Ministry of Health of the Republic of Moldova [600428]
I
Ministry of Health of the Republic of Moldova
State University of Medicine and Pharmacy
“Nicolae Testemiț anu”
FACULTY OF MEDICINE 2
Department of Surgery
License Thesis
OBSTRUCTIVE JAUNDICE
Prepared by:
Usman Mohammad
Group 1644
Scientific coordinator:
Tudor Timiș
MD. PhD. Associated Professor
CHISINA U, 2015
II
DECLARATION
I hereby declare that the diploma thesis entitled "Obstructive Jaundice " is written by me
and has not been presented before at another college or institution of higher education in
the country or abroad. Also, I declare that all sources used, including the Internet
sources, are indicated in the paper, considering the rules for avoiding plagiarism:
– All text fragments are reproduced exactly, even the proper translations from other
languages are written in quotes and have detailed reference source;
– Paraphrasing in own words of text written by other authors has detailed reference;
– Summary of the ideas of o ther authors has a detailed reference to the original text.
Date
Usman Mohammad
____________________
III
LIST OF ABBREVIATIONS
Abbreviation Definition
CBD Common bile duct
ERCP Endoscopic retrograde cholangiopancreatography
Na+ Sodium ion
K+ Potassium ion
Ca+2 Calcium ion
Cl- Chlorine ion
HCO 3- Bicarbonate
cm Centimeter
GGT Gamma -glutamyl -transpeptidase
RNA Ribonucleic acid
mg/dL Milligram per deciliter
mEq/L Milliequivalent per liter
µmol/L Micromole per liter
IU/L International unit per liter
SGOT Serum glutamic oxaloacetic transaminase
AST Aspartate transaminase
ALT Alanine transaminase
SGPT Serum glutamic pyruvic transaminase
g/L Gram per liter
A/G Albumin -globulin ratio
CT Computed tomography
3D 3 dimensional
Mm Millimeter
USG Ultrasonography
PTC Percutaneous trans -hepatic cholangiography
MRCP Magnetic resonance cholangiopancreatography
EU Endoscopic ultrasound
IDA Iminodiacetic acid derivative
CNS Central nervous system
Ml Milliliter
JAK Janus kinase
INR International normalized ratio
CBC Complete blood count
Lab Laboratory
WBC White blood cells
Hb Hemoglobin
IV
ALP Alkaline phosphatase
CRP C reactive protein
LDH Lactate dehydrogenase
HAV Hepatitis A virus
HCV Ab Hepatitis C virus antibody
HBs Ag Hepatitis B surfaces antigen
CMV Cytomegalovirus
Neg Negative
Pos Positive
nmol/L Nanomole per liter
ng/mL Nanogram per milliliter
EGD Esophageo -gastro -duodenoscopy
HIV Human immunodeficiency virus
BP Blood pressure
HEENT Head, ear, eye, nose and throat
BMI Body mass index
SpO 2 Oxygen saturation
PT Prothrombin time
PTT Partial thromboplastin time
RBC Red blood cells
Dx Diagnosis
IV Intravenous
ml/hr Milliliter per hour
GI Gastrointestinal
HBc Ab Hepatitis B core antibody
OJ Obstructive Jaundice
LIST OF TABLES
Nr. Name Page
1.1 TNM staging for gall bladder Cancer 24
1.2 American TNM Staging System for Cholangiocarcinoma 25
V
LIST OF FIGURES
Nr Name Page
1.1 Development of liver and extrahepatic biliary apparatus 5
1.2 Common bile duct anomalies 6
1.3 Common duct anomalies (continued) 6
1.4 The anatomy of intra – and extrahepatic biliary system 8
1.5 Normal vascular anatomy of extrahepatic biliary system 9
1.6 Vascular anomalies 10
1.7 Lymphatic drainage of biliary tree 11
1.8 Metabolism and excretion of bilirubin 13
1.9 Types of extrahepatic biliary atresia 19
1.10 Todani’s classification of choledochal cysts 20
1.11 Classification of bile duct stricture 23
1.12 Classification of cholangiocarcinoma 26
1.13 Algorithm of obstructive jaundice management 36
1.14 Exploration of the common bile duct 39
1.15 Sphincterotomy 40
1.16 Endoscopic papilla sphincterotomy 43
1.17 Cholecysto -jejunostomy 44
1.18 End-to-side Choledocho -jejunostomy 45
1.19 Side-to-side Choledocho -jejunostomy 45
1.20 Immediate repair of bile duct injury 46
1.21 Biliary -intestinal anastomosis for late repair of bile duct stricture 47
1.22 Biliary -intestinal anastomosis for low bile duct injuries 48
1.23 Mucosal graft for repair of bile duct 49
1.24 Percutaneous cholecystostomy 51
1.25 Endoscopic nasobiliary drainage 52
1.26 Internal -external biliary drain in a patient with obstruction of the CBD 53
1.27 Pancreatoduodenectomy 55
1.28 Sequential double palliative bypass on the same Roux -en-Y jejunal loop 55
2.1 Gallbladder distended with sludge, no stones 57
2.2 Intra – and extrahepatic bile duct dilated 58
2.3 Splenomegaly 58
2.4 Hepatic veins are patent 59
2.5 Portal vein 59
2.6 Acute on chronic portal vein thrombosis 60
2.7 MRCP of biliary system 61
2.8 Cavernous transformation of the portal vein 61
2.9 Examples of biliary stents 62
2.10 Intra -operative ERCP 63
2.11 Intra – and extrahepatic bile duct dilation 71
VI
CONTENTS
CHAPTER I: THEORETICAL MATERIAL
1. INTRODUC TION …………………..……………………………………… 1
2. OBJECTIVES OF THE ST UDY …………………………………………. 2
3. REVIEW OF LITERATURE …………………………………………….. 3
3.1 Anatomy of biliary system …………………………………………….. 5
3.2 Physiology ………………………………………………………… ……… 12
3.3 Pathogenesis ……………………………… ……………… ……… ……. 14
3.4 Etiology ………………………………………………………… ……. … 16
3.5 Clinical presentation ……………………………………… ……………… 28
3.6 Investigations …………………………………………… ……… ……. … 31
3.7 Preoperative preparation ……………………………………… ……… . 37
3.8 Surgical procedures …………………… ……………………….. ……….. 38
CHAPTER II: CLINICAL CASES
1. CASE PRESENTATION 1 ……………………………………………… .. 56
2. CASE PRESENTATION 2 ………………………………………………. . 65
3. CASE PRESENTATION 3 ………………………………………………. . 68
CHAPTER III: CO NCLUSION S ……………………………………………….. .. 72
CHAPTER IV: BIBLIOGRAPHY ……………………………… ……………….. 73
1
CHAPTER I
INTRODUCTION
Jaundice is a frequent manifestation of biliary tract disorders and the evaluation and management of
obstructive jaundice is a common problem faced by the general surgeon.
Obstructive jaundice is strictly defined as a condition occurring due to a block in the pathway between
the site of conjugation of bile in liver cells and t he entry of bile into the duodenum through the ampulla.
The block may be intrahepatic or extrahepatic in the bile duct. [1]
Despite the technical advances, the operative modes of management of obstructive jaundice were
associated with very high morbidity a nd mortality. Yet , during the last de cade significant advances
have been made in our understanding with regard to the pathogenesis, diagnosis, staging and the
efficacy of management of obstructive jaundice. [2]
Obstructive jaundice of varied etiology is one of the causes of admission to hospitals across the
Republic of Moldova. To diagnose the cause, site of obstruction and management of a case of surgical
jaundice is indeed a challenging task for the surgeon. He nce, a comprehensive study of the etiology,
clinical presentation and management of obstructive jaundice is of paramount importance in the
appropriate management of these patients.
2
OBJECTIVES OF THE STUDY
To study the clinical history and presentation of obstructive jaundice.
To study the various causes and sit es of obstruction of the biliary tree.
To study the different modalities of treatment of obstructive jaundice.
3
REVIEW OF LITERATURE
Jaundice is a generic term, which describes yellow pigmentation of the skin, mucus membrane or
sclera.
Mention of jaundice is made in t he works of Hippocrates (400 BC ) who pointed out that persistent
jaundice may be due to cancer or cirrhosis of liver. [3] Gallstones have been descri bed in Chilean
mummies since the second an d third centuries AD. Galen in second century AD in his humoral concept
of disease attributed abnormalities of yellow bile, black bile, blood and phlegm within the body to
cause disease. [3,4]
o Francis Glisson (164 0) , Abrahmson vater (1720) and Ruggero Oddi (1887) refined anatomy
with description of sphincteric mechanism. [3,4]
o Charcot (1877) , discussed the symptoms associated with the passage of CBD stones which
were jaundice, pain abdomen and fever (Charcot tria d).
o Telfer Reynold added hypotension and altered mental status to Charcot’s triad (Reynold’s
Pentad ) related to sepsis with cholagitis. [5]
o Langenbunch performed first cholecystectomy in the year 1882.
o Robert Abbe (1889) was the first to perform choledo chotomy.
o Lawson Trait performed choledocholithotomy.
o Ludwig Courvoisier (1843 -1918) stated Courvoisier’s law. [3]
Courvoisier’s law : In obstruction of the common bile duct due to a stone, distension of the gall
bladder seldom occurs, the organ usually is a lready shriveled. In obstruction from other causes,
distension is common. If there is no disease of gallbladder and the obstruction is due to a cancer of the
ampulla, pancreas or bile duct, then the gallbladder may well be distended.
o William Stewart Halste ad performed choledochoduodenal anastomosis for ampullary
carcinoma.
o Emil Theoder Kocher’s incision and kocher’s maneuver. [5]
o Charles McBurney – Transdoudenal choledochotomy.
o Hans Kehr – Invented T -tube. [3]
o John B. Murphy – Cholecystoenterostomy avoiding choledochotomy.
o The first mention of carcinoma of gallbladder was published in 1777 in Ratio Mendendi of
Maximillian Stall.
o Fredrich discussed carcinoma of gallbladder and suggested the relationship between gal l
bladder stone and cancer. [3]
o Graham Cole (1925) –Oral cholecystography.
o Mirrizzi (1931) – Intraoperative cholangiography.
o Okuda (1973) – CHIBA needle for percutaneous transhepatic cholangiography.
o Wildegans of Germany (1953) introduced modern choledochoscope.
o Shore and Shore (1965) – Flexible choledochoscope.
4
o Yamakawa (1975) – Percutaneous transhepatic cholangioscopy.
o McCune and Oi (1970) – ERCP.
o Kawai et al – Endoscopic papillotomy.
o First laparoscopic CBD exploration by Philips Peterson.
