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- •Contents
- •Contributors
- •Series Editors' preface
- •Editors' preface
- •Acknowledgements
- •Chronic liver failure
- •Metabolic liver function
- •Measuring liver volume
- •Blood tests of liver function
- •Tests of liver function measuring substance clearance
- •Indocyanine green (ICG)
- •Hepatobiliary scintigraphy
- •Lidocaine (MEG-X)
- •Aminopyrine breath test
- •Urea synthesis
- •Glutathione synthesis
- •Measuring liver blood flow
- •Effect of major liver resection on hepatic blood flow
- •Effect of major liver resection on innate immunity
- •Liver regeneration
- •Molecular signals for hepatic regeneration
- •Cell populations involved in liver regeneration
- •Evidence-based practice in surgery
- •Overview of liver functions and evolution
- •Symptoms of liver failure: acute and chronic
- •Common causes of acute liver failure: hepatic insufficiency following liver resections
- •Consequences of surgery
- •Small-for-size syndrome
- •Hepatic steatosis
- •Assessment of steatosis
- •Chemotherapy-induced liver changes
- •Portal vein embolisation
- •Technique
- •Therapy for liver failure
- •N -Acetyl cysteine
- •Nutritional support in liver failure
- •Artificial extracorporeal liver support
- •Artificial liver support
- •Bioartificial liver systems
- •Liver transplantation
- •Cell therapy for liver failure: general principles
- •Haemopoetic stem cell therapy for liver disease in humans
- •Future developments
- •References
- •Liver
- •Overview of hepatic anatomy and terminology
- •Divisions of the liver based on the hepatic artery
- •Resectional terminology
- •Surgical anatomy for liver resections
- •Hepatic arteries and liver resections
- •Bile ducts and liver resections
- •Prevailing pattern and important variations of bile ducts draining the right hemiliver
- •Prevailing pattern and important variations of bile ducts draining the left hemiliver
- •Prevailing pattern of bile ducts draining the caudate lobe (Sg1)
- •Portal veins and liver resections
- •Ramification of the left portal vein (Figs 2.10 and 2.11)
- •Hepatic veins and liver resection (Fig. 2.13)
- •The plate/sheath system of the liver
- •Liver capsule and attachments
- •Surface anatomy
- •Gallbladder and extrahepatic bile ducts
- •Gallbladder
- •Agenesis of the gallbladder
- •Double gallbladder
- •Cystic duct
- •Cystic artery
- •Extrahepatic bile ducts
- •Anomalies of extrahepatic bile ducts
- •Extrahepatic arteries
- •Blood supply of bile ducts
- •Pancreas
- •Pancreatic ducts
- •Blood supply of the pancreas
- •Lymphatics of the pancreas
- •References
- •Introduction
- •Colorectal liver metastases
- •Transabdominal ultrasound
- •Computed tomography and magnetic resonance imaging
- •Positron emission tomography
- •Diagnostic laparoscopy and laparoscopic ultrasound
- •Staging and assesment of resectability
- •Hepatocellular carcinoma
- •Transabdominal ultrasound
- •Computed tomography and magnetic resonance imaging
- •Diagnostic laparoscopy and laparoscopic ultrasound
- •Staging and assesment of resectability
- •Pancreatic and periampullary carcinoma
- •Transabdominal ultrasound
- •Computed tomography and magnetic resonance imaging
- •Endoscopic retrograde cholangiopancreatography (ERCP)
- •Endoscopic ultrasound
- •Positron emission tomography
- •Diagnostic laparoscopy and laparoscopic ultrasound
- •Staging and assesment of resectability
- •Positron emission tomography
- •Diagnostic laparoscopy and laparoscopic ultrasound
- •Staging and assesment of resectability
- •References
- •Introduction
- •Proximal bile duct tumours
- •Transabdominal ultrasound
- •Computed tomography and magnetic resonance imaging
- •Endoscopic retrograde cholangiopancreatography
- •Classification
- •Haemangiomas
- •Pathology
- •Clinical presentation
- •Management
- •Liver cell adenoma
- •Pathology
- •Clinical presentation
- •Management
- •Focal nodular hyperplasia
- •Pathology
- •Clinical features
- •Management
- •Nodular regenerative hyperplasia (macroregenerative nodules)
- •Bile duct adenoma (bile duct hamartoma)
- •Hepatic pseudotumours
- •Miscellaneous benign tumours
- •Liver abscess
- •Clinical presentation
- •Management
- •Amoebic abscess
- •Hydatid cyst
- •Clinical presentation
- •Management
- •Simple cysts of the liver
- •Clinical presentation
- •Management
- •Polycystic liver disease (PCLD)
- •Clinical presentation
- •Management
- •Cystadenoma
- •References
- •Introduction
- •Hepatocellular carcinoma
- •Incidence of HCC
- •Risk factors for HCC
- •Cirrhosis
- •HBV infection
- •HCV infection
- •Human immunodeficiency virus (HIV) infection
- •Other viral infections
- •Alcohol
- •Non-alcoholic fatty liver disease (NAFLD)
- •Hereditary haemochromatosis
- •Cirrhosis of other aetiologies
- •Aflatoxin
- •Metabolic liver diseases
- •Adenoma, contraceptives and androgens
- •Pathology of HCC and nodular lesions in chronic liver disease
- •Clinical presentation
- •Liver function tests and tumour markers
- •Liver function tests
- •Serum tumour markers
- •α-Fetoprotein
- •Others serum tumour markers
- •Radiological studies
- •Ultrasound
- •Computed tomography
- •Magnetic resonance imaging
- •Contrast-enhanced ultrasound
- •Other imaging
- •Angiography
- •Positron emission tomography
- •Accuracy of imaging techniques
- •Requirement for and reliability of histological assessment
- •Diagnosis of HCC
- •Natural history of HCC and staging systems
- •Screening for HCC
- •Treatment options
- •HCC in normal livers
- •Liver resection of HCC in cirrhotic patients
- •Liver resection
- •Main limitations
- •Risk of surgery and patient selection
- •Technique
- •Outcome after resection
- •Treatment of recurrence
- •Liver transplantation (LT)
- •Rationale
- •Patient selection
- •Treatment on the waiting list
- •Transarterial chemoembolisation (TACE)
- •Technique
- •Contraindications
- •Morbidity and mortality
- •Monitoring
- •Efficacy
- •Percutaneous local ablative therapy
- •Technique
- •Advantages and drawbacks
- •Contraindications and limitations
- •Methods and margins
- •Indication
- •Other palliative treatments
- •Conventional systemic chemotherapy
- •Anti-angiogenic targeted therapies
- •Radioembolisation
- •Other treatments
- •Defining a treatment strategy
- •Uncomplicated HCC associated with chronic liver disease
- •Treatment of complicated HCC
- •HCC with macroscopic portal vein invasion
- •HCC with macroscopic invasion of hepatic veins
- •Ruptured HCC
- •Fibrolamellar carcinoma (FLC)
- •Intrahepatic cholangiocarcinoma (ICCA)
- •Incidence
- •Risk factors
- •Classification and staging
- •Pathology and progression analysis
- •Clinical presentation and laboratory tests
- •Imaging studies
- •Diagnosis
- •Treatment
- •Angiosarcoma
- •Primary hepatic lymphoma
- •References
- •Introduction
- •Preoperative staging: the key to selection of candidates for curative treatment
- •Computed tomography (CT)
- •Magnetic resonance imaging (MRI)
- •Positron emission tomography (PET)
- •Staging laparoscopy
- •Cardiopulmonary exercise testing
- •Surgery: the old and the new standards for resection
- •Criteria for resection
- •Surgical strategies to improve resectability
- •Portal vein embolisation
- •Two-stage hepatectomy
- •Repeat hepatectomy
- •Extreme liver surgery
- •Extrahepatic colorectal disease
- •Techniques of surgical resection
- •Transection techniques
- •Fibrin sealants
- •Laparoscopic liver surgery: less is more?
