Biliary system
Anatomy
Plain x ray
GB stone in 10 %
Gas in biliary tree
Gall stone ileus
Gas in GB wall
Porcilin GB
Radiological investigations
Oral Cholecystography

We comment on
 Site
 Size
 Shape
 Filling
Defect
 Function
 Concentration
 contractility
of dye
Investigations
Imaging techniques
Ultrasound this is most useful
 Most important to show intrahepatic bile ducts
dilatation
 Measure the diameter of CBD (normal up to 7 mm)
 Comment on the status of the GB and its stones
 Visualize CBD diameter, stones or areas of narrowing
 Tumors in the region of the pancreas is seen
CT (conventional or helical) competes with the U/S
especially as regards the pancreatic tumors.
Radiological investigations
Ultrasound
cholangiogram

Preoperative cholangiogram
 IV
cholangiogram
 PTC
 ERCP
Intra operative
 T tube ( post operative )

Investigations for a case of
obstructive jaundice
ERCP
ERCP is an outpatient procedure that combines
endoscopic and radiologic modalities to visualize
both the biliary and pancreatic duct systems.
Endoscopically,
the ampulla of Vater is identified and
cannulated.
A contrast agent is injected into these ducts, and
x-ray images are taken to evaluate their caliber,
length, and course.
ERCP
is used to
get a final diagnosis and
do biopsy of ampullary tumors,
or brush cytology.
Investigations for a case of
obstructive jaundice
ERCP
 It can be also therapeutic for
stone extraction by Dormia basket or
insertion of a stent, both are preceded by
sphincterotomy.

It
has its risks
ascending infections,
 perforations,
pancreatitis, an
bleeding due to sphincterotomy done routinely
before CBD cannulation

ERCP
Congenital
caroli’s syndrome
Chledochal cyst (type I)
Investigations for a case of
obstructive jaundice
MRCP
a sensitive noninvasive method of
detecting biliary and pancreatic duct
stones, strictures, or dilatations within
the biliary system.
It is also sensitive for helping detect
cancer.

Investigations for a case of
obstructive jaundice
MRCP (contraindications)
Absolute include
the presence of a cardiac pacemaker,
cerebral aneurysm clips,
ocular or cochlear implants
 ocular foreign bodies.

Relative contraindications include
the presence of cardiac prosthetic valves,
 neurostimulators,
 metal prostheses,
 penile implants

Investigations for a case of
obstructive jaundice
PTC
 performed by a radiologist using fluoroscopic
guidance.
The liver is punctured to enter the peripheral
intrahepatic bile duct system.
An iodine-based contrast medium is injected into
the biliary system and flows through the ducts.
Obstruction can be identified on the fluoroscopic
monitor.
Investigations for a case of
obstructive jaundice
PTC
It
is especially useful for lesions proximal to the
common hepatic duct.
Still,
PTC
ERCP is generally preferred.
is reserved for use if ERCP fails or when
altered anatomy precludes accessing the ampulla.
Investigations for a case of
obstructive jaundice
PTC
Complications of this procedure include
 the possibility of allergic reaction to the
contrast medium.
 peritonitis.
 intraperitoneal hemorrhage, sepsis
 cholangitis.
 subphrenic abscess.
 lung collapse.
 Severe complications occur in 3% of cases
PTC
Investigations for a case of
obstructive jaundice
Endoscopic ultrasound (EUS) combines
endoscopy and US to provide remarkably
detailed images of the pancreas and biliary
tree.
 It uses higher-frequency ultrasonic waves
compared to traditional US (3.5 MHz vs 20
MHz)
 allows diagnostic tissue sampling via EUSguided fine-needle aspiration (EUS-FNA).

