Gall bladder & biliary tract

disease
Entry questions
1. Why does hemolytic anemia and cirrhosis cause pigmented stone?
2. What are the signs symptoms of acute cholecystitis?
3. How do you classify cholecystitis?
4. What are the classifications of gallbladder stone?
5. What are the different cause of GS?
6. The most common type of GS?
7. What differential do you consider for acute cholecystitis?
8. What are the characteristics of cholesterol gallstones?
9. What are the characteristics of pigment gallstones?
10. What are the characteristics of mixed gallstones?
11. How cholesterol stones are formed in the gallbladder?
12. Which factors determine solubility of cholesterol in bile?
13. When bile becomes supersaturated with cholesterol?
12/13/24 T.A 2
 …
14. In which form cholesterol remains in solution in
bile?
15. What is nucleation?
16. Which factors initiate cholesterol precipitation?
17. Which factors increase cholesterol secretion in
bile?
18. What are the conditions causing reduced bile
salts concentration in bile?
19. Why infection is important for development of
gallstones?
20. What are the compositions of mixed stones?
21. How chenodeoxycholic acid (CDCA) and
ursodeoxycholic acid (UDCA) may prevent
stone formation?
12/13/24 T.A 3
RUQ Anatomy: GB Location
 GB lies inferior to liver
 Between the right and quadrate hepatic lobes
 Hollow viscus in the gallbladder fossa
 Consists of funds, body , infundibulum and neck
 Neck tapers to cystic duct common site of stone
formation and pronged stay “Hartmann's pouch”
 The mucous membrane contains indentations
of the mucosa that sink into the muscle coat;
these are the crypts of Luschka.
 The mucosa of the cystic duct is arranged in
spiral folds known as the valves of Heister.
 Its wall is surrounded by a sphincter structure
called the sphincter of Lütkens

12/13/24 T.A 4
Cont…
 A pear-shaped reservoir 5 – 12 cm in length.
 Average capacity 30-50 ml , when obstruction occurs it
extends up to 300ml.
 250-1000ml bile /day produced from the liver.
 The normal ratio is 1:25 with critical of 1:13 chestrol to bile
acid
 Cystic artery supplies the GB.
 Venous return  through small veins  liver or large cystic
vein  portal vein.
 Lymphatic drains  cystic LN & posterior pancreatico
duodenal LN.
 Nerves  Vagus & sympathetic (T8 & T9)
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 …
 Cystic Duct:-2-4 cm in length, 3mm diam.
 Common hepatic duct  1 to 4 cm length. 4mm –
diameter.
 Common bile duct varies from 5 to 15 cm, 5 to 8 mm in
diam.
 CALOT’S TRIANGLE
 Formed by
 CD below and laterally,
 The Rt lobe of liver above,
 The CHD medially.
 Contents
 Rt hepatic A or aberrant Rt H.A.
 Cystic A & an aberrant BD.
 LN
 If the Calot's triangle is not visible during surgery
fundoectomy will be done up to the neck of gall
baldder.
12/13/24 T.A 6
12/13/24 T.A 7
RUQ Anatomy

Gallbladde Quadrate
r liver lobe
Right Left
liver liver
lobe lobe
Cystic
Hepatic
duct
artery

Portal
Commo vein
n Bile
Duct IVC

12/13/24 T.A 8
Bile duct anatomy
Supraduodenal
Retroduodenal
Infraduodenal
Intraduodenal

 Sphincter of Oddi surround it , and terminates by

opening on the summit of the Ampulla of Vater

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Gallbladder function

 Reservoir for bile ( contains 40–70 ml bile)

 Concentrates bile up to 5-10x
 Water is absorbed
 Bile salts and solutes become
concentrated
 NaCl will be absorbed and
 Cholesterol and Ca remain there
 Secretion of mucous up to 20 ml/d
 Contract &release bile into duodenum
12/13/24 T.A 10
Pathologic Conditions of the Biliary Tract

 Cholelithiasis & choledocholelitiasis

 Cholecystitis & cholangitis
 Acute
 Chronic
 Sclerosing cholangitis
 Obstructive jaundice
 Cancer
 Preampullary
 Cholangicarcinoma
 Gall bladder
 Duodenal tumor
 Adenomyomatosis
12/13/24 T.A 11
Cholithiasis
Incidence
 Most common biliary pathology
 Prevalence: 6-10 % men, 12-20 % women
 The “F” risk factors
 Fat,
 Fertile,
 Flatulent,
 Female ,
 Fourty
 Familial Hx.
 Majority of gallstones clinically silent
 18-50% become symptomatic over 10-15yr and only
1-2% become symptomatic per yrs and each year
increase by 1%.
12/13/24 T.A 12
Natural Hx of Cholithiasis
 70% are asymptomatic
 30% are symptomatic
 Only 2-3 % become symptomatic each year and the
accumulation of this make lastly 2/3 to be
symptomatic.

