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ACKNOWLEDGEMENT
It gives me immense pleasure to express my deep sense of gratitude and
sincere thanks to Dr. M. SHIVAKUMAR M.S., Professor of Surgery, J.J.M. Medical
College, Davangere for his dedicated professionalism, indefatigable efforts cheerful
guidance, and constant encouragement during the course of my study and preparation
of this dissertation.
I am highly indebted to Dr. B. PRADEEP M.S., Professor and Head of the
Department of Surgery who’s practical guidance during the course of my study is
without parallel.
I pay my humble thanks to Dr. M. MOHANDAS HEGDE, M.S., Hon.
Professor, Department of Surgery, J.J.M. Medical College Davangere.
My sincere thanks to my Professors Dr. P.J. PRABHAKAR, Dr. R.
SRINKANTIAH, Dr. R.L.CHANDRASHEKAR, Dr. R.M. SHEKHAR, Dr. G.C.
RAJENDRA, Dr. S.M. BYADGI, for allowing me to collect cases from their units
and for their valuable guidance.
I am extremely thankful to Associate Professors Dr. DINESH. M.G, Dr. J.T.
BASAVARAJ, Dr. U. MAHENDRANATH PATIL and Dr. RAVISHANKAR
PURANTHAR for their guidance.
I thank Dr. MANJUNATH GOWDA and Dr. M.C. ANUP KUMAR for
their constant encouragement and guidance during the course of my study.
VI
I would like to thank our Readers Dr. S.N. SOMASEKHAR, Dr. DEEPAK
UDAPUDI, Dr. RUDRAIAH H.G.M., Dr. RAJESHWAR REDDY, Dr. PATIL
VIRUPAKSHAGOWDA, Dr. JAGADEESH B.V.C., Dr. EDAGUNJI G.C.,
Dr. RAJENDRA PRASAD, Dr. NARASIMHASWAMY P., and Dr. PRAKASH
M.G. for their guidance, suggestions and advice during the course of my study and
preparation of this dissertation.
I also express my sincere thanks for the faculty of the paediatric surgery
Dr. N.K KADLI, Dr. HARSHA B.M., Dr. MOHAN MARULAIAH, for the
invaluable contributions and advice given during the course of completion of this
dissertation.
I also express my thanks to Dr. VIKRAM S, and Dr. JAYAPRABHU for
their help in collecting the operative photographs for this dissertation.
I also express my sincere thanks to the superintendents of Chigateri General
Hospital and Bapuji Hospital Davangere for allowing me to study the patients of their
hospital.
I express my special thanks to Dr. H. GURUPADAPPA M.D., director of post-
graduate studies and research and Dr. H.R. CHANDRASEKHAR Principal, J.J.M.
Medical College Davangere.
I would like to thank Sri P.S. MAHESH Liberian and his colleagues and
D.K. SANGAM Bio-Statistician for their help during the preparation of this
dissertation.
VII
I am thankful to my parents whose blessings and constant encouragement
have always been with me throughout my endeavour.
I am thankful to my brother Sri. K.S. VENKATESH PRABHU and my
Sisters for their abundant support, patience understanding and love.
I am thankful to my wife Dr. SUHASINI for her profound love and constant
support and showing me the excitement and joy of surgery, and to my daughters
P. Namratha and P. Namitha for making everything worth while.
My sincere thanks to M/S Zen Computer Technology for their meticulous
computerized typing.
My gratitude to the participant patients of this study without which this work
could not have been completed.
Date : / /2006 Signature of the candidate
Place : DAVANGERE Dr. PRAKASH. K.S.
VIII
LIST OF ABBREVIATIONS USED
% – Percentage
< – Less than
ALT – Alanine amino transferase
AST – Aspartate amino transferase
Ca – Carcinoma
CBD – Common bile duct
Cho Ca – Cholongaiocarcinoma
Cholido Cyst – Cholidochal cyst
CT – Computed tomography
DISIDA – Di-isopropyl iminodiacetic acid
ERCP – Endoscopic retrograde cholangio pancreatography
FNAC – Fine needle aspiration cytology
GGT – Gamma glutamyl transpeptidases
hr – Hour
IU/L – International units per liter
Mg/dl – Milligram / deciliter
MRCP – Magnetic resonance cholangio pancretography
MRI – Magnetic resonance imaging
Periamp Ca – Periampullary carcinoma
pH – Hydrogen ion concentration
PH Metastases – Porta hepatis metastases
PSC – Primary sclerosing cholangitis
PTC – Percutaneous trans hepatic cholangiography
RDA – Retroduodenal artery
RHA – Right hepatic artery
Sec in liver – Secondaries in liver
SGOT – Serum glutamic oxaloacetic transaminase
SGPT – Serum glutamic pyruvic transaminase
U/L – Units per liter
US – Ultrasound
IX
ABSTRACT
Background and Objectives : Patients with surgical jaundice need quick and precise
diagnosis established for the presence of an obstruction in the biliary tract, the level
and nature of the lesion. The importance of history and clinical examination in
arriving at a correct pre-operative diagnosis needs to be emphasized.
Our study attempts to determine the various causes, age and sex pattern in
extra hepatic obstructive jaundice.
Methods : 30 patients with surgical jaundice were studied during the period from
January 2004 to December 2005 who were diagnosed by investigation like
ultrasonography and liver function test.
Results : 76% of patients were between the age group of 50-80 years, there was a
slight male predominance in 53.33%, malignant cause for surgical jaundice
constituted in 66.67% with Carcinoma Head of pancreas the commonest cause in
33.33%, benign cause for surgical jaundice constituted in 33.33%, with
choledocholithiasis the commonest cause in 23.33%.
Interpretation and conclusion : Most common age group seen in surgical jaundice
was between 50-80 years. The sex ratio is near equalizing.
Most common cause of surgical jaundice was carcinoma head of pancreas and
choledocholithiasis.
Keywords : cholestasis; extrahepatic bile duct obstruction; bilirubin; bile duct stones;
TABLE OF CONTENTS
Page No.
1. Introduction 1
2. Objectives 3
3. Review of literature 4
4. Methodology 60
5. Results 62
6. Discussion 73
7. Conclusion 82
8. Summary 83
9. Bibliography 85
10. Annexures
I. Proforma 94
II. Consent form 102
III. Master chart 103
XI
LIST OF TABLES
Page
Sl. No. Tables
No.
Table 1 Age distribution among the surgical jaundice cases 62
Table 2 Sex distribution among the surgical jaundice cases 63
Table 3 Causes of surgical jaundice cases 64
Table 4 Clinical presentation in surgical jaundice causes 65
Table 5 Mean and range values of liver function test in surgical jaundice 67
cases
Table 6 Ultrasonographic findings in cases of surgical jaundice 69
Table 7 Various treatment modalities in surgical jaundice cases 71
Table 8 Sex ratio in various study of surgical jaundice cases 73
Table 9 Cause of surgical jaundice in various study 74
Table 10 Presentation in malignant jaundice various studies 76
Table 11 Prognosis of after treatment of patient with choledocholithiasis 81
XII
LIST OF GRAPHS
Page
Sl. No. Figures
No.
1 Age distribution among the surgical jaundice cases 62
2 Sex distribution among the surgical jaundice cases 63
3 Causes of surgical jaundice cases 64
4 Clinical presentation in benign and malignant surgical jaundice 66
5a Mean value of total bilirubin in benign and malignant surgical 68
jaundice
5b Mean value of alkaline phosphatase and SGOT in benign and 68
malignant surgical jaundice
6 Ultrasonographic findings in benign and malignant surgical 70
jaundice
XIII
LIST OF FIGURES
Sl. No. Figures
1 Anatomic division of the gall bladder and extrahepatic biliary tree 5
2 Component of sphincter of oddi 8
3 Arterial blood supply of the extrahepatic biliary tree 9
4 Extra hepatic effect of cholestasis 18
5 Yellowish discoloration of the sclera 18
6 Ultrasonography of choledochal cyst 27
7 Ultrasonography of porta hepatis calcification 27
8 C.T. of carcinoma head of pancreas 29
9 MRCP showing stones within the dilated bile duct 29
10 ERCP showing structures in the common hepatic duct 32
11 PTC showing the upper extent of the malignant CBD stricture 32
12 Cholangiography 35
13 Barium study showing inverted 3 sign in carcinoma head of the 35
pancreas
14 Operative photograph of choledoctomy with extraction of CBD 43
stones
15 Multiple CBD stones 43
16 Operative photograph of Whipple’s pancreaticoduodenectomy 58
17 Resected specimen of Whipple’s pancreaticoduodenectomy 58
18 Operative photograph of distended gall bladder 59
19 Operative photograph of cholecystojejunostomy with 59
jejunojenostomy
XIV
Introduction
INTRODUCTION
SURGICAL JAUNDICE is defined as structural or mechanical obstruction
whereby the outflow of bile has been obstructed anywhere from the liver to the
duodenum.1
JAUNDICE [JAWN’DIS] Fr, JAUNISSE, from JAUNE YELLOW /
ICTERUS [L., from Gr. IKTEROS 2 refers to Yellowish discolouration of the skin,
sclera and Mucous membrane due to increased bilirubin concentration in the body
fluids.3
Jaundice is frequently encountered by the general surgeons. The most frequent
presentation of a jaundice patient is due to choledocholithiasis, pancreatic and
periampullary carcinoma or benign biliary stricture.
Clear recognition and understanding of the problem demands adoption of a
broader view of biliary obstruction that presented by jaundiced patient.
The modern biliary imaging technique can display precisely the extent and
cause of biliary obstruction. Even in the absence of jaundice, it allows medical and
surgical cause of biliary obstruction to be differentiated with an accuracy of 95%.
“CHOLESTASIS” was coined by Berg has replaced the older term
“obstructive jaundice”. It means a reduction of bile flow and its cause can affect the
biliary tree anywhere from the tiny biliary canaliculi to the sphincter of oddi in the
duodenum.
Cholestatic syndrome
Comprises features that are characteristic of a failure of bile flow, Clinically
characterized by Jaundice, dark urine, pale stool, pruritus, Biochemically predominant
conjugated hyperbilirubinaemia and a moderate to marked increase in the serum
alkaline phosphatase level.
CHOLESTASIS may be due to intrahepatic disease, which is rarely amenable
to surgical treatment or due to extrahepatic biliary disease which is often amenable to
surgical treatment. The later is often called “SURGICAL JAUNDICE” and is the one
we are mainly concerned in this study.4
Patients with surgical jaundice need quick and precise diagnosis to establish
the level and nature of the obstruction in the biliary tree.
Objectives
OBJECTIVES
The objectives of this study is :
a) To study various causes of extra hepatic obstructive Jaundice.
b) To study age and sex pattern in extra hepatic obstructive jaundice.
Review of literature
REVIEW OF LITERATURE
HISTORICAL ASPECT
Operative management of the extrahepatic biliary obstruction evolved rapidly
in the late 19th century.
 Alexander Von Winiwarter a pupil of Theodar Billroth performed the first
bilio enteric anastomosis in Liege in 1880.
 Monastryski first performed a palliative biliary tract bypass
cholecystojejunostomy for malignant biliary obstruction in 1887.
 Oskar Sprengel in 1891 attempted choledocho dueodenostomy for impacted
common bile duct stone.5
 The first success resection of a peri-ampullary tumour was performed by
Halsted in 1899.
 In 1935 Whipple and his associates reported their first successful two stage
radical enbloc resection of the duodenum and head of pancrease for a growth
of the ampulla of vater, and the first successful one stage
pancreaticoduodenectomy was carried out by Whipple in 1940.6
First report of endoscopic retrograde cholangeio-pancreatography (ERCP)
in 1986 by Me cune and associates, which has progressed as one of the
standard modalities for diagnosis and treatment for pancreatobiliary diseases. 5
EXTRA HEPATIC BILIARY SYSTEM
DEVELOPMENT7 :
The liver, extrahepatic bile duct, gall bladder and ventral portion of the
pancreas originate from the hepatic diverticulum from the most caudal part of the
foregut during the 4th week of intrauterine life.
The hepatic diverticulum migrates superiorly into the ventral mesogastrium
which divides into cranial and caudal portion.
The caudal portion of the diverticulum develops into the gall bladder and
cystic duct. The original diverticulum from the duodenum is elongated and forms the
hepatic duct, common hepatic duct and common bile duct.
Lumina begins to develop within the gall bladder and extra hepatic biliary tree
during 7th week of gestation by vaculization.
By the end of the 12th week of gestation the liver begins to secrete bile that
passes through the patent extrahepatic tree into the duodeum.
GROSS ANATOMY7 : (fig.1)
Right hepatic duct Left hepatic duct

Cystic duct Common hepatic duct
Neck Supraduodenal
Retroduodenal
Gallbladder
Fundus Intrapancreatic Common bile
duct
Papilla of vater Intramural
Figure 1 : Anatomic division of the gall bladder and extra hepatic

biliary tree
The extra hepatic biliary tree consist of the common hepatic duct which is
formed by the union of the right and left hepatic ducts. Common bile duct formed by
the union of hepatic and cystic duct.
Left hepatic duct is formed from the biliary drainage of segment II, III and IV
of the liver.
Right hepatic duct drains segment V, VI, VII and VIII. In 80% of cases
segment I drain to both right and left hepatic duct.
Left hepatic duct crosses the base of segment IV in a horizontal direction,
having an extrahepatic length of 2 cms or more, and join right hepatic duct to form
common hepatic duct. Confluence of the right and left hepatic duct occur in an
extrahepatic location ventral to the portal venous bifurcation.
Common hepatic duct descends in the hepatoduodenal ligament ventral to
portal vein and medial to the hepatic artery proper and is joined by the cystic duct to
from the common bile duct.
Gall bladder is a pear shaped distensible reservoir with an average capacity of
30-50ml, measure 7-10 cm. Cystic duct arises from the gall bladder and joins the
common hepatic duct to form common bile duct. The length is variable, measures 2-4
cm, joins the lateral aspect of the supraduodenal position of the common hepatic duct
at an acute angle.7
Common bile duct formed by the union of cystic and common hepatic duct. Its
length is variable, approximately 8 cm.
a) Supraduodenal part of common bile duct courses downwards in the free edge
of lesser omentum anterior to portal vein and to the right of hepatic artery
proper.
b) Retroduodenal part of common bile duct passes behind the first part of
duodenum, lateral to the portal vein and anterior to the IVC with
gastroduodenal artery on its left.
c) Intrapancreatic portion of common bile duct traverse the posterior aspect of
the pancreas in a tunnel or groove to enter the second part of the duodenum,
which is joined by pancreatic duct.
d) Intra duodenal portion of common bile duct passes obliquely through the
duodenal wall to enter the duodenum at the papilla of vater, which is 8-10 cm
from pylorus on the posterior medial part of the duodenum at the junction of
upper 2/3rd with lower 1/3rd which appears like a small nipple like structure
protruding into the duodenal lumen and is marked by a longitudinal fold of
duodenal mucosa.
Minor papilla drains the accessory duct and lies 2 cms cranial and anterior to
the major papilla.
Union of CBD and pancreatic duct is variable.
i) Form a long common channel in 60%
ii) Form a short common channel in 38%
iii) Open independently in the duodenum in 2%
a) The ampulla of vater7 :
- The ampulla of vater is the dilated distal pancreatico-Biliary confluence below
the junction of the two ducts.
- Ampulla exists only when the two ducts join far enough from the papilla, the
common channel dilates as it passes through the duodenal wall.
- The greatest diameter of a normal duct is 3-4.5mm.
b) Sphincter of oddi / boyden 8 (fig.2)
It is a multisphincter complex varies as short as 5mm or extend into the
parenchyma of the pancreas. It consists of
i) Superior sphincter of choledochus
ii) Inferior (submucosal) sphincter
iii) Sphincter ampullae
iv) Pancreatic sphincter.