5
ANATOMY OF BILIARY SYSTEM
Development
Liver develops from an endodermal bud that arises from the ventral aspect of the gut, at the point of
junction between foregut and midgut. The bud enlarges and soon shows a division into :
Cranial part – Pars hepatica
Caudal part – Pars cystic
1. Pars hepatica : divides into right and left parts each of w hich forms one lobe of the liver.
2. Pars cystic : Gives origin to the gall bladder and to the cystic duct. The part of the hepatic bud
proximal to the pars cystic forms the bile duct. Bile duct at first opens on the ventral aspect of
the developing duodenum. But as a result of differential growth of the duodenal wall and as a
result of the rotation of the duodenal loop, it comes to open on the dorso -medial aspect of the
duodenum along with the ventral pancreatic bud. [6,7,8 ]
Fig. 1 .1: Development of liver and extrahepatic biliary appa ratus
Anomalies of the extrahepatic duct system
A. Abnormal length: Variation in the level at which the various ducts join each other.
B. Abnormal mode of termination
Cystic duct may join left side of the common hepatic duct .
Cystic duct may end in the right hepatic duct .
Cystic duct may pass anterior to the duodenum, before joining the common hepatic duct.
Bile duct may open into the pyloric, or even the cardiac end of the stomach.
6
C. Atresia: Parts of the duct system and sometimes the whole of it may be absent.
D. Duplication: Parts of duct system may be duplicated. [8]
Fig. 1.2: Common bile duct anomalies
a) Low fusion of right and left hepatic duct.
b) Double common duct.
c) Fusion of right hepatic and cystic duct.
d) Right hepatic duct draining into gall bladder.
Fig. 1.3: Common duct anomalies (continued)
a) Normal confluence of CBD and pancreatic
duct.
b) Indepen dent drainage of CBD and pancreatic
duct.
c) Dominant Santorini duct.
Anatomy of extra hepatic biliary system
Extrahepatic biliary system consists of:
1. Hepatic ducts: right and left
2. Common hepatic duct
3. Cystic duct
4. Common bile duct (CBD)
5. Hepato -pancreatic duct
6. Gall bladder
7
Liver is divided into two major portions, the right lobe. Which are respe ctively drained by right and left
hepatic ducts. The right and left hepatic d ucts converge at the liver hilum to constitute the common
hepatic duct. Cystic duct joins common hepatic duct to form common bile duct. The common bile duct
courses downward and backwards anterior to portal vein and lateral to hepatic artery, in the porta
hepatis. The common bile duct is divided into four parts : Supraduodenal, Retroduodenal, Paraduodenal
and Intraduodenal. The retroduodenal portion of the common bile duct approaches the second por tion
of duodenum obliquely accompanied by the terminal part of duct of Wirsung and opens in the
duodenum at papilla of V ater. [6,9]
The length of CBD is about 8 cm. it is joined by the main pancreatic duct (Wirsung’s duct), forming
the hepato -pancreatic ampulla or duct. This ampulla shows a dilation known as the ampulla of Vater,
and it opens in t he second part of the duodenum. The ampulla of Vater is guarded by a sphincter known
as, sphincter of Oddi. This is the junction of foregut and midgut.
The gall bladder is situated in fossa of gall bladder on the inferior surface of the liver. It is 7 cm long
and 3 cm wide. It consists of:
1. Fundus – The fundus is a rounded end that faces the front of the body.
2. Body – The body is in contact with the liver, lying in a depression at the bottom of the liver.
3. Neck – The neck tapers and is continuous with the cystic duct . At the junction of the neck of
the gallbladder and the cystic duct, there is an out -pouching of the gallbladder wall forming a
mucosal fold known as Hartmann 's pouch , where gallstones commonly get stuck.
8
Fig. 1.4: the anatomy of intra – and extrahepatic biliary system: The anterior border of the liver is
lifted upwards (brown arrow). Gallbladder with Longitudinal section, pancreas and duodenum
with frontal one. Intrahepatic ducts and stomach in transparency.
1. Bile ducts : 2. Intrahepatic bile ducts , 3. Left and right hepatic ducts , 4. Common hepatic duct ,
5. Cystic duct , 6. Common bile duct , 7. Ampulla of Vater , 8. Major duodenal papilla 9. Gallbladder,
10–11. Right and left lobes of liver. 12. Spleen . 13. Esophagus . 14. Stomach . Small intestine :
15. Duodenum , 16.Jejunum 17. Pancreas : 18: Accessory pancreatic duct , 19: Main pancreatic duct . 20–
21: Right and left kidneys (silhouette).
9
Blood supply
Gall bladder is supplied by cystic artery. The blood supply to the biliary ducts is derived from the
hepatic, cystic and superior pancreaticoduodenal arteries. Veins drain directly into liver or form
tributaries of the portal vein. Gas troduodenal branches to CBD run on the side of CBD at 3 O’clock
and 9 O’clock position. Retroportal artery from celiac plexus runs posterior to portal vein to supply
post-aspect of CBD.
Fig. 1.5: Normal vascular anatomy of extra hepatic biliary system
10
(e) (f)
Fig. 1.6: Vascular anomalies [7,8]
a) Accessory cystic arteries – arising from right hepatic artery.
b) Accessory cystic artery – arising from left hepatic artery.
c) Hepatic artery arising from superior mesenteric artery.
d) Accessory hepatic arteries arising from the coel aic trunk and superior mesenteric
arteries .
e) Anterior transposition of the right hepatic artery and cystic artery.
f) Recurrent (caterpillar hump) right hepatic artery.
11
Nerve supply
Consists of sympathetic and parasympathetic fibers passing in the hepatic plexus and being joined at
the porta -hepatis by branches from the anterior vagal trunk.
Lymphatic drainage
1. Cystic group
2. Hepatic group
3. Pancreatico -splenic group & ultimately to coeliac group
Fig. 1.7: Lymphatic drainage of biliary tree
12
PHYSIOLOGY
One of the major functions of the liver is to secret bile normally between 600 – 1200 ml/day.
Bile is secreted by the liver in two stages:
Initially bile is secreted by liver hepatocytes, which is rich in bile acids, cholesterol and other
organic constituents, which flow into bile canaliculi.
Next, the bile flows peripherally towards the interlobular septa, where the canaliculi empty into
larger ducts, the hepatic duct and comm on bile duct and then into duodenum or to gall bladder
through cystic duct. [10,11,12 ]
Composition of bile
Water 97.5 mg/dL
Bile salts 1.1 mg/dL
Bilirubin 0.04 mg/dL
Cholesterol 0.1 mg/dL
Fatty acids 0.12 mg/dL
Lecithin 0.04 mg/dL
Na+ 145 mEq /L
K+ 5 mEq/L
Ca+2 5 mEq/L
Cl- 100 mEq/L
HCO 3- 28 mEq/L
Metabolism
Hepatic metabolism of bilirubin occurs in three phases:
1. Uptake
2. Conjugation
3. Excretion
Bilirubin is a product of heme catabolism. Red cell hemoglobin accounts for approximately 85% of all
bilirubin.
Heme is catabolized to unconjugated bilirubin in the reticuloendothelial system. Unconjugated bilirubin
is bound to albumin in the plasma and transported bound to albumin to the liver and is conjugated with
glucuronic acid in the hepatocytes; the conjugation is catalyzed by glucuronyl transferase. Conjugated
bilirubin is secreted into the bile and enters the duodenum. In the small bowel, some of the bilirubin is
hydrolyzed to yield unconjugated bilirubin and glucuronic acid. Most unconjugated bilirubin is
13
excreted in the stool, but some is reabsorbed and returned to the liver for re -conjugation (enterohepatic
circulation).
Fig. 1.8: Metabolism and excretion of bilirubin
14
PATHOPHYSIOLOGY
Cholestasis is defined as the failure of normal bile to reach the duodenum. It is classified as:
1. Extrahepatic cholestasis.
2. Intrahepatic cholestasis.
Intrahepatic cholestasis: no demonstrable obstruction to the major bile ducts. They are ca used due to
drugs, hepatitis, hormons, primary biliary cirrhosis and septicemia.
Extrahepatic cholestasis: encompasses conditions where there is physical obstruction to the bile
ducts. Cholestasis begins with distension of the bile duct proximal to the obs truction, including
intrahepatic duct system. The bile stasis in the duct radicals within the portal triads leads to
proliferation of the epithelial lining cells, Sometimes accompanied by an increase in surrounding
fibrous tissue. Eventually the canaliculi become distended with bile. Distended canaliculi ruptures,
which leads to extravasation of bile, producing so, called bile lakes surrounded by injured or necrotic
liver cells. Because stasis of bile predisposes to ascending bacterial infections, extrahep atic cholestasis
may be complicated by cholangitis. Escherichia coli produce beta -glucuronidase, which may lead to
deconjugation of bilirubin in bile. This may lead to deformation of primary common bile duct stones
with a high bile pigment as contents.
If obstruction continues, the reticulin laid down in the periportal area matures to hard type, causing
fibrosis around the bile duct, which may further aggravate the cholestasis. [14,15]
Biochemical changes
Bilirubin
Conjugated hyperbilirubinemia is the classic biochemical feature of obstructive jaundice. Conjugated
bilirubin is water -soluble and penetration to body fluids is high, thus producing more jaundice than
unconjugated pigment.
Alkaline phosphatase
The level r ises in cholestasis and to a lesser extent when liver cells are damaged. The mechanisms of
the increase are complex. Hepatic synthesis of the alkaline phosphatase by the hepatocytes is increased
and this depends on intact protein and RNA synthesis.
Gamma g lutamyl transpeptidase (GGT)
Serum values are increased in cholestasis and hepatocellular diseases. Levels parallel serum alkaline
phosphatase in cholestasis and may be used to confirm that a raised serum phosphatase is of
15
hepatobiliary origin. It is also elevated in alcohol intake, pancreatitis, chronic lung disease, renal failure
and congestive heart failure.
Protein synthesis
The liver occupies a central role in protein synthesis and albumin is quantitatively the most important
of pl asma protein formed in the liver. The relatively long half -life of serum albumin (20 days) makes
the serum albumin level a better index of severity and prognosis in patients with chronic liver disease.
Alteration in serum albumin levels may reflect not onl y disturbances in synthesis but also changes in
the rate of catabolism, dilution by expanded plasma volume or enhanced loss from the gastrointestinal
tract and kidneys. The most important aspect of protein synthesis relates to the liver in the maintenance
of the normal blood coagulation process.
Clotting factors
Liver disease is a common cause of impaired coagulation. Normal serum activities of the vitamin K –
dependent coagulation factor proenzymes (factors II, VII, IX and X), as assessed by the one stage
prothrombin time, depend on both intact hepatic synthesis and adequate intestinal absorption of vitamin
K. In cholestatic disease prolonged prothrombin time can be improved by parenteral administration of
vitamin K. a characteristic pattern of abnormalities occurs in patients with severe liver dysfunction; it
consists of low plasma fibrinogen level, a prolonged prothrombin time, and a normal or prolonged
partial thromboplastin time. [10,16 ]
16
ETIOLOGY
A complete or partial obstruction of biliary flo w can cause jaundice and this may be intra or extra
hepatic.
