectomy. Close attention must be paid to portal venous anatomy when considering major hepatectomy in the presence of a left sided gallbladder [10].

The Cystic Duct

Fig. 1.7  Adenomyomatosis of the gallbladder fundus demonstrated on ultrasound (yellow arrow)

Fig. 1.8  Left sided gallbladder as seen at laparoscopy

The cystic duct connects the gallbladder to the extrahepatic biliary tree. It is typically 2–4 cm in length but can vary from 0.5 to 9 cm. The proximal cystic duct is commonly adherent to the gallbladder neck giving the morphologic appearance of Hartmann’s pouch (Fig. 1.4). Dissection of these adhesions will allow the surgeon to gain more length of the cystic duct for cholangiogram or clipping. The luminal diameter of the cystic duct is typically 2.6 ± 0.7 mm. It can dilate in the presence of obstruction or passage of stones. A

1  Operative Anatomy and Surgical Landmarks of the Biliary System

“wide” cystic duct however should be a warning sign for the surgeon who may have mistakenly dissected the CHD or CBD. The CBD will have blood vessels running at 3 and 9 o’clock whereas the cystic duct will not. Misidentification of the cystic duct, rather than anatomical anomalies, accounts for most CBD injuries (Chaps. 16 and 23). The lumen of the cystic duct is characterised by the spiral valves of Heister (Figs. 1.9a and  b). Heister, a German surgeon and anatomist, described the ‘valves’ in 1732. In fact these are not valves but crescentic folds in the mucosa, the function of which is incompletely understood, but they may be structural rather than partitioning. The cystic duct typically has 2–10 crescentic folds projecting into its lumen, they are concentrated in its proximal end and are larger and less frequent in the distal end [11]. Occasionally the surgeon will have to bear this in mind on c­ annulating the cystic duct

a

b

Fig. 1.9  A series of operative cholangiograms demonstrating some of the variations in the union of the cystic duct with the biliary tree. (a) The usual anatomy that occurs in 75% of individuals, with a union on the right side of the common hepatic duct some 1–3 cm from the confluence. (b) A low union of the cystic duct with the CHD. In this example the cystic duct runs parallel with the CHD for 3.5 cm. During operative dissection this may appear to be fused. (c) The union of the cystic duct is high at the

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for an operative cholangiogram or transcystic exploration of the common bile duct. There is great variability in the junction of the cystic duct with the extrahepatic biliary tree. In the majority the junction lies in the middle third of the combined lengths of the common hepatic and bile ducts (Fig. 1.9a) but in 10% it will drain into the lower third (Fig. 1.9b). More infrequently, the cystic duct may drain into a more proximal duct— the common hepatic, right, left or accessory right hepatic duct (Figs. 1.9c, e, and f). As for the circumferential position the cystic duct joins the CBD, in 50% of cases the cystic duct joins the right lateral aspect of the CHD, the medial aspect in 20% (Fig. 1.9e) and anteriorly or posteriorly in 30% [11, 12]. The cystic duct joins the CHD at an oblique angle in 73% with a slight internal septum created where the two ducts merge. In 17% the cystic duct will spiral around the CHD and in 10% it runs parallel before the ducts unite [11, 12] Fig. 1.9.

c

c­ onfluence of the right and left hepatic ducts. (d) The cystic duct spiralling either anterior or posterior to the CHD and uniting with the CHD on the left side. There is a stone in the distal CBD. (e) Union of the cystic duct with the right posterior sector duct. Other similar variations include union with the right hepatic duct or with the segment 6 duct. (f) A very short cystic duct. In this case it has a union close to the confluence

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d

e

f

Fig. 1.9 (continued)

Extrahepatic Biliary Anatomy The right anterior and posterior sectoral ducts should unite within the liver substance to form a short right hepatic duct. This will converge with the longer left hepatic duct in a Y shaped manner to form the common hepatic duct. The length of the common hepatic duct is variable and ­determined by where the cystic duct joins to form the common bile duct. The common bile duct continues in the free edge of the hepatoduodenal ligament, initially anterior to the portal vein and to the right of the hepatic artery in this supraduodenal portion. It runs posterior to the first part of the duodenum and in a groove in the head of the pancreas, often embedded in pancreatic tissue, to the ampulla of Vater in the posteromedial wall of the second part of the duodenum [13, 14]. The main variations of the hepatic duct confluence were described by Couinaud in

1953 [15]. The complex embryological process that is involved in duct genesis may explain the number of variations here. More contemporary studies demonstrate atypical branching patterns in the right and left hepatic ducts in 14% and 8%, respectively (Fig. 1.10) [16, 17]. The aberrant right posterior segmental duct can occur in 8% of the population and deserves special mention in relation to cholecystectomy. In 6% the cystic duct will join the right posterior duct (Type A4, Figs.1.9e,  1.10, and 1.11) and here it is at high risk of being mistaken as the cystic duct. Ligation or injury of this duct will led to cholestasis or bile leak that is not responsive to ERCP (Chap. 22), and will usually require repair with a Roux loop. In our series from Princess Alexandra Hospital, injury to the right posterior duct makes up for almost 30% of referrals for biliary injury [18].

1  Operative Anatomy and Surgical Landmarks of the Biliary System Type A1 (62.6%)

9 Type A3 (11%)

Type A2 (19%)

a RASD LHD

RASD

LHD

RASD c LHD RPSD

RPSD

RPSD

Type A5 (1.6%)

Type A4 (5.8%) RASD

LHD

RPSD

Fig. 1.10  The common variations of the branching patterns of the right and left hepatic ducts. From: Huang TL, Cheng YF, Chen CL, Chen TY, Lee TY (1996) Variants of

RASD

LHD

RPSD

the bile ducts: clinical application in the potential donor of living-related hepatic transplantation. Transpl Proc 128:1669–1670

Intraoperative Cholangiography The role of routine cholangiogram in cholecystectomy remains debated (Chaps. 6, 7, and 17). There is no doubt, however, that it is an immensely helpful tool to demonstrate both normal and abnormal biliary anatomy. This author believes routine use and study of the intrahepatic and extrahepatic anatomy is a safe practice that leads to increased knowledge of anatomical variations for the s­ urgeon. As shown in Fig. 1.12, what ducts are absent is as important as what ducts are present. Anatomical landmarks for each cholangiogram should include: Fig. 1.11  Aberrant right posterior duct (Type A4)

1. Cystic duct length and angle of junction with the bile duct.

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a

b

Fig. 1.12 (a) Operative cholangiogram—absence of filling of right posterior ducts. (b) At laparotomy for bile leak—cannulation of injured aberrant right posterior duct

(RPD) and cystic duct. The injured RPD was repaired by Roux-­en-­Y hepatico-jejunostomy

2 . Free flow of contrast into the duodenum. 3. Biliary dilatation. 4. Filling defects in the extra hepatic biliary tree. 5. Presence of all intrahepatic ducts—left, right anterior and right posterior.

the controversy in using the term duct of Luschka, with many preferring the term subvesicle bile duct [19]. A recent systematic review looked at all bile ducts near the gallbladder fossa that might be responsible for a bile leak from a “duct of Luschka” and categorized into four subtypes (Fig. 1.13) [19].

The practical anatomy to remember for easy routine cannulation of the cystic duct is outlined above. In brief, the cystic duct is often adherent to the GB so dissection will give extra length, the sometimes troublesome spiral valves are more frequent proximally, a wide cystic duct is a warning sign of possible misinterpretation of anatomy.