- •Morbidity, mortality and survival after liver resection for CRLMs
- •Classification of CRLMs
- •Staging systems and terminology
- •Chemotherapy for CRLMs
- •Agents
- •Clarifying the intent of chemotherapy in CRLMs
- •Conversion/induction chemotherapy
- •Perioperative chemotherapy
- •Pathological response to chemotherapy as a predictor of long-term outcome
- •Chemotherapy-associated hepatotoxicity
- •Liver-targeted therapies
- •Hepatic arterial infusion
- •Drug-eluting beads for TACE (DEB-TACE)
- •Selective internal radiation treatment (SIRT)
- •Ablative therapies for CRLMs
- •Radiofrequency ablation
- •Microwave ablation
- •Multidisciplinary team approach
- •Conclusions
- •References
- •Introduction
- •Pathophysiology and molecular basis of liver metastases
- •Treatment strategies
- •Neuroendocrine tumours
- •Gastrointestinal stromal tumours
- •Breast cancer
- •Ovarian cancer
- •Renal cell carcinoma
- •Melanoma
- •Non-colorectal gastrointestinal adenocarcinoma
- •Testicular cancer
- •Urothelial cancer
- •Lung cancer
- •Adrenocortical tumours
- •Endometrial cancer
- •Conclusion
- •References
- •Introduction
- •Aetiology and pathophysiology of portal hypertension
- •The natural history of portal hypertension
- •Presentation
- •Imaging
- •Management of varices
- •Therapeutic aims for pharmacological therapy in portal hypertension
- •Oesophageal varices
- •Primary prophylaxis for the prevention of variceal haemorrhage
- •Prevention of re-bleeding from oesophageal varices (secondary prophylaxis)
- •Treatment for bleeding oesophageal varices
- •Gastric varices
- •Portal hypertensive gastropathy
- •Second-line therapies
- •TIPS (transjugular intrahepatic portosystemic shunt)
- •TIPS for variceal bleeding
- •Surgical options
- •Portal systemic shunts
- •Liver transplantation
- •Selection of second-line therapy
- •Non-cirrhotic
- •Cirrhotic
- •Management of ascites
- •Budd–Chiari syndrome
- •Acute Budd–Chiari syndrome
- •Chronic Budd–Chiari syndrome
- •Non-cirrhotic portal hypertension
- •Portal vein thrombosis
- •Segmental portal hypertension
- •TIPS and portal vein thrombosis
- •References
- •Introduction
- •Postsplenectomy sepsis
- •Trauma
- •Elective indications for splenectomy
- •Immune thrombocytopenic purpura
- •Evans syndrome
- •Hereditary spherocytosis
- •Elliptocytosis
- •Thallassaemias
- •Sickle cell anaemia
- •Autoimmune haemolytic anaemia
- •Lymphoma
- •Myeloid disease
- •Volvulus
- •Haemangiomas
- •Cysts
- •Portal hypertension
- •Preparation for splenectomy
- •Technique
- •Open splenectomy
- •Laparoscopic splenectomy
- •Postoperative management and complications
- •Summary
- •References
- •Introduction
- •Composition, formation and risk factors
- •Presentation
- •Cholecystolithiasis
- •Pathophysiology
- •Clinical features
- •Choledocholithiasis
- •Pathophysiology
- •Clinical features
- •Investigation
- •Blood tests
- •Ultrasonography
- •Endoscopic ultrasound (EUS)
- •Computed tomography (CT)
- •Radioisotope scanning
- •Magnetic resonance cholangiopancreatography (MRCP)
- •Percutaneous transhepatic cholangiography (PTC)
- •Endoscopic retrograde cholangiopancreatography (ERCP)
- •Management of gallbladder stones
- •Asymptomatic stones
- •Non-operative treatments for gallstones
- •Dissolution
- •Lithotripsy
- •Operative treatment of gallbladder stones
- •Open cholecystectomy
- •Mini-laparotomy cholecystectomy
- •Laparoscopic cholecystectomy
- •Symptomatic gallstones
- •Acute cholecystitis
- •Complications
- •Day-case laparoscopic cholecystectomy
- •Needlescopic cholecystectomy
- •Bile duct injury
- •Cholecystostomy
- •Subtotal cholecystectomy
- •Intraoperative cholangiography (IOC)
- •Routine IOC
- •Selective IOC
- •Bile duct injury
- •Laparoscopic ultrasound (LUS)
- •Management of common bile duct stones
- •Laparoscopic transcystic common bile duct exploration
- •Laparoscopic choledochotomy
- •Open choledochotomy
- •Endoscopic retrograde cholangiopancreatography (ERCP)
- •ERCP stent insertion
- •Preoperative ERCP
- •Intraoperative ERCP
- •Postoperative ERCP
- •Laparoscopic exploration of the CBD versus preoperative or postoperative ERCP
- •Recurrent or retained CBD stones
- •Transhepatic stone retrieval
- •Acalculous biliary pain
- •References
- •Introduction
- •Congenital anomalies
- •Biliary atresia
- •Choledochal cysts
- •Classification
- •Risk of malignancy
- •Management
- •Special operative techniques
- •Iatrogenic biliary injury
- •Aetiology
- •Techniques to avoid injury
- •Classification
- •Presentation
- •Management
- •Intraoperative recognition
- •Postoperative recognition: biliary fistula
- •Postoperative recognition: biliary obstruction
- •The timing of repair
- •Early repair
- •Delayed repair
- •Associated vascular injury
- •Further imaging
- •Operative techniques
- •Management of complications related to repair
- •Revisional surgery
- •Liver resection and transplantation
- •Prognosis
- •Success of repair
- •Survival
- •Quality of life
- •Associated malignancy
- •Benign biliary strictures
- •Mirizzi's syndrome
- •Presentation
- •Management
- •Hepatolithiasis
- •Management
- •Parasitic infestation causing jaundice
- •Liver flukes (trematodes)
- •Echinococcus
- •Treatment
- •Ascaris lumbricoides
- •Primary sclerosing cholangitis
- •Aetiology
- •Presentation
- •Investigation
- •Management
- •Exclusion of associated malignant stricture
- •Biliary strictures imitating malignancy
- •Lymphoplasmacytic sclerosing pancreatitis
- •Functional biliary disorders
- •References
- •Introduction
- •Cholangiocarcinoma
- •General considerations
- •Epidemiology
- •Natural history
- •Aetiology
- •Histopathology
- •Cholangiocarcinoma involving the proximal bile ducts (hilar cholangiocarcinoma)
- •Clinical presentation and diagnosis
- •Radiological investigation
- •Direct cholangiography
- •Computed tomography
- •Duplex ultrasonography
- •Magnetic resonance cholangiopancreatography (MRCP)
- •Preoperative evaluation and assessment of resectability
- •Treatment options
- •Resection
- •Results of resection
- •Adjuvant therapy
- •Palliation
- •Percutaneous biliary drainage
- •Intrahepatic biliary-enteric bypass
- •Radiation therapy
- •Photodynamic therapy
- •Chemotherapy
- •Cholangiocarcinoma involving the distal bile duct