Causes of surgical jaundice are classified into: [13]
A. In the lumen of duct
Choledocholithiasis
Hemobilia
Parasitic infestation due to: Hydatid disease, Ascariasis
B. In the wall of duct
1. Congenital
Biliary atresia
Choledochal cyst
2. Acquired
Papillary stenosis
Strictures
a. Post-traumatic
b. Post-surgical :
o Injuries at cholecystectomy
o Exploration of CBD
o Pancreatic operation
o Gastrectomy
o Biliary enteric anastomosis
o Operation on liver and portal vein
c. Post-inflammatory strictures :
o Gallstones
o Chronic pancreatitis
o Chronic duodenal ulcer
o Parasitic inflammation
o Recurrent pyogenic cholangitis
d. Pimary sclerosing cholangitis
e. Following radiotherapy
f. Mirrizzi’s syndrome
3. Malignant causes
17
Cancer of Gall bladder
Cholangiocarcinoma
Cancer of ampulla of V ater
C. Outside the wall of duct
1. Benign: Pseudocyst of pancreas .
2. Malignant:
o Cancer of head of pancreas
o Enlarged lymph nodes at portahepa tis
o Periampullary Ca ncer
o Extra biliary malignancy
In the lumen of duct
A. Choledocholethiasis
Nearly all calculi found in the common bile duct were originally found in the gall bladder and
migrate down the cystic duct into the common bile duct. Calculi in common bile duct can be
divided into: [15,17 ]
1. Primary common bile duct sto nes
2. Secondary common bile duct stones
1. Primary common bile duct stones
These stones are formed primarily in the CBD and do not originate from gall bladder. These are
caused due to bile duct stasis or due to infection. Almost all calculi are pigment stones . They
are solitary, ovoid, light brown in color, soft and easily crushable.
Disturbance in the flow of bile as well as introduction of infected material into the biliary tract,
may be associated with previous operation that disturb the usual motility dyn amics of the
sphincter, such as shpincterotom y, sphincteroplasty and biliary -enteric anastomosis and also
condition that obstruct the flow of bile into duodenum such as sphincter fibrosis, chronic
pancreatitis and periampullary duodenal deverticula can lea d to stasis of bile resulting in bile
duct calculi and infection of biliary system. [18,19]
2. Secondary common bile duct stones
They a re those that have migrated into t he biliary system from the gall bladder.
3. Retained stones in common bile duct are those that present at some point in time following
cholecystectomy with or without concomitant bile duct stone.
18
B. Hemobilia
Hemobilia is a rare cause of upper GI bleeding that most often results from blunt or penetra ting
hepatic injury, with fistula formation within the liver between a vascular structure and the
biliary duct system. Jaundice occurs due to acute extrahepatic biliary obstruction owing to the
blood clot formation in the common bile duct. Non -traumatic ca use of hemobilia includes
hepatic abscesses, choledocholithiasis or oriental cholangiohepatitis.
C. Parasitic infestation of bile duct
1. Ascariasis : is the most common helminthic infestation of bile ducts, caused by Ascariasis
Lumbricoides . In the presence of massive duodenal infestation the worms can enter the
biliary system. [20]
2. Clonorchiasis : it is endemic to Asia and is caused by the liver fluke, Clonorchis Sinensis ,
which is transmitted by ingestion of infected raw fish. The intrahepatic ducts are the natural
habitat, where they cause obstruction, periductal inflammation and fibrosis. [21]
3. Echinococcus granulosus (Hydatid cyst) : it is the usual organism responsible for hydatid
disease. Large cysts in the liver may compress the intrahepatic biliary radic als and rupture
into the bile duct and may release daughter cysts causing obstructive jaundice and fibrotic
change in the biliary tree. [22]
In the wall of duct
1. CONGENITAL
a. Biliary atresia
The occurrence of biliary atresia is embryological. Failure of vacuolization of the solid
embryonic bile ducts filled by proliferating epithelial cells was supposed to produce this
malformation. Probably only a small percentage of cases are congenital malformations or
intrauterine catastr ophies. [23]
Types :
Type I: Atresia of CBD, with a common hepatic duct remnant.
Type II: Atresia of common hepatic duct and bile duct with right and left duct remnants.
Type III: Atresia of the extrahepatic ductal system.
19
Fig. 1.9: Types of extrahepatic biliary
atresia
b. Choledochal cyst
It is defined as an isolated or combined congenital dilatation of the extrahepatic and
intrahepatic biliary tree. Mostly confined to extrahepatic biliary tree starting from
bifurcation of right and left hepatic ducts to the opening of pancreatic duct. Three theories
have been stated for the formation of the cyst.
Anomalous pancreatic duct and biliary du ct junction causes pancreatic reflux into
CBD, leading to high pressure in CBD.
Abnormal canalization of the bile duct during embryogenesis, with distal obstruction
causing weakening of bile duct wall.
Abnormality of autonomic innervation of the extrahepat ic tree. [24,25 ]
Todani’s classification of choledochal cysts
Type I – dilatation of the extrahepatic biliary tree, a – cystic, b – focal, c – fusiform.
Type II – saccular diverticulum of extrahepatic bile duct.
Type III – biliary tree dilatation within the duodenum: choledochocele.
Type IVa – dilatation of intra & extra -hepatic biliary tree.
Type IVb – multiple extra hepatic cysts.
Type V – dilatation of intrahepatic ducts (Caroli’s disease)
20
Fig. 1.10: Todani’s classification of choledochal cysts
Type I
Type V Type III
Type I Vb Type I Va Type I I
21
Caroli’s disease
It is a rare, congenital, non -familial condition, characterized by multiple saccular dilatation of
intrahepatic ducts separated by segments of normal or stenotic ducts. Usually associated with
congenital hepatic fibrosis, medullary sponge kidney, cholangiocarcinoma and stone formation. [24,25 ]
2. ACQUIRED
Papillary stenosis: it has been defined as an obstructive disease of the papilla, which is organic
and benign. It is usually primary, of unknown pathogenesis or secondary to inflammation such
as duodenal ulcer or pancreatitis or passed out CBD calculi. [26]
Benign biliary strictures
Benign stenosis a nd strictures of the bile ducts occurs in number of conditions and may affect
intrahepatic or extrahepatic biliary tree.
Causes
A. Bile duct injuries [27-30]
I. Postoperative bile duct strictures
1. Cholecystectomy and exploration of common bile duct
2. Other operative procedures:
– Biliary – enteric anastomosis
– Operation of liver or portal vein
– Pancreatic operation
– Gastrectomy
II. Stricture after blunt or penetrating injury
B. Post-inflammatory stricture with: [27-30]
1. Cholelithiasis / choledocholithiasis
2. Chronic pancreatitis
3. Chronic duodenal ulcer
4. Abscess or inflammation in subhepatic region
5. Parasitic infection
6. Recurrent pyogenic cholangitis
C. Primary Sclerosing Cholangitis
D. Radiation -induced Cholangitis
E. Papillary Stenosis
22
Postoperative bile duct strictures
The g reat majority of injuries to the bile duct occur during cholecystectomy with or without exploration
of the CBD. They also occur in other operation on either the stomach, pancreas or liver, or during
surgeries for portal hypertension. [32]
Number of factors related to bile duct injury with cholecystectomy [29-32]
A. Anatomical variation
There are wide anatomical variations in extrahepatic biliary tree and adjacent hepatic artery and
portal venous structure. Anomalies of the vessels are in the tune of 20% and hence very
common. The most common for right hepatic artery to arise in whole or in part from the
superior mesenteric trunk. The important ductal anomalies are related to the manner of
confluence of right and left hepatic ducts and of the cystic duct with the common hepatic duct
and bile duct anomalies mentioned early.
B. Use of diathermy near Calot’s triangle .
C. Technical factors : bile duct injuries occur following cholecystectomy performed by surgeons
who are inadequately trained or inexperienced. Traction on the gall bladder while applying clips
on the cystic duct may include a part of th e CBD wall which leads to stricture formation. The
hepatic duct or common bile duct is often assumed as the cystic duct and has been excised. [27]
D. Attempts to control hemorrhage during cholecystectomy: there may be damage to the bile
duct if clamps are app lied blindly.
E. Bile duct ischemia: bile duct blood supply runs in three columns, one posterior and two lateral.
It is suggested that damage to these vessels may result in ischemia to the bile duct, with
consequent necrosis and stricture.
F. Pathological factor : acute cholecystitis may be accompanied by extensive edema in the region
of porta hepatis and Calot’s triangle and there may be considerable friability during dissection.
[28]
Primary Sclerosing cholangitis
It has an unknown etiology. It is a progressive cholestatic disorder characterized by a fibrosing
inflammatory process, which affects the intrahepatic and/or extrahepatic ducts. It may occur alone or in
association with inflammatory bowel disease. There st rictures are typically short and annular
alternating with normal or minimally dilated segments leading to characteristic beaded appearance.
[3,34]
23
Classification of bile duct stricture [32]
Type I: low common hepatic duct stricture; hepatic duct stump > 2cm.
Type II: mid common hepatic duct stump < 2cm.
Type III: high stricture (hilar)
Type IV: destruction of hilar confluence.
Type V: involvement of sectoral right branch alone or with common duct.
Fig. 1.11: Classification of bile duct stricture
24
3. MALIGNANT CAUSES
a. Cancer of gall bladder
This tumor represents only 2% of all cancers, but it is the most common site of cancer in
biliary tract.
Etiology
75-98% of patients with gall bladder cancer have gall stones and also common in the
presence of chronic cholecystitis. Others include porcelain gall bladder (10 -25% risk)
choledochal cyst, inflammatory bowel disease, polyposis coli and primary Sclerosing
cholangitis.
Pathology
85% of gall bladder carcinoma is adenocarcinoma, other variants common are mesenchymal
tumors, carcinoid, lymphoma, squamous and adenosquamous carcinoma.
Table 1.1: TNM staging for gall bladder Cancer
Tumor Nodes Metastasis
Stage 0 Tis N0 M0
Stage IA T1 N0 M0
Stage IB T2 N0 M0
Stage IIA T3 N0 M0
Stage IIB T1-3 M0 M0
Stage III T4 Any N M0
Stage IV Any T Any N M1
Tis: Cancer in situ
T1: tumor limited to mucosa or muscularis
T2: tumor invades perimuscular connective tissue or serosa
T3: tumor invades liver (< 2cm) or one adjacent organ
T4: tumor extends > 4cm into liver or two or more adjacent organ
25
Nevin classification for staging of gall bladder carcinoma [37]
Depth of tumor
Stage I: mucosa
Stage II: muscularis
Stage III: serosa
Stage IV: liver invasion
Stage V: adjacent organ or distant metastasis
b. Cholangiocarcinoma
The incidence of bile duct tumors increases with age. It has even distribution between men
and women. The most common is adenocarcinoma (95%) and remaining are squamous,
leiomyosarcoma, mucoepidermosis, carcinoid and cystadenocarcinoma.