12/13/24 T.A 13
Classification
Based on stone composition ,location & etiology.
 Composition
 Cholesterol stone (10%)----cholesterol>70%
 Pigment stone (10%)---cholesterol ---< 30%
 Mixed stone (80%)-----cholesterol 30-70%
 Location
 GB
 Extra hepatic BD
 Intra hepatic BD
 Major elements – cholesterol, bile pigments,
calcium.
 Others – Fe, P, CO3, mucus, debris
12/13/24 T.A 14
 Etiology
 The etiology of gallstones is multifactorial including
metabolic ,infective and bile stasis.
 Types of stones
 Cholesterol Stones
 Radiolucent

 10% of all stones

 (>70% by weight is cholesterol, <10% are

radiopaque)
 Pigment Stones
 Radiopaque

 15% of all stones

 (<30% by weight is cholesterol)

 Strawberry gallbladder
 Accumulation of cholesterol stain the GB wall mucosa
12/13/24 to yellow and is mostly associated with cholesterol 15

stone.
….
 Brown pigments stones
 Usually secondary to bacterial infection caused by bile
stasis or infestation by parasites) they are rare in the
GB.
 Black pigment stones
 Secondary to hemolytic disorders and cirrhosis )
Pathophysiology
 Cholesterol stones supersaturation of bile with
cholesterol
 Black pigment stones supersaturation of calcium
bilirubinate
 Mixed stone ---the most common type of gallbalader
stone accounting more than 70% and the cholestrole
12/13/24 T.A 16
amount is 30-70%
 RISK FACTORS
Age ----------- >40yr
Gender ------ female
Estrogens ----increasing cholesterol clearance
Pregnancy, ----multiparas---fertile----progesterone
induced smooth muscle relaxation and bile stasis
Hormone replacement, pills-----
Obesity -----fat increase cholesterol excretion
Intestine disease------ resection
Familial
Rapid wt loss ----decreased CCK resulting in stasis
Fasting ----- lack CCK and bile stasis
 Diabetes----increase cholesterol excretion
 SBS , TPN
Cirrhosis & hereditary blood disorders
Vagotomy ----b/c of stasis T.A
12/13/24 17
 Pathogenesis of Gallstone
Multifactorial
 Metabolic(non pigmented stone)
 Drug
 Obesity
 High calorie diet
 Bile stasis---mixed stone
 Estrogen in pregnancy
 Parenteral nutrition
 Vagotomy
 Infectious----the commonest cause
 Hemolysis
 Saint triads
 Colonic diverticula
 Hiatus hernia
 GB stone
 Parasitic infection
 Cystic fibrosis---abnormal mucous
 Others
 DM
 Gastric surgery-----CCK and reabsorption of bile acid will decrease
 Cirrhosis
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 Type 4 hyper protinimia
 Impaired GB function
Supersaturated bile
Emptying
Age
Absorption
Sex
Excretion
Genetics
Obesity
Diet

Absorption/EHC
Nucleating agents SBS
Mucus Fecal flora
Glycoprotein Ileal resection
Infection Cholestiramine

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Pathogenesis Cholesterol & mixed
stone
Occurs in three stages
Cholesterol saturation
 Mixed bile acids, lecithin & cholesterol…micelles
 Any alteration …cholesterol precipitation
 Due to ↑ed quantity or alteration of the vehicle ---
critical step
 Supersaturation can occur due to secretion of
hepatic bile with either high cholesterol or low
bile acids or lecithin …litogenic bile >13:1
normal is 1:25
Lithogenic bile
 Bile Supersaturation with cholesterol is called
Lithogenic b/c it is liable for GS.
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Nucleation
 Cholesterol monohydrate crystals form &
agglomerate ---- macroscopic stone
 Promoters or retarding agents
 Heat labile GP in the bile as potential
pronucleating factors (e.g GB mucus)
 Stasis of bile in the GB
 ↓ GB motility & emptying
 ↑ed calcium
 Alteration in GB secretion & absorption
 Stone Growth
 Due to cholesterol precipitation &
agglomeration
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 Pathogenesis of Pigmented
Stones
 Due to altered solubilisation of unconjugated bilirubin with
precipitation of ca bilirubinate & insoluble salts
 Cholesterol and bile acid form missile while cholesterol
and phospholipid form vesicle the movement of cholesterol
from the vesicle to the missile cause hypersaturation of the bile
and stone formation
2 types
1. Brown pigment stones
 Common in Asia
 Secondary to infection
 Release of beta glucuronidase
 Rare in the GB

2. Black pigment stones

12/13/24
 Pts with haemolytic
T.A
dd. & cirrhosis
22
 Clinical presentation of gall stone
 Asymptomatic/silent---70% of the cases 50%
incidental finding and 25% become
symptomatic for the next five years.
 Typical/classical
 Biliary “colic”---more at night and stay for hours and
radiate to right shoulder
 Associated with post prandial only in 50%of cases
 May be associated nausea/vomiting
 Fat intolerance
 Atypical
 Dyspepsia/indigestion
 Flatulence
 Belching
 Atypical sites(retrosternal)
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Complications of GS
 Gallbladder--- due to move's of
stones & infection
 Silent stones
 Cholecystitis →acute or chronic
 Gangrene --- BV obstruction
 Perforation
 Biliary peritonitis
 Biliary-enteric fistula
 Empyema
 Mucocele (hydrops)
 Carcinoma
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Cxn…cont’d
 IN THE BILE DUCTES
 Obstructive jaundice
 Cholangitis
 Acute pancreatitis

 IN THE INTESTINE
 Acute intestinal obstruction (GS ileus)

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Symptomatic cholelithiasis
 This is similar as chronic cholecystitis
 When the stone obstruct the cystic duct at the neck of
the GB the pt become symptomatic and it will relive
as the stone dislodges.
 If the stone stay more than 6 hrs it will progress to
acute cholecystitis b/c it will become ischemia .
 All symptoms of acute cholecystitis will present except
fever.