Acute Cholecystitis
Acute
obstructive
(Calcular)
Acute Acalcaus
Acute emphysematous
Acute obstructive (Calcular)
(Pathology)
Calcular obstruction
 GB become hyperemic, oedematous & distended
 Chemical inflammation



Release of Phosphlipases
Act on lecithin which is a mucosal protector
transforming it into



Lysolecithin (mucosal toxin
Arachidonic acid (PG precursor) (inflammation)
Sepsis

Ecoli, klebsilla & strept which occur later on
Acute obstructive (Calcular)
(Pathology)

Following acute inflammation the
condition end by one of the following
 Resolution
 Mucocele
 Empyema
 Gangrene
And perforation
 Bilo-enteric fistula
Acute Acalcular Cholecystitis
It form 8 %
 Risk factors are

 Sepsis
 Starvation
 Prolonged
TPN
 Ileus
 Morphine
use > 6 days
Acute Acalcular Cholecystitis

Pathology is not knowen
 Prolonged
distention of GB , Bile stasis &
inspissations lead to mucosal injury and vessel
thrombosis
 Hypersensitivity to concomitant antibiotics
 Gangrene occur in 25 % of cases
Acute emphysematous
GB
Caused by mixed poly-microbial infection
including gas forming bacteria
 70% male , diabetics
 Thrombosis of cystic artery is the cause
 It lead tom

 Gangrene
in 75 %
 Perforation in 15 %
Patient 5 F
 General
Clinical picture

 High
fever with shivering
 Nausea, vomiting & biliary dyspepsia

Local
 Biliary
colic
 Tenderness
 Murphy’s
sign
 Boa’s sign
 Complication
Clinical picture
The attack of biliary colic is the start with visceral type of
pain (diffuse, colicky, radiating, and associated with
vomiting)
 Later on after 6 to 8 hours, the pain localizes to the right
hypochondrium, and become associated with
tenderness, rebound T, and rigidity and mild fever
(somatic pain)
 The presence of distended gall bladder is the hallmark of
the disease, either discovered clinically or by U/S
 In 25% of cases the bilirubin rises, due to compression
of the CBD (Mirrizi syndrome) or less commonly due to
an associated stone CBD
 Serum amylase should be a routine as well as plain X ray
abdomen (pancreatitis, and perforation or gas in biliary
system

Acute calculous cholecystitis

Obstruction of GB outlet leads to chemical
inflammation, which persists for 72 h then a fate
of the following, will occur
Resolution (most common), with relief of obstruction
~>scarring and non-function of GB
 Resolution of the inflammatory process with
persistence of the obstruction (mucocele of the GB)
 Persistence of infection (empyema of the gall bladder)
with obstruction persistence
 Gangrene and acute perforation leading to localized
pericholecystic abscess or generalized frank biliary
peritonitis
 Chronic perforation with development of biliary
eneteric fistula

Investigation

Laboratory
 Leucocytosis
 Liver
function
 S. amylase

Radiological
 Plain
xray
 US
 Doppler
US
 HIDDA scan
 CT scan & MRI
Investigations: the best is
ultrasound
 An
ultrasound is the most common
screening test.
 It is 90-95% sensitive for cholecystitis
 It is 78-80% specific.
 For simple cholelithiasis, it is 98%
sensitive and specific.
Investigations: the best is
ultrasound

Findings include gallstones or sludge and one or more of
the following conditions:
 Gallbladder wall thickening (>2-4 mm)

Gallbladder distention (diameter >4 cm, length >10
cm)

Pericholecystic fluid from perforation or exudate

Air in the gallbladder wall (indicating gangrenous
cholecystitis)

Sonographic Murphy sign (86-92% sensitive, 35%
specific), pain when the probe is pushed directly on
the gallbladder (not related to breathing)
Treatment (conservative)
NPO, nasogastric & IV fluids
 Analgesic, antipyretic & spasmolytic
 Antibilotic
 Broad spectrum ( cephalosporins )
 Metronidazole & aminoglycoside
 Follow up and surgery
 In the same admission
 Interval cholecystectomy


Urgent if
Treatment (surgical)
 Doubt
in diagnosis
 Failure to improve
 Complication

