BILIARY SURGERY

Objectives:
 To review anatomical &physiological aspects

 To know the different diagnostic techniques

 To understand pathogenesis, types, complications

and management of gallstones

 To understand causes, presentations and management

of obstructive jaundice
 To know types, complications and management of

cholecystitis
 To be aware of other biliary tract diseases
 :Surgical Anatomy of Biliary Tract
2

 Gall bladder (GB):

pear-shaped,
7-12Cm long,5CC
Capacity: 30 – 50CC normally BUT
may accommodate: 300 CC
Parts: Fundus, Body, Neck
 Cystic duct: (Two way Duct)
3 Cm long,1-3 mm lumen (valve of
Heister), Sphincter of Lutkens
.
 Hepatic Ducts originate in liver
a. R(RHD)/L(LHD) hepatic ducts
b. Common hepatic duct(CHD)
(<2.5cm)
3
Surgical Anatomy of Biliary Tract:(cont)
 Common bile duct (CBD) (7.5 cm
long)
Parts: 4
i) Supraduodenal portion: (2.5cm)

ii) Retroduodenal portion

iii) infraduodenal portion

iv) Intraduodenal portion,

oblique course in wall of 2nd part of
duodenum surrounded by sphincter of
Oddi, terminating at the summit of Ampulla
OF Vater, at the middle of posteromedial
of the 2nd part of duodenum
4

 Arterial Supply of GB:

(Normally: Cystic a. from RHA passing behind CHD)
Anomalies: -accessory cystic a from gastrodeudenal artery
-In 15% RHA &/or Cystic a Cross INFRONT of CHD & Cystic Duct
- Caterpiller Turn or Moyenihan hump of RHA

 CALOT’S TRIANGLE: (the key for cholecystectomy):

Formed by: CHD, Cystic Duct & Inferior surface of the Liver

 Lymphatic Drainage of GB:

Subserosal and Submucosal lymphatics drain into Cystic LN Lund, a sentinel LN
(lies at the junction between cystic duct & CHD)
- Efferent Lymphatics: -from LN of Lund go to hilar LN then to coeliac nodes.
-from Subserosal lymphatics of GB connect to
subcapsular liver lymphatics (…mets)
 Biliary Anatomy

a. Right hepatic duct.

b. Left hepatic duct.
c. Common hepatic duct.
d. Portal vein.
e. Hepatic artery.
f. Gastroduodenal artery.
g. Right gastroepiploic artery.
h. Common bile duct.
i. Fundus of the gallbladder.
j. Body of the gallbladder.
k. Infundibulum.
l. Cystic duct.
m. Cystic artery.
n. Superior
pancreaticoduodenal artery.

Schwartz’s Principles of Surgery, 8th Ed.,McGraw-Hill Companies, 2005.

WHAT IS NORMAL ABOUT THE BILIARY
TREE IS THE ABNNORMALTY! (Glenn 1885)
 :Physiological Considerations
7
 Bile composition:
-water 97%
-Bile salts & bile pigments 1-2%
-cholesterol & fatty acids 1%
 Bile Excretion:

Rate: 40 cc per Hour

control by; cholecystokinin from duodenum
Functions of Gall Bladder:
i) Reservoir for bile
ii) Concentration of Bile (5-10X): By active
absorption of water, NaCl, -HCo3,(increase of
salts, pigments, cholesterol,and calcium)
iii) Mucous secretion (20 cc per 24 Hrs)
:INVESTIGATIONS IN BILIARY TRACT DISEASES
8

A) Specific:
 Ultrasound: stones, GB

wall & reactions around

 Plain X-Ray: 10% of GB

stones are radio opaque

 INVESTIGATIONS IN BILIARY TRACT
9 :DISEASES (cont)

 MRCP: pathological anatomy, stones

 CT scan: tumors, anatomy
 HIDA scan: function of GB & liver cell
 INVESTIGATIONS IN BILIARY TRACT
10
DISEASES:(cont)
ERCP: stones, tumors, stricture
11
12
ERCP
 INVESTIGATIONS IN BILIARY TRACT
13 DISEASES:(cont)