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Investigation of the biliary tree
 Ultrasound: stones and biliary dilatation
 Plain radiograph: calcification, R/O IO and viscus
perforation
 Magnetic resonance cholangiopancreatography:
anatomy and stones, radiation free but not Theraputic
 Multidetector row computerised tomography scan:
anatomy, liver, gall bladder and pancreas cancer
 Radioisotope scanning: function
 Endoscopic retrograde cholangiopancreatography:
anatomy, stones and biliary strictures
 Percutaneous transhepatic cholangiography: anatomy
and biliary strictures, better if the stone is higher up
 Endoscopic ultrasound: anatomy and stones
12/13/24  HIDA---golden standard with T.A IV dye with visibility of the GB 27
mucosa
RADIOLOGICAL INVESTIGATION OF THE
BILIARY TRACT

1. Plain radiograph
 A plain radiograph of the gall bladder will show radio-
opaque gallstones in 10% of patients with gallstones
“Mercedes-Benz’ or ‘seagull’ sign”.
 A plain X-ray may also show the rare cases of
calcification of the gall bladder, a so called ‘porcelain’
gall bladder
 Porcelain GB is 25% associated with malignancy
 Pigmented stone

12/13/24 T.A 28
2. Ultrasonography
 Transabdominal ultrasonography is the initial imaging
modality of choice as it is accurate, readily available,
inexpensive and quick to perform.
 However, it is operator dependent and may be suboptimal due
to excessive body fat and intraluminal bowel gas.
 It can show biliary calculi, the size of the gall bladder, the
thickness of the gall bladder wall, the presence of
inflammation around the gall bladder, the size of the
cystic duct, carcinoma of the pancreas
 Ultrasound criteria to Dx cholecystitis
 Pericholicystic fluid
 Probe tenderness
 Wall thickness > 4mm
 In the presence of GS two of the
12/13/24 T.A above three are diagnostic 29
3. Radioisotope scanning
 Non- visualization of the gall bladder is suggestive of
acute cholecystitis.
 The gall bladder is visualised within 30 min of isotope
injection in 90% of normal individuals and within 1
hour in the remainder
 Bowel in 1 hrs

12/13/24 T.A 30
4. Computerised tomography
 It is particularly useful in detecting hepatic and
pancreatic lesions and is the modality of choice in the
staging of cancers of the liver, gall bladder, bile ducts
and pancreas.
 It can identify the extent of the primary tumours and
defines its relationship to other organs and blood vessels
 It is not operator Dependant and used also to stage
malignancy's
 US is superior than CT in GBS and liver metastasis while
CT is used for resectablity assesment.
12/13/24 T.A 31
 5. Magnetic resonance
cholangiopancreatography
 MRCP based on the principles of nuclear magnetic
resonance used to image the gall bladder and biliary
system.
 It is non-invasive and can provide either cross-sectional or
projection images.
 Contrast is not required.
 The images obtained are comparable to those from
 ERCP or PTC without the potential complications of either
technique
 MRCP and ERCP are indicated only
 Clinical jaundice present
 Sign of cholangitis T.A
12/13/24 32
 US is inconclusive and suspicion of OJ
6. ERCPG
 This technique remains widely used.
 Can identify causes of obstruction such as
stones, malignant strictures
 ERCP, the technique has a role in the
assessment of the jaundiced patient.
 It is especially useful in determining the cause
and level of obstruction.
 Used for both Theraputic( put stent, crush stone
or do sphincteroectomy) and diagnostic purpose.
 The disadvantage is it can
 Perforatethe pancreatic, CBD
 Cause acute pancreatitis
12/13/24 T.A 33
8. PTCG
 This is an invasive technique in which the bile ducts
are cannulated Directly
 In general, in the jaundiced patient, if a malignant
stricture at the level of the confluence of the right and
left hepatic ducts or higher is suspected, a PTC is
preferred to an ERCP as successful drainage is more
likely.
 Used as therapeutic and diagnostic purpose as ERCP
but it is better than ERCP
 Contraindicated in pts having bleeding disorder.
12/13/24 T.A 34
Management of GB stones
 Category 1
 Gallstones on imaging studies but without symptoms
 Called asymptomatic Cholithiasis mostly incidental finding
 Category 2
 Typical biliary symptoms and gallstones on imaging
studies
 Category 3
 Atypical symptoms and gallstones on imaging studies
 Category 4
 Typical biliary symptoms but without gallstones on
imaging studies
 Has high risk of postcholcystoectomy syndrome

12/13/24 T.A 35
Definitive Rx
 Elective producer
 Removal of GB & stones after 6-8wks
 Open cholecystectomy
 Laparoscopic cholecystectomy
 Emergency cholecystectomy
 Pts not settling within 48 hrs.
 Pts with DM to prevent gangrene.
 Emphymatous GB
 Indication to manipulate CBD
 Icteric pt
 Elevated LFT
 Palpable mass intraoperative
 US or ERGC show stone in the CBD---dilated > 10mm