Causes of cholangiocarcinoma are primary Sclerosing cholangitis, choledochal cyst, liver
fluke infestation, CB D stone, thorotrast and asbestos exposure. [38,39 ]
Cholangiocarcinoma is best classified anatomically into three broad groups: [76]
TNM staging for extrahepatic cholangiocarcinoma [40]
T1: tumor limited to mucosa/muscle
T2: tumor invades to periductal tissue
T3: tumor invades adjacent structure
Table 1.2: Current American Joint Commission on Cancer
TNM Staging System for Cholangiocarcinoma [76]
1. Intrahepatic
2. Perihilar
3. Distal
Stage 0 Tis N0 M0
Stage I T1 N0 M0
Stage II T2 N0 M0
Stage III T1 or T2 N1 or N2 M0
Stage IVA T3 Any N M0
Stage IVB Any T Any N M1
26
Bismuth -Corlette classification
The Bismuth -Corlette classification is a classification system for perihilar cholangiocarcinomas , which
is based on the extent of ductal infiltration.
Classification :
Type I: limited to the common hepatic duct , below the level of the c onfluence of the right
and left hepatic ducts .
Type II (Klatskin tumor) : involves the confluence of the right and left hepatic ducts .
Type IIIa: type II and extends to the bifurcation of the right hepatic duct .
Type IIIb: type II and extends to the bifurcation of the left hepatic duct .
Type IV: extending to the bifurcations of bo th right and left hepatic ducts OR multifocal
involvement . [74]
Fig. 1.12: Classification of cholangiocarcinoma
C Bismuth classification [75]
27
c. Periampullary carcinoma
Periampullary cancers include a group of malignant neoplasms arising at or near the ampulla
of Vater, within 2 cm of radius from ampulla. Most of them are adenocarcinoma arising from
the head of pancreas (60%), ampulla of Vater (20%), distal common bile duct (10%) or
second part of duodenum (10%).
Risk factors [41]
Cigarette smoking
Diet rich in animal fat
Chronic pancreatitis
Post gastrectomy, cholecystectomy
Chemical exposure: naphthylamine, benzidine
Hereditary: familial polyposis, Gardener syndrome
Diabetes mellitus
d. Cancer of head of pancreas
Accounts for 60% of periampullary carcinomas. At least 2/3 of cases of pancreatic cancer
arise in the head of the gland. Ductal carcinoma of the pancreas accounts for more than 90%
of all malignant pancreatic exocrine tumors. Other variants are giant cell carcinoma,
adenosquamous carcinoma, mucinous carcinoma and acinar cell carcinoma.
Pancreatic cancer has a propensity for perineural invasion within and beyond the gland and
for a rapid lymphatic speed. The most common site for extralymphatic involvement are the
liver, peritoneum and lungs. [43]
e. Carcinoma of ampulla of Vater
Accounts for 20% of periampullary carcinomas. Most are adenocarcinomas. Though a
number of other tumor histologies such as carcinoids, other neuroendocrine tumors and
sarcomas may arise . Spread of the tumors is by local extention to involve the pancreas and
duodenum and metastasis to regional lymph node. [42]
28
CLINICAL PRESENTATION
Abdominal pain
Typically, the pain is felt in the right upper quadrant or epigastrium, with frequent radiation to the
interscapular area and typically lasts for 30 minutes to several hours.
The pain due to bile duct obstruction is due to distension and increased pressure within the bile duct.
With cholangitis both the pain and the initial phase o f fullness and discomfort are produced at lower
intraluminal pressure.
When inflammatory or malignant lesions spread to the surface of the liver or gall bladder, “somatic”
pain results.
Jaundice
Jaundice is the abnormal accumulation of bilirubin in body tissue , which occurs when the serum
bilirubin level exceeds 50 μmol/ L. Excess bilirubin causes a yellow tinting to the skin, sclera and
mucous membranes. Jaundice is an important feature of disease in the blood, liver or biliary system.
Pruritus
Pruritus is an important symptom of liver disease. It lasts longer than 3 – 4 weeks regardless of the
cause. It tends to be most marked on the extremities, is present less often on the trunk, rarely on the
neck and face. It is often more troublesome after a hot bath and at night, when the skin is warm. The
pruritus of liver disease has been attributed to the high plasma concentration of bile salts.
29
Anorexia
Anorexia is a common symptom of liver disease, particularly in jaundiced patients with either
hepat ocellular failure or biliary obstruction. Anorexia may be profound. Weight loss is probably due to
anorexia and reduced food intake.
Nausea, vomiting
Nausea and vomiting are often a striking feature in patient with acute biliary obstruction but may not be
present.
Bowel functions
A moderate increase in stool frequency with passage of soft or loose stools due to increased fecal fat
resulting from a lowered intraluminal concentration of bile salts. It is an uncommon presenting
symptom except in malignant bili ary obstruction – steatorrhea occurs with biliary obstruction but much
higher level of fecal fat results when pancreatic duct is blocked.
Stools and urine
Fecal color gives a good indication whether cholestasis is total, intermittent or decreasing. Occult blood
in stools – sign of malignancy.
Bile salts, deficient in the intestine in cholestasis are essential for the normal color of the stools. It is
usually pale in color in cholestasis.
Urine is dark in color in cholestatic jaundice because of increase in circulating conjugated bilirubin.
Mass per abdomen – gall bladder palpable or Courvosier’s gall bladder.
Bleeding
Patients may complain of spontaneous bleeding from the nose and gums or of easy bruising, because
the prothrombin time is prolonged due to decrease in vitamin K absorption.
Fever
This is secondary to acute cholangitis, which results from two factors, obstruction of the biliary tree
and bacteria in bile.
30
General physical examination
A parous middle -aged obese fema le is a candidate for gall stones while chances for cancerous
biliary obstruction increases with age.
Widely set eyes, a prominent forehead, flat nose and small chin are features of any form of
persistent intrahepatic cholestasis in childhood.
Xanthoma and xanthelasma around the eyes suggest chronic cholestasis. Elevated plasma
cholesterol levels are seen as deposits in palmar creases, below the breast, chest or back. The
tuberous lesions appear later and are found on extensor surfaces, especially the wrist s, elbows,
knees, ankles and buttocks.
Fever may be present in metastatic liver disease and with primary carcinoma of pancreas and
stomach.
Dyspnea and tachypnea are commonly seen due to ascites , abdominal organomegaly due to
elevated and restrict movement of the diaphragm.
Jaundice: yellowish discoloration of sclera, skin and mucous membrane due to increase in
serum bilirubin above 2 mg/dL. Patients with prolonged biliary obstruction have a deep
greenish hue compared with hemolytic jaundice where it is mil d yellow and in hepatocellular
jaundice where it is orange.
An increase in melanin pigmentation is seen with many chronic liver disease and chronic
cholestatic disorders.
Scratch marks result from severe pruritus.
Spider nevi, excessive bruising or tiny pe techial hemorrhages indicate the presence of chronic
liver disease . [44]
31
INVISTIGATION S
Laboratory examinations [44-46]
1. Urine bilirubin
When bilirubinuria is present the urine is unusually dark brown in color. Test strips can detect
as little as 1 -2 mol e of bilirubin per liter. Bilirubinuria occurs even with small increase in
plasma -conjugated bilirubin and usually precedes jaundice.
Absence of bilirubinuri a is important in a jaundiced patient, as it suggests an unconjugated
hyperbilirubinemia or hemolysis.
2. Urinary urobilinogen
Bilirubin esters entering the intestine undergo bacterial hydrolysis and degradation in the ileum
and colon with the production of u robilinogen. Normal level in the stools is 40 – 200
mg/24hours.
Urinary urobilinogen gives a reaction with Ehlirich’s aldehyde reagent. A normal value is 0 – 4
mg/24hours.
In the presence of liver damage more urobilinogen escapes hepatic uptake and biliar y excretion
and it is excreted in urine.
3. Liver function tests
a. Serum bilirubin
Normal values: To tal – upto 1.2 mg/dL (< 25 µmol/L)
Direct – upto 0.4 mg/dL (< 6 µmol/L)
Indirect – 0.4-0.8 mg/dL (< 18 µmol/L)
The standard test for bilirubin is the Vandenberg reaction. The basis for this colorimetric
test is the differing solubility of conjugated and unconjugated bilirubin.
Hepatocellular disease impairs excretory function of bile t o a greater degree than the ability
to conjugate bilirubin and therefore the hyperbilirubinemia in this setting is predominantly
of the conjugated type. It is very difficult to distinguish between hepatocellular disease and
extrahepatic biliary obstruction solely on the basis of conjugated hyperbilirubinemia.
In patients with jaundice secondary to extrahepatic obstruction, the determination of the
direct fraction of bilirubin is more sensitive index than total bilirubin.
b. Alkaline phosphatase
Normal values: 3 – 13 King Armstrong (K -A) units (or)
1.5 – 4 Bobansky units (or)
53 – 128 IU/L
The level of alkaline phosphatase rises in cholestasis and to a lesser extent when liver cells
are damaged.
The rise in alkaline phosphatase along with increase in Gamma Glutamyl Transpeptidase
(GGT) is specific for hepatobiliary origin.
32
c. GGT
Serum values are increased in cholestasis and hepatocellular diseases. Levels parallel to
serum alkaline phosphatase in cholestasis and may be used to confirm that a raised serum
phosphatase is of hepatobiliary origin. Normal range is (8 -78 IU/L).
d. Aminotransferases
1) Serum Glutamic Oxaloacetic Transaminase (SGOT) or Aspartate Transaminase (AST)
[46]
This is a mitochondrial en zyme present in large quantities in heart, skeletal muscles,
liver and kidney and the serum level increases whenever these tissues are actually
destroyed, presumably due to release from damaged cells.
Normal values: 6 – 40 units (Karmen)
5 – 40 IU/ml
0 – 15 IM/ml
2) Serum Glutamic Pyruvic Transaminase (SGPT) or Alanine Transpeptidase (ALT)
This is a cytosolic enzyme also present in liver. Compared to SGOT malor amount is
present in liver. Therefore, this is more specific for liver damage than SGOT. Normal
values: 6 – 36 units (Karmen)
5 – 35 IU/ml
0 – 15 IM/ml
e. Albumin: normal value 35 – 55 g/L
Synthesized in the hepatocytes. Its half -life is 15 -20 days. Hypoalbuminemia reflects severe
liver damage and decrease albumin synthesis. Other causes for hypoalbuminemia are:
protein losing enteropathies, nephritic syndrome and chronic infection.
f. Globulin: normal value 20 – 35 g/L
They are a group of protein mostly made up of gamma globulin, produced by B –
lymphocytes. Alpha and beta globulins are produced in hepatocytes. Globulin increase in
chronic liver disease.
g. A/G ratio: normal value 1.5 – 3 g/L
Any change or reve rsal in the ratio indicates liver damage.
h. Prothrombin time: normal value 12 – 16 seconds
It collectively measures factors II, V, VII and X. biosynthesis of these depends on vitamin
K. Prothrombin time may be elevated in hepatitis, cirrhosis and obstru ctive jaundice.
Marked prolongation of prothrombin time > 5 seconds above control is a poor prognostic
factor.