 Other investigations:
- OCG
- IV Cholangiography
- Radioisotope scan
- PTC (Percutaneou Transhepatic
Cholangiography)
- Peroperative Cholangiography
- Direct Chlangioscopy: Peroral, peroperative,
Per-T-Tube Tract,…
B) Other related labs: eg, CBC, LFTs, URINE, CXR,…….
 Cholangioscopy
14
CHOLELITHIASIS (Gallstone Formation)
15
 Commonest biliary pathology
 Incidence: ~ 10-15% of adults
 The 5Fs: Fat,Fertile,Flatulant,Female,Fifty
 85% asymptomatic;(up to 4% will be symptomatic in a year time)
TYPES OF GALLSTONES

CHOLESTEROL BLACK PIGMENTED BROWN PIGMENTED

 :Types of Gallstones
16

 Cholesterol stones:
Commonest, 51-99% cholesterol

 Black pigmented (mixed)

stones:
bilirubun pigment,Ca phosphate
& carbonate

 Brown pigmented stones:

Ca bilirubinate, Ca palmitate,Ca
stearate & cholesterol
 Formation of Cholesterol Gallstones:
(Admirand & Small Triangle)
17
 Causes of Gallstones Formation are 3: metabolic, infective & Bile stas
18

 Stages of cholesterol stone formation: (mostly metabolic)

i) saturation:
increase cholesterol in ratio to bile salts and lecithins
ii) crystallization:
initiated by a nidus of bacteria, intestinal content,bile pigment,mucoprotein starting
processes of nucleation, flocculation, and precepitation of supersaturated bile
iii) growth :
growth of tiny crystals to macroscopic stones
NB: causes of increased cholesterol blood level:
-elderly
-contraceptive pills
-antihyperlipoprotinaemic drugs
-inturrupted enterohepatic circulation
 Causes of gallstone formation:(cont.)
19
 Infection:
-Unclear role,
-Occasionally some organisms are cultured from the centre of a stone
 Bile stasis:
evidence: there is increase stones in cases of:
-increase estrogen blood level(this estrogen reduces contractility of GB
& reduces bile salts)
-post truncal vagotomy
-long term TPN ; cholecystokinin secretion is reduced if oral intake is reduced)
NB: Pigmented Stones: (increased in pts with haemolysis ie increased Bilirubin
- haemolytic anaemias
- prosthetic valve replacement
- malaria
-biliary tract strictures
- liver cirrhosis
- ascaris Luumbricoides, clonorchis siensis
- E. Coli ; leads to formation of Gluucuronidase which converts bilirubin in the insoluble unconjugated
 :Clinical manifestations of Gallstones
20

 I) IN THE GALLBLADDER:
*Asymptomatic: (silent gallstones)
*Acute cholecystitis:
-Mucocele of gall bladder
-Empyema of gall bladder
- Perforation of gall bladder
-gangrene of gall bladder
*Chronic cholecystitis
 II) IN THE CBD:
-obstructive jaundice
-cholangitis
-pancreatitis
 III) IN THE INTESTINE:
gall stone ileus
21
CHOLECYSTITIS
Types:
 I) Acute: - calculous
- noncalculous
.
Emphysematous
.
Gangrenous…… etc
 II) Chronic: calculous
noncalulous
 III) Acute on top of Chronic
Cholecystitis
 Acute Calculous Cholecytitis
22

 Features:
- gallstone impacted in Hartman’s pouch or cystic duct in 95% of cases
- occurs often in an already chronically inflammed GB
- common causative organisms: E.Coli, Bacteroids, Clostredia (..gangrene), Typhoid
(..perforation)

• Clinical picture:
• Sudden onset
• Pain: RHC,…..
• Nausea + vomiting
• Fever : 38 or more
• Positive Murphy’s sign
• Positive Boa’s sign (right sided hypersthesia between 9th & 11th rib post.
 :Diagnosis of acute cholecystitis
23

 Clinical picture
 Investigations:
- CBC: neutrophilia
- blood chemistry
- plain abdominal x ray
- biliary tree and abdominal ultrasound
- HIDA scan
 :SEQUALAE OF ACUTE CHOLECYSTITIS
24

 Resolution of the acute attack; the impacted

stone slipped back to the fundus of GB due to
increase distension of GB & elevation of its
mucous membrane around the stone pushing it
backwards

 Mucocele of GB; still neck is obstructed,

bilirbin absorbed, mucous in excess

 Empyema of GB; contents become infected, but

no bacteria can be cultured in 5% of cases,..