Figure 2 : Component of sphincter
of oddi
i) Superior and inferior sphincter of choledochus
Circular muscle fibers surrounding the intra mural and submucosal bile duct. It
stops bile flow into duodenum.
ii) Ampullary sphincter
Layer of longitudinal muscle fibers prevents reflux of intestinal content into
ampulla and controls entry of bile and pancreatic juice into duodenum.
iii) Pancreatic sphincter
Muscular septum between the bile duct and pancreatic duct controls pancreatic
secretion entering duodenum and bile into pancreatic duct.
Normal vascular anatomy 9: (fig.3)
The most important arteries to the supraduodenal bile duct run parallel to the
duct at the 3O clock and 9O clock position.
Approximately 60% of the blood supply
to the supraduodenal bile duct originate
inferiorly from the pancreaticoduodenal and
retroduodenal arteries whereas 38% of the blood
supply originates superiorly from the right
hepatic artery and cystic duct artery; 2% of the
arterial blood supply to the supraduodenal bile
duct is segmental arises directly from the
hepatic artery proper as it ascends in the hepato-
duodenal ligament adjacent to CBD. The blood
supply to the retroduodenal and intrapancreatic
bile duct is from the retroduodenal and

Figure 3 : Arterial blood supply of
pancreaticoduodenal arteries. the extra hepatic biliary tree
Physiology of bile secretion10
Bile is made up of the bile salt, bile pigment and other substance dissolved in
an alkaline electrolyte solution.
a) Function of bile
i) Bile salts reduces surface tension, and in conjugation with phospholipid and
monoglycerides are responsible for the emulsification of fat, preparatory to its
digestion and absorption in the small intestine.
ii) Bile salts have both hydrophilic and hydrophobic domains and tend to form
cylindrical disk “MICELLES” which keep lipid in solution and transporting
them to the brush border of the intestinal epithelial cells, where they are
absorbed.10
iii) Normally 600-1000 ml/day of bile is secreted by the liver hepatocytes into bile
canaliculi, terminal bile duct reaching hepatic duct and Common bile duct.
Bile is either emptied into duodenum or diverted through cystic duct into gall
bladder.11
Additional secretion watery in nature, sodium and bicarbonate ion is secreted
by secretory epithelial cells that lines the ductules and ducts. It is stimulated by
secretin which helps in neutralizing acid that empties into the duodenum from the
stomach.
Bile is secreted continuously by the liver cells and most of it is normally
stored in the gall bladder, it normally concentrates to 5-20 times, as water, sodium,
chloride and most other small electrolytes are continuously absorbed by gall bladder
mucosa.
Bile acid10 : Sodium and potassium salts of bile acid are synthesized from cholesterol
in the liver and conjugated with glycin or taurine. Primary bile acid is formed in the
liver, are cholic acid and chenodeoxycholic acid.
Secondary bile acid are formed in the colon, as bacterial metabolite of the
primary bile acid. Cholic acid is converted into deoxycholic acid and
chenodeoxycholic acid into lithocholic acid.
Bilirubin is a Tetra-pyrol pigment produced by the breakdown product of
heme. Bilirubin and biliverdin are responsible for the golden yellow color of the bile,
normal serum bilirubin is < 1mg/dl.
10
Bilirubin is conjugated with glucuronide by the enzyme glucuronyltransferase
to form water soluble conjugated bilurubin.
Conjugated bilirubin is filtered at the glomerulus and the majority is
reabsorbed by proximal convuluted tubule, a small fraction is excreted in the urine,
any bilirubin found in urine is conjugated bilirubin. It forms 30% (0.3mg /dl) of the
blood level.
Unconjugated bilirubin is always bound to albumin in the serum and is not
filtered by the kidney, hence is not found in urine. It constitute not more than 10% of
the total bilirubin concentration
In the intestine about one half of the conjugated bilirubin is converted by the
bacterial action into urobilinogen, which is highly soluable and is reabsorbed, about
5% is reexcreted in the urine.
The urobilinogen is oxidized to form stereocobilin and is excreted through
faces. Normal output of faecal bilinogen is 50-280 mg/day and urinary bilinogen is
less than 4mg / day.
Physiology of the biliary tract 12 :
The common bile duct does not exhibit any peristaltic or mechanical activity,
Bile flow enters the sphincter of oddi passively. Sphincter of oddi has two major
function.
i) It prevents reflux from the duodenum.
ii) Regulates the flow across the sphincter.
11
An active sphincter with phasic contraction resists the flow of bile, increasing
intra ductal pressure and diverting bile flow towards the cystic duct and gall bladder.
Bile in the fasting state flows through the extra hepatic ductal system with
variable pressure generated by the sustained secretion of hepatic bile and the
resistance of the sphincter of oddi.
Diversion of bile flow takes place when choleductal pressure exceeds the
resistance of the narrow and tortuous cystic duct and of the intra gall bladder pressure.
Extrahepatic biliary obstruction – pathophysiology 9
Classification :
1) Type I / Complete obstruction producing jaundice
 Tumour of head / body of pancreas
 Cholangio carcinoma
2) Type II – intermittent obstruction produces symptoms and typical biochemical
changes, but may or may not be associated with attack of clinical jaundice.
 Choledocholithiasis
 Periampullary tumour
 Duodenal diverticula
 Papilloma of bile duct
 Choledochus cyst
 Hemobilia
12
3) Type III : chronic incomplete obstruction associated with or without classic
symptoms or the observation of biochemical changes producing pathologic
changes in the bile duct or the liver.
 Stricture of the common bile duct
 Stenosed biliary enteric anastomosis
 Chronic pancreatitis
 Sphincter of oddi stenosis / or dyskinesia
4) Type IV : segmental obstruction includes intrahepatic biliary tree obstruction.
Physical effects :
i) Increased pressure : The normal secretory pressure of bile is 120-250mm of
water. Obstruction to bile flow increases biliary pressure with dilation of the
biliary tree. The degree of rise in biliary pressure depends upon the secretory
capacity of the hepatocyte and ductular cells and the distensibility of the biliary
tract, chronic obstruction with slow evolution fail to produce significant proximal
dilatation when associated with significant chronic cholangitis and ductal fibrosis.
ii) Bile reflux : Regurgitation of bile into the circulation occurs via the lymphatics
and also across the hepatocyte in intracellular vacuoles.
iii) Hepatocellular damage : Cholesterol and phoshpolipid secretion are more
readily reduced by high pressure than bile salt secretions altering the composition
of hepatic bile and less lithogenic. Prolonged obstruction leads to fall in serum
albumin, prolonged prothrombin time, malabsorption of vitamin K.
iv) Hepatic blood flow : Total hepatic tissue perfusion might be reduced in the face
of increasing hydrostatic pressure within the liver due to increased intraductal
pressure and ductal dilatation.
13
Pathological effect :
i) Bile duct and canaliculi :
Bile canaliculi become dilated and the microvilli distorted and swollen. Bile
pigment thrombi seen in the canaliculi and in adjacent hepatocytes leads to increase in
length and tortuousity of canaliculi.
Reabsorption of bile constituents from the ductules leads to a marked
inflammatory reaction in the portal tracts.
Retention of bilirubin and bile acid in periportal zone exert toxic effects within
hepatocytes leading to solubilization of canalicular membrane with increased release
of canalicular alkaline phosphatase into the blood stream.
Morphological changes are reversible if obstruction is relieved within two
weeks.
ii) Fibrotic changes :
Mucosal atrophy and squamous metaplasia followed by inflammatory
infiltration and fibrosis in the subepithelial layer of the ducts.
Irreversible changes is associated with mechanical obstruction to sinusoidal
flow results in secondary portal hypertension.
Benign iatrogenic biliary stricture which are chronic and incomplete have a
high association with portal hypertension.
14
iii) Atrophy :
In the early stage, unilateral hepatic duct obstruction leads to enlargement of
the obstructed lobe later on due to fibrosis and cellular atrophy of the obstructed liver
parenchyma leads to compensatory hyperplasia of the unaffected segment.
d) Biochemical effect :
i) Bilirubin :
 Conjugated hyperbilirubinemia is the classic feature of obstructive jaundice.
 Prolonged partial obstruction produces mixed biochemical picture.
 The mechanism of regurgitation of bilirubin include
o Initially biliary lymphatic regurgitation.
o Biliary venous regurgitation
o Transhepatocytic regurgitation
o Rupture of the dilated canaliculi into the sinusoids by necrosis of surrounding
liver cells.
ii) Alkaline phosphatase
Elevation of alkaline phosphatase is the most sensitive indicator of biliary tract
obstruction when other causes are excluded. But its return to normal following relief
of obstruction is extremely variable.
iii) Protein synthesis
Albumin is the most important plasma protein synthesized by the liver. Due to
its long half life in the circulation (20 days), only minimal changes may occur
secondary to the hepatocyte damage produced by biliary tract obstruction. Hence
serum prealbumin is most valuable (t½ 1.9 days).
15
Severe and prolonged obstructive jaundice is associated with reduced blood
fibrinogen, prothrombin and factor VII leading to impaired blood coagulation process.
iv) Lipids
Cholesterol level may be elevated in long standing biliary obstruction.
v) Bile salt circulation
Interruption of enterohepatic circulation leads to gross elevation of serum bile
acid levels. This leads to decrease in hepatic synthesis of bile acid, increased urinary
excretion and formation of abnormal bile acid by the liver. Absence of bile salts from
the intestine is associated with altered small bowel microflora and increased
absorption of endotoxin.
vi) Systemic effect :
The peripheral vascular resistance is reduced which may lead to prerenal renal
failure.
The combination of impaired systemic vasoconstrictor response to
hypotension and an increased renal vascular response to adrenergic stimuli favours
the development of renal hypoperfusion and renal ischeamia which leads to acute
tubular necrosis.
Other systemic complication include delayed wound healing, gastrointestinal
bleeding.
16
Clinical features 9, 13: (fig.4)
a) Jaundice : (fig.5)
If a stone obstructs the common bile duct in the absence of infected bile,
asymptomatic jaundice which often fluctuates with spontaneous complete resolution
as the stone floats up in ductal dilatation.
Painless jaundice is the classical symptoms of periampullary cancer, jaundice
fluctuate in ampullary tumours due to necrosis and sloughing.
Jaundice is late symptom in Carcinoma head of pancreas and it will be
persistent and progressive.
In case of benign biliary stricture jaundice is usually present, occasionally
intermittent or even absent depending upon whether bile duct obstruction is complete
or partial and whether an internal or external biliary fistula is present.
Progressive and unremitting jaundice is usually the predominant clinical
feature in case of cholangio carcinoma.
b) Itching : OTHER
Itching occur with any cause of biliary obstruction but tends to be more
frequent with malignant obstruction. It is generally worse just after going to bed and
favour extremities, forearm, hands, lower legs, and feet.
Itching is unusual in calculous obstruction as the obstruction is rarely
complete and sufficiently prolonged.
Bile acids are generally mediators of cholestatic itching. It cause injury to the
membrane of certain cells within the skin and a release of pruritogenic proteases.
17
18
c) Biliary pain :
 Biliary pain is characteristically felt in the epigastrium, radiates to the right
hypochondrium and to the right sub-scapular region, it is NOT COLICKY, most
commonly constant in nature with only minor fluctuation in intensity.
Stone producing “ball valve” obstruction presents as “Charcot’s triad
characterized by recurrent pain, fluctuating jaundice and intermittent fever with
rigor.14
Malignant obstruction classically produces painless jaundice. However there
may be a preceding history of pain in some patients with carcinoma of the pancreas,
bile duct or ampulla.
Pain of pancreatic disease is steadly severe, located under the umbilicus and
over back at T12-L1. As the pancreas is a retroperitoneal organ any edema swelling,
inflammation or enlargement make pain worse when the patient lies flat, as posterior
peritoneum is stretched over the mass, and pain is relieved when patient sits up and
leans forward.
d) Fever :
Fever is the most common presenting symptom of patients in acute
cholangitis.
Fever usually indicate choledocholithiasis as bacteria is usually present when
common bile duct stones are present, duct obstruction raises biliary pressure and
infected bile enters the circulation with systemic signs of sepsis.
19
Malignant bile duct obstruction is usually sterile hence fever is rare, except in
patient who has undergone previous diagnostic or therapeutic endoscopic procedure.
e) Dark urine :
Occur due to conjugated bilirubinuria. It occur several days before the onset of
jaundice and during the day the urine becomes lighter.
f) Light stools :
It depends on the degree of cholestasis or mechanical obstruction, the stools
may be pasty grayish ‘clay’ to light yellow in colour. If obstruction is only partial
stool color may remain normal despite bilirubin in urine.
g) Anorexia, malaise and fatigability :
Anorexia is loss of appetite or lack of desire for food. In biliary obstruction
nausea appears before jaundice. Pain from gall bladder disease is rarely associated
with much vomiting.
Weight loss and anorexia are characteristic symptoms of pancreatic
carcinoma. Weight loss occur more often with malignant obstruction, although it also
occur from benign cause with prolonged steatorrhoea.
General examination 9 :
Jaundice usually detected initially in the sclera as bilirubin has high affinity to
elastin content of sclera.
20
Spider naevi are vascular skin lesions supplied by a central arteriole which
blanch when the central arteriole is occluded with a pin head. It usually occur in the
distribution of the superior vena cava, the chest above the nipples, face, arms and
hand.
Palmar erythema is the red flushing of the plams which particularly effect the
thenar and hypothenar eminences and the base of the fingers.
Spontaneous bruising, ecchymoses, and bleeding around venepuncture sites
are all well recognized features of liver disease which is associated with abnormal
coagulation.
Itching is usually generalized but the palms and soles seem most affected.
Long standing cholestasis is associated with xanthomas found around the eye.
Ascites may be related to liver disease, hypoalbuminemia with portal
hypertension or malignancy.
Palpable gall bladder in the presence of obstructive jaundice suggests
malignant obstruction of the biliary tree (courvoisier’s law).
Investigation :
a) Urine urobilinogen 15:
Normally there are mere traces of urobilinogen in the urine. Normal urine
urobilinogen is 0-4mg/24hr. In complete obstruction of the bile duct no urobilinogen
is found in the urine as bilirubin has no access to the intestine where it can be
converted into urobilinogen.
21
b) Urine bilirubin 16:
Bilirubin cannot be detected in the urine of normal subjects or in patients with
unconjugated hyperbilirubinaemia.
In cholestatic patients a small fraction of the conjugated bilirubin is filtered by
the glomerulus which gives dark color to the urine.
‘Dip sticks’ are commercially available, easy to use and give satisfactory
results for the detection of conjugated bilirubin in urine.
c) Liver function test 17:
Prothrombin time and serum albumin are widely employed useful tests that
reflect hepatic synthesis and release.
i) Prothrombin time :
Liver synthesizes six coagulation factor I, II, V, VII, IX, and X.
Prothrombin time evaluate the extrinsic coagulation pathway by measuring the
rate of prothrombin conversion to thrombin. It is prolonged when factors I, II, V, VII
and X are deficient, singly or in combination.
Prolongation of the prothrombin time is often the earliest sign of impending
liver failure, but it is not specific for liver disease and occurs in many other condition.
ii) Albumin :
Albumin is the most important plasma protein synthesized by the liver and
thus is a useful indicator of hepatic function.
Albumin has a long half life in serum of 20 days, hence is not a good indicator
of hepatic protein synthesis in acute liver disease.
22
iii) Serum marker of cholestasis :
 Alkaline phosphatase :
It is the primary enzyme to catalyse hydrolyses a number of phosphate esters
at an alkaline pH. It is identified in liver, bone, intestine, kidney and leukocytes.
Alkaline phosphatase in liver is localized to the sinusoidal membrane and to
the microvilli of the biliary canaliculi. Obstraction with consequent irritation of
epithelial cell leads to secretion of alkaline phosphatase into serum. Isoenzyme of
liver alkaline phosphatase is heat resistant. Elevation of GGT (Gamma-Glutamyl
Transpeptidase) suggests a hepatic origin of an elevated alkaline phosphatase.
Normal serum level of alkaline phosphatase is 40-125 u/l, the highest
elevation of alkaline phosphatase in patients with liver disease occur in patients with
cholestasis and hepatic carcinoma.
 5' Nucleotidase :
5' nucleotidase catalyze the hydrolysis of nucleotides by releasing inorganic
phosphate from the 5 th position of the pentose ring.
It is present in liver, intestine, brain, heart, blood vessels and endocrine
pancreas.
Serum level of 5' nucleotidase correlate closely with serum alkaline
phosphatase and it is used to confirm that elevation of alkaline phosphatase reflect
liver disease.
23
 Leucine aminopeptidase :
Leucine aminopeptidase cleaves amino terminal amino acids from peptides
and has highest activity when leucine is the N-terminal residue.