Duct of Luschka A common culprit for post cholecystectomy bile leak is a Duct of Luschka (Chap. 22). German anatomist Hubert von Luschka published in detail the anatomy of various organ ­systems in 1863. His description of the gallbladder included intramural glands “Luschka crypts” but also a network of small ducts in the connective tissue surrounding the gallbladder on both the peritoneal surface and the cystic plate. In retrospect, perhaps Luschka was describing lymphatics rather than aberrant small bile ducts. Hence

1. Segmental subvesicle duct—a segmental duct draining into the main bile duct with an unusual superficial course (commonly the right posterior segmental duct) 2. Accessory subvesicle duct—a supernumerary bile duct from the formal biliary tree interconnecting between biliary channels and taking a superficial course 3. Hepaticocholecystic bile duct—a bile duct from the liver that drains directly into the gallbladder 4. Aberrant subvesicle bile duct—a network of small bile ducts in the connective tissue of the gallbladder fossa in continuity with the intrahepatic bile ducts Most injuries to subvesicle ducts are due to dissection deep to the cystic plate therefore exposing a superficial duct in the liver parenchyma. Many are recognized by a bile leak

1  Operative Anatomy and Surgical Landmarks of the Biliary System

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Type 1

Type 2

Type 3

Type 4

Fig. 1.13  Diagrams of the sub-vescicle ducts (Types 1 – 4). From: Schnelldorfer T, Sarr MG, Adams DB. What is the Duct of Luschka?-A systematic review. J Gastrointest Surg 2012;16:656–662

p­ ost-­operatively. If a leak from a subvesicle duct is recognized in the gallbladder fossa at the time of cholecystectomy then cholangiography by cannulating the subvesicle duct or the cystic duct is recommended to define anatomy. Most injuries can be managed by ERCP and stenting the sphincter (Fig. 22.5). Types 2–4 can be managed by clipping or oversewing the subvesicle duct (Fig. 22.17) (Chap. 22).

Cystic and Hepatic Arteries The cystic artery usually arises from the right hepatic artery, passes within Calot’s triangle, and divides into a superficial branch running along the peritoneal surface of the gallbladder and a deep branch running between the gallbladder and cystic plate. If dissection is close to the gallbladder and this branching is proximal, a posterior cystic artery will need to be ligated separately.

The prevalence of a true double cystic artery is reported at 2–22% [20–22]. The cystic artery will originate from the right hepatic artery (RHA) in 75% (Fig. 1.14a). It can as also originate from an accessory or replaced RHA (12%), the left hepatic artery (LHA) (6.2%), the gastroduodenal artery (2.6%) (Fig. 1.14c), the common hepatic artery (2.2%), the proper hepatic artery (0.6%) (Fig. 1.14d), the coeliac trunk (0.4%), or extremely rarely from the SMA or superior pancreaticoduodenal artery [4, 20]. When the cystic artery arises from an accessory or replaced RHA, the RHA may run through Calot’s triangle and give off a short cystic artery. When it arises from the LHA, common hepatic or coeliac trunk it will course anterior to the common hepatic duct but may also course through the liver before reaching the gallbladder. When the cystic artery arises from the SMA or GDA it is found inferior to the cystic duct and does not pass through Calot’s triangle [20].

T.R. O’Rourke

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In a large retrospective study of 600 elective laparoscopic cholecystectomies, 85.5% had a normal pattern of cystic artery in Calot’s triangle, in 13% the cystic artery approached the

gallbladder from outside the Calot’s triangle and in 1.5% there was more than one cystic artery, within or outside Calot’s triangle (Fig. 1.14) [23].

a A

B iii i ii i

b A

Fig. 1.14 Diagramatic representations of some of the variations in cystic artery anatomy. In each set “A” is the laparoscopic view and “B” is the anatomical diagram. (a) The classic cystic artery (i) arising from the right heaptic artery (ii). The cystic artery is above the cystic duct (iii). (b) A double cystic artery (i) arising from the right heaptic artery. Both are above the cystic duct (ii). (c) A cystic artery (ii) arising from the gastroduodenal artery (iii) passing inferior to the cystic duct (i). (d) Cystic artery (i) arsing from a variation of the right heaptic artery (iii) in close proximity to the cystic duct (ii). From: Ding YM, Wang B, Wang WX, Wang P, Yan JS. New classification of the anatomic variations of cystic artery during laparoscopic cholecystectomy. World J Gastroenterol. 2007; 13:5629–5634

B

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1  Operative Anatomy and Surgical Landmarks of the Biliary System

The RHA normally courses behind the common hepatic duct, before entering the liver (Fig. 1.14a) but in up to 25% it may run anterior. A tortuous RHA is not uncommon, making a “Caterpillar turn” or “Moynihan’s hump” close to the gallbladder before giving off a short cystic artery. This situation makes the RHA particularly prone to injury during cholecystectomy and should be suspected if an unusually large cystic artery is encountered [20, 22]. Nearly 20% of patients have a replaced RHA with its origin off the SMA or aorta. The replaced RHA will course upwards posterior to the portal vein and assume the normal position of the RHA posterior to the CHD before entering the liver. Rarely the replaced HA may run between the PV and CBD. Approximately 15% of patients will have a replaced LHA with its origin from the left gastric artery [4]. Variations in arterial anatomy are common (Fig. 1.14). As mentioned above, the arterial and extrahepatic biliary system develop in unison so if any abnormal anatomy is encountered, others should be expected.

Blood Supply to the CBD With respect to blood supply, the extrahepatic bile duct can be divided into 3 segments: hilar, supraduodenal and retropancreatic. The arteries of the supraduodenal bile duct arise from the superior pancreaticoduodenal artery, gastroduodenal artery, right hepatic artery and cystic artery. There are an average of eight small arteries, each measuring approximately 0.3 mm. The most important of these vessels runs the length of the duct along the lateral borders in the 3 o’clock and 9 o’clock position (Fig. 1.15). Of these vessels supplying the supraduodenal bile duct, 60% will run upwards from the major inferior vessels and 38% will run downward from the hepatic artery. Only 2% will have a non-axial blood supply, arising directly from the hepatic artery [14, 24]. The hilar bile duct has a rich atrial supply from copious small branches from the surrounding vessels. This arcade is in continuity with the blood vessels of the supraduodenal duct. There is a communicating arcade between the left and

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d a e b c

f g h

Fig. 1.15  Blood supply of the extrahepatic bile duct. a. Right hepatic artery. b. 9 o’clock artery. c. retroduodenal artery. d. left hepatic artery. e. hepatic artery. f. 3 o’clock artery. g common hepatic artery. h. gastroduodenal artery

right hepatic arteries here in the hilar plate, originating from the segment 4 artery and the right branch of the middle hepatic artery [14]. The retropancreatic bile duct receives its blood supply from the pancreaticoduodenal arteries. Small vessels form a mural plexus around the duct [14].

Venous and Lymphatic Drainage The veins that drain the bile duct usually exist parallel to existing arteries along the lateral border of the bile duct. These veins may drain into the portal vein of hepatic veins in the liver. In cases of portal hypertension or portal vein thrombosis these veins can be exceptionally large and a potential source of major haemorrhage [4, 14] (Chap. 19). Venous drainage of the gallbladder includes veins that drain directly into the middle hepatic

T.R. O’Rourke

14

vein or right portal vein in the liver. There are also veins that follow the cystic duct and hepatic duct to drain into the portal system. Again, large varices can be expected in cases of portal hypertension and the surgeon should be cautious [14, 24]. Lymphatic vessels in the gallbladder are located in the subserosal layer and drain into the cystic lymph node of Lund (or Calot’s node) (Fig.  16.6c) and from here to the nodes of the porta hepatis. Lymphatics can also pass directly into the liver along segments 5 and 4b until reaching nodes in the hepatoduodenal ligament. Thus, radical resection for gallbladder cancer involves resection of these segments of liver and radical lymphadenectomy. Lymphatics from the inferior bile duct will also drain to retropancreatic nodes and nodes between the aorta and vena cava [4, 14].

 alot’s Triangle and the Hepatocystic C Triangle Jean-Francoois Calot, a French surgeon, described anatomy of the right upper quadrant with particular reference to the gallbladder in his doctoral thesis, De la cholecystectomie, p­ ublished

in 1891 [25]. In his original description the triangle is bounded by the cystic duct inferiorly, the common hepatic duct medially and the cystic artery superiorly. The modern definition of Calot’s triangle differs from that original description in that the superior border is the inferior surface of the liver, medially the CHD and inferiorly the cystic duct—the hepatocystic triangle. Using the modern definition the contents of the triangle should include the RHA, cystic artery, the cystic lymph node of Lund, lymphatics and connective tissue (Fig. 1.16) [20].

The Plate System The plate system consists of bile ducts and blood vessels surrounded by a connective tissue sheath that is continuous with Glisson’s capsule, intrahepatically, and the hepatoduodenal ligament, extrahepatically. Four plates are recognized. The hilar plate located in the hilum with segment 4 at its superior border. The cystic plate in the gallbladder bed is continuous with the hilar plate and also the Glissonian sheath of the right anterior segment of the liver. The umbilical plate envelopes the umbilical portion

Liver Right hepatic artery Gallbladder Left hepatic artery Cystic artery Common hepatic duct Cystic duct Common bile duct Common hepatic artery

Fig. 1.16  Calot’s triangle. Red cross hatched area is the original discription of Calot. The blue cross hatched area is the modern definition of Calot’s traingle, which actually conforms to a quadralateral rather than a triangle.