 Perforation of GB; continued distension,

inflammation in thin walled GB
Common site: Fundus, Neck of GB
(impacted stone)
Effects: local abscess, adhesions,
generalized peritonitis (in 0.5% cases)
MR may reach 50%
 :TREATMENT OF ACUTE CHOLECYSTITIS
25

 Early Operation: (within 48 hours)

Cholecystectomy; open or laparoscopic
 Conservative followed by cholecystectomy:(90%)
PRINCIPLES:
- NPO
- NGT
- IVF
- Analgesics
- Antibiotics: (broad spectrum mainly against Gram negative)
eg: 3rd generation cephalosporin + aminoglycosid + Flagyl
(No conservative management if the diagnosis is uncertain)
Outcome of conservative TRT:
This is effected by:
- the RHC pain and tenderness
- temp
- other associated symptoms
TREATMENT OF ACUTE CHOLECYSTITIS:(cont)
26

Accordingly: one of the following two scenarios:

A) Recovery of the acute attack if:
pain subsided, temp normalized,..
So, remove NGT, start feeding, cholecystectomy 3 days
after

B) Deterioration: pain persists, tender with mass RHC, fever,

tachycardia, neutrophilia
So, emergency cholecystectomy
 Acute Acalculous Cholecystitis
27 ( common in elderly, bedridden, diabetic and patients recovering from major trauma or burns)
 Causes:
- nonspecific inflammation of gall bladder
- Cholecystoses:
- Cholesterosis: (strawberry GB)
mm of GB looks like strawberry
with streaks of yellowish spicks
(submucous aggregations of cholesterol crystals)
- Cholesterol polyposis of GB:
similar to cholesterosis of GB but with
filled projections of mm in the strawberry GB
- Cholecystits glandularis proliferans:
( syn: intramural diverticulosis of GB,)
- All layers of GB hypertrophy
- intramural stones &calculi with septum
- Diagnosis is by US and OCG
 Diagnosis:(clinically, US, OCG, Radioisotope scan, cholesterol crystals
in duodenal aspirate)
 TRT: CHOLECYSTECTOMY
28

: Definitive contraindications for laparoscopic cholecystectomy

1-Sever intraperitoneal adhesions (adhesolysis)
2- Peritonitis
3- Small Bowel obstruction
4- Coagulopathy
5- Large diaphragmatic hernia

Relative Contraindications for laparoscopic cholecystectomy:

1- Pregnancy
2- Cirrhosis
3- Previous abdominal surgery
4- some complicated acute Cholecystitis
29
:Preoperative Workup
 Good history and physical examination
(any other concomitent disease)
(check CBC, blood chemistry (LFTS),U/S,CxR, ECG,
 Coagulation profile ( especialy in jaundiced pt )
 Good hydration ( especially in jaundiced pt )
 Prophylactic antibiotics ( Usually 2nd or 3rd generation cephalosporin)
 Informed consent
 Blood preparation : - Group
- Group and X-Mach
 provision for prevention for peroperative cholangiogram
Open Retrograde/Antegrade Cholecystectomy
30

 Incision
 Right subcostal ( Kocher`s ) incion
 Right paramedian incion
 Midline incion

 Position :
 operating table and pt positioned possible peroperative cholangiograam
 Patient: supine on his back
 Surgeon on the right side of the patient .
 1st assistant infront of surgeon

changeable( once to the left of surgeon and another to the left of 1st
assistant to retract the liver)
 :Skin Preperation
31

 Skin shaving from nipple down to pubic hair

line ,the night before surgery or just before surgery,
preferable a hair epilating cream
 Painting and sterilizing the operative field with
povidine Iodine 10% .(technique…)
 Drapping : drapes around the field of surgery
 :Steps of Cholecystectomy
32

 Skin incision : layer by layer with haemostasis till the peritonium

which is opened in between two haemostats

 Exploratory laparotomy :
(examine all abdominal & pelvic organs for any other possible
incidental pathology )

NB: Basic principles in operative surgery are:

 Exposure
 Dissection and isolation of the organ to be operated
 Devesculaization of the organ to be operated
 Excision of the related pathology
 :Steps of Cholecystectomy (cont.)
33

 The GB is held by two ring forceps

one to the fundus and another to
Hartman’s pouch
 Calot`s triangle identified
 Cyst artery dissected legated and cut
 Cyst duct dissected; legated and cut
 Retrograde dissection of GB (from neck
to fundus )
 Secure haemostasis
 Drain
 Count instruments, swabs and needles
 Wound Closure layer by layer
( anatomical repair )
 specimen is sent for histopathology
 :Postoperative Orders
34