Even it is preset in virtually all human tissue, its elevation are seen only in
hepatobiliary disease and in pregnancy.
Leucine aminopeptidase elevation is in most hepatobiliary disease but the
highest elevation are seen in biliary obstruction.
 -glutamyl transpeptidase :
-glutamyl transpeptidase has been localized to the whole hepatobiliary tree
from hepatocytes to common bile duct. It is also present in pancreatic acinii and
ductules.
Serum -glutamyl transpeptidase activity correlates well with serum alkaline
phosphatase and is most sensitive indicator of biliary tract disease.
It also increases in other pathological condition like chronic alcoholism,
pancreatitis, myocardial infarction.
Lipoprotein disturbance in cholestasis :
The sera of patients with obstructive jaundice contains an abnormal
lipoprotein called lipoprotein X. which is sensitive and specific indicator of
cholestasis.
Lipoprotein X is present in 99% of patients with histologic evidence of
cholestasis and was undetectable in about 97% of patients without cholestasis.17
24
Aminotransferases :
Aspartate transaminase (AST)/ serum glutamic oxaloacetic transaminase
(SGOT) and Allanine transaminase (ALT) / serum glutamic pyruvic transaminase
(SGPT) are commonly measures of hepatocellular injury. Neither is specific for liver
tissue but ALT (SGPT) is more specific than AST (SGOT).
d) Ultrasound 18: (fig.6,7)
Ultrasound is the initial investigation of any patient suspected of disease of the
biliary tree.
Ultrasonography is an accurate and convenient method of imaging the liver
and biliary system. It is safe, widely available and relatively inexpensive.
Bile duct is a sonolucent tubular structure anterior to the portal vein, an
internal diameter of 6mm is considered the upper limit for the size of bile duct. The
intrahepatic tributaries of the bile duct are not normally seen unless dilated.
In choledocholithasis CBD diameter of 1 cms or greater indicates obstruction,
echogenic shadows consistent with calculi are visible in only 60-70% of patient with
common duct stones.
Pancreatic tumours that cause jaundice are usually large enough to be detected
as masses with irregular, predominantly low level echoes. Ampullary carcinoma are
too small to be detected. Their presence may be inferred from the combination of
dilated pancreatic and biliary ducts (“double duct sign”)9. Ultrasound examination in
case of pancreatic cancer can provide information about liver metastases, pancreatic
masses, peri pancreatic adenopathy and ascities. Ultrasound can be helpful in
25
evaluating tumor invasion and flow in the portal vein, an important guideline for
resectability of periampullary tumour. 7
Dilatation of the intrahepatic or extrahepatic bile ducts is the sonographic hall
mark of biliary obstruction, and assessment of gall bladder distension, contracted or
nonvisualization.18
Ultrasound examination in case of jaundiced infants with choledochal cyst
enable to confirm the diagnosis and information about cyst size and its relation to
intrahepatic ducts and portal vascular anatomy in antenatal sonogram may suggest the
diagnosis.7
e) Endoscopic ultrasound 18:
It is an ultrasound imaging technique performed within a luminal or hollow
organ which allows examination of the structural integrity of that and the adjacent
organs and viscera.
It helps in detection of pancreatic tumor, and assessing resectability of
pancreatic cancer, endoscopic ultrasound is highly accurate in tumor detection for
sizes ranging from 0.5cm to 2.5cm and location. It is also used to guide an FNAC,
criteria for unresectability such as vessel invasion, or lymph node metastasis.
Endoscopic US accurately differentiates stones from tumor masses and is also
quite accurate in identifying small pancreatic and periampullary tumors.
f) Barium studies : (fig. 13)
In barium study their may be double contour to the medial border of the loop
due to indentation by the mass and Frostberg’s reversed 3 sign is seen.
26
27
g) Computed tomography 9: (fig.8)
CT has advantages due to its high resolution images, short scan times and is
more accurate, and less operator dependent and more reproducible.
The CT diagnosis of biliary obstruction is based on the demonstration of
dilated intrahepatic or extrahepatic bile ducts, dilated intrahepatic ducts appear on CT
as linear branching or circular structures of near water density.
The extrahepatic bile duct normally measures less than 7mm.
CT is also able to predict the cause of obstruction in a majority of cases.
Abrupt termination of the extrahepatic duct suggests a malignant process, smooth
gradual tapering of bile duct favours benign disease.
Spiral CT scanning provides additional staging information including vascular
involvement in patients with periampullary tumour.19
CT provides more complete and accurate imaging of the pancreatic head and
surrounding structure. CT scanning provides useful information on the tumour size as
hypodense focal lesion, extent of the disease, spread to the liver, peripancreatic
lymphnodes or retroperitoneal structures and evaluate major vessels adjacent to the
pancreas for tumour invasion, encasement or thrombosis regarding resectability of the
tumour.
28
29
h) MRI / magnetic resonance imaging 9: (fig.9)
MRI is used to demonstrate the anatomical structure of living tissue, and it is
free of ionizing radiation. In contrast to CT it offers images in any plane of space.
MRI has sensitivity and specificity of 95% and 89% respectively at detecting
choledocholithiasis.20
MRI has not been shown to have a definitive advantage over modern CT
scanning.
MRCP (Magnetic resonance cholangiopancreatography) has the potential to
provide information about tumour size and extent, biliary and pancreatic ductal
anatomy and vascular involvement through a single, non invasive procedure, MRCP
can delineate the entire biliary tree on either side of an obstructing tumour without
risk of sepsis.
i) Endoscopic retrograde cholangio pancreatography (ERCP)7 : (fig.10)
ERCP is the primary method of direct cholangiography with considerable
therapeutic potential.
It consists of introduction of a side viewing flexible endoscope into the second
portion of the duodenum, cannulation of the papilla of vater and injection of contrast
material under fluoroscopic guidance. It helps to define the anatomy and pathology of
biliary and pancreatic ducts.
ERCP is a sensitive diagnostic test for pancreatic cancer. Cut off of both the
pancreatic and distal bile duct at the level of the genu of the pancreatic duct (Double
duct sings) is pathognomonic for pancreatic cancer.
30
ERCP helps to distinguish chronic pancreatitis from pancreatic cancer, The
former is characterized by multiple focal stenoses of the pancreatic duct.
ERCP can be used therapeutically for endoprostheses to decompress the
biliary tree. It also allows for biopsy whereas MRCP does not, hence ERCP is
advantage over MRCP in evaluation of the ampulla.
ERCP is advantagous over PTC. It is less patient discomfort, fewer
complication and its ability to examine the upper gastrointestinal tract, papilla of vater
and the pancreatic duct with direct biosy of the tumour.
The most common complication in ERCP includes acute pancreatitis, bleeding
and retroperitoneal perforation and cholangitis following inadequate biliary drainage.
j) Percutaneous transhepatic cholangiogram (PTC)7 : (fig.11)
PTC is better in defining proximal biliary anatomy, and the level of biliary
obstruction but its disadvantages include more invasive, traumatic nature, risk of
hemobilia and inability to visualize pancreatic duct Its complication include
hemorrhage, sepsis, intraperitoneal bile leak, rarely pneumothorax, hemothorax,
arteriovenous fistula and vasovagal reaction.
PTC is invasive diagnostic imaging test in which a needle is passed through
the skin into the biliary tree through hepatic parenchyma, iodinated contrast is
injected to opacify the bile duct.
PTC is contraindicated in coaugulopathy, ascites, severe allergy to contrast,
intrahepatic vascular tumour, uncooperative patient and lack of safe access.
31
32
It is indicated when
i) ERCP has failed to outline the duct system or to adequately define the
obstructing lesion.
ii) ERCP is technically impossible due to tumour or surgery deforming the
second part of duodenum.
iii) A high obstructing lesion as suggested by US or CT.
iv) It precedes an interventional procedure, Stent insertion, Biliary damage, Stone
extraction.21
k) Radionuclide scanning of the biliary tree 21;
The application of radionuclide scanning to the biliary tract depend on the
ability of the liver to take up and excrete radiolabelled agents into the bile ducts and
gall bladder.
Using the new generation of 99m Tc labelled Di-isopropyl-iminodiacetic acid
(DISIDA) helps to define the anatomy of the biliary tree as well as abnormalities
within the CBD with a high degree of accuracy. 9
Biliary leak following complication of surgery of the gall bladder or the biliary
tree can be confirmed and frequently localized by biliary scintigraphy.
Radionuclide technetium HIDA scanning is most useful in patients suspected
of having early post-operative bile duct injury, to assess biliary leakage or to
document a complete biliary obstruction.7
33
l) Operative cholangiography 7:
Operative choliangiography refers to radiographic image of the abdomen
acquired during direct injection of iodinated contrast into the biliary tree through the
gall bladder or cystic duct during open or laproscopic cholecystectomy.
Intra operative cholangiography is performed at the time of cholecytectomy,
not to miss and or to evaluate CBD pathology. It also helps to avoid unnecessary CBD
exploration based on clinical and bio-chemical grounds alone.
T-Tube cholangiography 7: refers to radiographic images obtained during direct
instillation of contrast into a surgically placed common bile duct drainage tube.
It is indicated to confirm or to exclude the status of a surgical biliary
anastomosis, it also helps to follow the results of endoscopic or percutaneous
intervention.
m) Staging laproscopy 7:
It is done using a 30 degree angled laproscope to evaluate the peritoneal
surfaces, the paracolic gutter, the hemidiaphragms, the pelvis and the surface of the
liver or omental nodules.
34
Fig. 12: Cholangiography
35
Classification of cause of surgical jaundice :
I. In the lumen of the duct
a) Choledocholithiasis
b) Parasitic infestation
 Clonorchis sinensis
 Opisthorchis viverrini
 Ascaris lumbricoides
c) Hemobilia
II. In the wall of the duct
a) Benign biliary stricture
i) Congenital
 Biliary Atresia
 Choledochal cyst
ii) Post operative strictures
- Injuries at primary biliary operation
 Laparoscopic cholecystectomy
 Open cholecystectomy
 Common bile duct exploration
- Injuries at other operative procedure
 Gastrectomy
 Duodenal ulcer procedures
 Hepatic resection
 Liver transplantation
 Pancreatic procedure
 Porta caval shunt.
36
iii) Post traumatic
iv) Strictures due to inflammatory condition
 Chronic pancreatitis
 Cholelithiasis and chledocholithiasis
 Primary sclerosing choleangitis
 Duodenal ulcer
 Crohn’s disease
 Sphincter of oddi stenosis
 Toxic drugs
 Radiation fibrosis
v) Mirizzis syndrome
vi) Benign bile duct tumors
b) Malignant causes
 Cholangio carcinoma
 Carcinoma of ampulla of vater
 Carcinoma of gall bladder
III Outside the wall
a) Benign
 Pseudocysts of pancreas
b) Malignant
 Carcinoma head of pancreas
 Enlarged lymphnode at portahepatis
 Periampullary carcinoma
 Extrabiliary malignancies
37
Preoperative management 9 :
1) Liver and renal function :
 Prognosis deteriorates as the depth and duration of the jaundice increases, the
effect of ischaemia and endotoxaemia.
 Cholaemia and liver damage are associated with adverse effects on renal
structure and function, hence patient with obstructive jaundice have an
increased risk of post operative acute renal failure.
2) Treat infection :
 Biliary tract infection associated with cholelithiasis or previous procedure.
 Aminoglycoside with metranidazole is given as first choice.
3) Correct pre renal deficits :
 Assessment of fluid balance with measurement of central venous pressure
before and after surgery
 Serum albumin < 30gm / lts denotes significant volume depletion.
 Routine coagulation screening, and administration of vitamin K before surgery
4) Avoid dangerous drugs :
 Avoid hepatotoxic and nephrotoxic drugs
 Prostaglandins used for maintenance of intrarenal blood flow.
Mannitol is an osmatic diuretic which is not metabolized but freely filtered by
the glomeruli, it is given for the prophylaxis of ischemic acute renal failure.
Adequate intravenous saline is given as a marked natriuresis during the first
two or three post operative days.
38
Postoperative care :
1) Extensive nursing care
2) Physiotherapy for improvement of pulmonary and musculo skeletal function.
3) Psychological support
4) Cardiovascular system : Adequate intravascular volume
5) Respiratory system : Arterial blood gas analysis
pH
Bicarbonate status
Partial pressure
6) Renal : Prevent oliguria
Correct intravascular volume and perfusion pressure
Mannitol and dopaminergic agent
7) Nutritional support :
Enternal and parenteral hyperalimentation
8) Infection control
9) Monitor haematological and coagulation parameters
10) Post operative analgesia.
Post operative complications :
1. Apart from various complications of any surgery those risks associated with
jaundice are :
a) Post operative lung collapse, consolidation and pulmonary embolism.
b) Septicemia : It is characterized by hypotension, tachypnoea and vasoconstriction.
Blood culture has to be done and intra venous broad spectrum antibiotics should
be started until sensitivity is known. Blood transfusion may be needed.
39
c) Hepato renal syndrome12 : Hepatorenal syndrome is defined as the progressive
renal failure that occurs as a result of intense renal arterial vasoconstriction due to
severe liver disease.
Hepatorenal syndrome results due to splanchnic steal, in which splanchnic
vasodilatation leads to renal vasoconstriction.
Glomerular filtration rate falls in response to anaesthesia or surgery, which
leads to rise in the secretion of antidiuretic hormone and aldosterone which results
in increased tubular reabsorption of salt, water and urea.
Surgery and anaesthesia can be associated with a significant fall in liver
perfusion. Liver anoxia results in further decrease in the clearance of endotoxins
from portal blood, and decrease clearance of lactic acid in the liver which further
decrease clearance results in profound metabolic acidosis.
d) Reactionary hemorrhage
e) Slow recovery of consciousness
f) Biliary fistula occurs after hepatic resection or bileduct surgery usually
conservative treatment is applied. A policy of wait and restricting bile flow with
parenteral supplementation of nutrition and electrolytes will result in closure of
fistula.
g) Pancreatic fistulas : are treated conservatively based on restriction of oral intake
and support with parenteral nutrition. Administration of H2 receptor antagonist
results in decrease fistula output.
Choledocholithiasis 12 :
Choledocholithiasis / CBD stones are classified as :
a) Primary stones arise denova in the bile duct.
40
- It is composed predominantly of calcium bilirubinate monomer with minor
quantities of cholesterol and calcium soaps of fatty acids.
- It appears as brownish yellow, and is often soft and friable.
- It depends on biliary stasis and bacterial infection predominantly due to E.coli,
klebsella.
- Bacterial enzyme catalyze deconjugation of bilirubin, and lysis of phospholipids
leads to deposition of calcium bilirubinate and calcium palmitate.
b) Secondary stones which are formed in the gall bladder and migrated into the CBD.
It has predominantly cholesterol or black pigment identical to gall bladder stones.
Presentation :
- Bile duct stones remains asymptomatic for months to years. About 2/3 rd of
asymptomatic patients with gall stone remain symptom free. Stones 3mm or less
almost invariably pass into the duodenum without causing symptoms.
- Incidence of CBD stones discovered at the time of cholecystectomy is about 10%.
Management7 :
Extraction :
a) Surgical duct exploration : CBD stones are generally removed through a
choledochotomy. The stones can be manipulated into the choledochotomy site
using the index finger and thumb. Stone retrieval instruments includes baskets,
balloon, forceps and a mechanical lithotriptor.
Complication of CBD exploration includes retained CBD stones, post
operative pancreatitis, stricture, bile leakage.
b) ERCP and sphincterotomy
41
c) Laparoscopic common bile duct exploration via the cystic duct or with formal
choledochotomy.
Laproscopic common bile duct exploration is a safe, feasible and single stage
option for the management of common bile duct stone. 22 and avoids the
potential morbidity of an endoscopic sphincterotomy.23
d) Percutaneous T-tube / transhepatic Dormia basket removal through T-tube
2) Stenting : Temporary nasobiliary endoscopic retrograde long term internal stent
3) Fragmentation / lithotripsy : Impacted stones can be fragmented using extra
corporeal shock wave lithotripor, yttrium aluminium garnet laser.
4) Dissolution : Cholesterol stone is dissolved using monoctanoin.
5) Sphincterotomy and sphincteroplasty is performed for impacted stones in the
ampullary area, multiple small stones or sludge, recurrent CBD stones and
stenosis of ampulla of vater.
6) Choledochoenterostomies is indicated for dilated duct secondary to CBD stones
and recurrent CBD stones.
Retained stones are stones deliberately left in place at the time of surgery or
diagnosed shortly after cholecystectomy. Recurrent stones are stones diagnosed two
years later. Both of which are best treated endoscopically or via the T tube, the stone
matures in 2-4 weeks, extraction is done using basket of balloon under fluoroscopic
guidance.
In recurrent choledocholithiasis who present with clinical and operative
findings, choledochoduodenostomy has to be considered the method of choice.24
42
43
Ascariasis lumbricoides 16:
 Ova of the round worm ascariasis lumbricoides arrive in the liver by