We perform
 Chole-cyst-ectomy
 retrograde
Chole-cyst-ectomy
 Chole-cyst-ostomy
 Subtotal Chole-cyst-ectomy
 Mini Chole-cyst-ectomy
 Laparscopic Chole-cyst-ectomy
Treatment (surgical)
Established
Non-progressive
disease
Interval Chole-cyst-ectomy
Early chole-cyst-ectomy
Gall stones
Increase bile pigments
Decrease phosphlipid
&bile salts
Increase
cholesterol
Metabolic
Gall
stones
Infection
Stasis
 75%
Cholesterol stone
of stones formed in sterile GB
(10% infection)
 Protein matrix
 cholesterol (70%)
 bile pigment
 Ca carbonate
 Ca palmitate (Ca salts deposited at
periphery, their amount determine
the radiolucency)
Cholesterol stone
 Two types
 Pure cholesterol
 Oval or rounded
 mamillated or mullbery-surfaced
 pale yellow in color
 solitary big size (100% cholesterol
rounded)
 60% cholesterol (mixed)
 Multiple mediums sized (60%
cholesterol, faceted)
 brownish polished surface
Gall stones
Formation involves 7 processes
1.
2.
3.
4.
5.
6.
7.
Super saturation with cholesterol
Incomplete transfer of cholesterol from vesicles
to micelles
Formation of vesicles with high cholesterol
Aggregation and fusion of unstable vesicles
Cholesterol crystallization (mucin is a nucleating
agent)
Biliary sludge formation (mucin+ cholesterol+
Ca+pigment ~precursor of stones)
Stone growth
Black Pigment Stone
25% of stones.
It is common in cirrhotics, after terminal ileum
resection and in hemolytic diseases. Formed in a
sterile GB (20% infection rate)
 Composed of bilirubin polymer without Ca
palmitate and +cholesterol (25%)+matrix of
organic material
 Usually multiple, small, irregular, dark green or
black in color
 Hard in consistency and cut surface is layered



Formation
Elevated concentration of mono-conjugated bilirubin
lower bile salt concentration is the usual constitution
in forming patients
 yet the exact pathogenesis is not known


Brown Pigment Stone
Rare ductal stones caused by infection by
gram -ve bacteria releasing B
glucuronidase releasing free bilirubin
 Composed mainly of

 Ca
bilirubinate,
 Ca palmitate + small amounts of cholesterol
 matrix of organic material

Amorphous soft stones
Gall stone disease

Symptom less


no interference
interference in





Diabetics
Acromegalic
Calcified
Patient under go surgical intervention
Symptomatic
Chronic cholecystitis
 Acute biliary colic, acute cholecystitis
 Jaundice

Clinical presentations









Acute cholecystitis
Empyema of the gallbladder
Mucocele of the gallbladder
Biliary colic
'Flatulent dyspepsia'
Mirrizi's syndrome
Obstructive jaundice
Pancreatitis
Acute cholangitis
Chronic calcular cholecystitis
Clinical picture
 Recurrent attacks of epigastric or right
hypochondrial pain (persistent pain)
 May be attacks of severe biliary colic
 Nausea &vomiting
 Flatulent dyspepsia with intolerance to fatty
meals
 Tenderness in right hypochondrium (Murphy’s
Treatment :
 Cholecystectomy
either conventional
or laparoscopic is the ideal treatment
for symptomatic patients.
 Patients with asymptomatic gall
stones can be left without surgery
specially if cirrhotics.
 However patients with a calcified or
porcelain gallbladder should consider
elective cholecystectomy due to the
increased risk of carcinoma (25%).
Laparoscopic cholecystectomy
(LC)
Shown to be equally as effective as open
cholecystectomy in controlled trials
 Pre-operative ERCP is indicated if:

 Recent
jaundice
 Abnormal liver function tests
 Significantly dilated common bile duct
 Ultrasonic suspicion of bile duct stones
cholecystectomy

Indication
 Trauma
 Inflammation
 Acute
& chronic
 Mucocele
 empyema
 Tumor
 Torsion
 As
a part of other operations
cholecystectomy
 Incisions
Subcostal
(Kocher’s)
Upper right paramedian
Right upper transverse
Upper midline
cholecystectomy
Technique

Preliminary exploration
 Signs of cholecystitis
 Associated pathology
Saint’s triade
Welkie’s triade
Pancrease
Stone in CBD
Saint’s triade
Welkie’s triade
Technique
 Packing
of the field & retractors
GB is grasped
Separation of GB
Artery
Duct
Identification of Calot’s

Operative complications
Injury to important structure

Common bile duct injury:




observed more frequently in the laparoscopic approach.
Iatrogenic common bile duct injury often results from a
combination of inexperience of the surgeon, the presence of
anomalous biliary anatomy, and acute inflammation.
Duodenum injury
Pancreatic and liver injury
Ligation of Rt hepatic artery
 Primary hge