33
Radiological studies [47-51]
1. Ultrasound
Ultrasound examination of the hepatobiliary system is an important first line, non -invasive
investigation. Patient preparation for ultrasound should include fasting for 12 hours. Dilated bile
ducts, gall bladder disease, hepatic tumors and some diffuse hepatic abnormalities are
identified. [48,49 ]
Normal ultrasound shows the liver to have mixed echogenicity. Portal and hepatic veins,
inferior vena cava and aorta are shown. Normal intrahepatic ducts measuring 1 -3 mm in
diameter and common bile duct 2 -7 mm in diameter are seen on ultrasound.
Ultrasoun d plays a vital role in the evaluation of focal liver disease, screening for liver
metastasis, hepatocellular carcinoma, portal hypertension, surgical obstructive jaundice and
hepatic veno -occlusive disease.
Sonography is ideally suited to study the intern al architecture of a focal mass and distinguish a
solid from a cystic lesion. The addition of color Doppler flow imaging further helps
characterizing mass lesions and assessing patency of vessels.
2. Computed tomography (CT)
CT also shows dilated bile ducts distinguishing obstructive from non -obstructive jaundice in
90% cases. But as a screening procedure it has no advantage over ultrasound. It is however,
more likely than ultrasound to show the level and cause of obstruction.
Advancement of CT technology inc luding the development of spiral scanners and more
recently, multi -detector row CT scanners and the development of 3D imaging software have
significantly improved the ability of CT to image patients with obstructive biliopathy. [52]
3. Endoscopic retrograde c holangiopancreatography (ERCP)
With the help of ERCP, diseases of the esophagus, stomach, duodenum, pancreas and the
biliary tract including duodenal diverticula and fistulae may be diagnosed. [53]
ERCP is performed with a side viewing endoscope, either video or fibre -optic. The stomach and
duodenum are inspected and biopsy and cytology specimen taken if indicated. The papilla is
identified. The cannula is then introduced under direct vision into the papilla and contrast
injected under fluoroscopic control. X -ray films are taken. The success rate of ERCP is 80 -90%,
but depends on experience. [54]
Indication:
o Used to show duct strictures.
o Gall bladder and common bile duct stones.
o Pancreatic and bile ju ice may be obtained for culture, aspiration cytology.
o After biliary surgery.
o Pancreatic disease.
o Cytology or biopsy from malignant growth or strictures.
Complication:
o Acute pancreatitis.
o Cholangitis.
34
4. Percutaneous trans -hepatic cholangiography (PTC)
Contrast is injected percutaneously into a bile duct within the liver. The procedure is done in the
radiology department. The “skinny” chiba needle is 22 G, is introduced in the 7th, 8th or 9th right
intercostals space at midaxillary line, with the help of USG and the contrast is injected. Biliary
tree is identified and if any dilated ducts are encountered, they should be catheterized and
external or internal biliary drainage established. [55]
The technique is easy and the success rate is 100% if intrahepat ic bile ducts are dilated.
Indication
o When ERCP has failed.
o Endoscopic access is difficult (hepaticoenterostomy, Billroth II).
o Brush cytology and biliary biopsy may be performed.
Complication
o Bleeding.
o Biliary peritonitis.
o Septicemia.
5. Magnetic resonance cholangiopancreatography (MRCP)
MRCP shows water containing bile and pancreatic juice within the bile duct and pancreatic duct
without the need for injection of contrast. MRCP is more expensive than USG and CT, and is
not available in all hospitals.
It has an overall accuracy of greater than 90% in showing CBD stones. It is highly accurate in
showing bile duct stricture and pancreatic carcinoma. [56,57 ]
6. Endoscopic ultrasound (EU)
This is done using an endoscope which has a miniature ultrasound transducer m ounted at its tip.
Most endoscopes used for ultrasonography have a mechanical rotating scanner at the tip and
side or oblique viewing. Recognizing the structures seen at endoscopic USG requires a
sufficient period at training and this has limited its gener al availability to specialist centers.
In the hepatobiliary system its prominent role is in the detection and evaluation of pancreatic
tumors. It also detects CBD stones and can be used for image -directed biopsy. Accuracy of EU
for choledocholithiasis is greater than 90%. [58]
7. Biliary scintigraphy
The technetium -labeled iminodiacetic acid derivative (IDA) is cleared from the plasma by
hepatocellular organic anion transport and excreted in the bile. The method may be used to
determine patency of the cystic duct in suspected acute cholecystitis. The gall bladder ejection
fraction can be calculated. Cholescintigraphy can show whether the bile duct is ob structed.
Scintigraphy is also useful in assessing the patency of biliary -enteric anastomosis and may
show biliary leaks after cholecystectomy or liver transplantation. [59]
35
8. Operative and postoperative cholangiography
They are indicated when there is st ones present in CBD. After exploration of the CBD,
cholangiography should always be performed, using high kilovolt peak technique and full
strength contrast.
Any debris may cause filling defects less sharply defined than those caused by gallstones.
Any obs truction of CBD, there will be no flow of contrast into the duodenum.
Postoperative cholangiography using contrast injected gently should be undertaken routinely
before final removal of a T -tube draining the biliary tree. It is essential to obtain filling of all
right and left intrahepatic radicals, the common hepatic duct and CBD and flow to duodenum
before removal of T -tube. [60]
With the development of newer investigative modalities, the remaining tests mentioned, are
rarely done nowadays for the diagno sis of obstructive jaundice.
9. Abdominal radiograph
10. Barium contrast upper gastrointestinal X -ray
11. Oral cholecystography
12. Intravenous cholangiography
36
Fig. 1.13: Algorithm of obstructive jaundice management [81]
37
PREOPERATIVE PREPARATION
Obesity increase the technical difficulties for the surgeon and makes post -operative
complication more likely. Weight reduction under the control of the dietician if possible.
Use of contraceptive pills and the risk of the venous thrombosis and it is advis able that OCP be
stopped prior to and after 6 weeks of surgery.
An abdominal prothrombin activity increases the risk of hemorrhage. Administration of vitamin
K dose will reduce this risk.
Preoperative antibiotic prophylactic is given.
Insertion of naso -gastric tube, intravenous fluid infusion and urinary catheter to monitor output
is a must.
The patient’s blood grouping in case of transfusion is necessary.
Nutritional status should be assessed and improved if necessary.
The renal, cardiovascular system and CNS should be evaluated before surgery.
Jaundice patients have a high risk of post operative renal failure which can be reduced by
operating during diuresis produced by mannitol with fluid supplementation.
Anesthesia
General anesthesia for biliary tract surgery is essentially no different from that of any intra -abdominal
operation. However, there are a few points of particular interest to the anesthetist.
The presence of abnormal liver function tests requires caution to be taken according to the
degree of abnormality with the dosage of all drugs used, as almost all depend on the liver for
their detoxification. Halothane is contraindicated in the presence of abnormal liver function.
General anesthesia must produce sleep, analgesic, good muscle relaxation an d stable blood
pressure.
Care must also be taken during the operation to avoid kinking of inferior vena cava during deep
retraction which results in drop in cardiac output.
IV atropine 0.6 mg given first before the operative cholangiogram helps to diminish any spasm
of the sphincter of Oddi .
Incision
Kocher’s right subcostal.
Midline incision.
Right upper paramedian.
38
SURGICAL PROCEDURES
In current surgical practice, various operative procedures have been performed for obstructive jaundice,
depending on the cause. The choice of procedure also depends on the experience and preference of the
surgeon.
Cholecystectomy with CBD exploration with stone removal/dilatation/sphincteroplasty and T –
tube drainage.
Cholecystectomy with choledochoduodenectomy with T -tube drainage.
Cholecystojejunostomy.
Pancreaticoduodenectomy (Whipple’s procedure)
Palliative operation for relieving obstructive jaundice due to malignant disease.
Pancreaticojejunostomy.
Non-surgical biliary drainage.
Different operations for biliary stric tures.
Exploration of the CBD
The operation of choledochotomy carries a mortality of at least 4 times greater than cholecystectomy
alone.
Indication:
o History of jaundice.
o Multiple small stones or single faceted stone in the gall bladder.
o A dilated cystic duct.
o Induration of head of the pancreas.
o Dilated common duct – more than 8 mm.
o A palpable stone in the CBD during surgery.
Operation
Opening of the duct
Stay sutures of catgut are inserted into the common duct near either side of the anterior aspect about 2
cm above the first part of the duodenum and a longitudinal incision is made with a fine knife.
39
Exploration (distal)
Fogarty catheter is inserted down the common bile duct into the duodenum and the balloon inflated.
The catheter is gently withdrawn until it is halted by the sphincter of Oddi. The lower end of the duct is
palpated and felt against the catheter, above the balloon. A bulldog clamp is placed across the common
duct above the opening to prevent any stones escaping into the proximal ducts. The balloon is deflated
and the catheter gently brought through the sphincter, this can be traced by the palpating fingers. The
balloon is reinflated and steadily withdrawn bringing the stone with it. This procedure is repeated until
no more stones are withdrawn.
Exploration (proximal)
The catheter is reinserted into the proximal segment and the procedure is repeated in the lef t and right
hepatic ducts. The bulldog clip is placed on the common duct bellow the opening to prevent stones
falling into the distal duct. The balloon is inflated until some resistance is felt and withdrawn with the
pressure maintained on the syringe. Thi s is necessary because the lumen of the duct increase in
diameter and unless the balloon continues to fill the lumen, a stone may slip past. [61,62]
Fig. 1.14: Exploration of the common bile duct
40
Assessment by X -ray
The catheter is inserted into the common duct so that the balloon lies just distal to the opening where it
is initiated to occlude the duct. After checking the position of the X -ray machine, about 10 ml of
hypaque is injected and films are taken. The ballo on is deflated and the procedure repeated with the
catheter in the common hepatic duct. For fixed stone Bougie’s or Desjardin’s forceps are used to
dislodge the stone and withdrawn.
Closure of the duct can be done with or without a T -tube. Catgut is used a nd usually it is continuous.
Gall bladder is removed, cystic duct, cystic artery ligatures are checked. Any bile leak from the CBD is
inspected.
Removal of T -tube post operatively
The T -tube is allowed to drain freely into a bile bag for 5 days when it is clipped for 1 hour after meals.
This is increased by 1 hour each day so that by the 10th day the tube is clipped all day. A T -tube
cholangiogram is obtained as a final check that the duct system is normal and if so the skin suture is
withdrawn and the tube is removed. [60]
Sphincterotomy
Sphincterotomy requires duodenotomy placed at the level of the sphincter of Oddi , division of the
sphincter and suture of the wall of CBD to the duodenum. It has advantages of facilitating inspection of
the papilla, biopsy and pancreatic radiography, if required. [63]
Indication
o CBD stone.
o Stricture at the lower end of the CBD.
Fig. 1.15: Sphincterotomy
41
Exploratory choledochoscopy
The choledo choscope permits visual inspection within the bile duct during surgical exploration for
gallstones and may greatly facilitate the exploration of the common and hepatic bile ducts and the
localization and retrieval of stones.