 V/S recording 2 hourly till stable, then ward routine,…

 NPO for at least 24 Hrs
 I.V fluids (pt dependent), usually 500 cc Q4Hr for an average
adult man
 Analgesic :usually narcotic analgesics for three doses at
least, according to age and weight
 Allow sips of water next day & progress ,normal diet
 Ambulate; the earlier the better….
 Remove drain (if inserted operatively) when discharge is
insignificant amount and character
 Stitches removed on the 7th postoperative days .
 Dischage usually after a week
 LAPAROSCOPIC
35
CHOLECYSTECTOMY
 Same indications and workup as open
cholecystectomy)
 Assure Empty urinary baldder
 Insertion of NGT. Same drap and skin prep
 Skin incisions :
- 4 stabs :
Two 5mm each: - One in
right MCL 5cm
below costal margin
(to hold Hartman’s pouch)

- One in ant axillary line at

level of umbilicus
(to hold the fundus of GB)

Two 10 mm each –One Epigastric

(dissecting)
-One Periumbilical
(camera)
36

 Pneumoperitonium creation:
Gas (Co2) insufflation:
By Veress needle insertion through a periumbilical stab
Flow rate: 2-4 L/min
Pressure: 12-14mmHg
 Insertion of ports :

The first 10mm port ( the umbilical camera port) inserted

with abdominal wall elevation
All other ports, the 10mm epigastric,the other two 5mm ports
are inserted respectively under very clear vision
 :OPERATING STAFF & PROCEDURE
37

 The camera man on Left side beside the

surgeon on his left side of the patient & the
other assistant on the right side

 Funds gripped and pushed shed upwards

wards by the assistance on Right side of
the patient to elevate the liver .

 The surgeon on the Left side of the pt

holds the Hartman’s pouch with the L
hand grasper and start dissection in
Calot’s triangle; cystic artery & duct;
Each clipped twice proximally one distally
and cut .

 Antegrade dissection of GB assuring

haemostasis

 Close umbilical and epigastric Ports , no

need to close 5mm stabs
 :Post Lap Cholecystectomy Orders
38

*SAME AS OPEN CHOLECYSTECTOMY BUT:

 V/S recording 2 hourly till stable, then ward routine,…

 NPO for about 12 Hrs

 I.V fluids (pt dependent), usually 500 cc Q4Hr for an average

adult man
 Analgesic: usually narcotic analgesics; one or two doses according to
age and weight
 Allow sips of water next day or 12 Hrs after surgery &
progress ,normal diet
 Ambulate; the earlier the better….

 Remove drain (if inserted operatively) when discharge is insignificant

amount and character
 Usually no Stitches but if inserted to epigastric and umbilical incision,
removed on the 7th postoperative days .
 Discharge usually the next day
39

OPEN CHOLECYSTECTOMY
VERSUS
LAPAROSCOPIC CHOLECYSTECTOMY
 JAUNDICE

Definition: DAY LIGHT

Accumulation of yellow pigment (Bilirubin) in the skin, sclera

and other tissues of the body. Clinically jaundice is apparent
when bilirubin is reaching around 2.5mg/dl (N=0.1-1mg/dl)
:Bilirubin Metabolism
 Formation of Bilirubin
 Transport of bilirubin in plasma
 Transport of hepatic bilirubin
 Hepatic uptake
 Conjugation
 Biliary excretion
 Enterohepatic circulation
Pathophysiologic classification of Jaundice
 Over production of Bilirubin (Hemolytic)
 From hemolysis of RBC
 Lysis of RBC precursors – Ineffective erythropoesis
 Impaired hepatic function (Hepatitic)
 Hepatocellular dysfunction in handling bilirubin
 Uptake, Metabolism and Excretion of bilirubin
 Obstruction to bile flow (Obstructive)
 Intrahepatic cholestasis
 Extrahepatic Obstruction (Surgical Jaundice)
Hemolytic Jaundice
Pathogenesis
Overproduction
 Hemolysis (intra and extra vascular)
 inherited or genetic disorders
 acquired immune hemolytic anemia

(Autoimmune hemolytic anemia)

 nonimmune hemolytic anemia

(paroxysmal nocturna Hemoglobinruia)