- •Clinical presentation and diagnosis
- •Staging and assessment of resectability
- •Treatment options
- •Cholangiocarcinoma involving the intrahepatic bile ducts
- •Clinical presentation
- •Diagnosis
- •Radiological investigations
- •Staging and assessment of resectability
- •Treatment options
- •Gallbladder cancer
- •Epidemiology/aetiology
- •Clinical presentation and diagnosis
- •Histopathology and staging
- •Evidence for an aggressive surgical approach
- •Surgical therapy
- •T1 tumours
- •T2 tumours
- •T3 tumours
- •T4 tumours
- •Preoperative suspicion of malignancy
- •Unsuspected malignancy at exploration
- •Malignancy diagnosed post-cholecystectomy
- •Adjuvant therapy
- •Palliation
- •References
- •General description
- •Pathophysiology
- •Natural history
- •Diagnosis
- •Aetiology
- •Obstructive factors
- •Biliary disease
- •Benign pancreatic duct stricture
- •Tumours of the ampulla or pancreas
- •Toxic factors
- •Metabolic factors
- •Genetic defects
- •Trauma
- •Iatrogenic causes
- •Inflammatory
- •Physiological
- •Sphincter manometric abnormalities
- •Assessment of severity
- •Single biochemical measures
- •C-reactive protein (CRP)
- •Other single predictive markers
- •Intra-abdominal hypertension (IAH)
- •Repeated clinical assessment
- •Imaging
- •Role of ultrasound (US)
- •Role of CT
- •Role of magnetic resonance (MR)/magnetic resonance cholangiopancreatography (MRCP)
- •Endoscopic ultrasound (EUS)
- •Management
- •Initial management
- •Supportive management
- •Specific medical management
- •Prevention of infection
- •Nutritional support
- •Nutritional delivery in the patient with acute pancreatitis
- •Disease modulation through content or mode of delivery
- •Other medical therapies
- •Inhibition of pancreatic secretion
- •Inhibition of pancreatic enzymes
- •Inhibition of the inflammatory response
- •Role of ERCP
- •Definitive management issues
- •Prevention of recurrent acute pancreatitis
- •Management of gallstones
- •Investigation of non-gallstone-associated pancreatitis
- •Peripancreatic fluid collections
- •Management of an early fluid collection
- •Management of a pseudocyst
- •Percutaneous drainage
- •Endoscopic drainage
- •Surgical drainage of an acute post-inflammatory collection
- •Management of a pancreatic duct fistula
- •Management of necrosis
- •Management of sterile necrosis
- •Management of infected necrosis (early phase, 2–6 weeks)
- •Methods of necrosectomy
- •Open laparotomy/debridement
- •Minimally invasive approaches to infected necrosis
- •Management of pancreatic abscess
- •Specific late complications
- •Haemorrhage
- •Segmental portal hypertension and gastrointestinal haemorrhage
- •Pancreatic duct stricture
- •Gastric outlet obstruction
- •References
- •Summary
- •Definition
- •Incidence
- •Aetiology
- •Clinical course
- •Pathophysiological findings and pain mechanisms in chronic pancreatitis
- •Calcifying CP
- •Autoimmune pancreatitis
- •Hereditary CP
- •Pathogenesis of pain in chronic pancreatitis
- •Preoperative assessment and investigations
- •Laboratory evaluation
- •Imaging studies
- •Treatment
- •Conservative therapy
- •Endoscopic and interventional treatment
- •Endoscopy
- •Surgical therapy, timing and indications
- •Surgical techniques
- •Selection of the surgical intervention
- •Pancreatico-duodenectomy
- •Distal and total pancreatectomy
- •Partington–Rochelle procedure
- •Longitudinal pancreatico-jejunostomy and cyst drainage
- •Beger procedure
- •Frey procedure
- •Berne procedure
- •Hamburg procedure
- •V-shaped excision
- •Selection of the procedure
- •Salvage procedures
- •Complications of chronic pancreatitis
- •References
- •Introduction
- •Epidemiology
- •Risk factors (see Box 15.1)
- •Smoking
- •Diet and alcohol
- •Occupation
- •Past medical history
- •Hereditary pancreatic cancer
- •Precursor lesions
- •Presentation
- •Investigation
- •Serology
- •Markers
- •Diagnosis
- •Imaging studies
- •Cytology/histology
- •Advanced staging techniques
- •Laparoscopy
- •Pathology
- •Treatment
- •Resection
- •Pancreatico-duodenectomy
- •Extended lymph node and vascular dissection
- •Distal pancreatectomy
- •Laparoscopic pancreatectomy
- •Total pancreatectomy
- •Central pancreatectomy
- •Surgical palliation
- •Obstructive jaundice
- •Upper GI tract outflow obstruction
- •Adjuvant therapies
- •Neoadjuvant therapy
- •Future areas of interest
- •References
- •Introduction
- •Intraductal papillary mucinous neoplasms
- •Clinical presentation
- •Investigation
- •Pathology
- •Management
- •Outcome
- •Pancreatic neuroendocrine tumours
- •Clinical presentation
- •Investigations
- •Biochemical
- •Radiology
- •Treatment
- •Metastatic disease
- •Pathology and outcome
- •Other tumours
- •References
- •Introduction
- •Liver trauma
- •Mechanisms of liver injury
- •Classification of liver injury
- •Diagnosis of liver injury
- •Other diagnostic/therapeutic modalities for the assessment and treatment of liver injury
- •Management of liver injury: selection of patients for non-operative management
- •Operative management of liver injury
- •General strategy
- •Choice of incision
- •Intraoperative assessment
- •Perihepatic packing
- •Techniques for surgical haemostasis
- •Resectional debridement
- •Anatomical liver resection
- •Selective ligation of the hepatic artery
- •Management of hepatic venous and retrohepatic caval injury
- •Ex vivo surgery and liver transplantation
- •Complications of liver trauma
- •Complications of non-operative management
- •Postoperative complications after surgery for liver trauma
- •Outcome after liver injury
- •Extrahepatic biliary tract trauma
- •Incidence of biliary injury
- •Classification of biliary injury
- •Presentation and diagnosis of biliary injury
- •Operative management of biliary injury
- •Outcome after biliary injury
- •Pancreatic trauma
- •Mechanisms of pancreatic injury
- •Diagnosis of pancreatic injury
- •Classification of pancreatic injury
- •Initial management of pancreatic injury
- •Operative management of pancreatic injury
- •Complications of pancreatic injury
- •Conclusion
- •References
- •Index

Chapter 11
staying as close as possible to the gallbladder. The
biliary tree and hepatic arterial anatomy is highly