Position of patient
The operating table should have facilities foe X -ray to enable the operative cholangiography to be
done. The patient should be positioned with a few degrees of feet down and lateral tilt to the right.
Incision
A transverse right upper abdominal incision.
Operation
Once the abdomen is opened, th e duodenum and the hepatic flexure of the colon are retracted
downwards. A clear exposure of anterior aspect of the supraduodenal CBD is done. The
choled ochotomy should be placed as low as possible, above the superior border of the duodenum.
The choledochoscope is introduced into the CBD in a distal direction. The interior of CBD is inspected
as the instrument is advanced distally. A gallstone may be retri eved from the CBD under direct vision.
A fine balloon catheter (Fogarty) is passed down the channel of the choledochoscope and passed
beyond the stone and inflated. The balloon, stone and instrument all withdrawn together.
For multiple mobile stones in the duct a retractable wired basket may be passed down the
choledochoscope channel. The basket should be used to open as a dragnet to avoid crushing of the
stones.
Proximal choledoch oscopy is done to view hepatic ducts. Choledochotomy is closed with 3/0 catgut,
either interrupted or continuous. [64]
Transduodenal exploration of bile duct (Biliary Sphincterotomy)
Indication
o Impacted stone to the lower end of the CBD.
o Stenosis of the papilla and sphincter.
o Re-exploration.
42
Contraindication
o A single large stone in the supraduodenal portion of the CBD that does not descend to the
sphincteric region.
o Multiple facetted stones locked in the bile duct.
o Long stricture of terminal CBD.
o Presence of acute pancreatitis.
Operation
Either a right paramedian or Kocher’s subcostal incision provides good access to the biliary tree once
the abdomen is opened, the hepatic flexure of the colon and proximal transverse colon are mobilized
and reflected caudally exposing the head of the pancreas and the duo denal.
Head of the pancreas and duodenum are mobilized forward and medially. Dissection continues until the
aorta is visualized and the 3rd part of the duodenum is free. Papilla is located on the medial wall of the
duodenum. A small bulldog clip is then pl aced across the supraduodenal part of the CBD in order to
prevent calculi slipping back into the common hepatic duct and its tributaries.
The duodenal walls are incised longitudinally or transversely. Babcock tissue forceps are applied to the
longitudinal fold, distal to the papilla and the later is drawn into duodenotomy incision. A grooved
director or lacrimal probe is passed into the papillary orifice and hence into the CBD.
Sphincterotomy is done at 10’ o’clock position. Stones are extracted with Desjar din’s forceps and
Fogarty balloon catheters. Clearance of the duct is confirmed by intraoperative post -exploratory
cholangiography.
Alternatively, choledochoscopy may be used. The duodenotomy is closed in its original axis using a
continuous suture (catgut ) and fine non -absorbable Lambert suture.
Complication
o Bleeding: persistent bleeding of the Sphincterotomy incision usually occurs from a divided
circumferential duodenal artery which is best secured by suture.
o Cholangitis: it is important to remove all ca lculi and provide an adequate sphincterotomy with
free drainage.
o Acute pancreatitis: probing into pancreatic duct should be avoided and to ensure that no suture
encircle the pancreatic duct. [63]
43
Duodenoscopic sphincterotomy for removal of duct stones
Fibro -optic -esophagogastroduodenoscopy is now a routine procedure. ERCP is performed by passing a
Teflon catheter through the biopsy channel of the duodenoscope and placing it directly in the orifice of
papilla of Vater under direct vision. Contrast materi al is then injected during fluoroscopy and
appropriate radiographs are taken. The technique is performed under sedation.
Sphincterotomy
After endoscopic cholangiogram has demonstrated stones, the Teflon catheter is replaced in the distal
bile duct by a diathermy wire.
After confirming its position radiographically the wire is withdrawn slightly and maid taut to produce a
bow, pressing on the root of the papilla.
Diathe rmy current is applied to produce a cut 15 -20 mm long. The aim is to ablate the biliary
sphincters and a view directly up the bile duct is obtained. [65,66 ]
Needle -knife sphincterotome , stent (+) Pull-type sphincterotome , stent ( -)
Fig. 1.1 6: Endoscopic papilla sphincterotomy [77]
Stone extraction
After sphincterotomy, some allow stones to pass spontaneously (< 1 cm in diameter). Few prefer to
remove all stones using balloon catheters or wire basket .
Complication
o Bleeding (mainly from the sphincterotomy site).
o Cholangitis.
o Pancreatitis.
o Retroperitoneal perforation.
44
Endoscopic treatment for patients without stones
Patients with convincing biliary symptoms following biliary surgery are suspected to have sphincter of
Oddi dysfunction or stenosis; this may result from the passage of stones or instruments.
Endoscopic sphincterotomy is a logical and effective form of tre atment when functional obstruction is
present.
For malignant biliary obstruction, when the patient unfit or unsuitable for surgery, jaundice can be
relieved by performing sphincterotomy through the tumor or by placing a prosthetic stent.
Palliative operati ons for jaundice due to malignant disease [67,68 ]
Indications
Non-resectable carcinoma of the pancreas and periampullary carcinoma
Two symptoms are readily palliated by operation: duodenal obstruction and jaundice.
For duodenal obstruction
Gastro -enterostomy with entero -enterostomy is done.
For jaundice
a. Cholecysto -enterostomy
Indication : tumor must at least be 5 cm below the junction between the cystic duct and the
common bile duct.
Procedure
o Gall bladder is emptied using a trocar suction apparatus .
o Jejuna loop is laid alongside the gall bladder of cholecysto -enterostomy done using 2/0
catgut.
Fig. 1.17: Cholecysto -jejunostomy
45
b. Choledocho -jejunostomy
Indication :
o Distal CBD malignant stricture.
o Malignant growth CB D/periampullary carcinoma
End-to-side anastomosis
The common duct is dissected free and transected, and the distal end is oversewn. The proximal
end is then sutured to the loop jejunum. The opening in the jejuna loop made at the apex, should
be a little smaller than the diameter of the common duct.
Anastomosis can be completed with or without T -tube.
Side-to-side anastomosis
If the bulk of the jejunum allows, then a series of accurate interrupted all coats sutures is placed
between the opening of the common duct and the opening in the jejunum. Anastomosis can be
completed with or without T -tube.
End-to-side Side-to-side
Fig. 1.18: Choledocho -jejun ostomy Fig. 1.19: Choledocho -jejunostomy
c. Choledocho -duodenostomy [69]
Indication:
o Dilated CBD containing infected bile and biliary sludge.
o Multiple intrahepatic stones.
o Suppurative cholangiohepatitis.
Contraindication:
o In patient with a bile duct of normal dimension .
Operation
o Incision: Kocher or paramedian.
46
o Exposure: first and second parts of duodenum with addition of the lesser sac and the free
edge of the lesser omentum and the liver.
Dissection
The CBD is opened and a specimen of bile is sent for culture. Stones are removed and the duct
is cleared by copious lavage with saline. The duodenum is freely mobilized by Kocher’s
maneuver in order to allow it to roll upwards over the anterior surface of the bile duct.
After t he duct has been dissected, a vertical incision 2 -5 cm long is made on its supraduodenal
portion and the duodenum is opened in such a way to allow the stoma to be made without
tension. The anastomosis is done with interrupted 3/0 chromic catgut.
Benign bi liary stricture – diagnosis & principles of treatment [70]
Damage to the bile duct may be recognized immediately (at operation), early postoperative period or
later after discharge.
Immediate repair of bile duct injury
The form of repair will depend upon the severity and site of the damage, but results are excellent.
a. Common duct laceration without tissue loss
Insertion of T -tube through the laceration and closure of the wound with interrupted absorbable
sutures. T -tube is removed after 10 days, after chola ngiogram.
b. Common duct laceration with minimum tissue loss
Loss of part of the wall of common duct occurs when the cystic duct is torn at its origin. Its
tissue loss is minimal; the edges are trimmed and closed transversely. T -tube is positioned in
CBD through a separate incision and removed after 4 weeks.
Fig. 1.20: I mmediate repair of bile duct injury
47
c. Common duct divided
End-to-end anastomosis
A clear division of common duct without tissue loss may be repaired by direct anastomosis at
the two ends with interrupted sutures over a T -tube, which should be left in situ for months.
Biliary -intestinal anastomosis
Accidental removal of a wall segment of CBD will necessitate some form of biliary -intestinal
anastomosis using a Roux loop at jejun um.
Late repair of bile duct stricture
a. Biliary intestinal anastomosis for low bile duct strictures
Treatment of a stricture at the lower end of the CBD will depend on its site and relationship to the
ampulla.
Fig. 1.21: Biliary -intestinal anastomosis for late repair of bile duct stricture
(Choledocho -jejunostomy )
1. Choledocho -duodenostomy
To avoid leaving an undrained stump, the common duct above the stricture is anastomosed
side-to-side to the second part of the duodenum establishing a wide stoma.
2. Choledocho -jejunostomy
Anastomosis of the common duct to a jejunal Roux -en-Y is theoretically more desirable
because food particles are less likely to enter biliary tree and obstru ct its lumen.
48
Fig. 1.2 2: Biliary -intestinal anastomosis for low bile duct injuries
(Choledocho -duodenostomy)
b. Biliary -intestinal anastomosis for mid bile duct strictures
Anastomosis of dilated common hepatic duct above the stricture to a jejunal Roux -en-Y loop using
interrupted catgut. A T -tube inserted into the common hepatic duct with one arm through the
anastomosis should remain in situ for 3 months.
c. Biliary -intestinal anastomosis for high bile duct strictures
The track, which will lea d to the mucosa -lined ducts, is first explored with a fine probe, it is
then enlarged with Baker’s dilators.
Once the mucosa -lined duct has been identified, a rubber catheter is positioned and
cholangiogram is performed. This will demonstrate anatomy, degr ee of dilation and any stones
present.
Positioning of a trans -hepatic tube: fully curved Randall’s forceps are now inserted into the
common hepatic duct and passed along the dilated intrahepatic duct system, usually of the left
lobe and then to the periphe ry. Then the tip of forceps grasps the end of the latex rubber tube
and is drawn along the ducts to appear at the porta hepatis.
Construction of Roux loop and exposure of the jejunal mucosa : a standard ante -colic jejunal
Roux -en-Y is fashioned and the end of the free limb closed in 2 layers. Just proximal to
disclosed end a 2 cm diameter disc of seromuscular wall is removed to expose the intact jejunal
mucosa.
The end of the trans -hepatic tube passed to the jejunal lumen and anchored.
49
Traction of the trans -hepatic tube from above, will draw the mucosa into the lumen of the
common duct to create sutureless anastomosis with mucosa -to-mucosa opposition.
Few interrupted catgut sutures are inserted between the jejunal serosa and liver capsul e to
maintain the graft in position.