Injury of cystic artery
Injury of Rt hepatic
Injury portal vein
GB bed
Post operative complications

General
 Chest
& abdomen
 DVT
 Infection:
 Spillage
of stones into the peritoneal cavity during
cholecystectomy increases the risk of infection and
abscess formation.
 Wound infections also are possible but are less
common in the laparoscopic approach..
Post operative complications

Local

Bleeding:



Ligation of






Reactionary slipped ligature
2 ry hge if infection which may lead to collection above IVC
( Waltman- Walter syndrome)
CBD or CHD
Hepatic artery
Biliary peritonitis
Biliary fistula
Subphrenic collection
Postcholecystectomy syndrome
Post cholecystectomy syndrome

Organic causes
 Long
stump of cystic duct
 Missed stone
 Stricture
 Stenos is of sphincter of Oddi

Non organic causes
 Psycho-somatic
 Biliary
dyskinesia
Long stump of cystic duct

If stone is formed
 Stump
must be excised with
 Stone extraction

If no stones

symptomatic treatment
Missed stone after cholecystectomy
Confirm diagnosis by US & ERCP
 Minimal invasive

 ERCP
sphincterectomy & stone extraction by
Dormia Basket
 PTC then choledochoscpic extrction

Surgical
 Supradoudenal
choledochotomy
 Transdoudenal sphincteroplasty
Stricture
 Minimal
invasive by stent insertion
 Surgical
Roux
en Y choledocho
jujunostomy
Roux en Y hepatico jujunostomy
Post cholecystectomy syndrome

Organic causes
 Long
stump of cystic duct
 Missed stone
 Stricture
 Stenos is of sphincter of Oddi

Non organic causes
 Psycho-somatic
 Biliary
dyskinesia
Post cholecystectomy syndrome

Stenos is of sphincter of Oddi
 Endoscopic
papillotomy and sphincterotomy
 Sphincteroplasty
 Choledocho doudenotomy

Biliary dyskinesia
 Endoscopic
papillotomy and sphincterotomy
Stone in CBD
Aetiology
GB stone (commonest)
 Primary stones of CBD usually (Brown)

 Parasites
 Stasis
 FB
 cholangitis
Clinical picture
Symptom less 20 %
 Symptoms

 Charcot’s
triade
 Jaundice
 Pain
 Fever
 Raynaud’s
 Charcot’s
pentale
triade
 Hypotension
 Altered mental status
Investigations

Laboratory
 CBC
 Liver
function
 urine

Radiological
 US
 ERCP
 MRCP
 PTC
Management of stone CBD
Support liver by correction of the general
condition by I.V. fluids for hydration
 Support kidney by Mannitol
(hypotension and hyperbilirubinemia
together causes renal shut down)
 Prevent infection by antibiotics,
 Prevent bleeding by correction of the
avitaminosis K by parentral vitamin
administration

Concurrent common bile duct and
gallbladder stones
 Preoperative
ERCP, with clearance of the
common bile duct, followed by LC
 Open cholecystectomy and common bile duct
exploration
 Combined laparoscopic-endoscopic
management:
Endoscopic sphincterotomy and stone extraction
are performed on the operation table
 after the surgeon has passed a guidewire through
the cystic duct into the duodenum
 to help the endoscopist because the procedure is
performed with the patient in the supine position.

Management of a case of stone
CBD
Minimal invasive
 Endoscopic extraction of calculi
followed by cholecystectomy whether
surgical or most commonly
laparoscopic
 PTC which provide drainage and
subsequent choledochoscopy & stone
extraction
Management of a case of stone
CBD
 Conventional
choledochtomy
 Chole cystectomy and supra
doudenal choledochtomy
choledocholithotomy (exploration of
the common bile duct)
 Trans doudenal sphincterotomy
 Choledocho douden ostomy
Indications of common bile duct
exploration (supra doudenal