From: Abdalla S, Pierre S, Ellis H. Calot’s triangle. Clin Anat 2013;26:493–501. Red = Calot’s original triangle. Blue = modern interpretation or hepatocystic triangle

1  Operative Anatomy and Surgical Landmarks of the Biliary System

of the portal vein, it is connected to the ligamentum teres ventrally and the Arantian plate

15

covering the ligamentum venosum dorsally (Fig. 1.17) [26, 27].

A umbilical plate

hilar plate

round ligament

cystic plate

S4a

S5

S6 S7

Rouviere sulcus hepatoduodental ligament

B

umbilical plate

Glisson’s sheath of anterior segment hilar plate G4a

cystic plate

G3

G8 G4b

G2

Fig. 1.17  The hepatic plate sytem. (A) Location of the different hepatic plates. (B) Components and contents of the hepatic plates. From: Kawarada Y, Das BC, Taoka H. Anatomy of the hepatic hilar area: the plate system. J Hepatobiliary Pancreat Surg 2000; 7: 580–586

GB

umbilical plate Glisson’s sheath of posterior segment hilar plate

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The importance of an understanding of the plate system is clear for liver resection but can also help the surgeon performing cholecystectomy. When there is a normal plane of connective tissue between the gallbladder and the cystic plate dissection is straightforward and major vascular structures are avoided. In severe inflammation this plane of dissection is often not clear. If the surgeon finds himself or herself behind the cystic plate in a fundus down approach then the dissection will continue onto the right portal pedicle. Strasberg and Gouma have shown an association of extreme vasculobiliary injuries in this circumstance [28].

Rouviere’s Sulcus Described by Henri Rouviere in 1924, this 2–3 cm sulcus runs to the right of the liver hilum anterior to segment 1 and usually contains the right portal triad or its branches [29]. In a study of 40 normal livers at autopsy, Rouviere’s sulcus was identified in 82%, of these 70% were open and 12% were fused with only a small cleft visible. 18% had no recognizable sulcus [30]. The branches of the right posterior pedicle were identified in the sulcus in 70%. Importantly the sulcus indicates the plane of the common bile duct accurately. The cystic duct and artery lie anterosuperior to the sulcus and the common bile duct lies below the level of the sulcus. For laparoscopic cholecystectomy this is an important landmark. Hugh has shown by beginning dissection ventral to the sulcus there is a low rate of bile duct injury [31]. When the Hartmann’s pouch is grasped and lifted up towards the falciform liga-

T.R. O’Rourke

ment, the line drawn between Rouviere’s sulcus and the base of segment 4 indicates the level below which dissection should not occur (Figs. 1.18 and 16.6) [32].

The Critical View of Safety (CVS) The CVS was first described by Strasberg in 1995 [33]. The rational is to provide the surgeon with a system of reference prior to dividing any structures during cholecystectomy to avoid iatrogenic bile duct injury. The cystic duct and artery are dissected free and the gallbladder mobilised off the cystic plate so that only two structures enter the gallbladder (Figs. 1.19 and 16.15). This is a clearance of the fat and fibrous tissue from the modern Calot’s triangle to positively identify the cystic duct and artery. The difficulty of the CVS comes with the high rate of anatomical variability in the hepatocystic triangle and the pathology or inflammation that make dissection and clearance of all the fibrofatty tissue hazardous. Bile duct injury can occur whilst attempting to safely establish the critical view [32]. It is recognized that in dense fibrosis, the surgeon should not continue dangerous dissection but rather consider early cholangiogram, conversion to open or solicit the help of a colleague [34]. Anatomically, the critical view is a tool for safe cholecystectomy and display of normal anatomy. In cases of anatomical variation or dense fibrosis it should not be considered a compulsory part of the surgeon’s dissection, rather a part of the surgeon’s armamentarium along with all the other anatomical knowledge outlined above (Chap. 16).

1  Operative Anatomy and Surgical Landmarks of the Biliary System Fig. 1.18 Rouviere’s sulcus (a) Diagramatic representation of the anatomy. The green tirangle is above the sulcus and is safe to be dissectiong in this area. The red quadrangle is below the sulcus and is not safe. (b) A laparoscopic view of the dissection represented in the diagram

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a

Cystic duct

Safe dissection triangle

Rouviere’s sulcus Right hepatic duct Common bile duct

b

Pla

n

f eo

cus

sul

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T.R. O’Rourke

Fig. 1.19  Critical view of safety

References 1. Eisendrath DM. Anomalies of the bile ducts and blood vessels: as the cause of accidents in biliary surgery. JAMA. 1918;71(11):864–7. 2. Stazzbabosco M, Fabris L. Development of the bile ducts: Essentials for the clinical hepatologist. J Hepatol. 2012;56:1159–70. 3. Roskanis T, Desmet V. Embryology of extra- and intrahepatic bile ducts, the ductal plate. Anat Rec. 2008;291:628–35. 4. Keplinger KM, Bloomston M. Anatomy and embryology of the biliary tract. Surg Clin N Am. 2014;9:203–17. 5. Moosman DA. The surgical significance of six anomalies of the biliary duct system. Surg Gynaecol Obstet. 1970;131:660–5. 6. Schorlemmer GR, Wild RE, Maudell V, Newsome JF. Cholecystohepatic connections in a case of extrahepatic biliary atresia. JAMA. 1984;252(10):1319–20. 7. Van Eijck FC, van Veen RN, Kleinrensink GJ, Lange JF. Hartmann’s gallbladder pouch revisited 60 years later. Surg Endosc. 2007;21:1122–5. 8. Van Kamp M-J. A Phrygian cap. Case Rep Gastroenterol. 2013;7:347–51. 9. Hammad AY. A literature review of radiological findings to guide the diagnosis of gallbladder adenomyomatosis. HPB. 2016;18:129–35. 10. Strong RW, Fawcett J, Hatzifotis M, et al. Surgical implications of a left sided gallbladder. Am J Surg. 2013;206:59–63.

11. Dasgupta D, Stringer MD. Cystic duct and Heister’s “Valves”. Clin Anat. 2005;18:81–7. 12. Shaw MJ, Dorsher PJ, Vennes JA. Cystic duct anatomy: an endoscopic perspective. Am J Gastroenterol. 1993;88:2202–106. 13. Sinnatamby CS. Last’s anatomy regional and applied. 10th ed. London: Churchill Livingstone; 1999. 14. Blumgart LH, Fong Y. Surgery of the liver and biliary tract. 3rd ed. New York: W.B. Saunders Company Ltd.; 2000. 15. CouinaudC. Lefoie.EtudesAnatomiquesetchirurgicales. France: Edition Masson; 1957. 16. Chaib E, Kanas AF, Galvao FH, et al. Bile duct confluence: anatomic variations and its classification. Surg Radiol Anat. 2014;36:105–9. 17. Huang TL, Cheng YF, Chen CL, Chen TY, Lee TY. Variants of the bile ducts: clinical application in the potential donor of living-related hepatic transplantation. Transpl Proc. 1996;128: 1669–70. 18. Slater K, Strong RW, Wall DR, Lynch SV. Iatrogenic bile duct injury: The scourge of laparoscopic cholecystectomy. ANZ J Surg. 2002;72:83–8. 19. Schnelldorfer T, Sarr MG, Adams DB. What is the Duct of Luschka?—A systematic review. J Gastrointest Surg. 2012;16:656–62. 20. Abdalla S, Pierre S, Ellis H. Calot’s triangle. Clin Anat. 2013;26:493–501. 21. Nagral S. Anatomy relevant to cholecystectomy. J Minim Access Surg. 2005;1(2):53–8. 22. Hugh TB, Kelly MD, Li B. Laparoscopic anatomy of the cystic artery. Am J Surg. 1992;163:593–5.