retrograde flow in the bile ducts. They exert an immunological reaction with
eggs. Giant cells and granulomas are surrounded by a dense eosinophil
infiltrate.
 The adult worm is 10-20 cms long. It may lodge in the common bile duct
producing partial bile duct obstruction and secondary cholangitic abscesses.
 Treatment is by ERCP with endoscopic worm extraction with or without

sphincterotomy.
Hemobilia 5:
 Hemobilia refers to bleeding within the biliary tract, it may arise anywhere
within the biliary system – from liver parenchyma, intrahepatic or extra
hepatic bile ducts, gall bladder, pancreas or the ampullary region.
 It presents as pain, Jaundice, hematemesis and melena
 It may be caused by laceration (operative trauma), pressure necrosis, tumor,

infection, or thrombolysis in bile, the arterial system is involved more often
than the venous system due to its high pressure .
Management :
 General evaluation and resuscitation with blood transfusion

a) Intrahepatic false aneurysms is effectively treated with anteriographic
techniques such as embolization with clot, steel coils, or other emboli.
b) Hepatic parenchymal bleeding is controlled either by direct ligation of the
exposed vessel and resection, packing or ligation of the proper hepatic artery,
right or left hepatic artery.
44
c) Cholecystectomy is curative with bleeding into the gall bladder
d) Management of iatrogenic causes of hemobilia depends on the severity of the
bleeding and the type of manipulation. It is usually controlled with
arteriography.
Neonatal biliary atresia, and choledochal cyst 7;
 Neonatal jaundice may be the result of intrahepatic cholestasis or structural

abnormalities causing biliary obstruction. The latter includes biliary atresia
and choledochial cyst.
a) Biliary atresia 25
 Biliary atresia causes prolonged neonatal jaundice, for more than 2 weeks. It is
accompanied by pale stools and dark urine, extrahepatic bile ducts remains
obliterated fibrous cord.
Type I : Entire extra hepatic ductal system is obliterated [common type].
Type II : Gall bladder, cystic duct and the common ducts remain patent
Type III : Atresia of the right and left hepatic duct
Fibrous cord representing the gall bladder, the remaining biliary tree is scanty
to absent.
Management :
 Kasai portoenterostomy with Roux-en-Y-limb. Infants operated on or before they
are 70 days old have better results, and the success of the operation depends on the
microscopically patent biliary channels.
 Kasai portoenterostomy continues to be the definitive primary treatment for the
vast majority of patients with biliary atresia.26
45
 Infants who fail to drain bile after portoenterostomy can be salvaged only by
organ transplantation.
b) Choledochal cyst 6:
Choledochal cyst is defined as an isolated or combined congenital dilation of
the extrahepatic or intrahepatic biliary tree.
Classification :
Type I – Dilation of the extrahepatic biliary tree
Type II – Saccular diverticulum of extrahepatic bile duct.
Type III – Biliary tree dilation within the duodenum “Choledochocele”.
Type IV a – Dilation of the intrahepatic and extraheptic biliary tree.
IVb – Multiple extrahepatic cyst.
Type V – Dilation confined to the intrahepatic duct “Caroli’s disease”
It is associated with increased risk of developing cholangiocarcinoma
Management :
 Complete or near complete excision of the choledochol cyst with reconstruction
by roux-en-y choledocho-jejunostomy or hepatic duct-jejunostomy.
Benign biliary stricture 25
The most common cause of benign biliary stricture is latrogenic bile duct
trauma during cholecystectomy. The incidence of major bile duct injury after
laproscopic cholecystectomy is 0.16 – 2.35 % and for open cholecystectomy is 0.07 –
0.9 %. 27
46
Bismuth classification of stricture of the bile duct :
Based on the anatomic pattern of involvement
Type I – low common bile duct ; stump > 2 cms
Type II – middle common hepatic duct ; stump < 2 cms
Type III – Hilar – confluence of right and left hepatic duct intact
Type IV – right and left ducts separated
Type V – involvement of the intrahepatic duct
Higher the location of the stricture the more difficult is the repair and the
greater is the recurrence rate
 Post operative bile duct stricture accounts for more than 80% of bile duct stricture.
The rate of bile duct injury has doubled since the introduction of laparoscopic
cholecystectomy
i. Blind plung application of a haemostat to a bleeding cystic or accessory
cystic artery or to the right hepatic artery is likely to damage the common
hepatic duct.
ii. Too much traction applied in fundus first procedure, may tent the common
bile duct and any forceps intended for the cystic duct grasp the angulated
main channel.
iii. Failure to identify the anatomy in calot’s triangle, the common hepatic
duct is tied instead of the cystic duct.
iv. Dissection around the common bile duct particularly at the sides of the
duct may lead to ischemic stricture formation.
47
Management :
a) Immediate repair of intra operative bile duct injury
 Unexpected bile leakage observed during surgery or the suspicious of
abberrant ductal anatomy should raise concern for a biliary injury.
 Conversion of laparoscopic cholecystectomy to an open procedure will
facilitate identification of the biliary anatomy and allow repair.
 Partial transections of the biliary duct less than 180 0 is primarily closed over a
‘T’-tube.
 Injury more than 1800 or complete transection and if possible to oppose the
two ends : end to end ductal repair with placement of a ‘T’ tube through a
separate choledochotomy with additional mobilization of the duodenum
(Kocher’s maneuver)
 High ductal transections with significant loss of the length of the biliary tree is
repaired with a tension free biliaryenteric anastomosis via Roux-en-Y jejunal
limb.
b) Elective repair of post operative injuries or strictures
 Percutaneous or endoscopic biliary drainage
 In treatment of post cholecystectomy bile duct stricture surgery provides a
better long term out come over the endoscopy. As patient with total
obstruction are not amendable to endoscopic approach.28
 Metallic endobiliary stents should not be used for benign strictures, in those
patients with a predicted life expectancy greater than 2 years. 29
 End to side Roux-en-Y hepatico or choledochojejunostomy.
48
Primary sclerosing cholangitis :
 PSC is a chronic fibrosing inflammatory condition of the biliary tree which affects
both intra hepatic and extra hepatic duct, it may also involve gall bladder and
pancrease.
 It usually occur in male (70%) and around 30-40 years. it is usually associated
with inflammatory bowel disease (75%) [ulcerative colitis 65% Crohn’s disease
10%], pancreatitis (20%) and diabetes mellitus (5%).
 PSC progress silently leads to cirrhosis, portal hypertension and liver failure.
 It is associated with greater risk of developing a bile duct carcinoma.
 The median length of survival from the time of diagnosis is 12 years,
Immunosuppressive, antifibrotic and anti-inflammatory agents have been used to
treat PSC.
 Dominant stricture of the extrahepatic biliary tree is treated by endoscopic balloon
dilatation, endoscopic stenting or percutaneous transhepatic approaches. Surgical
management with resection of the extrahepatic biliary tree and hepatico
jejunostomy.
 If liver failure supervenes these patients are suitable candidates for liver
transplantation.
Stenosis of the sphincter of oddi 30:
A benign stenosis of the outlet of the common bile duct is usually associated
with inflammation, fibrosis or muscular hypertrophy.
A dilated common bile duct that is difficult to cannulate, with delayed
emptying of the contrast are diagnostic features.
It is managed by endoscopic or operative sphincterotomy.
49
Mirizzi’s syndrome 6:
Mirizzi’s syndrome is characterized by long cystic duct parallel to the
common hepatic duct with a low opening into hepatic duct with an impacted stone. It
produces extrinsic obstruction in the common hepatic duct with clinical features of
obstructive jaundice.
Type I - Impacted cystic duct stone without fistula, pericholecystic inflammation
causes partial or complete obstruction of the common hepatic duct.
Type II – Impacted cystic duct stone with bilio biliary fistula “cholecysto choledochal
fistula”.
Management :
Type I – Cholecystectomy with reconstruction of the defect in the wall of the common
bile duct.
Type II – partial cholecystectomy with stone extraction and construction of a
cholecystocholedocho-jejunostomy or cholecystocholedocho duodenostomy.
Cholangiocarcinoma / carcinoma of the bile duct 7,16, 25 :
 Cholangiocarcinoma may arise at any point in the biliary tree from the small intra
hepatic bile ducts to the common bile duct.
 The majority occur proximal to cystic duct in the upper third (58%) and the
incidence in middle third is 17%, lower third is 18% and 7% are diffuse.
 Risk factor of malignant tumors of the extrahepatic bile ducts are chronic
ulcerative colitis and sclerosing cholangitis and with liver flukes (clonorchis
sinensis) choledochal cysts, hepatolithiasis, biliary enteric anastomosis and
chronic typhoid carriers.
50
 It is common in male (2:1)
 In case of extrahepatic bile duct cancer, resection should be considered and efforts
should be made to obtain a tumor free margin. An aggressive surgical approach
will give some survival benefit to the patients with even advanced disease.31
 Treatment options include curative resection, palliative resection, palliative
biliary–enteric by pass and palliative percutaneous, endoscopic or intraoperative
stenting.