 Ineffective erythropoiesis

Overproduction may overload the liver with UB

Hemolytic Jaundice

Symptoms
weakness, anemia,
Icterus, splenomegaly
Labs:
 Urobilinogen(UB) without bilirubinuria
 fecal and urine urobilinogen
 hemolytic anemia
 hemoglobinuria (in acute intravascular hemolysis)
 Reticulocyte counts
Hepatic (Hepatocellular) Jaundice

Due to a disease affecting hepatic tissue

(cells) either congenital or acquired
diffuse hepatocellular injury
Hepatic Jaundice
Pathogenesis
 Impaired or absent hepatic conjugation of bilirubin
 decreased GT activity (Gilbert‘s syndrome)
 hereditary absence or deficiency of UDPGT (Grigler-Najjar
Syndrome)
 Familiar or hereditary disorders
 Dubin-Johnson Syndrome
 Rotor syndrome
 Acquired disorders
 hepatocellular necrosis
 intrahepatic cholestasis
(Hepatitis, Cirrhosis, Drug-related)
 Hepatic Jaundice
Symptoms
weakness, loss appetite, hepatomegaly, palmar
erythema, spider
Lab Findings
• liver function tests are abnormal
• both CB and UCB
• Bilirubinuria 
Obstructive Jaundice
Pathogenesis
 it is due to intra- and/or extra hepatic
obstruction of bile ducts
 intrahepatic Jaundice: Hepatitis,
tumours,Drugs,….
 Extra Hepatic Biliary Obstruction: Stones,
Stricture, Inflammation, Tumors, (Ampulla of
Vater)
Obstructive Jaundice
symptoms
 Pruritus
 Jaundice may vary in intensity
 Chill+fever+gall bladder enlargement
stone+cholangitis
NB: courvoirser’ Law
Obstructive Jaundice
Lab Findings:
 Serum Bilirubin
 Feceal urobilinogen (incomplete obstruction)
 Feceal urobilinogen absence (complete obstruction)
 urobilinogenuria is absent in complete obstructive
jaundice
 bilirubinuria 
 ALP 
 cholesterol 
CT Abdomen

A large mass with a hepatoma.

Primary sclerosing cholangitis in childhood
Jaundice- Differential Diagnosis
The Approach:

 UCB (Unconjugated Bilirubin) or CB (Conjugated Bilirubin)

 Exclude UCB (e.g. hemolysis or Gilbert Synd.)
 Distinguish hepatocellular from obstructive
 Distinguish intrahepatic from extra hepatic
cholestasis
Indirect hyperbilirubinemia
A. Hemolytic disorders
 Inherited

 Acquired

B.Ineffective erythropoiesis
C.Drugs
D.Inherited conditions: Crigler-Najjar types I and II
Gilbert’s syndrome
Indirect (Nonconjugated) Hyperbilirubinemia
Hemolytic disorders-----Inherited
 Spherocytosis,elliptocytosis

 Glucose-6phosphate dehydrogenase and pyruvate kinase

deficiencies
 Sickle cell anemia

Hemolytic disorders-----Acquired
 Microangiopathic

 Paroxysmal nocturnal hemoglobinuria

 Immune hemolysis
Direct hyperbilirubinemia
 Viral hepatitis

 Alcohol

 Drug toxicity

 Environmental toxins

 Wilson’s disease

 Autoimmune hepatitis

 Inherited conditions:Dubin-Johnson syndrome

Rotor’s syndrome
:CHOLESTATIC Jaundice

ANATOMICALLY:
 Intrahepatic

 Extrahepatic
Drugs causing Cholestasis
 Anabolic steroids (testosterone, norethandrolone)
 Antithyroid agents (methimazole)
 Azathioprine (Immunosuppressive drug)
 Chlorpromazine HCI (Largactil)
 Clofibrate, Erythromycin estolate
 Oral contraceptives (containing estrogens)
 Oral hypoglycemics (especially chlorpropamide)
CHOLESCTATIC CONDITINS THAT MAY PRODUCE
JAUNDICE

Vanishing bile duct syndrome

 Chronic rejection of liver transplants

 Sarcoidosis

 Drugs
CHOLESCTATIC CONDITINS THAT MAY PRODUCE
JAUNDICE

Extrahepatic
Malignant
•

Benign
•
CHOLESCTATIC CONDITINS THAT MAY PRODUCE
JAUNDICE

Extrahepatic------Malignant
 Cholangiocarcinoma

 Pancreatic cancer

 Gallbladder cancer

 Ampullary cancer

 Malignant involvement of the porta hepatis

lymph node
Peri-Ampullary Tumours, Endoscopic
View
Pathology
Adenocarcinoma accounts for 95%
Arises from 4 different tissues of origin
 Head of pancreas