1  Operative Anatomy and Surgical Landmarks of the Biliary System 23. Ding YM, Wang B, Wang WX, Wang P, Yan JS. New classification of the anatomic variations of cystic artery during laparoscopic cholecystectomy. World J Gastroenterol. 2007;13:5629–34. 24. Castaing D. Surgical anatomy of the biliary tract. HPB. 2008;10:72–6. 25. Calot JF. De la cholecstectomie. 1891. Med Frc de Paris, Dissertation. 26. Kawarada Y, Das BC, Taoka H. Anatomy of the hepatic hilar area: the plate system. J Hepato-Biliary-­ Pancreat Surg. 2000;7:580–6. 27. Masunari H, Shimada H, Endo I, Fujii Y, Tanaka K, Sekido H, Togo S. Surgical anatomy of the hepatic hilum with special reference of the plate system and extrahepatic duct. J Gastrointest Surg. 2008;12:1047–53. 28. Strasberg SM, Gouma DJ. ‘Extreme’ vasculobili ary injuries: association with fundus-down cholecystectomy in severely inflamed gallbladders. HPB. 2012;14:1–8.

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29. Rouviere H. Sur la configuration et la signification du sillon du processus caude. Bulletins et Memoirs de la Societe Anatomique de Paris. 1924;94:355–8. 30. Dahmane R, Morjane A, Starc A. Anatomy and Surgical relevance of Rouviere’s sulcus. Sci World J. 2013;2013:254287. 4 pages 31. Hugh TB, Kelly MD, Mekisic A. Rouviere’s sulcus: a useful landmark in laparoscopic cholecystectomy. Br J Surg. 1997;84:1253–4. 32. Connor SJ, Perry W, Nathanson L, Hugh TB, Hugh TJ. Using a standardized method for laparoscopic cholecystectomy to create a concept operation-­ specific checklist. HPB. 2014;16:422–9. 33. Strasberg SM, Hertl M, Soper NJ. An analysis of the problem of biliary injury during laparoscopic cholecystectomy. J Am Coll Surg. 1995;180: 101–5. 34. Strasberg SM, Brunt LM. Rationale and use of the critical view of safety in laparoscopic cholecystectomy. J Am Coll Surg. 2010;211:132–8.

2

Biliary Imaging for Gallstone Disease Piers Dugdale

Introduction Medical imaging of the abdomen is of vital importance when assessing upper abdominal pain, both in the acute patient and in post-­operative patients. It supports the clinical assessment and provides guidance when there is difficulty in evaluating the patient. Imaging allows the clinician to more accurately follow the outcomes of non-surgical treatment or the post-­surgical course and intervene earlier or delay intervention if there is concern of complications.

Imaging Modalities Ultrasound Ultrasound is the modality of choice when initially evaluating the gallbladder and biliary tree (Fig. 2.1). It has good resolution, particularly when using modern ultrasound machines with technologically more capable probes and more complex acoustic algorithms. Ultrasound is readily available, fast and requires minimal patient preparation in the acute setting. It is also capable of being used as a point-of-care modality, so the P. Dugdale, M.B.B.S., F.R.A.N.Z.C.R Department of Medical Imaging, Nepean Hospital, Sydney, NSW, Australia e-mail: [email protected]

patient does not have to be moved but can be assessed at the bedside if required. It does not use ionising radiation and there are no known sideeffects from the ultrasound. It demonstrates gallstones and the gallbladder wall well due to their strong reflective interfaces compared to bile. Ultrasound can also provide functional information, assessing gallbladder emptying by imaging pre and post ingestion of a fatty meal. Assessment of blood flow in the portal venous system can also be useful. Ultrasound does have its limitations, particularly in bariatric patients, where depth of imaging reduces visualisation due to lack of acoustic return. The presence of fatty infiltration of the liver is commonly seen, reducing through transmission, particularly when scanning intercostally. Evaluation of the biliary tree for choledocholithiasis is limited by non-visualisation of the distal common bile duct (CBD) as it passes posterior to the duodenum, mainly due to the presence of gas with the duodenal lumen. The large bowel can also intervene, limiting the visual window. Ultrasound is a more subjective modality, requiring significant sonographer experience to provide the best study. Although sonographic studies are highly structured, there is still significant variation in study quality due to variation in patient anatomy. The anatomy is more difficult to visualise in three dimensions as images can be obtained in a variety of planes to show any abnormalities at their best.

© Springer International Publishing AG, part of Springer Nature 2018 M.R. Cox et al. (eds.), The Management of Gallstone Disease, https://doi.org/10.1007/978-3-319-63884-3_2

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P. Dugdale

22 Fig. 2.1 (a) Ultrasound in the erect posture of the gallbladder with a normal wall (white arrow) and stones in the fundus (yellow arrow). (b) Ultrasound of a nondilated CBD

a

b

CT Computed tomography (Fig. 2.2) is a more objective modality that is readily available and fast. The study parameters are pre-configured so there is minimal difference between studies performed by different CT radiographers. The standardised acquisition allows far more objectivity when assessing anatomy and any abnormalities. If imaging is obtained before and after IV contrast,

enhancement of structures can provide important information. CT study quality and interpretation can reduce significantly in bariatric patients due to reduced penetration of the X-rays causing a reduced signal-­to-noise ratio. More recent CT scanners, particularly those designed for overweight or obese patients have higher capacity X-ray tubes that can sustain higher voltage (kVp) and amperage (mAs) to punch the X-rays through the extra

2  Biliary Imaging for Gallstone Disease

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liver, the hepatic vessels, stomach, adrenals, duodenum or pancreas.

Multiphase CT Multiple contrast phases allow the Radiologist to differentiate tissues based on their enhancement profiles, making abnormal tissues more conspicuous and vascular lesions more visible. The usual phases are:

Fig. 2.2  A portal phase CT scan demonstrating a normal gallbladder and gallbladder wall (arrow). Note the outline of the vessels and the perfusion of the solid organs during the portal phase

tissue and create enough signal in the detectors. Bariatric scanners also generally have a wider bore so that large patients can more easily fit through and are still contained within the scanner’s field of view. The CT image grey scale is based on the Hounsfield Unit (HU), a direct measurement of the density of tissue in the body at any given point. Although review of the reconstructed axial imaging on a standard PACS viewing platform is powerful, the review of the source fine slice images in an advanced viewing program takes CT interpretation to a new level. This allows viewing of the 3D data in multiple ways, from standard multiplane reconstruction (MPR), maximum intensity projection (MIP) and full 3D reconstruction in limited circumstances. CT uses ionising radiation which can be significant, particularly if a multiphase technique is used. CT scanners are utilising progressively lower radiation doses to produce diagnostic studies, due to improved collimation of the radiation, more sensitive detectors, more powerful iterative image reconstruction algorithms and a multitude of other dose reduction techniques. CT is commonly used when there is concern for complications or involvement of adjacent anatomy, such as the hepatic flexure, adjacent

1. Non-contrast—This allows delineation of subtle calcific densities and acts as a baseline for assessing the amplitude of enhancement of the other phases. 2. Arterial phase—This outlines the arteries and any early enhancing tissues, such as tumours and vascular abnormalities. 3. Portal venous phase—This is the optimum phase for maximum difference in contrast enhancement between the tissues in the abdomen (Fig. 2.2). 4. Delayed phase—This is sometimes used when there is expectation of a long washout of contrast from a lesion.

CT Cholangiogram (Fig. 2.3) Instead of imaging using standard contrast that is almost exclusively excreted via the kidneys, imaging can also be performed using a contrast media that has a high excretion rate through the biliary tree, such as Biliscopin (Meglumine iotroxate). This contrast media has a much larger molecule that is preferentially taken up by the liver and excreted into the bile. However, the larger molecule increases the risk of contrast reaction compared to standard non-ionic contrast. This requires infusion of the Biliscopin over 1h prior to the scan, with monitoring of the patient’s vital signs. Nausea and drop in blood pressure is not uncommon and can be minimised by titrating the rate of infusion to the speed where the patient does not experience symptoms. The risk of adverse reactions such as rash, hives and nausea ranges from 0.8% to 3.4%. There are no recorded episodes of anaphylaxis [1]. This study is often limited if there is either high bilirubin levels or hepatocellular dysfunction, as there is competitive excretion between

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P. Dugdale

Fig. 2.3  A CT cholangiogram demonstrating a normal biliary tree post cholecystectomy

the liver and kidneys and there will not be sufficient biliary excretion for a meaningful contrast density difference between the biliary tree and surrounding tissues. CT Cholangiography can also demonstrate non-filling of the gallbladder either from mechanical or functional causes.