The upper end of the trans -hepatic tube is brought out through a separate stab incision in the
abdominal wall and fixed securely to the skin with non -absorbable suture.
d. Bilateral mucosal grafts
For very high stricture involve the carina, or the right and left ducts individually. In this event, both
ducts are intubated, and the trans -hepatic tubes are inserted separately, through the exposed jejunal
mucosa to create an epithelial bridge between the two ducts.
Fig. 1.23: Mucosal graft for repair of bile duct
Management of the trans -hepatic tube and vacuum drain
First 3 postoperative days – low-pressure suction (Robert’s pump at 5 cm Hg).
Later replaced by plastic bag into which bile drains freely.
On the 10th day cholangiogram to confirm patency of the anastomosis.
End of the trans -hepatic duct is closed with a spigot.
Patients are taught to irrigate the tube daily with 20 ml sterile water to maintain patency.
3 months later, the trans -hepatic tube is removed.
Alternative methods of biliary decompression
1. Intrahepatic cholangio -jejunostomy (long wire operation): involves the anastomosis of an
exposed peripheral intrahepatic duct to a defunctional limb of jejunum.
2. Percutaneous trans -hepatic bile drainage.
50
Malign ant biliary stricture [70]
Proximal tumors
Hepatic bifurcation tumors.
Hepatic duct tumors.
a. Parts to be excised are: (radical excision)
o Gall bladder.
o Entire supraduodenal common hepatic duct system as for right and left hepatic ducts.
b. Join the several hepatic duct openings for 2 biliary -enteric anastomosis.
c. Silastic drains through the substance of liver is brought to the inferior surface of the liver.
d. Roux -en-Y loop is constructed and sutured to the jejunum with silastic tube inside (in ternal),
and the other end is brought outside the abdominal wall. The tubes are removed after 2 -3
months after cholangiogram.
Distal tumors
Tumors of the bile duct below the cystic duct are treated with Pancreaticoduodenectomy .
Whipple’s surgery.
Pylorus preserving Pancreat oduodenectomy.
Total Pancreatectomy.
Double Palliative By -pass with a Single Roux -en-Y Jejunal Loop, for unresectable pancreatic
head cancer.
Non-surgical biliary drainage
External drainage.
Internal drainage.
External drainage :
Percutaneous cholecystostomy
Indication
Calculous or acalculous cholecystitis, cholangitis, biliary obstruction and opacification of biliary ducts.
[78]
51
Procedure
Under aseptic conditions and ultrasound guidance, using local anesthesia, the procedure is carried out
by using either m odified Seldinger technique or T rocar technique. Trans -hepatic or transperitoneal
puncture can be performed as an access route. Several days after the procedure transcatheter
cholangiography is performed to assess the patency o f cystic duct, presence of gallstones and catheter
position. The tract is considered mature in the absence of leakage to the peritoneal cavity, subhepatic,
subcapsular, or subdiaphragmatic spaces . [78]
Complications
Complications associated with PC usually occur immediately or within days and include haemorrhage,
vagal reactions, sepsis, bile peritonitis, pneumothorax, perforation of the intestinal loop, secondary
infection or colonisation of the gallbladder and cathe ter dislodgment. Late complications have been
reported as catheter dislodgment and recurrent cholecystitis. [78]
Fig. 1.24: Percutaneous cholecystostomy
Endoscopic nasobiliary drainage
Endoscopic nasobiliary drainage (ENBD) is a well established mode of biliary decompression.
Although ENBD is certainly an uncomfortable procedure with the potential risk of spontaneous
dislocation or removal of the drainage catheter by disoriented patients, it has several advan tages over
endoscopic biliary drainage ( EBD) using an indwelling stent. [80]
52
Indications
o Temporary drainage to treat obstructive jaundice and cholangitis caused by maligna nt or
benign biliary stricture.
o Urgent drainage to treat suppurative cholangitis primarily caused by common bile duct
stones .
o Temporary drainage after stone removal in patients with suspected incomplete clearance
and/or with cholangitis.
o Biliary leaks that occur primarily after surgery. [80]
Fig. 1.25: Endoscopic nasobiliary drainage
Internal drainage :
Percutaneous trans -hepatic Biliary Drainage
Indication
53
o Obstruction of biliary ducts, especially those due to unresectable malignant tumors .
o Calculous or acalculous cholecystitis .
o Cholangitis secondary to biliary obstruction .
o It also provides a potential route for stone dissolution therapy and stone extraction . [79]
Procedure
Percutaneous transhepatic cholangiography (PTC) is performed [79]. Once the needle is in the bile
duct, a guide wire is passed beyond the stricture and then the stent is passed. After the insertion of the
stent through the stricture, the guide wire is removed allowing internal decompression of t he
cholestasis.
Complications
Bile leakage, bilorrhea, hemobilia, cholangitis, hemothorax, and pancreatitis can develop. [79]
Fig. 1.26: Internal -external biliary drain in a patient with obstruction of the CBD
Other methods of Internal drainage :
o Standard ERCP and stenting – explained earlier.
o Endoscopic ultrasound -guided biliary drainage (EUS -BD). 3 subtypes:
• EUS-ERCP rendezvous technique .
• EUS -guided antegrade biliary drainage .
• EUS -guided transluminal biliary drainage . [79]
o Palliative operation for jaundice due to malignant disease.
54
Pancreat oduodenectomy (Whipple’s procedure)
The purpose of the operation of pancreat oduodenectomy is to remove the tumor en bloc with adjacent
lymph nodes. The head of the pancreas, the duodenum, the pylorus and distal half of stomach, the gall
bladder and the lower end of CBD and to restore biliary -pancreatic and GI continuity.
Pancreat oduodenectomy is the treatment of choice for operable malignant tumors of the ampulla of
Vater, the lower end of the CBD, the duodenum and the periampullary region of the head of pancreas.
Incision
o Right Mayo -Robson.
o Bilateral subcostal incision.
Procedure
I. Retraction of CBD: exposure and ligation of right gastric and gastroduodenal arteries.
II. Finger dissection between pancreas and portal vein from above, and finger dissection
between pancreas and superior mesenteric vein from below. If both index fingers meet ,
lifting the pancreas forward and then resection can be carried out.
III. Division of stomach (partial gastrectomy).
IV. Division of CBD with the gall bladder.
V. Division of the pancreas in front of the portal vein.
VI. Division and mobilization of the jejunum.
VII. Detachme nt of duodenum and uncinate process of pancreas from superior mesenteric
vessels.
VIII. Anastomosis of bile duct to jejunum. Anastom osis of pancreas to jejunum, gastro –
jejunostomy.
Complication
o Disruption of pancreato -jejunal anastomosis.
o Postoperative hemorrhag e from GI tract.
Pylorus -preserving Pancreat oduodenectomy
A modification to Whipple’s surgery is by preserving stomach and pylorus. The duodenum is
transected, usually 3 x 4 cm distal to the pylorus and re -anastomosed to the jejunum at the point where
a gastrojejunostomy would have been done in the standard operation. The remaining aspects of the
procedure are not different.
55
Fig. 1.27: Pancreatoduodenectomy
Double Palliative By -pass with a Single Roux -en-Y Jejunal Loop
After a careful abdominal exploration, a cholecystectomy is performed, followed by dissection and
transection of the common bile duct. Then, a Roux -en-Y intestinal loop, long 70 -80 cm is prepared
dividing the jejunum 20 -30 cm from the ligament of Treitz, a nd selecting the segment which can be
easily brought up to the sub -hepatic space through a window in the right transverse mesocolon, and
approximated to the cut end of the common bile duct.
A hepatico -jejunostomy, usually termino -lateral, is constructed . A trans -anastomotic Kehr’s T tube can
assure a temporarily external bile drainage. At a distance of 40 cm , and through a second incision in
the mesocolon, left to the middle colic vessels, the same jejunal loop is used for a posterior retrocolic
gastro -enterostomy, well away from the site of neoplastic involvement of the stomach or duodenum .
Finally the intestinal continuity is restored 20 cm downstream , by a termino -lateral jejuno -jejunal
anastomosis. A chemical splancnicectomy can be added.
Fig. 1.28: Sequential double palliative bypass
on the same Roux -en-Y jejunal loop:
1. hepatico -jejunostomy.
2. gastro -enterostomy.
3. jejuno -jejunal anastomosis
56
CHAPTER II
CASE PRESENTA TION 1
25 year -old male . Hospitalized on 28.07.2011, because of :
– Pain in upper abdomen radiating to his back for the previous 5 days
– Jaundice
– Dark urine, pale stools
– No fever
Medical history
Myeloproliferative disease
– Splenomegaly first noted in 2003 (age 17)
– Splenic and portal vein thrombosis 6/2008 (age 22)
• Thrombocytosis, bone marrow biopsy, JAK 2 positive
• Cavernous transformation
• Portal hypertension
– EGD 15.06.08: esophageal varices grade 1, fundic varices
Warfarin, propranolol, hydroxyurea
Ear infection 7/2011, one week prior to hospitalization
– Amo xicillin
o INR not well adjusted
Physical examination
Good general condition
Jaundice
Liver enlarged, not tend er
Spleen massively enlarged
No ascites
57
Lab studies
– CBC
– Liver function test
– Kidney function test
– Viral Hepatitis markers
WBC (4-9) 5.6 *109/L Urea (7-20) 16 mg/dL
Hb (136-177) 161 g/L Creatinine (0.6-1.2) 0.6 mg/dL
Platelets (150-450) 332 *109/L Amylase (23-85) 40 IU/L
INR (0.9-1.2) 2.75 LDH (105-333) 384 IU/L
AST (8-40) 95 IU/L D-DIMER (<500) 1117 ng/mL
ALT (6-56) 166 IU/L HAV IgM neg
ALP (53-128) 254 IU/L HBs Ag neg
GGT (8-78) 233 IU/L HCV Ab neg
Bilirubin (0.1-1.4)
Direct (0 -0.4) 7.0
4.9 mg/dL CMV IgG pos
CRP (200-240) 22.7 nmol/L CMV IgM neg
Ultrasonography
Fig. 2.1: G allbladder distended with sludge, no stones
58
Fig. 2.2: Intra- and extrahepatic bile ducts dilated
Fig. 2.3: S plenomegaly
59
Fig. 2.4: H epatic veins are patent
Fig. 2.5: P ortal vein
60
Computed Tomography
Fig. 2.6: Acute on chronic portal vein thrombosis
Summary 1
25 year -old patient
Abdominal pain
ELFT
Obstructive jaundice
Dilated intrahepatic and extrahepatic bile d ucts
Distended gallbladder, sludge
Acute on chronic portal vein thrombosis
61
Fig. 2.7: MRCP of biliay system
Fig. 2.8: C avernous transformation of the portal vein
62
Diagnosis
Portal Hypertensive Biliopathy . Obstructive jaundice caused by compression on CBD.
Management
Since the patient had worsening jaundice and ascending cholangitis , the following measures were
taken:
o Urgent ERCP
– CBD ir regular with distal stricture
– Precut s phincterotomy (no bleeding !)
– Placement of plastic stent 10 Fr
o Surgical consultation
– Portosystemic shunt technically not feasible !