 Distal Bile duct

 Ampulla of Vater

 Periampullary duodenum
 Pathology
Prognosis for each of these are different.
 Five year survival for pancreas: 18%

 Five year for ampulla: 36%

 Five year for distal bile duct: 34%

 Five year for duodenum: 33%

“Determination of tissue origin is important for prognosis,

extent of resection.”
“Determination of tissue origin BY CT scan, ERCP CT scan,
ERCP FNA, endoscopic biopsy.”
“Determination of k-Ras also helps (95% of pancreatic
cancer).”
Spread
 Locoregional spread results from lymphatic
invasion and direct tumor spread to adjacent soft
tissue.
 Ampullary lesions spread to LN 33%, typically to
a single LN in the posterior pancreatcoduodenal
group.
 Duodenal has intermediate spread.
 Pancreas metastasizes 88% to multiple sites.
Treatment
 Standard Whipple pancreaticoduodenectomy
thought to provide adequate tumor clearance in the
case of non-pancreatic ampullary tumor, because
tumor spread is localized.
 Biopsy proven paraduodenal LN is thought by
most to preclude curative resection
Surgery and Chemotherapy

 OUTCOME:
 Low risk: limited to ampulla or duodenum, well
differentiated, negative margins and LN.

 High risk: tumor invasion of pancreas, poorly

differentiated, positive margin, positive LN.
Surgery and Chemotherapy

 Low risk patients had 5 year local control and

survival of 100% and 80% respectively.
 High risk patients had 5 year local control and
survival of 50% and 38%, respectively.
 Based on these findings, some have proposed a
course of preoperative chemoradiation to improve
local disease control in these high risk patients.
Whipple Procedure
Five basic techniques are used to resect pancreatic
cancers:
 Standard pancreaticoduodenectomy

 Pylorus preserving pancreaticoduodenectomy

 Total pancreatectomy

 Regional pancreatectomy

 Extended resection (MD Anderson)

Whipple Procedure
CHOLESCTATIC CONDITINS THAT MAY PRODUCE
JAUNDICE

Extrahepatic------ Benign
 Choledocholithiasis

 Primary sclerosing cholangitis

 Chronic pancreatitis
 :The approach to Obstructive Jaundice
 Jaundice--- Diagnostic Procedures
 History:….Pain, colour of urine,stool,sclera,….
Charcot’s triad; jaundice, fever, rigors
(French physician)

 O/E ……… Courvoiser low (French physician)

 Family History of Jaundice

 Duodenal biliary drainage
 Imagine techniques
 Ultrasonography
 ERCP (Endoscopic Retrograde cholangiopancratography )
 PTC
 X-ray (GI, Angiography)
Jaundice- Differential Diagnosis
 Jaundice- Differential diagnosis
1. Once Jaundice is recognized, it is important to determine whether
hyperbilirubinemia is predominantly Conjugated or Unconjugated
Hyperbilirubinemia?
2. Differentiation of hemolytic from other type of Jaundice is usually not
difficult.
3. The laboratory findings are in constant in partial biliary obstruction
and differentiation from intrahepatic cholestesis is particularly
difficult.
Jaundice- Differential diagnosis

Differential Diagnosis
 UCB or CB
 Exclude UCB (e.g. hemolysis or Gilbert Syndrome)
 Distinguish hepatocellular from obstructive
 Distinguish intrahepatic from extra hepatic
cholestasis
 :Preoperative preperation of jaundiced patient

 Full CBC, Blood chemistry, ECG, CxR

 Prepare and cross mach at least two units of blood

TO AVOID HEPATPRENAL SYNDROME

PERIOPERATIVELY:
 - well hydration, parentral + enteral

 - correction of coagulopathy (PT prolongation) by

Vit K 10mg iv once or twice aday

 - Prophylactic antibiotics, to avoid what is called

hepatorenal syndrome
 Lab Diagnosis of Jaundice – D.D

Prehepatic Intrahepatic Posthepatic

Features
)Heamolytic( )Hepatocellular( )Obstructive(

Unconjugated ↑ Normal Normal

Conjugated Normal ↑ ↑
AST or ALT Normal ↑↑ Normal

.Alkaline phos
and GGT
Normal Normal ↑↑
Urine bilirubin Absent Present Increased

Urobilinogen Increased Present Absent

Interpretation of Liver Function
Tests
LFT Utility of the test
ALT/SGPT ALT ↓than AST in alcoholism
Albumin Assess severity / chronicity
Alk. phosphatase Cholestasis, hepatic infiltrations
AST/SGOT Early Dx. of Liver disease, F/up
Bilirubin (Total) /Conjug. Diagnose jaundice
Gamma-globulin Dx. F/up Chronic hepatitis & cirrhosis
GGT Dx alcohol abuse, Dilantin toxicity
Non Hepatic causes of abnormal LFT