MRI Magnetic Resonance Imaging (MRI) (Fig. 2.4) has been gaining more utility in evaluation of the upper abdomen including the biliary system, due to increasing magnet strength, improved gradient coil technology and more advanced sequences. This allows shorter breath-holds reducing motion artefact, increased spatial resolution and improved signal-to-noise ratio. Respiratory gated acquisitions can also be performed. MRI also suffers from reduced image quality in bariatric patients, although technological improvements are reducing this issue. There is also the physical limitation of the bore size of the MRI machine. Most MRI manufacturers are now producing bariatric scanners to cope with this issue.

One of the significant advances in MRI imaging is the advent of MRI contrast that is at least partially biliary excreted. Approximately 50% of a contrast agent such as Gd-EOB-DTPA is taken up by hepatocytes and excreted into the biliary system [2]. This provides an additional biliary phase to imaging at approximately 15–20 min that assesses hepatocyte function of the liver tissue or lesion in question. The excreted contrast can also be used to outline the biliary tree on T1 weighted images. There can be very limited excretion of contrast in the presence of high levels of bilirubin or hepatocellular dysfunction causing preferential excretion via the kidneys. The lumen of the biliary tree can be accurately assessed in non-contrast sequences by using the water component of bile as the ‘contrast agent’. These sequences also outline the pancreatic duct, useful additional information, particularly when evaluating the distal common bile duct. Administration of foods high in Molybdenum (Blueberries) to reduce artefact from the stomach and duodenum have been tried and are of limited utility. MRI is increasingly being used as a problem solving tool for patients who have been incompletely assessed by other modalities or have a dif-

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Fig. 2.4 MR Cholangiopancreato­ graphy (MRCP) – Thin slice T2 weighted sequence. The central intrahepatic ducts, CHD, cystic duct, CBD and pancreatic ducts are well demonstrated on this coronal image. The ducts demonstrate normal morphology

Nuclear Medicine

Fig. 2.5  MRCP in an 80-year-old man with multiple medical comorbidities demonstrating a dilated CBD with a distal CBD stone

ficult clinical presentation (Fig. 2.5). It is also an important modality for assessment of biliary anatomy pre-surgery.

Cholescintigraphy (Figs. 10.1 and 10.2) Nuclear Medicine hepatobiliary imaging utilises Technetium-99m attached to a chemical or blood component to enhance uptake in particular tissues. Images are acquired using gamma cameras to capture the photons emitted from the decay of Technetium. Biliary imaging uses the HIDA radiopharmaceutical to assess biliary function/physiology by mimicking bilirubin. Using the HIDA radiotracer allows assessment of uptake into the liver, excretion into the biliary tree and filling of the gallbladder. Standard gamma cameras can capture 2-dimensional information over time, which limits anatomic information. More advanced gamma cameras (SPECT cameras) can acquire information in 3-dimensions, giving more anatomic information. Nuclear Medicine imaging is most powerful however, when combined with the superior spatial information provided by CT or MRI. CT/SPECT or MRI/SPECT fusion imaging is a developing field of imaging. At this stage it has limited application in gallstone related disease, but may be of assistance as a problem solving tool when assessing potential complications such

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as bile leak or functional gallbladder disease. PET/CT has its main strength in assessment of neoplasia of the biliary system.

PET Positron Emission Tomography is currently utilised only for evaluation/staging of neoplastic disease of the liver, bile ducts and gallbladder with minimal application in stone disease.

Pre-operative Imaging

P. Dugdale

accounting for >80% of all gallstones in the United States. Most gallstones remain asymptomatic, with approximately 1% per year causing symptomatic disease (Chap. 5). Ultrasound is the most commonly used modality to assess for presence of gallstones (Fig. 2.6), with a sensitivity of 95% and specificity of >95% for stones larger than 2 mm [3–5]. When using CT, gallstones can only be demonstrated if they have a different density to the bile they are immersed in (Fig. 2.7). Increasing the

Introduction Cholelithiasis is prevalent, found in about 10% of the general population. Gallstones are twice as prevalent in women as in men, increasing in incidence with age. As a consequence of gallstone related disease, cholecystectomy is the most common elective abdominal surgery performed in the United States. There are two types of gallstones; cholesterol stones are composed greater than 70% cholesterol and pigment stones which contain predominantly calcium bilirubinate (Chap. 3). Cholesterol stones are the most common,

Fig. 2.7  CT – Multiple layering calcified gallstones in an otherwise normal gallbladder

Fig. 2.6 An ultrasound demonstrating multiple gallstones and a normal gallbladder wall

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2  Biliary Imaging for Gallstone Disease Fig. 2.8  MRI – T2 weighted fat suppressed acquisition. Multiple layering gallstones in an otherwise normal gallbladder. There is an impression of fissuring in several of the stones

Table 2.1  Gallstone signal characteristics Gallstone type Cholesterol Pigment

T1 signal intensity T2 signal intensity Decreased Decreased Increased Decreased

kVp to 140, sensitivity can be increased to 81–86% compared to 52–67% at lower settings [3]. On MRI, cholesterol stones usually have low signal intensity on both T1 and T2 weighted sequences [6] (Figs. 2.5 and 2.8, Table 2.1). Pigment stones also demonstrate decreased signal on T2 weighted sequences compared to the bile surrounding them, but have more variability in signal, often higher on T1 sequences. This is thought to be due in large part to the presence of metal ions [7]. Larger stones may exhibit a Mercedes-Benz sign, due to fluid or gas within faults in the stones. Biliary sludge or microlithiasis can be distinguished from concentrated bile on MRCP, usually seen as T2 hypointense particles less than 2 mm in diameter floating in the bile [8, 9]. It is worth commenting on in reports, because although the stones can resolve over time and are usually asymptomatic, they can go on to develop into larger stones or cause acute cholecystitis, cholangitis or pancreatitis if they cannot pass readily through the sphincter of Oddi [10].

The reported sensitivity for diagnosing gallstones in the gallbladder using MRCP is 89–100% with specificity of 83–100% [11, 12], with improved results when images are acquired with a thickness of 3 mm or less [13]. However, the real strength of MRCP is in diagnosing choledocholithiasis (Fig. 2.5) and stones in the cystic duct, with sensitivity of 91–98% and specificity of 88%, comparable to ERCP and endoscopic sonography, even with smaller stones 40 mm short axis) are secondary supporting features that provide a ­ more complete diagnostic picture. Wall thickening greater than 3 mm is the most common but least specific finding. In the absence of a positive Murphy’s sign or impacted gallstone, the list of possible causes include hepatitis, cirrhosis, ascites, hypoproteinaemic states, ­congestive right heart failure, kidney failure and pancreatitis. Chronic wall thickening causes include; chronic cholecystitis, adenomyomatosis, xanthogranulomatous cholecystitis and diffuse neoplastic infiltration [15].

a

b

Fig. 2.9 (a) Ultrasound in a patient with acute cholecystitis. (a) 1.36 cm stone lodged in the neck of the gallbladder. The wall is thickened and pericholecystic fluid is present. There is minor layering of sludge. The patient

was sonographic Murphy’s negative. (b) Ultrasound for acute cholecystitis. Multiple small stones are demonstrated, as well as marked wall thickening, pericholecystic fluid and increased vascularity in the wall

2  Biliary Imaging for Gallstone Disease

Computed Tomography CT is commonly performed, usually in the setting of more non-specific abdominal pain. CT is used to evaluate approximately one-third of patients aged 60 years and older who present to the emergency department with abdominal pain, with biliary disease diagnosed in approximately 10% of these patients [16]. Other findings on CT include gallstones, gallbladder wall thickening more than 3 mm, gallbladder distention more than 5 cm in the short axis or more than 8 cm in the long axis, pericholecystic fluid, inflammatory stranding adjacent to the gallbladder and subserosal oedema (Fig. 2.10) [17]. If CT is performed with contrast, the feature of transient curvilinear arterial hepatic enhancement adjacent to the inflamed gallbladder caused by reactive hepatic arterial hyperaemia may be helpful [18]. The negative predictive value of CT for diagnosis of acute cholecystitis is 89%. This is lower than that for ultrasound, but indicates that CT can exclude acute cholecystitis with confidence in a setting of relatively non-specific symptoms [19]. MRI MRI is usually used as a problem solving tool and is a third line investigation, most commonly to help distinguish between an atypical presenta-

a

Fig. 2.10  CT in acute cholecystitis (a) axial and (b) coronal views. The gallbladder is significantly dilated, with an irregular wall almost absent in several places. There is