variable and therefore great care must be taken in
identifying all structures within Calot's triangle
before ligation. In Couinaud's published study of
biliary anatomy, 25% had drainage of a right sectoral duct directly into the common hepatic duct.23
Sometimes this structure may follow a prolonged
extrahepatic course, where it can be at greater risk
from cholecystectomy. The right hepatic artery may
also course through this area. All structures should
be traced into the gallbladder to minimise the risk of
injury (Fig. 11.4 and 11.5).
Calot's original description of gallbladder anatomy
described a triangle formed by the cystic duct, common hepatic duct and superior border of the cystic
artery.24 For satisfactory visualisation of the structures, dissection should also extend above the cystic artery to the liver. Extensive dissection should
be avoided in Calot's triangle as diathermy injury
may occur to the lateral wall of the common hepatic
duct. Furthermore, arterial bleeding in this area
should not be cauterised or clipped blindly. Most
bleeding can be controlled with several minutes of
direct pressure with a laparoscopic forceps compressing Hartmann's pouch on to the bleed point.
During the era of open cholecystectomy many
advocated complete excision of the cystic duct to
its insertion into the common bile duct to avoid a
cystic duct stump syndrome. However, extensive
dissection around the common bile duct with or
without diathermy may cause an ischaemic stricture
due to damage to the intricate blood supply of the
common hepatic duct.
Many authors argue that operative cholangiogra-
phy is essential to avoid biliary injury.
16,19
Fletcher
et al. reported an overall twofold reduction in
biliary injuries with the use of operative cholangiography, with an eightfold decrease in complex
cases.19 Flum and colleagues analysed retrospectively the Medicare database in the USA and identified 7911 common bile duct injuries following
cholecystectomy. After adjusting for patient-level
factors and surgeon-level factors the relative risk
a b
Figure11.4 • Aberrant biliary anatomy. The normal biliary anatomy is a trifurcation of the right sectoral and left hepatic
ducts forming the common hepatic duct which receives the cystic duct after a variable distance. Operative photograph
(a) and a cholangiogram (b) of a short cystic duct (single arrow) draining into the right posterior sectoral duct (double
arrow), which has a long extrahepatic course.
Figure11.5 • Operative cholangiography of an aberrant right sectoral duct. The injury was recognised after division of the
duct following cholangiography. The cholangiogram catheter was used to obtain a cholangiogram of the aberrant duct. The
surgeon obtained advice by telephone and a decision was made to ligate the duct. The patient remains asymptomatic.
200

Benign biliary tract diseases
was 1.49 when intraoperative cholangiography was
not used.16 When the use of intraoperative cholangiography has undergone cost analysis, routine
cholangiography has been found to be the most
cost-effective during high-risk operations when employed by less experienced surgeons.
25
Unfortunately, many operative cholangiograms
are interpreted incorrectly and injuries are missed.
Although this event should be less frequent with the
use of modern C-arm imaging, in reported series of
biliary injuries only 6–33% of operative cholangiograms are interpreted correctly.
20,26
For correct
anatomical interpretation of the proximal biliary
tree, both right sectoral/sectional ducts and the left
hepatic duct should be visualised. In the presence
of an endoscopic sphincterotomy, contrast will preferentially flow into the duodenum and the patient
may need to be placed in a head-down position to
fill the intrahepatic ducts. If the anatomy is unclear
no proximal clip should be placed on what is presumed to be the cystic duct, to avoid a crush injury
to what may be the common hepatic duct.
Retrograde cholecystectomy has been described
previously as a safe technique when inflammation
around Calot's triangle makes identification of the
anatomy difficult. Nonetheless, care still needs to be
exercised during dissection to avoid injury to the right
hepatic artery and common hepatic duct, which may
be adherent to an inflamed gallbladder. Eight such
patients have recently been described by Strasberg
and Gouma.27 If identification remains impossible
then the gallbladder can be opened to facilitate
identification of the cystic duct. A subtotal cholecystectomy should be considered if a safe plane of dissection cannot be established, thus avoiding injury to
the common hepatic or left hepatic ducts. Originally
described for open cholecystectomy, these techniques
have now also been performed laparoscopically.
Bile duct injury can be avoided by careful
identification of the biliary anatomy, dissection close
to the gallbladder and avoidance of diathermy in
Calot's triangle. The use of operative cholangiography
and its correct interpretation is associated with a
reduced incidence of bile duct injury.
28
Classification
Injury to the distal biliary tree is less technically demanding to repair than involvement of the biliary
confluence. The success of reconstruction depends
on the type of injury and the anatomical location.29
Bismuth first described a classification system for
biliary strictures reflecting the relationship of the
injury to the biliary confluence (Table 11.1).30
Strasberg et al. further proposed a broader classification to include a number of biliary complications,
Table11.1 • Bismuth classification of biliary strictures
Bismuth
classification Definition
Bismuth 1 Low common hepatic duct stricture –
hepatic duct stump >2 cm
Bismuth 2 Proximal common hepatic duct
stricture – hepatic duct stump <2 cm
Bismuth 3 Hilar stricture with no residual
common hepatic duct – hepatic duct
confluence intact
Bismuth 4 Destruction of hepatic duct
confluence – right and left hepatic
ducts separated
Bismuth 5 Involvement of aberrant right
sectoral hepatic duct alone or with
concomitant stricture of the common
hepatic duct
including cystic stump leaks, biliary leaks and partial injuries to the biliary tree (Fig. 11.6).