12/13/24 T.A 36
Surgery
 Early cholecystectomy within 72 hrs
 Currently it is becoming popular even for those
done for elective base
 Laparoscopic cholecystectomy
 Changed to open if
 Extensively fibroid GB
 Difficult GB
 Advantages over open in
 Short hospital stay
 Less pain
 Minimum complication
 Good cosmetics
 Accepted by the client
 Open cholecystectomy
 Minicholescystectomy
 Done with a small 5cm incision over the right
subcoastal area with good out come
12/13/24 T.A 37
Sites for open cholsystectomy

12/13/24 T.A 38
Prophylaxis cholecystectomy
 Indicated in case of
1. DM---the risk of Emphymatous GB is high.
2. Patients on immunosuppressive therapy
3. Candidate for renal transplant
4. Large stone > 3cm
5. Multiple small GS---risk of pancreatitis
6. Porcelain GB
7. Area is endemic for GB cancer
8. Hemolytic anemia
12/13/24 T.A 39
Cholecystitis
 Could be
 Acute or chronic inflammation
 Calculous ,acalculous or emphysematous
 Risk factors: obstruction and bile stasis
 The most common cause is calculous cholecystitis

12/13/24 T.A 40
ACUTE CHOLECYSTITIS
 Most common complication of GSD
 In 95%....GS impacted at Hartman’s pouch
 Acute inflammation of GB
 30% bacteria cultured
 Middle aged & elderly
 Hx of episodic biliary colic pain Unremitting for days

12/13/24 T.A 41
Hx
 Persistence RUQ pain > 4 hrs radiate to the
right shoulder b/c of phrenic nerve irritation but if it
is pancreatitis the radiation will be to the back.
+ Nausea & Vomiting---b/c of reflex pylurospasm
+/- Pyrexia
 P/E
 Murphy’s sign +ve
 Boa’s sign ---hyperesthesia of the posterior 7-11th rib area
 Direct & rebound tenderness & guarding
 In 50% mass in RUQ … 20%
 Leukocytosis (12,000 to 15,000 cells/µL),

12/13/24 T.A 42
Murphy’s sign positive
 Acute cholecystitis
 Chronic cholecystitis
 Cholecystoses
 Cholestrosis
 Cholesterol polyp
 Cholecystitis glandulari’s prolifrance

12/13/24 T.A 43
Pathology
 Inflammation either due to obstruction or infectious
agent
 Perforation ----b/c of mucosal erosion due to
inflammation
 Obstruction by the already formed stone or newly
formed stone
 Mucocele ---used as a good proliferation area for
bacteria…..clostridium perphyringe (emphysematous
GB)
 Gangrenous GB---thrombosed blood vessles and
ischemia
12/13/24 T.A 44
 …
 Normally the GB mucosa secret glycoproteins which are protective
from bile irritation.
 In case of cholecystitis this will not happen b/c of ischemia resulting
from compression of the cystic artery by the GS pressure.
 This ischemia is also a cause in acalculous cholecystitis where blood
flow decrease to the mucosal resulting stasis and inflammation.
 In both case the initial inflammation is sterile resulting early culture
negative but later b/c of translocation it will be contaminated.
 In perforation there will be bile peritonitis which is a severest form
of peritonitis and infected b/c perforation happen in late stage.

12/13/24 T.A 45
 DDx
1. Perforated PUD ----epigastric pain
2. Appendicitis----- retrocaecal
3. Acute pancreatitis----radiation of pain will be to the back
4. Lobar pneumonia
5. Hepatitis
6. Liver abscess
7. Hydratic disease ----
8. Complicated PID
9. Pyelonephritis
10. AMI
11. Nephrolithiasis
12. Cholithiasis
13. Chronic cholicystis

12/13/24 T.A 46
 ACALCULAS CHOLECYSTITIS
 Pts with major abdominal & thoracic surgery & TPN
 Recovering from major trauma, severe burn, IC
patients
 It is the severest form
 Had poor prognosis than calculous cholystitis
 Difficult to manage b/c patients will not be stable
 Subtotal cholyscytectomy or cholicystostmy will be
done
 Associated with emphysematous cholicystis and other
complications.
Acute emphysematous cholecycistitis
 Serious form of Ac.
 Xized by gas in the lumen or wall of the GB
 In the elderly pts
 25% have DM and immunosuppressed pt.
 CF as AC but pts are more toxic
 DX ….air in the gallbladder or wall on plain abd. Film
 GS in 75% of pts
12/13/24  Emergency cholecystectomy T.A
is indicated 47
 Investigations
 CBC ----elevated
 Plain x-R show us
 Pigmented stone---radio opaque mass anterior to the vertebra
 Proclaim GB
 R/O other cause like perforated PUD
 65-70% of perforated PUD has air under the diaphrambut only
10% of perforated GB.
 RBS and urine glucose ---to r/o DM
 Emergency ultrasound
 Posterior acoustic shadow---this is b/c the stone dose not pass
the wave –sign of stone and in the presence of this two of the
three below is diagnostic
 Thickened wall >4mm
 Distended GB
 Pericholicystic collection and dilated CBD
 Liver enzyme and function test--- mostly amylase b/c it rise
early but the most specific one is lipase
 Serum alkaline phosphatase
12/13/24
 Serum lipase and amylases T.A 48
Cause of increase alkaline phosphatase
 Obstructive jaundice
 Biliary cirrhosis
 Bone disease
 Hepatitis
 Prostatic Ca or prostatitis
 Hepatic abscess