Preoperative




confirmation of the presence of CBD stones (U/S, ERCP, or
operative cholangiography)
Jaundice or history of jaundice
History of pancreatitis (although it is usually due to a passing
stone)
Operative




choledochtomy)
Stone palpable in CBD
Dilated CBD with thick lusterless fibrous wall, with mud inside
Dilated cystic duct specially if there is multiple small stones in
the gall bladde
Postoperative

Surgical Jaundice
Management of a case of stone
CBD
T tube insertion which should be
 Widest possible diameter
 Latex or red rubber (never plastic)
 Exist from one side of the choledochotomy
wound
 Horizontal limb is cut to lie below the carina and
above the common channel
 Vertical limb comes out straight from the
abdomen
 T tube cholangiography is done on the 4 th days
and tube is extracted at the 10-12 days after 24hour occlusion without problems (fever, leakage,
or pain)
Management of stone CBD
Sphincterotomy or sphincteroplasty done In
the presence of
 stenosed termination of CBD or
 an impacted stone in its lower end that
cannot be extracted from the
choledochotomy wound
the ampulla is attacked through a duodenal
incision and the ampulla should undergo
either sphincterotomy or sphincteroplasty
at 10 or 11-oclock positions to avoid
pancreatic duct injury
Management of a stone CBD
Chole docho duodenostomy is done (in the
following situations)
 In dilated CBD (more than one cm)
 In case there is multiple stones (> 4
stones in CBD) because of the high
possibility of missing a stone inside
 Presence of intrahepatic biliary stones
 Stricture of the lower end of CBD
Missed stone after CBD exploration
Confirm diagnosis bt US & ERCP
 Wait for 6 weeks
 Hydrostatic pressure
 Minimal invasive




ERCP sphincterectomy & stone extraction by Dormia
Basket
PTC then choledochoscpic extrction
Surgical


Supradoudenal choledochotomy
Transdoudenal sphincteroplasty
Jaundice
Jaundice
Pre-hepatic
(Hemolytic)
Hepatic
Post
hepatic (Obstructive)
Pre-hepatic (Hemolytic)

Congenital abnormal
 Shape
 spherocytosis,
 eleptocytosis
 Hb
 thalssemia,
 sickle
cell
 Enzymes
 G6

PD,
pyruvate kinase
Pre-hepatic (Hemolytic)

Acquired

Immune hemolytic





Collagenic SLE, Rheumatoid
Tumor lekemia, lymphoma
Infections malaria, syphilis
Drugs penicillin tetracycline, quinidine, aSPIRIN
Non immune






Septicemia
Burn
Metal poisoning
Mismatch blood transfusion
Haematoma
Snake venum

Hepatic
Acute
 Viral
 Amoebic
or bacterial
 Alcoholic
 Liver
cell necrosiis
 Drugs
 Direct

hepatotoxic
A antibiotics (Tetracycline),
 Analgesic (salycilate, paracetamol)
 Antihelminthic carbon tetra chloride
 Anaesthestics fluthane
 Arsenic
Hepatic
 Drugs
 Direct hepatotoxic
 B benzidine dervative TNT
 C cytotoxic 5FU
 Intra hepatic cholestasis
 Non sensitivity methyl testosterone
 Sensitivity
neomercazole, thiuracil, chloropromazine
 Hypersensitivity
PASA

Chronic
 Chronic
active
 Cirrhosis
 Primary hepatic cirrhosis
 Space occuping lesions
Obstructive jaundice (Etiology)

Common
 Common
bile duct stones
 Carcinoma of the head of pancreas
 Malignant porta hepatis lymph nodes

Infrequent
 Ampullary
carcinoma
 Pancreatitis
 Liver secondaries
Obstructive jaundice (Etiology)

Rare
 Benign
strictures - iatrogenic, trauma
 Recurrent cholangitis
 Mirrizi's syndrome
 Sclerosing cholangitis
 Cholangiocarcinoma
 Biliary atresia
 Choledochal cysts
Calcular obstruction
 Intermittent
(can be progressive if
stone is impacted)
 Usually no reaching high levels
 Pain is colicky in nature, and typical
for biliary colic
 G.B not palpable except very rarely if
its neck is obstructed too (double
stone)
Malignant obstruction
Progressive except very rarely in
ampullary tumors where sloughing can
give temporary decrease
 Usually reaching high levels
 Pain is constant and referred to the back
in pancreatic tumor, while it is absent in
CBD tumors
 G.B is palpable except in Klatskin tumors