17
Presentation
It is preferable that injuries are recognised at the time
of surgery to allow the best chance of repair, but this
occurs in less than a third of patients. An unrecognised injury may present early with a postoperative
biliary fistula, symptoms of biliary peritonitis or
jaundice. Early symptoms or signs may be lacking
but ductal injury should be suspected in the patient
whose recovery is not immediate or is complicated
by symptoms of peritoneal or diaphragmatic irritation and/or associated with deranged liver function
tests in the first 24–48 hours of surgery. Signs may
range from localised abdominal tenderness through
to generalised peritonitis with overwhelming sepsis. Ligation of the bile duct will present early with
jaundice; however, later presentation may occur as
a result of stricture formation from a partial injury,
localised inflammation or ischaemic insult.
Ligation of sectoral ducts may cause subsequent
or late atrophy of the drained liver segments, which
may become infected secondarily. Occasionally liver
resection or transplantation may be required for
fulminant hepatic failure secondary to combined
biliary and vascular injuries.
injuries may present late with secondary biliary
cirrhosis, which may require liver transplantation
when liver failure results.
In many patients there is a delay until referral,
despite evidence of a biliary injury. In a report by
Mirza et al., the median interval until referral was
26 days.33 This delay is not inconsequential as the
31,32
More commonly,
31,32
201

Chapter 11
a b
c d
<2 cm
>2 cm
e1
e3
e5
Figure11.6 • Strasberg classification. Type A injuries include leakage from the cystic duct or subvesical ducts. Type
B involves occlusion of part of the biliary tree, most usually an aberrant right hepatic duct. If the former injury involves
transection without ligation this is termed a type C injury. A lateral injury to the biliary tree is a type D injury. Type E injuries
are those described by Bismuth and subdivided into his classification (Table 11.1). Adapted from Strasberg SM, Hertl M,
Soper NJ et al. An analysis of the problem of biliary injury during laparoscopic chole cystectomy. J Am Coll Surg 1995;
180:102–25. With permission from the American College of Surgeons.
e2
e4
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Benign biliary tract diseases
opportunity for an early repair is lost and results in
the liver sustaining further damage.
Management
Intraoperative recognition
In a review by Carroll et al., only 27% of patients underwent a successful repair by the primary surgeon
responsible for the injury, whilst 79% of repairs performed following referral had a successful outcome.34
If experienced help is not at hand, no attempt should
be made to remedy the situation since this may compromise subsequent successful management. A T-tube
or similar drain should be placed to the biliary injury
and drains left in the subhepatic space, followed by referral to a specialist centre. No attempt should be made
to repair a transection or excision of the bile duct.
A partial injury to the bile duct may sometimes be
managed by direct closure with placement of a T-tube
through a separate choledochotomy. Primary repair
with or without a T-tube for complete transection of
the common bile duct is nearly always unsuccessful.
This may result from unappreciated loss of common
duct or an associated arterial injury, or result from local diathermy injury or devascularisation of the duct
from overzealous dissection of the common bile duct35
(Fig. 11.7a,b). Succesful endoscopic treatment is possible for failed primary repair; however, as many as
32% will require subsequent hepatico-jejunostomy.
If an injury to the biliary tree is suspected
during cholecystectomy, help must be sought from
an experienced hepatobiliary surgeon. A successful
repair by the surgeon who has caused the injury
is far less likely than one performed by a surgeon
experienced in performing a hepatico-jejunostomy.
Postoperative recognition: biliary fistula
Any patient who is not fit for discharge at 24 hours
due to ongoing abdominal pain, vomiting, fever or
bile in an abdominal drain should be considered to
have a biliary leak. The lack of bile in an abdominal
drain does not exclude the possibility of a biliary
leak, particularly if there is liver function test derangement. Symptoms and signs vary widely, and
widespread soiling of the abdominal cavity may be
present with few signs.
Initial investigation should include full blood ex-
amination and determination of serum levels of
urea, electrolytes, creatinine and liver function tests.
Ultrasound is usually the initial investigation but it
cannot readily differentiate bile and blood from a residual fluid collection following uneventful cholecystectomy. It may provide important information about
the presence of intra-abdominal or pelvic fluid, biliary
dilatation or retained stones within the bile duct.
36
If there is evidence of significant peritoneal irritation from widespread biliary peritonitis, laparoscopy allows confirmation of this and provides an
opportunity for abdominal lavage. The porta hepatis can be inspected to determine the cause of the
bile leak. Whilst dislodged clips from the cystic duct
can be managed by application of further clips or
suture, any other form of bile leak should lead to
specialist referral. Drains can be placed to the subhepatic space as well as the subdiaphragmatic space
and pelvis if required. No attempt should be made
to repair an injury laparoscopically. If laparotomy
is required, this should be considered in conjunction with specialist assistance if bile duct injury is
suspected.
Further assessment depends on the clinical situation. The majority of biliary fistulas are due to leaks
from the cystic duct stump or subvesicle ducts, and
endoscopic retrograde cholangiopancreatography
(ERCP) allows anatomical definition, endoscopic
sphincterotomy or stent placement. As complete
transection of the bile duct precludes ERCP, computed tomography intravenous cholangiography
(CT-IVC) or MRCP can determine continuity of
the biliary tree prior to endoscopy. Occasionally,
persistent bile drainage is associated with choledocholithiasis requiring sphincterotomy and stone extraction. Most simple cystic duct stump leaks can
be resolved by endoscopic stenting if cannulation is
possible at ERCP37 and occasionally side injury to
the biliary tree can be controlled with endoscopic
stent placement.
38
If ERCP is unsuccessful or the bile duct is ligated or
occluded by clips, percutaneous transhepatic cholangiography may facilitate biliary decompression but it
is less frequently employed for diagnosis or delineation of the biliary anatomy. Occasionally, both sides
of the liver may need to be externally drained to gain
control of a biliary fistula, especially with E4 injuries
to the biliary confluence. However, injury to the biliary tree detected in this way may allow surgical repair to be considered within the first week of injury
in the stable non-septic patient, and again such further investigation or management decisions should
only be considered following specialist referral.
Where the diagnosis of bile duct injury has been
delayed, the aim should be to control the biliary
fistula with external drainage using surgical or radiologically placed drains. Further control may be
required with endoscopic stenting or external biliary drainage. Delayed repair can be considered subsequently once sepsis and intra-abdominal soiling
have resolved, as a planned elective procedure in a
specialist unit usually 2–3 months following injury.