In 69% of patients with non resectable hilar cholangiocarcinoma insertion of the
wallstent is feasible and safe, it provides successful palliation without the need for
biliary reintervention.32
 Tumour of distal bile duct require pylorus preserving pancreatio-duodenectomy.
Perihilar cholangiocarcinoma / Klatskin s tumor’s
Bismuth – Corlette classification :
Type I – involving common hepatic duct
Type II – involving bifurcation of common hepatic duct
Type III a – involving common hepatic duct with right hepatic duct
Type III b – involving common hepatic duct with left hepatic duct
Type IV – involving common hepatic duct with right and left hepatic duct
Pancreatic and periampullary carcinoma 7:
 Ductal adenocarcinoma is the most common primary malignant disease of the
pancreas and periampullary region.
 It accounts for more than 75% of all non endocrine tumors arising in the region,
and ampullary, distal common bile duct and duodenal adenocarcinoma are less
common and accounts 15% - 20%.
51
 Risk factors :
i. Demographic patterns
 Advancing age 60-80 years
 Slightly higher in male
 Black race
ii. Host factors – genetic syndrome associated with increased risk
 Hereditary non polyposis colo-rectal cancer (HNPCC)
 Familial breast cancer associated with BRAC 2
 Peutz Jegher’s syndrome
 Ataxia telangiectasia syndrome
 Familial atypical multiple mole melanoma syndrome
 Hereditary pancreatitis.
iii. Environmental factors
Nitrosamines and tobacco smoke are carcinogenic for the pancreas.
Risk factors for other periampullary cancers includes inflammatory bowel
disease, sclerosing cholangitis, choledochal cysts and intrahepatic or common bile
duct stones.
 The head, neck and uncinate process of the pancreas harbor 65% of all ductal
adenocarcinoma.
 Approximately 65-75% of patients with pancreatic cancer come to medical
attention when they develop obstructive jaundice secondary to obstruction of the
intrapancreatic portion of the common bile duct.33
 CA 19-9 is the carbohydrate antigen 19-9 a tumors marker for pancreatic cancer,
significant level is more than 37 units / ml.
52
Management :
a) Non-operative therapy :
 The candidates for non-operative palliation includes unresectable local disease,
distant metastases, disseminated intra abdominal tumors or patients with
debilitating disease in whom anesthesia and surgery are unsafe.
i) Biliary decompression is achieved by either endoscopic or percutaneous
transhepatic techniques.
The complication of PTC or Percutaneous biliary drainage include
hemobilia, bile peritonitis, bile pleural effusion, cholangitis, pancreatitis and
acute cholecystitis.
ii) Tumor associated pain include tumor infiltration into the celiac plexus, pain
associated with early satiety, gastroduodenal obstruction and gall bladder or
biliary obstruction is palliated by
 CT guided percutaneous celiac nerve block
 External beam radiation therapy
 Thoracoscopic or endoscopic chemical splanchnicectomy.

iii) 30-50% of patients with pancreatic cancer have mechanical obstruction of the
duodenum, which is dealt by endoluminal approaches with biliary type expandable
metallic stents.
b) Operative palliation :
Palliative surgery is indicated in patients whose tumors are found to be
unnresectable at the time of laparotomy, and in patients considered with good
operative risks.33
53
i) Obstructive jaundice :
 Choledochoduodenostomy : is associated with higher rates of recurrent jaundice
due to its proximity of the tumor to the anastomosis, it is avoided in malignant
biliary obstruction.
 Cholecystojejunostomy : similarly it is not done if tumors is located less than 2-3
cms from the cystic duct- common hepatic duct junction.
 Cholecystoenteric with choledochoenteric bypass has better long term relief of
jaundice.
ii) Pain :
 Intra operative chemical splanchincetomy is performed during surgery by
injecting 20ml of 50% alcohol on either side of the aorta at the level of the celiac
plexus.
iii) Duodenal obstruction :
Prophylactic gastro jujenostomy significantly reduces the incidence of late gastric
outlet obstruction and relaprotomies without increases the incidence of post operative
complication.34
c) Resectional therapy :
 Only 15-20% of patients with pancreatic cancer have tumors that are resectable
for cure at the time of presentation. Upto 40% of patient with a pre-operative
diagnosis of a resectable tumor are found to have irrestectable disease during
exploration and undergo a double bypass procedure. 35
i) Pancreaticoduodenectomy is done for the resectable tumor ; finding that
contraindicate resection at exploration.30
- Liver metastases
54
- Celiac lymphnode involvement
- Peritoneal implants
- Invasion of transverse mesocolon
- Hepatic hilar lymph node involvement
Finding not contraindicated for resection at exploration
- Invasion at duodenum or distal stomach
- Involved peripancreatic lymph node
- Involved lymph node along the porta hepatis that can be swept down with the
specimen.

Preoperative biliary drainage should be avoided wherever possible in patients with
potentially resectable pancreatic and peripancreatic lesions. 36
 Pancreaticojejunostomy or pancreaticogastrostomy is done with either an end to
end, or a end to side fashion.
 Biliary anastomosis is performed as an end-to-side hepaticojejunostomy, 10cms
distal to the pancreatic anastomosis.
 Duodenojejunostomy is performed 10-20 cms downstream from the
hepaticojejunostomy.
Pylorus preserving whipple resection offer some minor advantage in the early
postoperative period but not in the long term.37
Complication following pancreaticoduodenectomy :
 Post operative complication remains as high as 40-50%,38 includes delayed gastric
emptying, pancreatic fistula, wound infection, intraabdominal abscess, cholangitis,
pneumonia, bile leak and pancreatitis.
55
Chemoradiation therapy :
The most important predictors of survival for patient with resected pancreatic
cancer is post operative adjuvant chemoradiation therapy.39
a) Radio therapy : External beam radiation therapy
Intra operative radiation therapy
Brachytherapy
b) Chemotherapy – 5 Flurouracil
Adjuvent radiotherapy combined with 5 FU is safe and tolerated
Neoadjuvant therapy :
 Neoadjuvant therapy involves the use of chemoradiation before surgical
exploration and attempted resection.
Palliative therapy
 Gemcitabine inhibits DNA replication and repair, Gematabine is a powerful
radiosensitizer.
 Other agents currently being evaluated include paclitaxel (taxol), matrix metallo-
proteinaseinhibitor (marimastat), perillyl alcohol and angiogenesis inhibition. 40
Common bile duct obstruction following pancreatitis :
 Pancreatic inflammation and edema may cause transient partial obstruction of the
common bile duct in patients with acute pancreatitis.
 CBD obstruction is the second most common complication of chronic pancreatitis
after pseudocyst formation, because the CBD courses posteriorly through the
substance of diseased pancreas which is vulnerable to stricture or compression by
pancreatic fibrosis, inflammation or pseudocyst.41
56
 Biliary obstruction may be associated with pancreatic pseudocysts located in the
head of the gland causing extrinsic compression of the bile duct.
 Any elevation of the serum bilirubin and alkaline phosphatase in a patient with
chronic pancreatitis should suggest the presence of a common bile duct stricture.
Management :
 Biliary decompression should be considered in any patient with a documented
persistent bile duct stricture.
 Endoscopic and percutaneous transhepatic stenting procedure has not been proven
effective in the long term management of benign biliary stricture.
i. Surgical biliary enteric drainage
Roux-Eu-Y hepatico jejunostomy combined with gastrojejunostomy offers
effective palliation for irresectable pancreatic head cancer and can be performed
with low mortality and acceptable morbidity rates.42
Choledochoduodenostomy – is preferred as it maintain normal flow of bile and is
technically easier and leaves the jejunum free for subsequent procedures to drain
the pancreatic duct.
ii. Choledochojejunostomy is done when choledochoduodenostomy cannot be safely
performed or when the diameter of the common bile duct above the stricture is not
2 cms.
Pancreatic ductal drainage is performed accompanied with biliary enteric
bypass “side to side longitudinal pancreaticojejunostomy”.
Frey procedure (local resection of pancreatic head combined with lateral
pancreatico jejunostomy) is the ideal operation for chronic pancreatitis, it provides
long lasting pain relief and correct the local complication. 43
57
58
59
Methodology
METHODOLOGY
Source of data :
The materials for the clinical study were collected from cases admitted in
Chigateri General Hospital and Bapuji Hospital attached to J.J.M. Medical College,
Davangere during January 2004 to December 2005.
Ethical clearance has been obtained from research and dissertation committee/
ethical committee of the institution for this study.
Type of study :
This is a cross sectional observational study of patients admitted and
positively diagnosed as extra hepatic obstructive jaundice.
Inclusion criteria :
Patients admitted and positively diagnosed as extra hepatic obstructive
jaundice by investigation like ultrasonography and liver function test were included in
this study.
Exclusion criteria :
Patients with jaundice other than extra hepatic obstructive pathology like
hemolytic jaundice, hepatocellular jaundice and intra hepatic obstructive jaundice
were excluded from the study.
Method of collection of data :
Clinical study of 30 cases of surgical jaundice of different aetiology were
analyzed. Following admission individual cases were examined systematically and
clinical data were recorded according to the proforma. Investigation like urine bile
60
salt, bile pigment, liver function test, ultrasonographic study of the abdomen were
done in all the cases. The cases were followed upto discharge and than upto 6 months.
Statistical analysis :
Results are presented as mean, standard deviation and proportion.
61
Results
RESULTS
The results obtained in the present study were analyzed as follows, 30 patients
with surgical jaundice were studied.
Table 1 : Age distribution among the surgical jaundice cases:
Age in years Number of patients Percentage

0–9 01 3.3%
10 – 19 01 3.3%
20 – 29 - -
30 – 39 - -
40 – 49 05 16.7%
50 – 59 08 26.7%
60 – 69 08 26.7%
70 – 79 07 23.3%
Interpretation ;
The age group varied from 3 years to 75 years, the average age was 55.5 years,
76% of patients are between the age group of 50 – 80 years.
Graph 1 : Age distribution among the surgical jaundice cases
30.0 26.7
26.7
23.3
25.0
20.0
Percentage
16.7
15.0
10.0
3.3 3.3
5.0
0.0 0.0
0.0
0–9 10–19 20–29 30–39 40–49 50–59 60–69 70–79
Age in years
62
Table 2 : Sex distribution among the surgical jaundice cases
Sex Number of patients Percentage

Male 16 53.3%
Female 14 46.7%
Interpretation :
There were 16 (53.3%) male and 14 (46.7%) female in our study with slight
male predominance
Graph 2 : Sex distribution among the surgical jaundice cases
46.7
Male
Female
53.3
63
Table 3 : Causes of surgical jaundice cases
Number of patients Percentage

A. Malignant cause 19 66.7%
1. Ca head of pancreas 10 33.4%
2. Periampullary Ca 3 13.3%
3. Cholangiocarcinoma 3 10.0%
4. Secondaries in liver 2 6.7%
5. Porta hepatic metastases 1 3.3%
B. Benign causes 11 33.3%
1. Choledocholithiasis 7 23.3%
2. Benign biliary stricture 3 6.7%
3. Choledochal cyst 1 3.3%
Total 30 100%
Interpretation :
Of the 30 cases in this study 19 patient presented with malignant causes
(66.7%), out of which carcinoma head of pancreas was commonest in 10 (33.4%)
cases, and out of 11 cases (33.3%) of benign cause of surgical jaundice, the
commonest cause was choledocholithiasis in 7 cases (23.3%).
Graph 3 : Causes of surgical jaundice cases
35.0 33.4
30.0
25.0 23.3
Percentage
20.0
15.0 13.3
10.0
10.0
6.7 6.7
5.0 3.3 3.3
0.0
Ca HOP Periamp Ca Cho Ca. Sec. in liver PH CBD stones Benign Choledo cyst
metastases biliary
stricture
A. Malignant cause B. Benign causes
64
Table 4 : Clinical presentation in surgical jaundice causes
Total Pain Mass Fever with Loss of Loss of Dark

Jaundice Itching Steatorea
cases abdomen abdomen chills appetite weight urine
Malignant 18 14 5 9 17 13 13
19 2 (10.5%) 17 (89.5%)
jaundice (94.7%) (73.9%) (26.3%) (47.4%) (89.5%) (68.4%) (68.4%)
Benign
10 11 1 5 11 1 1 8 9
surgical 11
(90.9%) (100%) (9.1) (45.5%) (100%) (9.1%) (9.1%) (72.7%) (81.8%)
jaundice
28 25 5 14 13 18 21 22
30 18 (63.3%)
(93.3%) (83.3%) (16.7%) (46.7%) (43.3%) (63.3%) (70%) (73.3%)
Interpretation :
In malignant jaundice the most common symptom was jaundice 94.7% loss of weight 89.5%.
In benign surgical jaundice the commonest symptom was pain abdomen 100%, fever with chills 100% jaundice 90.9%.
65
d) Clinical presentation : Table no 4
Jaundice was seen in 28 patients (93.3%) the duration of jaundice varied from
3 days to 3 months about 18 cases (6%) had jaundice of less than 1 month duration.
Pain abdomen was present in 25 cases (83.3%). The pain was felt in the
epigastrium and radiates to the right hypochondrium in 8 cases (26.7%). Pain was
recurrent in 6 cases (20%) and continuous with minor fluctuation in intensity in 11
cases (47.8%).
Dark urine was seen in 22 cases (73.3%). Pale coloured stool was seen in 21
cases (70%). Loss of appetite and weight was observed in 18 cases (63.3%). Itching
was noticed in 14 cases (46.7%). Fever with chills in 13 cases (43.3%) and mass
abdomen in 4 cases (13.3% ).
Graph 4 : Clinical presentation in benign and malignant surgical jaundice
Dark urine 81.8