Obstructive jaundice
Calcular
Complications of obstructive
jaundice

Ascending cholangitis
 Charcot's
triad is classical clinical picture
which is formed of intermittent pain, jaundice
and fever
 Cholangitis can lead to hepatic abscesses
 Need parenteral antibiotics and biliary
decompression
 Operative mortality in elderly of up to 20%
Complications of obstructive
jaundice

Clotting disorders
 Vitamin
K required for gamma-carboxylation
of Factors II, VII, IX, XI
 Vitamin K is fat-soluble. No absorbed. So it
needs to be given parenterally
 Urgent correction will need Fresh Frozen
Plasma
 Also endotoxin activation of complement
system
Complications of obstructive
jaundice
Hepato-renal syndrome
 Poorly understood
 Renal failure post intervention
 Most probably due to gram negative
endotoxinaemia from gut
 Preoperative lactulose may improve outcome
by improving altered systemic and renal
haemodynamics
 Drug Metabolism
 Half-life of some drugs prolonged. (E.g.
morphine)
 Impaired wound healing.

Investigations for a case of
obstructive jaundice
Laboratory
 Raised
 Direct bilirubin (in most of the cases the
indirect bilirubin also rises due to
hepatic cellular malfunction).
 Alkaline phosphatase
 Gamma glutamyl transferase
 5 nucleotidase
Investigations for a case of
obstructive jaundice
Laboratory
 Mild elevation or normal
 SGOT & SGPT (these are shooting in
viral hepatitis)
 Slightly depressed or normal
 Prothrombin time (due to avitaminosis
K)
 Urine urobilinogen
Investigations for a case of
obstructive jaundice
Imaging techniques
 Ultrasound this is most useful
 CT (conventional or helical) competes with
the U/S especially as regards the pancreatic
tumors.
 ERCP
 MRCP
 PTC
 EUS
malignant
Treatment for
cholangiocarcinoma of CBD
Palliative
Plastic stent insertion through ERCP
 Stent insertion through percutanous
transhepatic route
 Self-expanding stainless steel wire biliary
endoprosthesis is new modality with high
patency rate, and less infection rate

Treatment for
cholangiocarcinoma of CBD
Palliative
 Bypass surgery
 Round
ligament approach for Klatiskin tumors
(on condition that the carina is permitting
right to left communication)
 Hepatico jujenostomy for middle and low
tumors
 Cholecystojujenostomy for low tumors.
 usually we add gastrojujenostomy and
enteroanastomosis (triple anastomosis) for
pancreatic head tumors
Treatment for
cholangiocarcinoma of CBD
For operable cancers
 For Klastiskin tumor,


segment IV excision provides good access to the
confluence
allows good proximal clearance and facilitates
hepaticojujenostomy

For middle tumors excision of the tumor from
just below the carina to the duodenum is done
with hepaticojujenostomy

For distal tumors. Whipple operation is done
Biliary stricture
Etiology
Congenital (biliary atresia)
 Traumatic (most important, and usually follow
cholecystectomy)




Complete ligation of CBD
Narrowing of the duct by partial inclusion in a ligature
Ischemia of the duct, or diathermy injury
Inflammatory Sclerosing cholangitis (multiple
strictures separated by normal or dilated
segments).
 Cholangiocarcinoma

Sclerosing cholangitis
PSC (primary sclerosing choangitis ) is a
chronic cholestatic biliary disease
characterized by non suppurative
inflammation and fibrosis of the biliary
ductal system.
 The cause is unknown but is associated
with autoimmune inflammatory diseases
such as chronic ulcerative colitis.

Sclerosing cholangitis
 Most
patients present with fatigue
and pruritus and, occasionally,
jaundice.
 The natural history is variable but
involves progressive destruction
of the bile ducts, leading to
cirrhosis and liver failure.
Biliary stricture

Investigations used are similar to those
used in any case of obstructive jaundice
(U/S then CT, ERCP, MRCP or PTC

Treatment is centered on creating a biliary
enteric anastomosis with mucosa-tomucosa sutures without compromising the
blood supply of any of the ends.