12/13/24 T.A 49
…
Oral cholecystography (OCG)
- replaced by U/S
- used to assess GB function
IV cholangiography
-to see extrahepatic biliary tree
-effective in jaundiced pts.
CT & MRI
- to R/O pancreatic head tumour

12/13/24 T.A 50
….
PTC & ERCP
- in pts with comp. acute biliary dd. & jaundice
- clotting studies before PTC
- prophylactic antibiotics
Indicated in pts.
- known GBS with increased bilirubin >10 mg/dl
- Sx pts with previous cholecystectomy
- pts with biliary Sx & inconclusive evidence
9. HIDA
10. OCG
12/13/24 T.A 51
Treatment of acute cholicystis
 Supportive
 Admission
 Gastric content aspiration with Ryle tube
 Antispasmodic agent
 Analgesics---tramadol 75mg IM TID
 IV fluid
 Broad spectrum antibiotics –cover both G-ve and
+ve( ceftriaxone and metronidazole or if ceftriaxone not
available ampicillin/ gentamycin.
 NPO for 2-3 days and start with oral fluid and if
symptoms relived start normal diet.
12/13/24 T.A 52
….
 Definitive
 Early cholsystectomy
 If presented within 72hrs of symptom unless b/c the
surrounding edema will obscure the adjacent
structure and damage to CBD and CD is likely.
 Elective ----after 6 weeks of acute attack
 The preferred one is laparoscopic which has
advantage of
 Better cosmetic effect
 Less pain and hospital stay

 Less complication
12/13/24 T.A 53
Emergency cholecystectomy
 Indicated in case of
 Any complication
 Not relived within 48 hrs
 Pt presented within 72 hrs of the onset of symptom
 Reason for not relived during 48 hrs
 Incorrect Dx
 Gangrenous GB
 Mucocele
 Perforation---sever form of peritonitis
 Emphysematous GB
 Patient classification in emergency surgery
 Stable ----total cholecystectomy
 Unstable ----partial cholecystectomy or cholicystostmy

12/13/24 T.A 54
CHRONIC CHOLECYSTITIS
 Incompletely resolved AC
 Contracted fibrotic GB
 Dyspepsia …belching ,abdominal
bloating ,fullness epigastric burning & Nausea
& Vomiting
 Stone is invariably present
 The diagnosis is made by ultrasonography
 The treatment is cholecystectomy
12/13/24 T.A 55
Complication
 Complication GB surgery include
 Bleeding
 Most common site is the cystic artery and liver capsular
damage resulting parenchymal hemorrhage
 Damage to the Calot’s triangle
 Gall stone ileus
 If there is fistula especially dodunocystic
 Bile peritonitis
 If the is biliary leak---the most pain full peritonitis

12/13/24 T.A 56
….
 Post cholecystectomy syndrome
 This is re appearance of previous symptoms after
cholecystectomy is done.
 This can be due to
 Missed stone in the CBD
 Cystic duct stump stone
 Biliary duct damage
 PUD
 GERG
 Hiatal herina
 Biliary duct stricture
12/13/24 T.A 57
Post operative complications
1.Bleeding.
 Pts. With liver cirrhosis & portal HPN.
 Inadvertent division of the cystic or hepatic artery.
 Inadequately legated CA.
 The most commonly injured one is cystic artery
Management
1. Intra operative
 Insert a hot pack & adequate suctioning.
 Compress HA with index finger & thumb (Pringle’s
maneuver )
 After few minutes remove the pack & identify the source
of bleeding & secure by legation .

12/13/24 T.A 58
 …
 Bleeding from GB bed satisfactorily controlled
using hot packs followed diathermy using
forceps.
 Sutures
 During LC:-Suck out the blood & cot, apply
local pressure.
 Remove the pressure apply diathermy & clip.
 Bleeding continues  Laparotomy.
2.If it occurs late.
-Usually in the evening following surgery.
-Pts.->tachycardia, hypotension, tachypnea,
pallor, abd. Distension, bleeding from drain
Mx.: -Immediate exploration is mandatory.
-Transfusion of whole blood & FFP
12/13/24 T.A 59
Cont…
2. Post operative bile leakage.
-occurs in abought 3% of Pts.
Cause –Transected hepatico-cholecystic duct
-commonly CD leak, CBD injury.
Mx.- Small leak  Close spontaneously & the drain
should be kept until it occurs .
-Copious drainage persists or there is sign of intra-
abdominal collections or peritonitis  Reoperation.