68.42
Steatorea 72.7
68.42
Loss of weight 9.1

89.47
Clinical presentation
Loss of appetite 9.1

89.47
Fever with chills 100.0

10.53 Benign surgical jaundice
45.5
Malignant jaundice
Itching 47.37
Mass abdomen 9.1

26.32
100.0
Pain abdomen 73.68
Jaundice 90.9
94.74
0 20 40 60 80 100 120
Percentage
66
Table no 5 : Mean and range values of liver function test in surgical jaundice cases
Total Total bilirubin Direct bilirubin Indirect bilirubin Alkaline SGOT SGPT
cases mg/dl mg/dl mg/dl phosphatase iu/l iu/l iu/l
Malignant 20.9  6.7 16.7  5.3 4.2  1.4 284.5  127.5 118  55.9 124.2  59
19
jaundice (0.8-29.6) (0.6-23.6) (0.2-6) (79-557) (20-255) (22-308)
Benign
8.1 5.3 6.3  4.3 1.8  1 200.8  76.1 98.6  66.1 123.9  108.4
surgical 11
(2.3-19.4) (1.5-15.4) (0.5-4) (125-405) (25-245) (29-391)
jaundice
14.5 11.5 3.0 242.7 108.2 124.1

30
(0.8-29.6) (0.6-23.6) (0.2-6) (79-557) (20-255) (22-391)
Interpretation :
In this study the mean total bilirubin in malignant jaundice was 20.9  6.7 mg/dl.
Mean alkaline phosphatase in malignant jaundice was 284.5  127.5 IU/L.
67
Investigation : Table no 5
I. Liver function test :
i) Serum Bilirubin :
Serum bilirubin was elevated in 28 patients. Total bilirubin was below
29.6mg/dl and the direct fraction being the predominant one, the mean total bilirubin
was 14.5 mg/dl, and mean direct bilirubin was 11.5 mg/dl.
ii) Alkaline phosphatase was elevated in 29 patients (96.7%). The level varied from
79 IU/L to 557 IU/L the mean level was 242.7 IU/L about 3 –4 times the upper
limit.
iii) SGOT and SGPT was elevated in 29 patients (96.7%). The level varied from 20
U/L and 22 U/L to 255 U/L and 391 U/L respectively the average level of SGOT
was 108.2 U/L and SGPT was 124.1 U/L.
iv) The urine examination for bile salts and bile pigment were positive in all
malignant jaundice cases and out of benign obstruction it was positive in 9 cases
(81.8%).
Graph 5a : Mean value of total Graph 5b : Mean value of alkaline

bilirubin in benign and malignant phosphatase and SGOT in benign
surgical jaundice and malignant surgical jaundice
284.5
300
25 20.7
250
200.8
20
200
15 1 50 118
98.6 Mal i gnant
8.1 Beni gn
1 00
10
50
5
0
Al kal i ne phosphatase SGOT
0
Mali gnant Beni gn
68
Table 6 : Ultrasonographic findings in cases of surgical jaundice
Dilated Dilated biliary Distended gall Mass in
Total cases Stone in CBD Ascites
CBD radicles bladder pancreas
Malignant
19 18 (94.7%) 16 (84.2%) 15 (79%) 1 (5.3%) 9 (47.4%) 10 (52.6%)
jaundice
Benign surgical
11 10 (90.9%) 9 (81.8%) 3 (27.3%) 7 (63.6%) - 2 (18.2%)
jaundice
Total 30 28 (92.8%) 25 (83%) 18 (53.1%) 8 (34.5%) 9 (23.7%) 12 (35.4%)
Interpretation :
In our study distended CBD in malignant jaundice in 94.7%.
Dilated biliary radicles in malignant jaundice in 84.2%.
Distended gall bladder in malignant jaundice in 79%.
69
II. Ultrasonography : Table 6 :
Ultrasonography done on all the cases showed dilated common bile duct in 28
cases (92.8%), and dilated intra hepatic biliary radicals in 25 cases (83%), information
about the liver metastases, pancreatic masses, and ascites was assessed in 12 cases
(35.4%).
Graph 6 : Ultrasonographic findings in benign and malignant surgical jaundice
100.0 94.7
90.9
90.0 84.2
81.8 79.0
80.0
70.0
63.6
Percentage
60.0
52.6
50.0 47.4
40.0
27.3
30.0
18.2
20.0
10.0 5.3 0.0
0.0
Dilated CBD Dilated biliary Distended Stone in CBD Mass in Ascites
radicles gall bladder pancreas
Malignant jaundice Benign surgical jaundice
70
Table 7 : Various treatment modalities in surgical jaundice cases
Cholecysto Choledoctomy Referred Mortality
Whipple’s Cyst excision with Post
Total jejunostomy with to during
pancreatico roux –en –y operative
cases with extraction of cancer Follow-
duodenectomy hepaticojejunostomy mortality
jejunojejnostomy stone center up
Carcinoma head of
10 - 6 - - 2 - 2
pancreas
Periampullary
03 01 2 - - - - -
carcinoma
Cholangio
03 01 - - - 2 - -
carcinoma
Secondaries in
02 - 1 - - - - 1
liver
Porta hepatic
01 - 1 - - - - -
metastasis
02 10 04 03
19 - - -
(10.5%) (52.6%) (2%) (15.8%)
Choledocholithasis 7 - - - 07 - - -
Benign biliary
3 - 3 - - - 1 -
stricture
Choledochal cyst 1 - - 01 - - - -
11 - 3 (27.3%) 1 (9.1%) 7 (63.6%) - 1(9.1%) -
02 13 1 7 4 1 3
Total 30
(6.7%) (43.3%) (3.3%) (23.3%) (13.3%) (3.3%) (10%)
Interpretation :
In malignant jaundice Whipple’s PD was done in 10.52%, and CJ with JJ was done in 52.63%.
71
Treatment given : Table no 7
1. Malignant causes of surgical jaundice :
a) Whipple’s pancreaticoduodenectomy(PD) was performed on 2 patients out of
19 malignant cases (10.5%) and was followed up to 6 months one patient had
mild intra abdominal collection which was drained by ultrasound guide.
b) Cholecysto jejunostomy and jejunojejunostomy was performed on 10 cases
(52.6%) and was followed upto 6 months.
2. Benign cause of surgical jaundice :
a) Cholecysto Jejunostomy with Jejunojenostomy was performed on 2 cases of
(18.2%) benign biliary stricture and in one case (9.1%) Cholecysto
jejunostomy was performed which were followed up to 6 months.
b) CBD exploration and stone extraction was done on all 7 cases of
choledocholithiasis, and post operatively followed upto 6 months.
c) choledochal cyst excision with roux-en-y hepatico jejunostomy was done in
lone case of choledochal cyst, during 6 months of follow up patient was
healthy with no attack of fever, chills or jaundice.
3. Mortality : 4 cases (13.3%) of the total cases were not fit for any procedure due to
hepatic metastases, old age and emaciation which were referred to cancer centers.
One patient died during 7th postoperative day due to pancreatic fistule and
three patient died during follow up within 3 months (13.3%). All the patients were
followed up to 6 months. In the benign causes of surgical jaundice. all Patient with
choledocholithiasis patient were healthy at the end of 6 months.
In malignant jaundice 3 patient died during follow up within 3 months
(15.8%) and out of 12 patient who underwent surgery 2 patient who underwent
pancreatico duodenectomy (PD) followed till the end of 6 months without mortality.
72
Discussion
DISCUSSION
In this clinical study of 30 cases of surgical jaundice, the age distribution
range between 3 – 75 years. The youngest patients was 3 years with choledochal cyst
and oldest was 75years with carcinoma head of pancreas. The mean age was 56 years
and there were 16 male patients (53.3%), and 14 female patients (46.7%). The results
obtained were compared with previously conducted study.
Table 8 : Sex ratio in various study of surgical jaundice cases
Total cases M F M: F
a) Pellegrini et al44 (1982) 178 86 92 1 : 1.07
b) Pain JA45 (1987) 30 17 13 1 : 0.76
C Parks RW46 (1997) 121 61 60 1:0.98
d) Present study (2006) 30 16 14 1: 0.88
Interpretation :
In our study of 30 cases of surgical jaundice there was slight male
predominance at sex ratio 1:0.8 which correlates with similar studies by Pain JA45
(1987) 1:0.76 and Parks RW46 (1997) at 1: 0.98.
The sex ratio of malignant jaundice was 1:0.9 with slight male predominance.
This was compared with various authors.
Lillemoe KD, Cameron JL. In Mangot’s abdominal operation6 has stated that
there were slight male predilection in malignant jaundice. Steer ML in Sabiston
textbook of surgery5 reported that malignant jaundice was common in men than
women. Russel RCG, in bailey and love’s short practice of surgery25 reported that
male and female are affected to the same degree. Yoe CJ, Cameron JL. In Oxford
73
textbook of surgery47 reported that the sex ratio is equalizing over the recent years. It
was inferred that sex ratio is equalizing in malignant jaundice.
Causes of surgical jaundice :
In our study carcinoma head of pancreas was 33.3%, Choledocholithiasis was
23.3%, Cholangiocarcinoma was 10%, Benign biliary stricture was 6.7%, and porta
hepatis metastases was 3.3% and periampullary carcinoma was 13.3%. This results
correlates with study conducted by Parks RW et al46 (1995) who studied 121
patients during January 1986 to December 1994 reported that various causes of
obstructive jaundice as carcinoma of head of pancreas 34.7%, choledocholithiasis
20.7%, cholangiocarcinoma 9.9%, benign biliary stricture 4.1%, and porta hepatis
48
metastases 1.7%. Carlos Chan MD et al (1995) states that carcinoma of the
ampulla of vater represents 4%-10% of patient with peripancreatic carcinoma.
Table no 9 : Cause of surgical jaundice in various study
Pellegrini J.A. R.W. Parks et Present

et al44 Pain45 al46 study
Sl. No.
(1982) (1987) (1997) (2006)
178 cases 30 cases 121 cases 30 cases
13 42 10
1 Ca head of pancreas 36 (20.2%)
(43.3%) (34.7%) (33.3%)
2 Periampullary Ca - - 2 (1.7%) 3 (13.3%)
Choledocholithiasis 14 25 7
3 46 (25.8%)
stones (46.7%) (20.7%) (23.3%)
Cholangio 1 12 3
4 29 (16.3%)
carcinoma (3.3%) (9.9%) (10%)
Benign biliary 5 3
5 49 (27.5%) -
stricture (4.1%) (6.7%)
1
6 Choledochal cyst - - -
(3.3%)
2
7 Secondaries in liver - - -
(6.7%)
Porta hepatis 1 2 1
8 -
metastases (3.3%) (1.7%) (3.3%)
33
9 Others 18 (10.1%) 1 -
(27.3%)
74
Interpretation :
a) Malignant jaundice :
In the present study there were 19 cases of malignant jaundice, which includs
carcinoma head of pancreas (10), periampullary carcinoma (3), cholangio carcinoma
(3), secondaries in liver (2); and porta hepatis metastases (1). The age range was
between 12 – 75 years, mean age was 57.21 years, with 80% of cases were between
the age group of 50-80 years.
Of the 11 cases of Benign extra hepatic biliary tract disease which included
choledocholithiasis (7), benign biliary stricture (3), choledochal cyst (1), the age range
was between 3 – 72 years with mean age of 52 .45 years.
Clinical presentation in various studies of surgical jaundice :
In our study the presenting symptom and signs in malignant jaundice is
jaundice 95%, abdominal pain 74%, loss of weight 89%, pruritus 47%, fever
cholangitis 10.5%, hepatomagaly 66.7% and epigastric mass in 15.8%. This results
correlates with study conducted by Warren et al49 (1983) who studied 191 patients
and reported that the presenting symptoms in malignant jaundice as follows
abdominal pain 82.8%, loss of weight 90%, pruritus 41.3%, fever 4.9%,
hepatomegaly 64.4%. Brooks et al50 (1981) stated that epigastric mass was present in
18%. Van Wagensveld BA et al51 (1997) who studied 126 patient and reported
jaundice as a presenting symptom in 90%, loss of weight in 82%.
75
Table 10 : Presentation in malignant jaundice various studies
Warren et Brooks et Van Wagensveld Present