Such an initial conservative approach renders a potentially difficult operation into a repair that will be
considerably easier.
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Chapter 11
a
b
Figure11.7 • (a) Failure of primary repair with T-tube. Primary repair was performed for an injury to the common bile
duct presenting with biliary peritonitis. A T-tube was inserted through the anastomosis and this was removed at 4 weeks.
An anastomotic stricture developed and the patient required a hepatico-jejunostomy 2 months later. (b) Failure of primary
repair for ligation of the common bile duct. A complete transection of the common bile duct identified at postoperative
endoscopic retrograde cholangiopancreatography (ERCP). Immediate repair was performed with a direct duct-to-duct
repair. (c) A tight anastomotic stricture is demonstrated at a later ERCP.
Diagnosis of a bile duct injury in the
postoperative period should lead to immediate
referral to a specialist centre since inappropriate
attempts to manage this outwith a specialist centre
will compromise the outcome.
c
Postoperative recognition: biliary obstruction
Ligation or inadvertent clipping of the biliary tree
presents early in the postoperative period with jaundice. Later, stricture formation may occur as a result
204

Benign biliary tract diseases
of direct trauma during dissection, clips placed inadvertently on the cystic duct but compromising the
bile duct, or from damage to the intricate vascular
supply of the bile duct by extensive mobilisation
or diathermy. Initial investigation should include
haematology, assessment of coagulation by estimation of prothrombin time, and liver function tests.
Ultrasound may indicate the level of obstruction or
exclude the presence of a correctable cause of obstructive jaundice, such as a retained stone in the
common bile duct.
ERCP will identify a stricture or complete transection of the bile duct; however, identification
of complete transection with MRCP will avoid
the risks of an unnecessary ERCP. Overzealous
instillation of contrast should be avoided, and
placement of an endoscopic stent should only
be considered after consultation with a specialist unit since this may introduce sepsis into the
biliary tree and compromise further management.
Furthermore, an undrained biliary tree may allow
proximal biliary dilatation, thereby facilitating
later reconstruction. Although some have reported satisfactory resolution of biliary strictures
with endoscopic stenting alone, the follow-up has
usually been short and almost all patients require
later surgery in our experience. Partial occlusion
of the duct by a clip may be remedied by balloon
dilatation with or without placement of a stent;
however, delay in diagnosis may result in subsequent recurrent stricture formation. Nonetheless,
de Reuver et al. reported 110 patients with bile
duct strictures following cholecystectomy that
were treated with endoscopic stenting, 48 (44%)
of which had already undergone attempted surgical repair. At a mean follow-up of 7.6 years, 74%
of patients had a successful outcome.37 The development of removable endoscopic expandable
metal stents has recently been described, although
long-term results and large series are not yet available. Furthermore stent migration can complicate
treatment.
For strictures that declare late, appropriate
indications for stent placement are the presence
of sepsis, severe itch resistant to medical therapy,
or significant hepatic dysfunction.
The timing of repair
Early repair
When an injury is recognised in the early postoperative period and there is minimal peritoneal
contamination or sepsis, a definitive repair by an
experienced surgeon can be successful (Fig. 11.8).
In our series of 123 patients referred with injury to
the biliary tree, 22 patients underwent primary biliary repair in the first 2 weeks following injury and
three had revision of a failed biliary repair. Between
2 weeks and 6 months, a further 22 injuries were
repaired selectively. Successful repair was possible
in 22 of 25 early repairs compared with 20 of 22
delayed repairs.
Delayed repair
Many injuries continue to be unrecognised or referral delayed. In a prospective audit of major bile duct
injuries from Australia, the median delay before referral was 9 days (2–28 days), and this included five
patients with generalised peritonitis.
Controlling the biliary injury and associated sep-
sis is the first treatment aim, which may require
endoscopic or percutaneous biliary decompression, allowing jaundice to settle or biliary sepsis
to be drained. Intra-abdominal collections may be
drained percutaneously, or in the early postoperative period this may be better achieved by laparoscopic means. It is accepted, however, that bile
collections are frequently loculated and difficult to
39
20
If the diagnosis of ductal obstruction is made
early within the first week postsurgery, the bilirubin
level is only moderately elevated and there is no
coexisting coagulopathy or sepsis, immediate
repair offers the best chance of a successful
outcome.
If repair needs to be delayed, stent placement
may still be avoidable and a decision will
generally be made based on the individual patient
circumstances. Suspicion or evidence of arterial
injury may influence the management decision.
Figure11.8 • Operative picture of an early repair of an
E4 injury. A right-angle forceps is placed in the opening of
the left hepatic duct whilst the open right hepatic duct is
visible below. The portal vein is skeletonised with ligation
and excision of both the extrahepatic biliary tree and right
hepatic artery (held by forceps).
205

Chapter 11
eradicate in patients with intra-abdominal sepsis
or widespread biliary contamination or peritonitis.
The most effective treatment may be laparotomy
with extensive lavage and the placement of large
intra-abdominal drains. Definitive repair should not
be contemplated if there is severe peritoneal soiling
since injudicious attempts to repair the injury may
aggravate the injury and result in a poor outcome.
Once these objectives have been met, the patient
should be allowed to recover from the combined
insult of surgery and sepsis. A period of rehabilitation at home is generally required before repair
is contemplated in these compromised patients.
Abdominal and biliary drainage can be managed on
an outpatient basis with community nursing support. Nutritional supplementation may be required,
particularly in those who have required a prolonged
admission to the intensive care unit and hospital.
Attention should be paid to the consequences of
prolonged external biliary drainage and consideration given to recycling of bile.
Associated vascular injury
Abdominal CT is required to ensure resolution of
intra-abdominal collections and before repair to
exclude the presence of liver atrophy. Atrophy can
occur from prolonged obstruction to the segmental,
sectional or hepatic ducts, but is generally associated with the presence of a vascular injury, most
usually of the right hepatic artery. Liver resection
may occasionally be needed at the time of definitive
repair to remove a source of ongoing sepsis, or if
satisfactory reconstruction to the left or right duct
is not possible.