12/13/24 T.A 60
Cont…
3. Bile duct injury.
Incidence
-During open cholecystectomy 0.1 - 0.2%.
->> LC -major injury -> 0.55%, minor injury & bile leak  0.3%.
Diagnosis:-
only 25% of BD injuries recognized at the time of operation.
>1/2 of Pt. with BD injury presented within 1st post op month.
the rest present months or yrs. Later with recurrent cholangitis
or cirrhosis.
Early post op. progressive increase LFT., Bile leak, pain & fever.
-U/S or CT  collection or free fluid in the peritoneum.
Demonstrate dilated biliary tree proximal to
stenosis.
-Injection of water soluble contrast through surgical drain or
percutanously placed catheter define site & anatomy.
-Percutanous cholagiogram outline extent of injury &
decompression.
12/13/24 -ERCP Demonstrate the anatomy T.A distal to injury. 61
 Cont…

4. Retained stone
-occurs in 1% of Pts after cholecystectomy.
- >> 5% >> >> CBD exploration.
Diagnosis Post op T-tube cholangiography.
ERCP.
Rx. T-tube extraction of retained stone after 6 wks
with grasping forceps or baskets.
Endoscopic sphincterotomy & extraction.
Irrigation of T-tube to flush the stone in to
duodenum.
Reoperation.

12/13/24 T.A 62
….
5. Post cholecystectomy syndrome.
Persistent or recurrent Sxs after cholecystectomy.
This can be due to
 Hiatal hernia
 Missed stone
 PUD
 Stone in the cystic stump
 Operative damage to the biliary tree

12/13/24 T.A 63
Cont…
 Affects abought 10-15% of Pts.
 More common in middle age Pts.

Etiology
Retained or recurrent stones in the bile duct.
Stump cholelithiasis.
Bile duct stricture.
 Pancreatic or liver disease. ‘ Saint
triads’
 PUD or Bile gastritis.
 Irritable bowel syndrome.
 Diverticular disease.
 Psychiatric problems ( anxiety or depression )

12/13/24 T.A 64
Jaundice
Jaundice or icterus,
 Yellowish discoloration:
 Skin, mucous membranes, sclera.
 Excess plasma Bilirubin

 Normal range : 0.2 – 1.2 mg/dL)

< 5% - Conjugated
 Clinically obvious : (>1.5 mg/dl)

12/13/24 T.A 65
Classification
Classical: 1.Prehepatic- Hemolytic
2.Hepatic - Hepatocellular
3.Post hepatic - Obstructive
Bilirubin: 1.Conjugated
2.Unconjugated
Bile Flow
1.Cholestatice (Obstructive): Intrahepatic
Extrahepatic
2.Noncholestatic
. Medical
12/13/24
. Surgical T.A 66
Abnormal Metabolism
 Depending on the stages it may be disturbed
 Excessive production (hemolytic jaundice):-
 Inherited hemolytic anemia's
 Acquired hemolytic anemia's
 Hemolytic anemia's
 Hemolysins
 Absorption of sequestered blood
 Burns
 Mismatched or massive blood transfusions

12/13/24 T.A 67
 Abnormal Metabolism
II. Impaired transport to liver:-
-Gilbert’s syndrome( some forms)
III. Impaired hepatic conjugation:-
A. Inborn errors
1. Crigler - Najar syndrome
2. Gilbert syndrome
B. Immaturity of enzymes
1. Physiologic jaundice of newborn
2. Jaundice of prematurity
Unconjugated Hyperbilirubinemia
Retention Jaundice

12/13/24 T.A 68
Abnormal Metabolism
IV. Impaired excretion(hepatocellular
jaundice)
A. Acquired liver diseases
1.Hepatitis
2.Cirrhocis
3.Neoplasms,etc
B. Intrahepatic cholestasis
1.Drug induced
2.Disease related
3.Idiopatic
C. Dubin - Jonson & Rotor
syndrome
 Regurgitation jaundice
12/13/24  Direct & Indirect
T.A Bilirubinemia 69
 Abnormal Metabolism
V. Bile duct obstruction(obstructive
jaundice)
A. Extra hepatic
1. Stone
2. Neoplasms
3. Stricture
4. Atresia,ect
B. Intrahepatic

12/13/24 T.A 70
Surgical Jaundice
9. Klat skin tumour
1. CBD stones.
(Carcinoma at the
2. Carcinoma of head and confluence of hepatic
Preampullary region of ducts above the level
the pancreas of the cystic duct and
3. Biliary atresia so will cause
4. Choledochal cyst hydrohepatosis without
5. Ascending cholangitis. GB enlargement).
6. Biliary strictures. 10. Extrinsic compression
of CBD by lymph nodes
7. Sclerosing cholangitis. or tumours.
8. Cholangicarcinoma. 11. Parasitic infestations
12/13/24 T.A 71
Classification of Causes of Obstructive Jaundice

Based on the origion

1. Congenital: Biliary atresia, Choledochal cyst.
2. Inflammatory: Ascending cholangitis, sclerosing cholangitis.
3. Obstructive: CBD stones.
4. Neoplastic: Carcinoma of head or Preampullary region of pancreas,
cholangiocarcinomas, Klatskin tumours.
5. Extrinsic compression of CBD by lymph nodes
or tumours.
Based on the site
 Intraluminal
 Intramural----wall
 Extra mural----external compression
12/13/24 T.A 72
Approach to the jaundiced pt.
 With Hx ,P/E & LFT ≈
85% ► Accurate Dx  Occupation
 History:  Travel
 Rapidity of onset & course
of jaundice  Exposure to
 Color of urine & stools hepatotoxines
 Wight loss  Alcohol consumption
 Abdominal pain
 Digestive symptoms  Ingestion of drugs
 Malaise  Transfusions
 Anorexia
 Yellowish discoloration of  Injections
eye  Previous operations
 Skin itching