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tion of acute/subacute cholecystitis and more chronic gallbladder diseases. MRI may be useful in distinguishing the impacted stone deep in the neck or cystic duct, an area that ultrasound and CT have more difficulty visualising. T2 weighted images may show gallbladder wall thickening (>3 mm) and increased wall signal intensity. Bile is often more hypointense on T1 weighted images due to impairment of gallbladder bile concentrating capability, typical of the acute inflammatory state. Post-contrast imaging with fat suppression demonstrates increased enhancement of the gallbladder wall, the adjacent fat and the liver in the gallbladder fossa [20]. As in computed ­tomography, transient enhancement of pericholecystic hepatic parenchyma on dynamic images is a highly specific sign found in 70% of patients with acute cholecystitis [4, 5, 21]. Functional MRI using gadolinium contrast agents that have some biliary excretion have been used to problem solve patients with difficult diagnostic settings. Agents such as Primovist are excreted into the biliary tree. Non-filling of the gallbladder indicates either obstruction of the cystic duct or dysfunction of the gallbladder, often found in acute cholecystitis. Excellent correlation with HIDA scans, functional MRI and

b

pericholecystic fluid and stranding of the adjacent abdominal fat indicating oedema/inflammation. Note the lack of gallstones

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surgical findings has been found, with up to 100% positive predictive values for diagnosis of acute cholecystitis by functional MRI cholangiography [20, 22].

Sludge Biliary sludge is a mixture of sediments that have formed from concentrated bile, usually due to stasis of the gallbladder (Chap. 9). These sediments are made up of cholesterol crystals, calcium bilirubinate pigments and other calcium salts as well as mucous secreted by the gallbladder. Sludge has a wide variety of underlying causes, including pregnancy and rapid weight loss, particularly in the obese. It is also seen in patients with prolonged periods of nil by mouth often in the setting of significant and prolonged illness in ICU, as well as in patients receiving total parenteral nutrition (TPN). It is also associated with gallstones, certain drugs such as ceftriaxone and octreotide and bone marrow or solid organ transplantation [23]. Sludge is usually identified on ultrasound as an echogenic layering of material in the dependent part of the gallbladder (Figs. 2.11 and 8.2b). It is non-shadowing and usually mobile with changes in patient position. If the sludge is very

Fig. 2.11  Ultrasound with sludge lying in the dependent part of the gallbladder. Note the echoic echogenic sludge does not cast an acoustic shadow (green arrow)

thick, it may form lobulated structures that may be adherent to the wall of the gallbladder, so called tumefactive sludge (Fig. 2.12). When this is extensive, it can mimic a gallbladder tumour, although it will not demonstrate any vascular flow. Sludge often co-exists with gallstones. On CT, sludge may be visible as a mildly hyperdense dependent layer in the gallbladder, although it may be difficult to differentiate this from multiple small gallstones. On MRI, sludge presents as a dependent layer of T1 hyperintense and T2 iso to mildly hyperintense material. Concentrated bile can also layer out in the gallbladder prior to becoming sludge, with similar imaging characteristics [20]. If the underlying cause of the sludge is removed, the sludge usually disappears rapidly. Sludge will often recur even if there is interval resolution. In a small percentage of patients, the sludge persists or may amalgamate to become true gallstones [24]. Complications secondary to biliary sludge include biliary colic, acute cholangitis and acute pancreatitis from impaction of sludge material at the ampulla of Vater [23].

Adenomyomatosis Also called adenomyosis or adenomatous hyperplasia of the gallbladder, this is a common benign condition, seen in at least 9% of cholecystectomy specimens. It has no intrinsic malignant potential and frequently is associated with cholelithiasis [25]. The wall thickening of adenomyomatosis involves hyperplasia of the mucosa and muscularis propria. There is deposition of cholesterol crystals in Rokitanski-Aschoff sinuses which become dilated (Chap. 9, Fig. 9.1). Ultrasound is the investigation of choice. There is thickening of the gallbladder wall. This is most often focal, often visualised in the fundus (Figs. 1.7, 2.13 and 9.2). In this location it can appear mass-like or polypoid, when it is termed an adenomyoma. The segmental form of ­adenomyomatosis more often affects the body and when there is circumferential thickening it

2  Biliary Imaging for Gallstone Disease

31

Fig. 2.12 Ultrasound with lobulated sludge is demonstrated in the dependent aspect of the gallbladder. Buried at the bottom of the sludge are three gallstones causing acoustic shadowing. There is no cholecystitis

Fig. 2.13 Ultrasound of focal adenomyomatosis in the body of the gallbladder

gives rise to an hourglass appearance. Sludge and gallstones may also be seen. More diffuse adenomyomatosis can also be diagnosed. The more specific features of adenomyomatosis are intramural diverticula (Fig. 2.13) appear-

ing as cystic spaces, anaechoic on ultrasound. They may contain cholesterol crystals that demonstrate ring-­down or comet-tail artefact on noncompound/harmonic ultrasound due to the multiple acoustic interfaces resonating at the

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32 Fig. 2.14 Ultrasound of gallbladder adenomyomatosis. The arrow marks the comet-tail artefact produced by resonance of cholesterol crystals with the ultrasound waves in a diverticulum in the wall of the gallbladder

ultrasound frequency (Fig. 2.14). These findings are virtually specific to adenomyomatosis, particularly when they are visualised in the nondependent wall. On CT, the wall thickening is readily visible and larger diverticulae can be seen (Fig. 2.15). This can help differentiate between adenomyomatosis and cancer, particularly for the focal form in the fundus. On MR imaging, the Rokitansky-Aschoff sinuses form a ‘pearl necklace’ of multiple T1 hypointense/T2 hyperintense spaces within the thickened wall, reported to have 92% specificity for adenomyomatosis [26]. Note should be made that there have been reports of increased uptake of fluorine-18 flurodeoyglucose (FDG) within areas of adenomyomatosis at PET that can be a cause of difficulty when assessing gallbladder lesions for neoplasia [27].

a

b

Polyps Gallbladder polyps (Chap. 9) are quite common with a reported prevalence of 3–7% on abdominal ultrasound and in 2–12% of cholecystectomy specimens [28–31].

Fig. 2.15  CT (a) axial (b) coronal of gallbladder adenomyomatosis. There is thickening of the gallbladder wall with wasting of the body due to some contraction caused by the inflammatory process. The mucosa is fairly evenly enhancing, with lower density in the rest of the wall

2  Biliary Imaging for Gallstone Disease

By far most of gallbladder polyps are benign. However, it is important to recognise gallbladder cancer when it is in its early stages and potentially curative with resection. Most polyps are identified at ultrasound (Figs.  2.16 and 9.4) but are being identified on CT and MRI with increasing frequency. When using ultrasound, lesions should be imaged in more than one position to help rule out mobile lesions such as non-calcified gallstones or sludge balls. Polyps can be placed into three different groups; pseudotumours, benign tumours or malignant tumours.

Pseudotumours Cholesterol polyps, adenomyomatosis and inflammatory polyps make up the vast majority of polypoid pseudotumours, in decreasing order of frequency. Cholesterol polyps and adenomyomatosis are hyperplastic non-inflammatory conditions that differ in their histology. Adenomyomatosis is thickening of both the mucosa and muscularis propria, with accumulation of cholesterol crystals in dilated Rokitanski-Aschoff sinuses lined with mucosa. In contrast, cholesterol polyps demonstrate accumu-

Fig. 2.16 Ultrasound of a cholesterol polyp. A non-enhancing, non-vascular lesion on the non-dependent wall of an otherwise normal appearing gallbladder. It exhibits the classic ball-on-the-wall appearance

33

lation of triglycerides and cholesterol esters in the lamina propria within macrophages, covered by normal mucosa.

Cholesterol Polyps Cholesterol polyps are the most frequent pseudopolyp of the gallbladder, accounting for up to 60–70% of lesions in some studies [25, 29]. They occur typically in middle aged women and are multiple. They are not necessarily associated with gallstones [32]. There is no malignant potential. On ultrasound, cholesterol polyps appear as small, round, smoothly contoured intraluminal lesions that are attached to the wall. There is rarely a stalk, giving the classic “ball-on-the-­ wall” sign [33] (Figs. 2.16 and 9.4). They are usually echogenic and demonstrate no acoustic shadowing. If there are confluent polyps or polyps larger than 1 cm, they cannot be accurately differentiated from other benign or malignant lesions at imaging [34]. CT is poor at visualising cholesterol polyps due to the minor differential density with surrounding bile, particularly when they are less than 10 mm in diameter. MRI is also little used, due to lack of spatial resolution and contrast.