Abnormal LFT Non hepatic causes

PLE, Nephrotic syndrome
Albumin
Malnutrition, CHF
Bone disease, Pregnancy,
AKP
Malignancy , Adv age
AST MI, Myositis, I.M.injections
Hemolysis, Sepsis,
Bilirubin
Ineffective erythropoiesis
Antibiotics, Anticoagulant,
PTT
Steatorrhea, Dietary
 : Management CBD stone
 This is dependent on the Following:
- General condition of the patient and cardiopulmonary fitness
- Degree of jaundice and the state of liver function
- Presence or absence of cholangitis
- Coagulopathy status and PT
- Post biliary tract surgery/trauma or de nove CBD stone and if
operated whether a T-Tube inserted or not
- Size and location of the CBD stone
- Available resources; surgical skills, biliary endoscopy + lithotripsy
fascility,
 :THE OPTIONS OF CBD STONE MANAGEMEN
 ERCP: in stable jaundiced, not operated or operated patient, with no
coagulopathy defect
-Sphinctorotomy/Papillotomy; stone may slip in duodenum otherwise
-Dormia basket extraction otherwise
- Stone fragmentation (by ESWL, LASER, OR MECHANICAL) then extraction
-Nasobiliary Drainage
 Through the T-Tube tract (6/52 after operation)
using- Durhane steerable basket
or- Fogarty catheter
or- Long choledochoscope
or- Dissolution of cholesterol stone b bile salts and Heparine ,….
 Surgical Exploration of the CBD and stone Extraction, in……
 PTC & PTD (Percutaneous Transhepatic Cholangiography & Drainage), in…..Then
81
82
83
 :Management of Biliary stricture
 History… the course of jaundice, associations…
surgery, neoplasia,
 Examination:
 Investigations:
CBS, coagulation profile; PT
Blood chemistry: LFT, Kidney functions,…
Ultrasound; Biliary tree, abdominal
ERCP, diagnostic, biopsy; cytology, brush or tissue
+ PTC to delineate the nature of the stricture
85
TREATMENT:
:(Option depends upon the charactaristics of the stricture) ie
 Whether the stricture is benign or malignant
 How long is the proximal hepatic segment
 Patency of the stricure
 Available resourses

Options:
- ERCP & Stent insertion, Cholangioscopy
- Cholecystojujenostomy
- Choledochodudenostomy
- Hepaticojujenostomy
- Triple bypass in non-operable malignant distal cholangiocarcinoma, periampullary
tumour or pancreatic tumour
- Whipple’s operation in malignant distal cholangiocarcinoma, periampullary tumour
or pancreatic tumour
- PTC, PTD
Pancreas

Diagnostic approach to pancreatic mass:

 CA 19-9, CEA levels
 3-phasic CT scan (PO + IV contrast)
 MRI
 PET CT
 Endoscopic US with FNA
Pancreas
Diseases that require surgical treatment:
- adeno CA
- Functional endocrine tumors: insulinoma, gastrinoma,
glucoganoma, somatostatinoma, VIPoma
- Mucinous cystic neoplasm
- Intraductal papillary mucinous neoplasm
- Persistent pseudocyst
- Infected pseudocyst
- Necrotizing pancreatitis
- Chronic pancreatitis, resistan to medical Tx
 Pancreas – surgical technique

 Enucleation of islet cell tumors: open or laparoscopic

 Distal pancreatectomy with splenectomy: open or laparoscopic
 Distal pancreatectomy with splenic preservation: open or
laparoscopic
 Central pancreatectomy
 Trans-gastric pancreatic debridment: open or laparoscopic
 Pancreaticoduodenectomy
 Total pancreatectomy
“Islet cell tumors”. Mittendorf EA, Shifrin AL, Inabnet WB, Libutti SK, McHenry CR, Demeure MJ.
Current Problems in Surgery, Volume 43, Issue 10, Pp 685-765