12/13/24 T.A 73
Approach to the jaundiced pt.
Physical exam:-
Nutritional status ---- assed by serum albumin level.
Scleral icterus
Virchoff's nodes
The abdominal exam should focus on :-
 Size and consistency of liver
 Whether the spleen is enlarged
 Whether there is Ascites
 Grossly enlarged nodular liver/abdominal mass---
malignancy
 Bruit heard over the liver ---- hematoma
 Large, tender liver with rounded edge ---
viral/alcoholic hepatitis
 Murphy's sign --- A. cholecystitis
 Courvoisier's gall bladder--- malignant obstruction
 Blood on DRE---malignancy
 Stigmas of CLD

12/13/24 T.A 74
Investigations for Obstructive Jaundice

1. Serum bilirubin.
Normal value is less than 1.0 mg%.
Direct is increased in obstructive jaundice
2. Serum albumin
Globulin and A: G ratio. Normal S. albumin is more
than 3.5 gm%.
3. Prothrombin time.
Normal value is 12-16 seconds.
If more than 4 from the control or more than one and
half times the control is significant.
It is corrected by injection vitamin K 10 mg IM od for 5
12/13/24
days or by fresh blood transfusion
T.A 75
 …..
4. Serum alkaline phosphatase
SGPT, SGOT, 5‘nucleotidase.
Normal value is 60-200ul/l and if > 600 sign of
obstructive jaundice
5. U/S
6. ERCP
To visualize site of obstruction, brush biopsy, bile sample for
analysis.
Used as both diagnostic and Theraputic purpose
7. MRCP—Noninvasive diagnostic tool.
8. CT scan in case of tumours to assess operability.
9. Urine tests:
 Fouchet’s test for bile pigments,
 Hay’s test for bile salts and T.A
12/13/24 76
 Test for urobilinogen in urine
1. Choledocholithiasis
 The commonest cause of surgical jaundice
 1o stones originate in the CBD
 2o stones -- Most CBD stones originate in the GB
 Cxn of CBD stone
 Obst. Jaundice
 Cholangitis fever
RUQ pain
Charcot’s triad
Jaundice
altered mental status
Reynolds’s pentad
+
shock
 Suppurative cholangitis=>liver abscess
 Impaired LF =>Biliary cirrhosis
12/13/24 T.A 77
Courvoisier’s law….
 In a jaundice patient if GB is palpable it is unlikely
due to choledocholithiasis b/c the GB being
fibrosed by the previous cholicystis with the
exception of
 Double impaction of stone one at common bile duct and another at cystic
duct „
 Primary CBD stone „
 Distended gallbladder due to large stone load.

12/13/24 T.A 78
DDx for obstructive jaundice
CBD stones  Investigation
Pancreatic head tumor  LFT
 Biliary stricture  U/S
Preampullary tumor  ERCP
 Drug induced jaundice,  PTC
Hepatitis (viral)  MRI
 CT
Parasitic infection
Reginal LN enlargment
Chronic pancreatitis
Sclerosing cholangitis
12/13/24 T.A 79
12/13/24 T.A 80
12/13/24 T.A 81
12/13/24 T.A 82
 Difference b/n surgical and medical jaundice

 Surgical jaundice  Medical jaundice

 Clinical May/may not be
 Blurring of vision
 bleeding
Pruritus
 May not be bluing of
Pale stool
 Dark urine vision
 Lab results Normal stool and
 Bleeding diastasis urine
 Increase direct Increase either
biluribin
 Increase alkaline indirect or both
phosphatase PT may be normal
 Increase PT
12/13/24 T.A 83
Management
 Endoscopic removal/drainage(ERCP
 Open/lap
 Choledochotomy
 Spincterotomy / plasty
 Drainage
 Choledochduedunostomy
 Choledochjejunostomy

12/13/24 T.A 84
 Choledochotomy
Indications
 Palpable CBD stones
 Multiple stone in the GB
 Biluribin level > 1g/dl
 If there is jaundice or

Hx of jaundice or
Cholangitis
 Dilated CBD > 12 mm size 11 mm is
acceptable
 Abnormal LFT, in particular, the alkaline

12/13/24 phosphatase is raised.

T.A 85
Types of surgery for CBD stone
1. Supradodunal cholidocholilitotmy
 The CBD is incised and the stones are removed
 T- tube will be left
 After 8-10 days cholangiography will be done and if
patent the tube will be discharged after 10-12 days
2. Cholecystectomy + cholidocholilitotmy +
cholidododunostomy
 Done if the stone size is more than 2-3cm in size and
the CBD is dilated more than 15mm
 It is a permanent solution for stricture
 Bile leak will not be there
12/13/24 T.A 86
…

3. ERCPG +sphincteroectomy
 Indicated in case of
Lower CBD stricture


 Multiple intrahepatic stone

 Recurrent attack

4. ESWL=> with addition of bile salts

12/13/24 T.A 87
2. Preampullary tumors
 These are tumors arising from within 2 cm of the
sphincter of Oddi
 These tumors include
 Pancreatic head tumor-----40-60%
 Distal Cholangicarcinoma---10%
 Duodenal tumor ---10%
 Tumor arising from the sphincter of Oddi it self—20-40%
 The most common one is pancreatic head tumor
 The investigations and the DDx are the same as
choledocholithiasis.
 All had similar clinical feature and treated similarly but
prognosis differ.
12/13/24 T.A 88
…
 Double duct sign
 In ERCP or MRCP or other imaging if both the bile duct
and the pancreatic duct show dilatation with
constriction of both the ducts in the region of
head of pancreas it is called double duct sign.
 This is found in Preampullary carcinoma (or
carcinoma of head of pancreas).
 This may also be found in chronic pancreatitis