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Adenomyomatosis Adenomyomatosis accounts for approximately 25% of all polypoid lesions in the gallbladder [25, 35]. Please refer to the section on adenomyomatosis earlier in the chapter. Inflammatory Polyps This group represent approximately 10% of all gallbladder polyps in surgical specimens. They are usually small and multiple, mostly less than 10 mm diameter [25]. They are usually seen in the context of gallstones and chronic inflammation. It is speculated that they originate from depositions of cholesterol in the gallbladder wall that induces an inflammatory response with granulation and fibrous tissue. It may lead to epithelial dysplasia [36]. There is no definite evidence for progression to gallbladder cancer. Imaging features are poorly defined in the literature. Case reports describe a wide range of features such as iso and hypoechogenicity as well as hyperechogenicity. This is described both within and surrounding the lesion [37–39]. It is evident that the appearance of inflammatory polyps is non-specific on imaging and diagnosis of inflammatory polyps cannot usually be made.

Tumorous Polyps The most important of these lesions to consider are adenoma and adenocarcinoma. Other lesions such as leiomyomas, lipomas, neurofibromas and neuroendocrine tumours account for 1% of gallbladder polyps [25]. Rarely, metastases and lymphoma may manifest as polypoid gallbladder lesions. Adenomas Gallbladder polyps are quite rare, present in only 0.15% of cholecystectomy specimens, accounting for 4–7% of all gallbladder polyps [25, 40]. Adenomas are typically found incidentally. They are more frequently found in patients with primary sclerosing cholangitis (PSC) and gastrointestinal polyposis syndromes such as Peutz-­ Jegher and Gardner syndromes. On ultrasound adenomas vary in size up to 20 mm, can be sessile or pedunculated, demonstrate internal vascularity at colour Doppler and are usually solitary.

CT and MRI imaging characteristics are similar to that of adenocarcinoma and thus adenomas cannot be reliably differentiated from gallbladder malignancy at imaging [34]. Gallbladder Carcinoma The most common of the gallbladder primary malignancies is adenocarcinoma. It is the fifth most common gastrointestinal malignancyv and the most common malignancy of the biliary tract, accounting for 80–95% of biliary tract cancers, with higher rates in South American Indians and in North India. Its incidence rapidly increases with increasing age, particularly over 65 years of age [41]. Gallbladder carcinoma usually presents as a mass replacing the gallbladder in 40–65% of cases or focal or diffuse gallbladder wall thickening in 20–30%. However, in 15–25% it presents as an intraluminal polyp [42]. On ultrasound, adenocarcinoma should be suspected if the polyp is larger than 1 cm, it has a wide base, there is focal wall thickening of >3 mm and there are co-existing gallstones [43] (Chap. 9). On vascular ultrasound, colour within or at the base of the polyp and an increased resistive index may indicate malignancy [44]. Endoscopic ultrasound or specific use of high frequency transabdominal transducers supplementing the standard transducer during an abdominal ultrasound study may provide more information due to increased resolution. The American Joint Committee on Cancer (AJCC) provided a T categorisation standard for gallbladder cancer staging using ultrasound (Table 2.2) [45, 46]. Table 2.2  T staging for gallbladder staging using ultrasound (AJCC) T1a

T1b

T2

T3

When the tumour invades the lamina propria. This presents as a polypoid or focal wall thickening with preserved inner hypoechoic layers Tumour invades the muscular layer. These lesions tends to be polypoid or focal wall thickening that causes irregularity in the inner hypoechoic layer of the gallbladder wall Invasion of the perimuscular connective tissue. This is a polypoid or focal wall thickening that causes irregularity of the outer hyperechoic layer of the gallbladder wall Perforation of the serosa. There is disruption of the entire layer structure of the gallbladder wall or extension to the liver

2  Biliary Imaging for Gallstone Disease

35

CT (Fig. 2.17) and MRI can provide similar diagnostic information such as shape, size, number and location of lesions. Early prolonged irregular enhancement without washout is more common in malignant lesions than in benign ones [47]. Diffusion Weighted Imaging (DWI) has been reported to be useful, with increased signal on the DWI images and reduced signal on the corresponding ADC images. However, a significant proportion of inflammatory wall thickening can also demonstrate similar findings, indicating DWI/ADC findings need to be used in conjunction with other imaging features to be useful [48]. Axial imaging also provides further anatomic detail when there is suspicion of T4 or nodal spread, with better clarity in assessing involvement of adjacent structures such as the liver, colon, duodenum, vessels, ducts and

a

regional lymph nodes and the presence of fistula formation. Use of PET imaging (Fig. 2.18) is more of a problem solving tool. Increased FDG uptake in the lesion greater than background liver is suspicious for malignancy, although it is limited by false positives in the presence of inflammation such as acute cholecystitis [49].

Complicated Cholecystitis It is important to accurately characterise acute cholecystitis to allow the planning of best management, whether that is non-operative medical management, cholecystostomy, laparoscopic cholecystectomy or open cholecystectomy. Clinical features such as delayed presentation,

b

Fig. 2.17  CT of a gallbladder carcinoma with invasion into the adjacent liver. The gallbladder lies in the posterior aspect of the mass, containing a calcified gallstone. There has been invasion into the porta hepatis as well

Fig. 2.18  PET of a gallbladder carcinoma. There is avid uptake of the isotope into the tumour. Note is made of multiple hotspots in the liver parenchyma consistent with metastases

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deteriorating patient, diabetes, immunosuppression, signs of sepsis or acute abdomen should prompt a search for complications of acute cholecystitis, as it will often significantly alter the management plan. The following subtypes of complicated cholecystitis may co-exist, but are described separately as they each have their own particular imaging findings.

Emphysematous Cholecystitis Please refer to the section under acalculous cholecystitis.

Gangrenous Cholecystitis Gangrenous cholecystitis is a relatively common complication of cholecystitis, presenting in around 26–39% of cases of acute calculous cholecystitis [50, 51]. It has a higher morbidity and mortality rate than uncomplicated calculous cholecystitis. Gangrenous cholecystitis should be considered in patients with diabetes mellitus, a white cell count >15,000 cells/mL and the elderly. Ultrasonographic hallmark findings of gangrenous cholecystitis are heterogeneous or striated thickening of the gallbladder wall, often irregular with projections into the lumen, as well as pericholecystic fluid collections [52, 53]. Intraluminal membranes indicating desquamative gallbladder mucosa is a specific but less common finding. Care should be taken in diagnosing these patients because in one study, up to 28% had a negative sonographic Murphy’s sign and a wall thickness of less than 3 mm [54], while another study found only 33% of patients had a positive Murphy’s sign [55]. This is postulated to be due to denervation of the gallbladder wall due to the disease process. Although CT is highly specific for the diagnosis of acute gangrenous cholecystitis, it is insensitive. As it not uncommonly co-exists with emphysematous cholecystitis, there may be intramural or intraluminal gas. As with ultra-

sound, intraluminal membranes, an irregular or absent gallbladder wall, lack of gallbladder wall enhancement and co-existent pericholecystic abscess formation are other findings. Less specific findings including pericholecystic fluid, striation of the gallbladder wall and transient enhancement of the adjacent hepatic parenchyma can also be seen in uncomplicated severe cholecystitis. The more distended the gallbladder in the short axis, the more likely gangrenous cholecystitis becomes in the presence of the above findings [56]. Multisequence MRI can demonstrate features of gangrenous cholecystitis, such as ulceration/erosion, haemorrhage, necrosis or micro-­ abscesses in the gallbladder wall. Thickening of the gallbladder wall can be seen on fat suppressed T1-weighted or T2-weighted images and contrast-­enhanced T1 weighted fat suppressed images. Ulceration can be seen as T2 hyperintense divots in the wall. Haemorrhage in the wall, wall necrosis and abscesses will often appear as mixed signal areas on fat suppressed T2 weighted imaging. A lack of mucosal enhancement of part of the wall when accompanied by mixed enhancement elsewhere is a characteristic finding. A pericholecystic fluid collection may also be demonstrated [57].