 
90
Biliary Duct injury and Strictures
 LC has been associated
with a higher incidence of
IA bile duct injuries
 LC—0.4 to 0.8%
 Traditional OC—0.1-0.3%
Classic Laparoscopic Injury
Mistaking the common bile duct for the cystic duct --
 Thermal Injuries

Inappropriate use of 

electrocautery near
biliary ducts

May lead to stricture 

and/or bile leaks

Mechanical trauma can 

have similar effects

Lahey Clinic, Burlington, MA.1994

 Strasburg Classification
 Type A Cystic duct leaks or leaks from
small ducts in the liver bed

 Type B Occlusion of a part of the biliary

tree, almost invariably the
aberrant right hepatic ducts

 Type C Transection without ligation of

the aberrant right hepatic
ducts

 Type D Lateral injuries to major bile ducts

 Type E Subdivided as per Bismuth

classification into E1 to E5
 Strasburg Classification, cont’d
 E: injury to main duct (Bismuth)
 E1: Transection >2cm from
confluence
 E2: Transection <2cm from
confluence
 E3: Transection in hilum
 E4: Seperation of major ducts in
hilum
 E5: Type C plus injury in hilum
Management of Bile Duct Injuries
 Corrective Treatment (Lao)
 Endoscopic stenting for strictures

 T-tube placement for minor lacerations

 Primary duct-to-duct repair only if tension free

anastomosis available

 Biliary anastomosis with jejunal loop for major

excisional injuries
Choledoco/Hepaticojejunostomy
 Indications

 Benign, mainly iatrogenic biliary strictures

 Malignant obstruction of the biliary system, caused by

pancreatic or duct wall tumors.

 Rarely indicated for traumatic lesions or select

instances of sclerosing cholangitis.
Choledoco/Hepaticojejunostomy
 Preoperative assessment of the anatomy should be
attained by percutaneous or endoscopic cholagiography.

 These catheters can be left in place to help the surgeon

exploring a previously damaged or transected ductal
system.

 Removed once the anastomosis is healed and patent (1

to 2 weeks following repair)
Choledoco/Hepaticojejunostomy
 These patients may require the use of prophilactic
abx, parenteral vitamin K and possibly FFP.

 Combination of ampicillin and gentamycin/amikacin

or a third generation cephalosporin.

 E coli, Klebsiella and streptococcus.

 Bowel preparation is not always required.

Choledoco/Hepaticojejunostomy

 Surgical technique
 Right subcostal, right
paramedian or chevron
incision.
 Kocher maneuver
 Meticulous dissection
between duodenum and R
lobe of liver.
 Localization of the dilated
bile duct.
Choledoco/Hepaticojejunostomy

 Two 4-0 traction sutures

above the stricture.
 The common duct
ligated with 00 suture
below the stricture and
divided below the
traction sutures.
 Bile for C+S should be
sent.
Choledoco/Hepaticojejunostomy
 Creation of a Roux-en-Y
conduit.
 The proximal (afferent)
limb is anastomosed to 45 to
75cm
the distal
defuntionalized jejunum.
 The distal limb is
brought to the bile duct
in a retrocolic fashion.
Choledoco/Hepaticojejunostomy
 When dealing with greatly dilated ducts and end
to end anastomosis can be performed.
Choledoco/
Hepaticojejunostomy
 End to side anastomosis
is more commonly Electrocautery
performed.
 Seromuscular stitches
are placed to fix the two
structures to each other.
4-0 seromuscular
 5cm away from the
jejunal closure, at the
antimesenteric aspect.
Choledoco/Hepaticojejunostomy

A first row of sutures Appropriate Once the posterior

placed in the anterior retraction to allow wall closed should
duct wall posterior wall complete the anterior
closure wall.
Choledoco/Hepaticojejunostomy
Choledoco/Hepaticojejunostomy

 When dealing with

malignant obstruction,
a simple biliary enteric
bypass is advisable.
Choledoco/Hepaticojejunostomy

 Also an end-to-side
choledocojejunostomy
can be done
Choledoco/Hepaticojejunostomy
Postoperative care:
 If the use of drain seems appropriate a closed system
drain is left in the foramen of Winslow.

 Removed 3-5 days postop if no bile leak.

 Nasogastric tube and NPO 3 to 5 days depending on

the patient’s condition and the return of bowel
sounds and function.