al 49 al 50 et al 51 study (2006)
1 Jaundice 145 77% 113 (90%) 95%
(75.9%)
2 Abdominal pain 157 51% 60 (48%) 74%)
(82.8%)
3 Loss of weight 172 (90%) 55% 103 (82) 89%)
4 Pruritus 79 (41.3%) 47%
5 Fever; 9 (4.9% 10.5%
cholangitis
6 Hepatomagaly 123 66.7%
(64.4%)
7 Palpable gall 54 (28.3%)
bladder
8 Epigastric mass 32 (16.7%) 18% 15.8%
Interpretation :
The commonest presentation in malignant jaundice is jaundice and loss of
weight.
Presentation in various cause of benign extra hepatic biliary tract disease :
In our study there were 7 cases of choledocholithiasis with presentation as
jaundice in 85.7% pain abdomen in 100%, fever with chills in 100%, lightening of the
stool in 85.7%, darkening of urine in 85.7%, and itching in 28.6%.
Abrendt SA, Pitt HA in sabiston textbook of surgery5 stated the presentation
of choledocholithiasis includes biliary colic, jaundice, lightening of the stool and
darkening of the urine with fever and chills.
In our study there were 3 cases of benign biliary stricture, 2 cases of post
operative biliary stricture, and the lone case following chronic pancreatitis presented
with jaundice in 100%, pain abdomen in 100%, itching in 100%, fever with chills in
100%, loss of appetite and weight in 33.3%, and steatorea in 66.7%.
76
The most common cause of benign biliary stricture is iatrogenic bile duct
trauma during cholecystectomy. 37
CBD stricture occurs in 3 – 29% of patient with chronic alcoholic
pancreatitis52 usually present with history intermittent jaundice, abdominal pain.
In this study there was only one case of choledocal cyst presented at the age of
3 years with jaundice, pain abdomen, mass abdomen, fever, loss of weight and
appetite.
Lypsett PA et al53 (1994) studied 11 children with choledochal cyst and
reported that symptoms and signs at presentation were abdominal mass 8%,
abdominal pain 36%, Jaundice 64%, fever 18%, nausea / vomiting 18%.
3) Investigation :
In our study the value of total bilirubin in malignant obstruction varied from
0.8 mg/dl to 29.6 mg/dl with the mean value at 20.9  6.7 mg/dl. Of the 19 cases
malignant obstruction the value of alkaline phosphatase varied from 79 IU/L to 557
IU/L with mean value of 284.5  127.5 IU/L. The value of SGOT varied from 20 –
255 IU/L with mean value of 118  55.9 IU/L.
Steer ML in Sabiston textbook of surgery5 has stated that the highest
elevation in serum bilirubin are usually found in the patient with malignant
obstruction was more than 20 mg/dl.
44
Pellegrini et al has reported that average bilirubin values are higher in
patient with biliary obstruction caused by malignant disease.
77
Warren et al48 studied the laboratory values on 191 patients of carcinoma
pancreas and reported that the mean values of total bilirubin was 8-9 mg/dl, alkaline
phosphatase 269.1 IU/L, SGOT 111.5 IU/L.
In our study of 7 cases of choledocholithiasis the value of total bilirubin varied
from 2.3 mg/dl to 19.9 mg/dl with mean value of 10.3 mg/dl.
Ahrendt SA, Pitt HA in Sabiston textbook of surgery5 has stated that CBD
stone is associated with moderate increase in serum bilirubin at 10 – 12 mg/dl.
Pellegrini et al44 (1982) has reported that serum bilirubin value >14 mg/dl are
not usually caused by CBD stones.
In our study of 7 cases of choledocholithiasis the value of alkaline phosphatase
ranged from 125 IU/L to 405 IU/L the mean value was 207 IU/L.
Pellegrini et al44 (1982) reported that alkaline phosphatase more than 5 times
or clinical jaundice present for longer than 1month are uncommon manifestation of
CBD stones.
In our study the ultrasound examination was done in all the patients and
dilated CBD was noted in 94.7% of malignant disease, and 90.9% in benign cause,
distended gall bladder was noted in 79% of malignant cause and 27.3% in benign
cause, pancreatic mass was noted in 47.4% of malignant jaundice, ascites was noted
in 52.6% of malignant jaundice.
Galati P et al54 (1994) concluded that sonographic finding characteristic of
periampullary tumor are intrahepatic ductal dilatation, dilated CBD and hypoechoeic
mass in ampullary region and distended gall bladder seen in more than 50% of the
patients.
78
Treatment :
Malignant jaundice :
a) Curative treatment :
In our study curative resection of malignant disease was done in 2 cases
(10.5%). Whipples pancreatico duodenectomy was done in one case of periampullary
carcinoma and pylorus preserving pancreatico duodenectomy was done in one case of
cholangio carcinoma.
Singh SM and Reber HA55 (1989) reported that only 10-15% of patients with
pancreatic cancer have disease suitable for resection and possible cure by the time the
diagnosis is made.
b) Palliative treatment :
In this study palliative cholecysto-jejunostomy and jejuno-jejunostomy bypass
procedure was done in 10 cases of 19 malignant jaundice (52.5%) of which 6 cases of
carcinoma head of pancreas, 2 cases of periampullary carcinoma, 1 case with porta
hepatis metastases and secondaries in liver each. 4 cases presented in the late stage
who were not fit for any procedure and were referred to cancer center, 2 each from
carcinoma head of pancreas and cholangio carcinoma.
Singh SM and Reber HA55 (1989) reported that 85 – 90% of patients with
malignant jaundice requires some form of palliation.
c) Mortality :
In this study 3 (15.8%) patients died during follow up out of 19 malignant
jaundice patient within 30 day which included 2 patients of carcinoma head of
pancreas and 1 patients with secondary liver.
79
Van Wagensveld BA et al51 reported that in obstructive jaundice
postoperative mortality ranges from 2.5 – 19%.
d) Survival :
In our study both patient who underwent PD were followed till 6 months
without mortality.
Fisher WE, Andersen DK, Bell RH, Saluja AK, and Brunicaidi FC in
Schwartz textbook of surgery30 has stated that mean survival after PD was about 12 –
15 months.
Steer ML in Sabiston textbook of surgery5 has stated that the mean survival
for patient with stage III tumor range from 8 – 12 months and patient with stage IV
tumor is 3 – 6 months.
2. Benign extra hepatic surgical jaundice :
In our study choledocholithotomy and T tube drainage was successfully done
in all the 7 choledocholithiasis patients with recurrence in 1 case (14.3%).
Ahrendt SA, Pitt HA Sabiston textbook of surgery5 has stated that open
CBD exploration is associated with low operative mortality in 0 - 2%, and operative
morbidity 8% - 16%.
Uchiyama et al56 (2003) reported that recurrence rates in choledocholithiasis
was high when only choledochotomy and T tube drainage are performed in 10.3%.
80
Table 11 : Prognosis of after treatment of patient with choledocholithiasis
Uchiyama et al56
Present study 2006
1982 – 1986
Patients 87 7
Age (mean  SD) 64.5  13.3 57  15
Gender male : Female 41 : 46 (1:1.12) 3:4 (1:1.33)
Recurrence rate 10.3% 14.3%
Interpretation :
The sex ratio in patients with choledocholithasis was 1:1.33 and recurrence in
14.3%
In our study the lone patient of chronic pancreatitis with obstructive jaundice
underwent choledochoduodenostomy with internal drainage but the patient died on 7 th
postoperative day due to pancreatic fistula. The other 2 cases of benign biliary
stricture secondary to iatrogenic trauma patient underwent double bypass procedure.
Sonnenday CJ, Lillemoe KD, Yeo CJ in shakelfords surgery of the
alimentary tract7 has stated that patient who undergo surgical procedure for biliary
obstruction secondary to chronic pancreatitis are treated with
choledochoduodenostomy.
In our study the lone case of choledochol cyst was treated surgically with cyst
excision with roux en-y hepaticojejunostomy, during follow up patient was healthy
with no attack of fever, chills or jaundice.
Lipsett PA53 has stated that current treatment of choldedochal cyst is excision
of the cyst with hepatico-jejunostomy with roux en-y reconstruction of the biliary
tree.
81
Conclusion
CONCLUSION
From our study of 30 cases of surgical jaundice the following can be
concluded.
 Most common age group seen is between 50-80 years and the sex ratio is near
equalizing.
 Most common cause of surgical jaundice is carcinoma head of pancreas and
 Jaundice is the most common presentation of surgical jaundice followed by
pain abdomen, dark urine, pale stool and loss of weight.
 Early diagnosis and management helps to reduce the mortality and morbidity
rate.
82
Summary
SUMMARY
 A clinical study of 30 cases of surgical jaundice who were admitted to
Chigateri General hospital and Bapuji Hospital Davangere during the period
from Jan 2004 to Dec 2005.
 76% of patients are between the age group of 50-80 years with sex ratio of
1:0.88 with slight male predominance.
 The commonest cause of malignant jaundice was carcinoma head of pancreas
at 33.4% and in benign cases was choledocholithiasis at 23.3%.
 The commonest presentation in malignant jaundice is jaundice 94.7%
abdominal pain 73.9%, loss of weight 89.5% pruritus 47.4%, fever 10.5%.
 The commonest presentation in choledocholithiasis was jaundice 85.7%, pain
abdomen 100%, fever with chills 100% lightening of the stool 85.7%,
darkening of urine 85.7% and itching 28.6%.
 Total Bilirubin was highest in carcinoma head of pancreas and lowest in
choledochal cyst of which direct Bilirubin was more.
 The mean valueof total bilirubin in malignant jaundice was 20.9  6.7 mg/dl
and in benign cause of surgical jaundice is 8.1 5.3 mg/dl.
 Alkaline phosphatase was highest in cholangio carcinoma and lowest in
cholidocholithiasis.
 The mean value of alkaline phosphatase in malignant jaundice was 284.5 
127.5 IU/l and in benign cause of surgical jaundice is 200.8  76.1.
 Ultrasonography was more effective in detecting distended CBD (92.8%),
dilated intra hepatic biliary radicals (83%) and distended gall bladder in
(53%).
83
 10.5% of malignant jaundice underwent curative resection while 52.6%
underwent palliative surgery.
 All the benign extra hepatic obstructive jaundice patient underwent curative
surgery with 9% mortality due to pancreatic fistula.
 3 patient (10%) died during the follow up period within 30 days due to
extensive metastases of malignancy.
84
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93
Annexures
ANNEXURE I
Case No. :
PROFORMA
Name : Hospital : CGH /BH

Age : Unit :
Sex : I.P. No. :
Religion : Ward :
Occupation : DOA :
Address : DOO :
DOD :
Chief complaints :
History of presenting illness :

1. Jaundice : Yes / No
a) Duration
b) Mode of onset – Acute / Gradual
c) Progressiveness – gradual / intermittent
d) Depth – mild / moderate / severe
2. Abdominal pain : Yes / No
a) Site
b) Mode of onset
c) Character
d) Progress
e) Time
f) Radiation
g) Relation to food
h) Aggravating factor
i) Reliving factor
94
3. Mass per abdomen
a) Duration
b) Onset
c) Site
d) Progress
e) Presence of other lump
4. Fever : Yes / No
a) Pattern : Continuous / intermittent
b) Associated with chills and rigors : Yes / No
5. Loss of Appetite : Yes / No
6. Loss of weight : Yes / No
7. Nausea / vomiting : Yes / No
- Character
- Colour
- Frequency
- Quantity
8. Itching : Yes / No
9. Bleeding manifestation : Yes / No
a) Haemetemesis d) Haematuria
b) Malena e) Others
c) Epistasis
10. Flatulent dyspepsia
11. Fatty intolerance
12. Bowels
a) Constipations d) Blood and mucus
b) Diarrhea e) Foul smelling
c) Steatorrhoea f) Clay coloured stools
13. High coloured urine
14. Oedema
15. Bony pain /arthralgia
16. Any others
95
Past history :
1. History of previous jaundice
2. History of blood transfusion
3. History of DM / HTN / TB / Enteric fever / Syphilis
4. History of previous surgery
Drug history :
Personal history :
1. Diet 7. Addiction
2. Sleep a) Alcoholic
3. Appetite - Type
4. Bowel and bladder - Amount
5. Marital status - Duration
6. Menstrual history b) Smoking
- Type
- Amount
- Duration
Family history :
General physical examination :

1. Built 5. Pedal oedema
2. Nourishment 6. Lymphadenopathy
3. Icterus : Mild (+), Mod. (++), Sev. (+++) 7. Clubbing
4. Pallor 8. Skin - Colour
- Texture
- Scratch mark
9. Vital statistics 10. Eyes
- Pulse 11. Oral cavity
- BP
- Temperature
- Respiration rate
96
SYSTEMIC EXAMINATION :
A. PER ABDOMEN
I. Inspection :
1) Skin and subcutaneous tissue
2) Shape :
3) Umbilicus :
4) Engorged veins :
5) Movement with respiration
6) Visible peristalsis
7) Hernial orifices
8) Visible mass
Site
Size
Shape
Surface
Skin over the swelling
Extent
Number
9) Left supra clavicular lymphnode
II. Palpation :
1) Temperature
2) Tenderness
3) Liver : Palpable /not palpable

Size : cms from costal margin (R) MCL
Surface :
Extent :
Border :
Consistency :
Movement with respiration
4) Gall bladder
97
5) Mass per abdomen
- Local temperature
- Tenderness
- Position
- Size
- Shape
- Surface
- Margin
- Consistency
- Movement with respiration
- Plain of the swelling
6) Other organs
III. Percussion :
1) Liver dullness upper limit _______ICS in (R) MAL
2) Shifting dullness / fluid thrill
3) Percussion over the mass
IV. Auscultation :
1) Bowel sound
2) Bruit / hum
V. P.R. Examination
B. EXAMINATION OF LYMPHATIC SYSTEM
C. CARDIOVASCULAR SYSTEM
D. RESPIRATORY SYSTEM
E. CENTRAL NERVOUS SYSTEM
PROVISIONAL DIAGNOSIS :
98
INVESTIGATION
Normal value Observed value
I. Urine : Sugar -
Albumin -
Microscopy -
Bile salt -
Bile pigment -
Urobilnogen -
II. Blood : HB%: male 14-18gm/dl

female 12-16gm/dl
TC 4300-11,000/mm3
DC
ESR: male < 10mm/1st hr
female < 20 mm/1st hr
Bleeding time 1-4 min
Clotting time 2-15 min
Urea 20-40mg/dl
Fasting blood sugar 80-110 mg/dl
Random blood sugar
Grouping Rh typing
Prothrombine time 11-15 sec
Control
Index
INR
III. Serum Creatinine 1-1.4 mg/dl
Amylase 50-120 IU/L
S.Alkaline phsophatase 40-125 IU/L
SGOT 6-18 IU/L
SGPT 10-40 IU/L
99
IV. Blood
picture :
V. LFT : Serum bilirubin

Total 0.3-1 mg/dl Mild : < 6mg/dl
Mod.: 6-15mg/dl
Seve.: > 15mg/dl
Direct 0.1-0.3 mg/dl
Indirect 0.2-0.7 mg/dl
Serum protein
Total 5.5-8gm /dl
Albumin 3.5 – 5.5 g/dl
Globulin 2-3.5 g/dl
A / G ratio
VI. Others : Casoni’s test

HBs Ag
HIV I and II
VII. Radiological study :
- Plain X-ray abdomen
- Plain X-ray chest
- I.V. cholanigiography
- Percutaneous transhepatic cholanigiography
- Barium meal series
- C.T. Scan
- ERCP
VIII. Sonographic study
100
IV. Endoscopy
X. ECG
XI. Any other
FINAL DIAGNOSIS :
Treatment :
Operating Surgeon :
I. Surgery
- Date of surgery
- Procedure : operative findings
- Post operative period

POD 1 2 3 4 5 6 7 8 9 10
Urine output
Drain output
Vitals
Icterus
Pruritis
T tube
POD 11 12 13 14 15 16 17 18 19 20
Urine output
Drain output
Vitals
Icterus
Pruritis
T tube
II. Conservative treatment
III. Follow up
101
ANNEXURE II
CONSENT FORM
For Operation / Anesthesia
I______________Hosp. No._______________ in my full senses hereby give
my complete consent for ______________ or any other procedure deemed fit which is
a/ and diagnostic procedure / biopsy / transfusion / operation to be performed on me /
my ward______________ age ____________under any anesthesia deemed fit. The
nature and risks involved in the procedure have been explained to me to my
satisfaction. For academic and scientific purpose, the operation / procedure may be
televised or photographed.
Date: Signature / Thumb impression