Haemorrhagic Cholecystitis This is a rare complication of acute calculous or acalculous cholecystitis. It can also be caused by trauma, anticoagulation, malignancy or iatrogenic causes [58, 59]. Haemorrhage may be from inflamed mucosa that infarcts and erodes. Clot may obstruct the cystic duct and cause acute acalculous cholecystitis symptoms. Haemobilia may manifest as haematemesis or melena. If there is perforation there can be haemoperitoneum [60]. Perforation in this circumstance is a life threatening event that requires urgent cholecystectomy. Findings on CT include hyperdense bile that may have a fluid-fluid level or graduated haematocrit effect as well as findings typical of acute cholecystitis. If there is significant active bleed-

2  Biliary Imaging for Gallstone Disease

ing, extravasation of contrast may be seen on arterial phase, [60] with accumulation of contrast on the portal venous phase. It needs to be differentiated from other causes of hyperdense bile such as vicarious excretion of contrast via the biliary tree from previous intravenous contrast, biliary sludge, layering gallstones and milk of calcium bile. MRI is not usually used in the acute setting. It can be used for trouble-shooting unclear clinical presentations. On multisequence imaging, ­haemorrhage in the wall and lumen of the gallbladder is seen as high signal intensity on T1 weighted images due to methaemogloblin. Blood clots and haemorrhage may appear as low signal lesions or defects on T2 weighted images. This can result in lack of visualisation of the gallbladder or bile ducts. There may be a graduated change in signal intensity in the gallbladder due to the haematocrit effect, with reducing signal into the dependent areas on T2 weighted imaging [61].

Perforation This complication is usually associated with gangrenous cholecystitis, with a mortality rate of up to 15% [62]. Perforation can also occur in emphysematous and haemorrhagic cholecystitis. The high rate of mortality is usually due to delay in diagnosis and the consequent late surgical intervention.

Fig. 2.19  Ultrasound of a gangrenous gallbladder with perforation. The wall of the gallbladder remains thin, but there is significant pericholecystic fluid and a perforation at the apex of the fundus with a local collection. This is the commonest location for perforation

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Gallbladder perforation is commoner in men, occurring at an average age of 60 years [63]. Three types of gallbladder perforation are described: type I (or acute) is free perforation and generalised peritonitis; type II (subacute) is pericholecystic abscess formation and localised peritonitis; and type III (chronic) is formation of a cholecystoenteric fistula [64]. Type II is the most common. Because of its poor blood supply, the fundus of the gallbladder (Figs. 2.19 and 6.8b) is the most common site of perforation. Acute perforation can also result from trauma. Impending perforation may be demonstrated as a focal bulge in the gallbladder wall best seen on CT, but can also be identified on ultrasound or MRI. An extraluminal gallstone is specific for gallbladder perforation. On ultrasound there may be a ‘hole sign’ indicating the defect in the gallbladder wall. This can also be identified on CT and MRI as a defect in the gallbladder wall in a region with heterogenous density or signal. The region of the defect does not show any enhancement. In the type II perforation, the pericholecystic abscess communicates with the gallbladder lumen. Other findings include loculated ascites, particularly around the liver and oedematous thickened omentum.

38

In the setting of trauma, there will often be fluid exhibiting increased density on CT and variable signal on MRI depending on the volume and age of the blood within the gallbladder, gallbladder fossa, around the liver or in the dependent areas of the peritoneum. Complications of perforation include free intraperitoneal air, bile leak, formation of regional abscess in adjacent fat or within the liver and bowel obstruction [65].

Hepatic Abscess Hepatic abscesses associated with acute cholecystitis are usually as a result of direct extension through the gallbladder fossa of a pericholecystic abscess into the adjacent liver parenchyma (Fig. 2.20). The liver abscess may be walled off or directly communicating with the pericholecystic abscess and gallbladder lumen. If there is a liver abscess elsewhere in the liver, it can be due to ascending cholangitis from bili-

Fig. 2.20  CT of an hepatic abscess in the liver adjacent to the gallbladder

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ary tree obstruction associated with the acute cholecystitis (often due to stones within the bile duct), subcapsular extension or as a result of haematogenous spread via the portal vein [66]. On ultrasound a hepatic abscess has a hypoechoic appearance with mixed echogenicity at its margin and peripheral increased vasculature. CT demonstrates a hypodense collection, with either a single enhancing rim (single target sign) or an inner enhancing rim with an outer hypoattenuating zone indicating adjacent liver oedema (double target sign) [67, 68]. There may be segmental enhancement around the liver abscess, due to reduced portal venous flow due to inflammation and vessel stenosis, with consequent increase in hepatic arterial flow [67]. If the hepatic abscess is large enough and mature enough, percutaneous drainage with placement of a catheter under imaging guidance can be performed on abscesses down to 4–5 cm in size. Smaller abscesses can be aspirated under imaging guidance.

2  Biliary Imaging for Gallstone Disease

Chronic Cholecystitis Chronic cholecystitis represents prolonged inflammation of the gallbladder and is the most frequent presentation of symptomatic gallbladder disease. It is almost always associated with gallstones. The patient will often have vague signs and symptoms including epigastric discomfort, abdominal distention or nausea [5]. There may be a history of recurrent cholecystitis or biliary colic. Some patients are asymptomatic [69]. The gallbladder can be distended with a thickened wall, due to dysmotility from the inflammation. In more long-term chronic cholecystitis, the g­ allbladder is often contracted and small secondary to fibrotic change in the wall from the chronic inflammation. The walls are thickened and may be irregular (Fig. 2.21). Pericholecystic inflammation is usually absent [70, 71]. There is a possible connection between chronic cholecystitis and infection with Helicobacter pylori [72]. The appearance on ultrasound demonstrates a thickened gallbladder wall (>3–5 mm), almost always with cholelithiasis present. Pericholecystic fluid is usually absent. If the gallbladder is contracted, there will be a wall-echoshadow complex. CT will also show the cholelithiasis and thickened wall, with a lack of adjacent fat stranding. On MRI, enhancement of the gallbladder wall is usually smooth, slow and prolonged, unlike gallbladder carcinoma where

Fig. 2.21  Ultrasound of chronic cholecystitis. The wall is markedly thickened and the gallbladder contracted. There is a focal defect in the wall of gallbladder (green

39

enhancement is irregular, early and prolonged [73, 74]. Nuclear medicine can be useful in evaluating gallbladder function with cholescintigraphy (HIDA scan) (Fig. 10.1). If there are features such as delayed accumulation or non-accumulation of isotope in the gallbladder, irregular gallbladder filling, photopenic areas and septations, then chronic cholecystitis should be considered. A gallbladder ejection fraction of 3–5 mm), pericholecystic fluid in the absence of ascites and sludge.

2  Biliary Imaging for Gallstone Disease

41

CT is not uncommonly the primary investigation when the patient first presents, as the clinical picture may be non-specific. The main criteria are gallbladder wall thickening greater than 3 mm, subserosal halo (gallbladder wall oedema), pericholecystic fatty stranding, pericholecystic fluid in the absence of ascites or hypoalbuminaemia, mucosal sloughing and intramural gas. Minor criteria include gallbladder distension >5 cm in transverse, increased enhancement of the adjacent liver and high attenuation sludge [85]. Features to look for that indicates complicated acalculous cholecystitis are intraluminal haemorrhage (haemorrhagic cholecystitis), localised pericholecystic collections (perforation), gas within the lumen or wall (emphysematous cholecystitis) and regions of non-enhancing gallbladder wall (gangrenous cholecystitis). MRI is not commonly performed on patients with acalculous cholecystitis due to the often critical nature of the patients. When MRI is performed, findings are similar to ultrasound and CT, such as gallbladder distension, gallbladder wall thickening and adjacent inflammation in the absence of gallstones [57]. If there is uncertainty regarding the diagnosis, nuclear medicine cholescintigraphy can be per-

a

formed. The study has been largely relegated however, due to the difficulty in performing the procedure on the critically ill patient. If there is good excretion but non-filling of the gallbladder by 1h in the absence of gallstones, acalculous cholecystitis can be diagnosed. To increase the accuracy of the study, morphine can be given to increase biliary pressures. If there is no filling of the gallbladder 30 min after injection of morphine, it is considered a positive study for acalculous cholecystitis. If there is early filling (