Fig. 2.9: Examples of biliary stents (Illustrative image )
63
Postoperative complications
Hospital ized on 30.10.2011 because of
– Ascending cholangitis
– E. coli and Klebsiella oxytoca on blood cultures
o ERCP
– Removal of old stent
– Hemobilia
– Glypressin 2mg
– Placement of two stents 10 Fr
Fig. 2.10: Intra-operative ERCP
64
Hospital ized on 09.11.2011 because of:
– Acute cholecystitis
• Treated conservatively
– On 10.11.2011 hematemesis
• EGD Esophageal varices grade 2 -3 with red signs, not bleeding
Band ligation
• Mild portal hypertensive ga stropathy, no gastric varices
• Normal duodenum, stents in place, no hemobilia
Since 11/2011 doing well
– Propranolol, enoxaparin, ursodeoxycholic acid, omeprazole
– Periodic band ligation until obliteration of esophageal varices
– Periodic ERCP and stent exchange
– Portosystemic shunt ???
– Metal stent ???
Summary 2
25 year -old patient
Myeloproliferative disease
Obstructive jaundice
Acute on c hronic portal vein thrombosis
Portal hypertensive Biliopathy
ERCP and periodic stent exchange
65
CASE PRESENTA TION 2
64 years old woman addresses the hospital for
Presenting complaints
Epigastric pain
Gradual onset of dull epigastric & right hypochondriac pain radiating to the back, aggravated by
eating food and relieved by analgesics.
Itching
Generalized body itching with no rash.
jaundice
Unremitting yellow discoloration of the eyes.
Pale stool and dark urine.
On and off low grade fevers.
No nausea & vomiting, l oss of weight , or loss of appetite .
No history of blood transfusion or conta ct with anyone with yellow eyes .
Past medical history
No history of hypertension, diabetes mellitus, or HIV.
Past surgical history
No history of major surgery or trauma.
Allergic history
No known allergy to anything.
Social history
Married. No history of smoking or alcohol.
66
Physical examination
General i nspection:
Mildly wasted, afebrile, deep jaundice, scratch marks. No stigmata of liver disease.
Abdominal inspection :
Normal fullness, no collaterals.
Abdominal palpation:
No tenderness. Two masses in the right hypochondrium. A firm globular mass 3cm in the
widest diameter (gall bladder), liver is palpable, liver span 16cm, 3cm BCM. No ascites.
Patient formed pale yellow stool.
Cardio -vascular system:
Heart rate – 89 beats/min, B lood Pressure – 140/80.
Nervous system:
Fully conscious, oriented.
Investigations
Lab studies
– CBC
– Liver function test
– Renal function test is normal
– Bleeding time: 2min 45sec (2-7 )
– Clotting time: 5 min (5-11)
RBC (3.9-5.03) 3.8 *1012/L AST 70.6 IU/L
Hb (120-155) 104 g/L ALT 44.2 IU/L
Platelets (150-450) 332 *109/L Albumin (31 -43) 31.3 g/L
WBC (4-9) 5.9 *109/L GGT (8-78) 162 U/L
Neutrophils 4 *109/L Bilirubin total (0 -17)
Direct (0 -7) 358
236 µmol /L
Lymphocytes 0.1 *109/L
Hematocrit (34.9 -44.5) 31.2 %
Imaging studies:
• Abdominal Ultrasonography (Dec ember 2010):
Showed dilated biliary tract, grossly dilated gall bladder, no mass in the pancreas.
Concl usion : possible stricture at the ampulla .
67
• CT scan (Dec ember 2010):
Showed dilated common bile duct & small gall stones but demonstrated no pancreatic mass .
• Abdominal Ultrasonography (F ebruary 2011)
Liver is enlarged , intra and extra biliary ducts, and gallbladder are grossly distended, CBD and
pancreatic duct are dilated. L ymphadenopathy around the porta hepatis, hyper -echoic mass
around the head of the pancreas. Spleen and kidneys are normal, no ascites.
Diagnosis
1. Stricture of the Ampulla of Vater.
2. Obstructive jaundice.
3. Mild anemia.
Treatment
Supportive
Vitamin k, rehydration, cephalexin , Paracetamol, cholestyramine.
Specific
Preoperative biliary decompression , rehydration, IV antibiotics, catheterization, vit amin k.
Surgery
Operation: cholecystojejunostomy and jejunojejunostomy .
Postoperative care:
– Nasogastric tube
– IV fluids
– IV antibiotics
– Tramadol
68
CASE PRESENTA TION 3
56 years old male, presents with the following complaints:
– Dark colored urine for 3 weeks, with pain during urination. Associate with pain in
suprapubic area. He went to family doctor and was prescribed ciprofloxacin.
– Yellow coloration of the skin (didn’t remember for how long).
– Lost 9 kg in the last 4 weeks, due to decreased appetite.
– He didn’t notice any change in stool color.
History of disease:
– After the blood work, he was referred by the family doctor for abnormal liver function
test.
– He denied any fever, chills, viral infection, dyspnea, nausea, vomiting, chest pain , rash,
recent surgery. No history of travel.
Past medical history:
Arterial hyperte nsion, neuropathy, stroke, peripheral vascular disease, bipolar disorder, slipped disk.
Review of systems:
No other relevant symptoms apart from the above.
Past surgical history:
Negative.
Social history:
Current every day smoker 3 cigarettes/day. No alcoh ol. Former abuser of: cocaine, heroin, marihuana,
stopped 1 year ago. Sexually active, uses safe methods.
Family history:
Not significant.
Allergic history:
No known drug allergies.
69
Home medicines:
– Aspirin 81 mg daily.
– Lasix 40 mg daily.
– Lisinopril 10 mg daily.
– Nifedipine 30 mg 24hr daily.
– Duloxentine 30 mg daily.
– Gaba 600 mg tid
– Zolpidem 10 mg hs
Physical examination:
Vitals on admission:
BP 120/78 mmHg ; pulse 77/min
Temperature 37 C; respiratory rate 18/min; SpO 2 98%; BMI 30.56 kg/m2.
Awake, alert and oriented. No distress.
HEENT: icterus (+), no cyanosis, no thyroid or lymph nodes enlargement.
Heart: normal S1, S2, regular rate and rhythm, no rubs/gallops/murmurs , no jugular vein
distension, no carotid bruit.
Lungs: normal breath sounds bilateral.
Abdomen: soft, present bowel sounds, no dullness, no tenderness, shifting dullness negative,
slight tenderness on deep palpation in suprapubic area, Murphy’s sign ( -).
Extremities: bilateral edema (+), no tenderness, pulses are normal, atrophy of left hand due to
neuropathy.
Neurology: grossly normal except for left hand neuropathy.
Lab studies:
RBC (3.9 -5.03) 5.2 *1012/L AST 201 IU/L
Hb (120 -155) 107 g/L ALT 349 IU/L
Platelets (150 -450) 144 *109/L Albumin (31 -43) 39 g/L
WBC (4 -9) 8.6 *109/L LDH (105-333) 797 IU/L
Hematocrit (34.9 -44.5) 32 % Bilirubin total (0 -17)
Direct (0 -7) 8.8
5.2 µmol /L
Alkaline phos . (53-128) 511 U/L
Creatinine (0.6-1.2) 1.5 mg/dL Amylase (23-85) 55 U/L
Potassium K+ (3.6-5.2) 3.5 mmol/L Lipase (0-160) 402 U/L
INR: 1.1
PT: 12.6
PTT: 33.1
70
Initial diagnosis and treatment:
Presumptive Dx: obstructive jaundice, probably secondary to gallstone. Hypokalemia.
– Admit to floor.
– IV fluids normal saline at 100 ml/hr.
– Check LDH now.
– GI evaluation.
– Replace K+ and repeat blood metabolic profile.
– No fever, no leukocytosis – no antibiotics.
– If fever or leukocytosis – blood culture and start antibiotics.
– Hold home medication duloxetine and suboxone.
– Deep vein prophylaxis.
– Aspiration / fall precaution.
To confirm the diagnosis we need additional imaging tests
Abdominal ultrasound:
1. Hepatomegaly with diffuse heterogeneity, seen throughout the liver.
2. Intrahepatic biliary dilation is seen. CBD is mildly dilated.
3. Gallbladder is distended. Sludge and tiny stones are seen within the gallbladder. There is no gall
bladder wall thickening or pericholecystic fluid.
From old records:
1. Blood urea nitrogen, Creatinine, liver function test are all normal 4 months ago.
2. Urine toxins negative.
3. HBsAg, HCV Ab and HBc Ab are neg. HBsAb p os. > 1000 vaccinated.
MRCP:
Impression: dilated biliary tree with distended gallbladder, intra -and extrahepatic duct dilation. CBD
measures up to 11 mm. distal common duct abruptly tapers and appears isolated from the dilated
pancreatic duct.
Rule -out obstructing mass at the level of the pancreatic head or ampulla.
Recommend dedicated CT of the pancreas with contrast for further evaluation.
71
Fig. 2.11 : Intra -and extrahepatic bile duct dilation
ERCP:
Findings:
Esophagus: normal esophagus, stomach and duodenum.
Stomach: normal esophagus, stomach and duodenum.
Duodenum: normal esophagus, stomach and duodenum.
Pancreatic duct: markedly dilated with a tapering at the ampulla.
CBD: cannulated and stent placed.
Specimens: none.
Complications: none. Patient t olerated the procedure well.
Impression: markedly dilated pancreatic duct, rule -out pancreatic neoplasm.
72
CHAPTER III
CONCLUSION S
1. The incidence of OJ is higher amongst the older age group.
2. The most common clinical manifestation of OJ is jaundice.
3. Other common manifestation, but to a lesser extent, are: dark -colored urine, steatorrhea, itching
and abdominal pain (dyspepsia).
4. The most common cause of OJ is CBD stones .
5. USG is the cheapest, safest and most reliable diagnostic tool in the management of OJ. Thus,
indicated as fist line investigative method.
6. High serum bilirubin (total and direct fraction), alkaline phosphatase and GGT are almost an
absolute indicator of OJ.
7. The recent increase in utilizing ERCP and MRCP to image the biliary tract, has he lped to
diagnose the pathology earlier, and hence early intervention can be initiated.
8. ERCP has proved its worth as a diagnostic method and a treatment option, especially in
extracting CBD stones, placing stents, sphincterotomy and placing drainage tubes.
9. Pancreatoduodenectomy (Whipple’s procedure) is the treatment of choice for operable
malignant tumors of the ampulla of Vater, the lower end of the CBD, the duodenum and the
periampullary region of the head of pancreas.
10. For benign biliary stricture is best done: choledocho -/cholecysto -/hepatico -jejunostomy with
jejuno -jejunostomy (entero -enterostomy).
73
CHAPTER IV
BIBLIOGRAPHY
1. Scharsschmidt GF, Goldberg HI, Schmidt R. Approach to the patient with cholestatic jaundice .
N Engl J Med 1983; 308: 1515 -1519.
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