Buell et al. identified associated vascular injury
as an independent predictor of mortality, with
38% of patients dying compared to 3% (P<0.001)
where no arterial injury was present.40 Some authors advocate arteriography before repair to identify such associated vascular injury as a repair is
less likely to be successful,41 or for consideration
of hepatic arterial reconstruction at the time of
hepatico- jejunostomy.
described 55 patients with postcholecystectomy
strictures who underwent surgical reconstruction with a left duct approach and preoperative
coeliac axis and superior mesenteric artery angiography.43 Twenty-six patients (47%) had an associated vascular injury, of which 20 (36%) were
of the right hepatic artery. In this series only one
patient in each group (vascular injury vs. no injury) developed a recurrent stricture after repair.43
A proximal anastomosis may offer a better blood
supply, minimising the risk of anastomotic stricturing (Fig. 11.9). In support of this theory, Mercado
et al. demonstrated that an anastomosis fashioned
below the biliary confluence was more likely to
41,42
However, a recent paper
Figure11.9 • Anastomotic stricture following repair of
biliary injury. Percutaneous transjejunal cholangiogram
(PTJC) of a Bismuth 1 injury repaired by hepaticojejunostomy at the level of the transection of the common
bile duct (not to the left hepatic duct). Three months later
the patient required reconstruction of the anastomotic
stricture.
require revisional surgery (16%) compared to an
anastomosis performed at the biliary confluence
(0%; P<0.05).44 Recent improvements in magnetic
resonance imaging (MRI) and spiral CT are producing impressive arterial and venous anatomical
reconstructions, which may negate the need for invasive arteriography.
Injury to the hepatic arterial supply (usually the
right hepatic artery) may present with haemobilia or intra-abdominal haemorrhage from a false
aneurysm, usually associated with ongoing subhepatic sepsis. If suspected, urgent angiography is required (Fig. 11.10). Haemorrhage may be controlled
by embolisation of the feeding vessel, although rebleeding can occur and necessitate further embolisation. However, in our experience, further bleeding
in the presence of ongoing sepsis usually requires
laparotomy for control of bleeding and drainage of
any subhepatic collection.
Rarely, combined injury to the hepatic artery and
portal vein can occur with resultant infarction of
the affected hepatic parenchyma, usually the right
liver. Such injuries may require urgent hepatic resection or transplantation.
31,32,45
Further imaging
For patients with injury to the biliary confluence
(E3 and E4), preoperative imaging will help in
the planning of future repair. In the presence of
a biliary stricture, invasive cholangiography by
206

Benign biliary tract diseases
Figure11.10 • Digital subtraction angiogram demonstrating a false aneurysm of the common hepatic artery.
Embolisation was required for control. The patient has undergone a primary repair for a complete transection of the
common bile duct. FA, false aneurysm; GDA, gastroduodenal artery; HA, common hepatic artery; LHA, left hepatic artery;
RHA, right hepatic artery.
ERCP or percutaneous transhepatic cholangiogram (PTC) risks introducing sepsis. However, if
PTC is required for external biliary drainage, an
adequate cholangiogram may be obtained at this
time. The quality of MRCP continues to improve,
and detailed biliary anatomical reconstructions can
be produced, thereby negating the need for more
invasive imaging.
Operative techniques
Biliary reconstruction should be performed under
optimal circumstances at the time of injury or soon
thereafter. Once this opportunity has been lost, repair should only be considered when the patient has
been optimised, in the absence of intra-abdominal
sepsis, and when sufficient time has elapsed to allow for maturation of adhesions and the tissues at
the porta hepatis.
A right subcostal incision is used for access,
which can be extended across the midline if required. Retraction is provided with Doyen's blades
and the Omni-tract® (Omni-tract surgical, St Paul,
MN) mechanical retractor. Laparotomy is undertaken to assess the liver and to allow adhesiolysis,
thereby freeing the small bowel for reconstruction.
Frequently the omentum, hepatic flexure, duodenum and hepatoduodenal ligament are involved in
a dense inflammatory mass, and occasionally an unsuspected fistula between bile duct and duodenum
or colon is identified. Dissection is often easier if
commenced laterally and then directed towards the
biliary structures. The common bile duct can be difficult to identify, particularly in the presence of extensive fibrosis, and intraoperative ultrasound is a
useful tool in allowing its location and relationship
to vessels to be determined.
For injuries that involve the biliary confluence,
lowering of the hilar plate allows easier identification of the left and right hepatic ducts. This may be
aided by the use of an ultrasonic dissector (CUSA),
which is also employed to break down the contracted fibrotic tissue in the gallbladder bed and
facilitate the division of any bridge of liver tissue between segments 3 and 4. Opening these two planes
on the right and left sides facilitates identification of
and access to the biliary confluence.
Since the blood supply to the bile duct is often
damaged at the time of injury, the common hepatic
duct should be opened as proximally as possible,
although frequently there has been retraction of
the fibrotic remnant superiorly. Extension of the
incision into the left hepatic duct allows a wide
anastomosis to be fashioned with adequate views
of the left- and right-sided ducts. Care should be
taken since there may be a small superficial arterial
branch crossing the left duct anteriorly and running
above to segment 4. For injuries with separation
of the confluence, the right and left hepatic ducts
can be anastomosed together before formation of
a hepatico-jejunostomy, allowing a single biliary
207

Chapter 11
anastomosis. If possible, injuries to an isolated right
sectoral duct are best repaired or drained into a
Roux limb of bowel (Fig. 11.5). Simple ligation will
lead to atrophy of the drained segments, which may
become a nidus for sepsis. However, enteric drainage of a small sectoral duct may also lead to sepsis
if an anastomotic stricture occurs.
Repair should be effected by a hepatico- jejunostomy
with a 70-cm Roux limb of jejunum, thereby minimising the risk of enteric reflux and chronic damage to the biliary tree. Moraca et al. advocate
hepatico-duodenostomy for biliary injury on the basis that it is more physiological, quicker to perform,
and allows later ERCP for imaging and intervention.46 They found no difference in outcome following hepatico-duodenostomy when compared with
hepatico-jejunostomy, although median follow-up
was only 54 months. Hepatico-duodenostomy has
largely been abandoned in the treatment of other
benign biliary disease due to ongoing enteric reflux.
There have been anecdotal reports of the late development of cholangiocarcinoma,47 as well as the need to
undertake liver transplantation in patients so managed
when secondary biliary cirrhosis due to enteric reflux
has resulted. Our own view is that hepatico-duodenostomy has no role in the management of bile duct injury.
Fine absorbable interrupted sutures of 4/0 or 5/0
polydioxanone sulphate (PDS II) should be used to
fashion an end-to-side hepatico-jejunostomy, with
care being taken to produce good mucosal apposition. Some authors advocate the use of an access
limb, particularly for E3 and E4 injuries, to allow
subsequent radiological intervention for dilatation
of recurrent strictures.48 However, others believe that
advances in percutaneous transhepatic techniques
have made this unnecessary and have achieved satisfactory results without using this surgical approach.