Name: of patient / Guardian
Designation:
Guardian
Relationship:
Full Address
102
ANNEXURE III
MAST ER CHART
Loss Total
Sl. Age. Pain Mass Loss Dark Dir. B Indi. B Hb% Alk. SGOT SGPT Ab. Follow-
Name Sex Place I.P. No. DOA DOD Jaundice Itch. Fever of Steatorea GPE Bilirubin BS BP USG CT Diagnosis Surgery
No. Yrs Ab. AB of w t. urine mg/dl mg/dl g/dl Phosp.IU/L IU/L IU/L exam. up
app. mg/dl
OC with CBD
1 B. Hunamanthappa 51 M Ho.Durga 455737 23.2.04 8.3.04 + + - + + - - + + I +++ 19.4 15.4 4 14 + + 174 141 156 L - GB - CBD+IHBR+Calcui+ CBD calculi
exploration
L + GB
2 Nanjappa 48 M Dvg. 5125 7.3.04 15.4.04 + + - + 0 + + + + I +++ 20.4 16.4 4 12.8 + + 279 107 116 H+CBD+IHBR+GB+SOL+ Ca HOP CJ with JJ
+
OC with CBD Rec of
3 E. Karyanna 63 M Dvg. 456405 7.3.04 11.4.04 + + - + + - - + + I ++ 13.7 10.5 3.2 12 + + 251 151 234 L - GB - GB-multicaluli+CBD+IHBR+ Calculi in GB &CBD CBD calculi
exploration stone
L + GB
4 Neelamma 57 F Taralubalu 6123 15.3.04 11.4.04 - + - - - - - - I- 0.8 0.6 0.2 9.8 + + 221 118 129 IHBR+CBD+GB+FF+SOL+ Ca HOP CJ with JJ
+
CJ patient
L + GB CBD+IHBR+GB+smooth narrowing BBS (chronic
5 Girijamma 60 F Madhugiri 11082 25.4.04 14.5.04 + + - + + + + + + I+ 4 3 1 11 + + 184 76 82 expired on 7th
+ of distal CBD pancreatitis)
pod
L + GB OC with CBD
6 Deveramma 70 F Dvg. 460232 18.5.04 17.6.04 + + - - + - - + + I+ 2.3 1.8 0.5 12 - - 405 63 43 CBD+IHBR+GB- Multiple caculi in CBD+ CBD calculi
- exploration
OC with CBD
7 Mangalamma 42 F Chinngiri 460691 26.5.04 1.6.04 + + - - + - - + + I+ 6.7 5.4 1.3 14 + + 186 245 391 L - GB - Calculi in CBD, CBD+GB- CBD calculi
exploration
Caluli in lower 1/3rd or CBD, OC with CBD
8 K.S. Nagappa 46 M Honnur 460690 26.5.04 1.6.04 + + - - + - - + + I ++ 10.6 8.4 2.2 9.9 + + 174 140 152 L - GB - CBD calculi
CBD+IHBR+ exploration
L + GB OC with CBD
9 Thimmamma 72 F Honnalli 461548 10.6.04 30.6.04 + + - - + - - + + I ++ 12.3 9.8 2.5 9.7 - - 134 25 53 CBD+Calculi+IHBR+GB- CBD calculi
- exploration
L + GB Referred to
10 Neelamma 50 F Madhugiri 18042 22.6.04 28.6.04 + + - + + - - + + I +++ 22.4 17.9 4.5 8 + + 311 120 131 SOL+CBD+IHBR+GB+ Ca HOP sec. liver
+ cancer center
Malignant
L + GB Malignant stricture of Referred to
11 Hanumanthappa 45 M Arsikere 22842 3.8.04 18.9.04 + + - + - + + + + I+ 13 10.4 2.6 114 + + 557 284 308 CBD+IHBR+GB+FF+ stricture of dsital
+ distal CBD cancer center
CBD
L + GB Bulky pancreas (head)
12 Kenchamma 70 F Kadur 26682 6.9.04 2.10.04 + - - - - + + - - I +++ 29.6 23.6 6 9.8 + + 239 136 109 IHBR+CBD+GB+FF+SOL+ Ca HOP CJ with JJ
+ CBD+
Periampullary
13 Chandrappa 65 M Harihar 27402 12.9.04 3.10.04 + + - - - + + + + I ++ 26.66 21.36 5.3 10 + + 164 99 108 L - GB + IHBR+FF+GB+CBD+ CJ with JJ
carcinoma
Cholangio
L + GB IHBR+CBD+GB+SOL in right lobe Cholingoca with hepatic Referred to
14 Hemakka 55 F Harapanalli 31482 16.10.04 26.10.04 + - - + - + - - - I ++ 13.97 11.17 2.8 7.4 + + 125 99 108 carcinoma with
+ of liver metastasis cancer center
liver metastasis
L + GB
15 Shekharappa 64 M Holalu 32922 28.10.04 13.11.04 + - - - - + + - - I +++ 22.4 17.9 4.5 13 + + 159 115 126 CBD+IHBR+GB+Mass+ SOL in HOP Ca HOP CJ with JJ
+
16 Revanasiddappa 52 M Dvg. 478443 16.11.04 6.12.04 + + + - - + + + + I ++ 17.6 14.6 3 6 + + 175 92 101 L + GB - CBD+IHBR+FF+ Secondary in liver
CJ with JJ
17 B. Eshwarappa 62 M H. Durga 470307 18.12.04 28.12.04 + + - - - + + - - I +++ 22.4 17.6 4.8 7.5 + + 304 119 131 L + GB+ CBD+IHBR+GB+SOL in HOP Ca HOP CJ with JJ
L + GB Referred to
18 Devaiah 70 M C. Durga 39132 22.12.04 18.1.05 + + - + - + + + + I +++ 23.3 18.6 4.7 11 + + 390 131 143 CBD+IHBR+GB+SOL in HOP Ca HOP
+ cancer center
Cyst excision
Type I
19 Simran 3 M Dvg. 41172 10.1.05 15.3.05 + + + - + + + - - I+ 2.5 1.5 1 11 + + 164 36 29 L + GB - H+Cystic mass+ at hilum, CBD+ & roux en-y
Choledochal cyst
HJ
L + GB Periampullary
20 Gowaramma 60 F Haulilu 43932 4.2.05 28.3.05 + - - - - - - - - I ++ 25.55 20.45 5.1 10.4 + + 296 129 141 IHBR+terminal CBD growth Periampullary carcinoma Whipples PD
+ carcinoma
L + GB Multiple enlarged LN in porta Porta hepatis
21 Murpanna 12 M Badagi 56194 27.2.05 10.3.05 + + + - - + + + + I +++ 24.1 19.1 5 9.8 + + 427 163 178 CJ with JJ
+ hepatis IHBR+GB+FF+ metastasis
IHBR+peritonial Carcinoma HOP
L + GB
22 Ramakka 70 F Shimoga 48252 13.3.05 28.3.05 + + - + - + + + + I +++ 24.6 19.6 5 7.92 + + 426 131 143 CBD+GB+IHBR+SOL metastasis+pleural with liver - Expired
+
effusion+ secondary
L + GB IHBR+abrupt termination
23 Rudrappa 54 M Dvg. 49572 24.3.05 7.4.05 + + - + + - - + + I ++ 6.4 5 1.4 12.4 + + 216 84 92 CBD+IHBR+GB+ BBS CJ with JJ
+ FF + of CBD
L + GB
24 Laxshmappa 55 M Holalkere 50292 1.4.05 26.5.05 + + - + + - - - + I+ 4.6 3 1.6 11.9 + + 196 94 98 H+CBD+IHBR+GB+FF+ BBS CJ with JJ
+
L + GB Periampullary
25 Anjanappa 45 M Ballary 51012 7.5.05 3.5.05 + + - - - + + + + I ++ 18 14.4 3.6 9.6 + + 79 53 58 H+CBD+IHBR+GB- CJ with JJ
+ carcinoma
Carcinoma HOP
L + GB CBD+GB+SOL in HOP with liver
26 Kamalamma 75 F Hirehalli 55572 16.6.05 19.6.05 + + - + + + + + + I +++ 26 20.8 5.2 8 + + 423 168 135 with liver - Expired
+ metastasis
secondary
L +GB Cholangio Whipples PP
27 Rudramma 52 F Tumbigere 55932 19.6.05 30.6.05 + + - + - + + + + I ++ 15 12 3 11 + + 287 29 32 CBD+GB+IHBR+ IHBR-cholingoca
+ FF + carcinoma PD
CBD+IHBR-GB-calculi in terminal OC with CBD
28 Rishmabanu 61 F Jagulur 62652 21.6.05 28.6.05 - + - - + - - - - I- 6.8 5.4 1.4 8 + + 125 30 33 L - GB - CBD calculi
CBD exploration
L + GB Metastastic nodule in left lobe liver
29 Mallamma 60 F Haveri 62892 22.6.05 25.6.05 + + + + - + + + + I +++ 23.3 18.6 4.7 12 - - 394 129 141 Secondary in liver - Expired
+ FF+
L + GB
30 Malleshappa 75 M Kondajji 484791 23.6.05 30.6.05 + - - - - + + + + I ++ 27.35 21.35 6 9 + + 149 20 22 IHBR+CBD+GB+FF+ Carcinoma HOP CJ with JJ
+
103
KEY TO MASTER CHART
Ab – Abdomen
Alk Phosph – alkaline phosphatase
BBS – Benign biliary stricture
Ca – Carcinoma
CBD – Common bile duct
CJ – Cholecysto- jejunostomy
CT – Computed tomography
Dir B – Direct bilirubin
DOA – Date of admission
DOD – Date of discharge
DOO – Date of operation
F – Female
FF – Free fluid
GB – Gall bladder
H – Hepatomagely
Hb% – Hemoglobin
HJ – Hepatico-jejunostomy
HOP – Head of pancreas
I – icterus
IHBR – Intra hepatic biliary radicals
Ind B – Indirect bilirubin
IP. No. – In patient number
Itch – Itching
JJ – Jejuno- jejunostomy
104
L – Liver
Loss of app – Loss of appetite
Loss of wt – Loss of weight
M – Male
mg/dl – Milligram deciliter
OC – Open cholecystectmy
PD – Pancreatico duodenectomy
Rec – Recurrence
SGOT – Serum glutamic oxaloacetic transaminase
SGPT – Serum glutamic pyruvic transaminase
SOL – Space occupating lesion
USG – Ultrasonography
105

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I

It gives me immense pleasure to express my deep sense of gratitude and

sincere thanks to Dr. M. SHIVAKUMAR M.S., Professor of Surgery, J.J.M. Medical

College, Davangere for his dedicated professionalism, indefatigable efforts cheerful

I am highly indebted to Dr. B. PRADEEP M.S., Professor and Head of the

Department of Surgery who’s practical guidance during the course of my study is

I pay my humble thanks to Dr. M. MOHANDAS HEGDE, M.S., Hon.

Professor, Department of Surgery, J.J.M. Medical College Davangere.

My sincere thanks to my Professors Dr. P.J. PRABHAKAR, Dr. R.

SRINKANTIAH, Dr. R.L.CHANDRASHEKAR, Dr. R.M. SHEKHAR, Dr. G.C.

and for their valuable guidance.

I am extremely thankful to Associate Professors Dr. DINESH. M.G, Dr. J.T.

BASAVARAJ, Dr. U. MAHENDRANATH PATIL and Dr. RAVISHANKAR

PURANTHAR for their guidance.

their constant encouragement and guidance during the course of my study.

UDAPUDI, Dr. RUDRAIAH H.G.M., Dr. RAJESHWAR REDDY, Dr. PATIL

VIRUPAKSHAGOWDA, Dr. JAGADEESH B.V.C., Dr. EDAGUNJI G.C.,

Dr. RAJENDRA PRASAD, Dr. NARASIMHASWAMY P., and Dr. PRAKASH

preparation of this dissertation.

I also express my thanks to Dr. VIKRAM S, and Dr. JAYAPRABHU for

their help in collecting the operative photographs for this dissertation.

I also express my sincere thanks to the superintendents of Chigateri General

I express my special thanks to Dr. H. GURUPADAPPA M.D., director of post-

Medical College Davangere.

have always been with me throughout my endeavour.

I am thankful to my brother Sri. K.S. VENKATESH PRABHU and my

Sisters for their abundant support, patience understanding and love.

P. Namratha and P. Namitha for making everything worth while.

My sincere thanks to M/S Zen Computer Technology for their meticulous

could not have been completed.

Date : / /2006 Signature of the candidate

Place : DAVANGERE Dr. PRAKASH. K.S.

arriving at a correct pre-operative diagnosis needs to be emphasized.

extra hepatic obstructive jaundice.

January 2004 to December 2005 who were diagnosed by investigation like

ultrasonography and liver function test.

slight male predominance in 53.33%, malignant cause for surgical jaundice

constituted in 66.67% with Carcinoma Head of pancreas the commonest cause in

33.33%, benign cause for surgical jaundice constituted in 33.33%, with

choledocholithiasis the commonest cause in 23.33%.

was between 50-80 years. The sex ratio is near equalizing.

II. Consent form 102

III. Master chart 103

Table 2 Sex distribution among the surgical jaundice cases 63

Table 3 Causes of surgical jaundice cases 64

Table 4 Clinical presentation in surgical jaundice causes 65

Table 6 Ultrasonographic findings in cases of surgical jaundice 69

Table 7 Various treatment modalities in surgical jaundice cases 71

Table 8 Sex ratio in various study of surgical jaundice cases 73

Table 9 Cause of surgical jaundice in various study 74

Table 10 Presentation in malignant jaundice various studies 76

Table 11 Prognosis of after treatment of patient with choledocholithiasis 81

2 Sex distribution among the surgical jaundice cases 63

3 Causes of surgical jaundice cases 64

4 Clinical presentation in benign and malignant surgical jaundice 66

5a Mean value of total bilirubin in benign and malignant surgical 68

5b Mean value of alkaline phosphatase and SGOT in benign and 68

malignant surgical jaundice

6 Ultrasonographic findings in benign and malignant surgical 70

Sl. No. Figures

1 Anatomic division of the gall bladder and extrahepatic biliary tree 5

2 Component of sphincter of oddi 8