Rarely, there may be no recognisable bile ducts
visible in the porta hepatis. In such cases a variation
of porto-enterostomy (Kasai procedure) can be considered with the Roux limb sutured to the fibrous
structure of the hilar plate (S.W. Banting, personal
communication).
Partial injury to the biliary tree can be repaired
with fine interrupted sutures, although when resulting from diathermy dissection, formal hepaticojejunostomy may be necessary as conduction of the
thermal injury may cause later stricture formation. If
a T-tube is placed to protect a primary duct repair, this
should be placed through a separate choledochotomy.
49
Management of complications related to repair
Revisional surgery
Many patients with biliary injury continue to suffer
from complications despite reconstruction. Factors
such as the experience of the initial surgeon, the
level of injury, the associated sepsis and liver atrophy all increase the chance of an unsuccessful repair.
Following primary repair of a ductal tear or laceration, further stricture formation may result if there
has been extensive dissection around the common
hepatic duct. In such instances, surgical revision
with the formation of a Roux-en-Y hepatico-jejunostomy is indicated.
The majority of patients requiring revisional surgery will have undergone a previous biliary enteric
drainage procedure. Anastomotic stricturing will
require revision of the anastomosis, with extension
of the choledochotomy into the left hepatic duct
(Fig. 11.9).
Liver resection and transplantation
In the acute setting of bile duct injury, long-term
damage to the hepatic parenchyma is difficult to
predict. Major vascular injury or unrecognised segmental biliary obstruction may lead to atrophy of
the liver, chronic intrahepatic infection, abscess formation or secondary biliary cirrhosis. In such patients, careful operative assessment is required; CT
should be performed to identify areas of associated
liver atrophy and to exclude portal vein thrombosis.
In our experience, the majority of patients requiring liver resection are those with ongoing sepsis in
an obstructed segment or those where drainage of
the extrahepatic biliary tree is not possible due to
sectoral duct damage or fibrosis.31 A recent review
identified 99 patients (5.6%) requiring hepatectomy
among 1756 postcholecystectomy bile duct injury
patients,50 with combined arterial and Strasberg
E4 and E5 injuries more likely to require hepatic
resection.50 Occasionally, early hepatic resection is
required for combined arterial, portal venous and
biliary injury, although results are poor.45 Very
rarely, resection may be needed to gain access to the
biliary tree, especially when the injury involves the
biliary confluence (E4), although some authors routinely advocate resection of segments IVb and V for
access to the right hepatic ducts.51 The right lobe
is most commonly affected by sepsis and atrophy
as the right-sided sectoral ducts and arterial supply
are more likely to be damaged during cholecystectomy, although both left- and right-sided hepatic
resections have been reported in patients with severe biliary injury. Resection of the right liver can
be performed, for example at the time of delayed
reconstruction if there is any doubt regarding the
integrity of the anastomosis to the right sectoral or
hepatic duct and when a satisfactory anastomosis
can be achieved to the long extrahepatic left duct.
Failed reconstruction and persistent cholangitis
may lead to end-stage liver failure within a few years
and this may require liver transplantation31
(Fig. 11.11). A long interval between injury and
208

Figure11.11 • Contrast-enhanced CT image of the
liver after unsuccessful revisional hepatico-jejunostomy.
The surgeon who performed the laparoscopic
cholecystectomy performed the hepatico-jejunostomy
for an E4 injury. A revisional hepatico-jejunostomy was
performed before referral, which was complicated by
an anastomotic stricture and portal vein thrombosis.
The CT scan shows evidence of right lobe atrophy and
splenomegaly as well as a percutaneous biliary drain.
referral is known to be associated with end-stage
liver disease.52 Rarely, liver transplantation may be
needed when the combined biliary and vascular injury is so severe as to preclude attempted reconstruction, although the results are universally poor.
31
Prognosis
Success of repair
Successful repair has been well described and can
be achieved in 90% of patients in a specialised
20,26
unit.
learning curve for biliary repair has also been described for tertiary centres managing bile duct injury. Over a 20-year period, Mercado et al. reported
an improvement with experience and a reduction of
post-repair strictures from 13% to 5%.53 As well
as anastomotic strictures, liver atrophy and cirrhosis may also occur many years following repair.
Predictors of a poor outcome include involvement
of the biliary confluence,
surgeon,
repairs29 and recent active inflammation.
Survival
Mortality following injury to the biliary tree is significant. Death may follow the acute injury itself,
following the biliary repair, or occur later as a result
of biliary sepsis or cirrhosis. In a recent report of
As for laparoscopic cholecystectomy, a
29,52
34,54,55
three or more previous attempted
repair by the injuring
55
Benign biliary tract diseases
a nationwide analysis of survival following biliary
injury after cholecystectomy, Flum et al. identified
7911 (0.5%) injuries from 1 570 361 cholecystectomies.54 Within the first year after cholecystectomy
the mortality rate was 6.6% in the uninjured group
and 26.1% in those with injury to the common
bile duct. The adjusted hazard ratio for death during follow-up was higher for those with an injury
(2.79; 95% confidence interval 2.71–2.88). The
risk of death increased significantly with advancing
age and comorbidities. If the initial repair was performed by the injuring surgeon then the adjusted
hazard of death increased by 11%.
Quality of life
Boerma et al. first undertook an assessment of quality of life in patients who had sustained biliary injury or leak that required additional intervention.56
Five years after injury, quality of life in the physical
and mental domains was significantly worse than
controls, despite a successful outcome in 84% of
treated patients and regardless of the type of treatment or severity of injury. However, the length of
treatment was an independent predictor of a poor
mental quality of life. Melton et al. report that quality of life in 89 patients who had undergone biliary repair following laparoscopic cholecystectomy
showed no difference in the physical or social domains when compared to controls.57 However, in
the psychological domain, patients were significantly worse, particularly in the 31% of patients
who sought legal recourse for their injury.
Associated malignancy
A small number of reports exist about the development of cholangiocarcinoma at the site of anastomosis 20–30 years following repair.47 It is possible
that enteric reflux into the biliary tree with sepsis
and the production of mutagenic secondary bile
salts may be responsible. Furthermore, hepatocellular carcinoma may develop due to secondary biliary
cirrhosis (Fig. 11.12).
Benign biliary strictures
Mirizzi's syndrome
Mirizzi first described the syndrome of extrahepatic
biliary stricture in association with cholelithiasis in
1948,58 a condition that occurs in fewer than 0.5%
of cholecystectomies.59 Obstruction of the common
hepatic duct may occur for two reasons: (i) a stone
impacted in the cystic duct may cause direct pressure or oedema (Mirizzi type I; Fig. 11.13), or (ii) occasionally the stone may erode through the wall of
the gallbladder or cystic duct and into the common
hepatic duct (Mirizzi type II).
209
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