12/13/24 T.A 89
…
 Trousseau’s sign
 Migratory thrombophlebitis in patients with an
underlying abdominal malignancy is known as
Trousseau’s sign.
 This may be found in pancreatic malignancy and in
other gastrointestinal malignancy.
 Troisier’s sign
 Left supraclavicular lymph node enlargement due
to metastasis from an intra-abdominal
malignancy is known as Troisier’s sign.
12/13/24 T.A 90
Treatment and type of surgery
 Whipple’s procedure( radical
pancraticododunoectomy)
 The C loop of the duodenum
upto the DJ junction and the
head of pancreases up to
the neck will be resected.
 Triple anastomosis will be done

Gastrojejunostomy

Pancraticojjejunostomy and

Cholidojejunostmoy
 This procedure is indicated in a
stable patient
 The gastric motility will be
affected.
12/13/24 T.A 91
…
 Pylorus preserving
pancreaticododunostomy
 The pylorus is preserved
 The gastric motility will not
be affected
 Triple by pass
 This is a palliative treatment
 Chocystojejunostomy +
entro-entrostomy +
Gastrojejunostomy will be
done
 This is to prevent the entry
of food through the biliary
system
12/13/24 T.A 92
Whipple's producer

12/13/24 T.A 93
 Before anastomosis After anastomosis

12/13/24 T.A 94
 2. Carcinoma of the
Gallbladder
 Is a rare malignancy that occurs predominantly in
the elderly.
 It is an aggressive tumor, with poor prognosis.
 The overall reported 5-year survival rate is about
5%.
 Is the fifth most common gastrointestinal
malignancy in Western countries.
 However, it accounts for only 2 to 4% of all malignant
gastrointestinal tumors,

12/13/24 T.A 95
Etiology
 90% of patients have gallstones.
 However, the 20-year risk of developing cancer for
patients with gallstones is less than 0.5% overall
popn. and 1.5% for high-risk groups.
 Larger stones (3 cm), symptomatic than
asymptomatic gallstones.
 Proclaim GB has risk of 25%.

12/13/24 T.A 96
Risk factors
1. Gallstone
2. Carcinogen exposure
3. Choledochal cyst
4. Proclaim GB
5. Sclerosing cholangitis
6. Anomalous pancreatic bacillary duct junction
7. GB polyp >1cm
8. Adenomyomatosis of GB
9. Chronic Thyphoid carrier
10. Inflamatory bowel disease
11. HBV and HCV infection
12/13/24 T.A 97
Pathology
 80 - 90% of the tumors are  Cancer of the gallbladder
 Adenocarcinomas. spreads through
 Lymphatics
Squamous cell,
 Venous drainage
Adenosquamous,
 Blood born
Oat cell, and other
 Intraductal spread
Carconoid tumor
 Direct invasion into the
Anaplastic lesions occur
rarely.
liver parenchyma.
 The histologic subtypes include
Papillary,
Nodular, and
Tubular.

12/13/24 T.A 98
Nevins staging of GBC
Stage 1 Intramucosal

Stage 2 Extend up to the

muscular’s propria
Stage 3 Transmural
involvement ( involve
serosa)
Stage 4 Trans mural + cystic
LN involvement
Stage 5 Extension to the liver
12/13/24
or distal metastasis
T.A 99
 Clinical Manifestations and
Diagnosis
 Signs and symptoms are generally indistinguishable
from those with cholecystitis and Cholelithiasis.
 These include abdominal discomfort, right upper
quadrant pain, nausea, and vomiting.
 Jaundice, weight loss, anorexia, ascites, and
abdominal mass are less common presenting
symptoms.
 More than one half are not diagnosed before surgery.
 Common misdiagnoses include chronic cholecystitis,
acute cholecystitis, choledocholithiasis, hydrops of
the gallbladder, and pancreatic cancer.
12/13/24 T.A 100
Treatment
 Surgery remains the only curative option.
However, palliative procedures for patients with
unrespectable cancer and jaundice or duodenal
obstruction remain the most frequently performed
surgery.
 Patients with obstructive jaundice can managed with
either endoscopic or percutaneous-placed biliary
stents.
 There are no proven effective options for
adjuvant radiation or chemotherapy.
12/13/24 T.A 101
3. Bile Duct Carcinoma
 Incidence is about 0.3%.
 Arises from the biliary epithelium and may occur
anywhere along the biliary tree.
 The gall balader is not palpable unlike Preampullary
tumor.
 About two-thirds are located at the hepatic duct
bifurcation.
 Surgical resection offers the only chance for cure.
 The management is difficult since most are higher up
and disseminate through portal vein.
12/13/24 T.A 102
Etiology
 Risk factors include
 Primary sclerosing cholangitis,
Stone
Choledochal cysts,
Ulcerative colitis,
Hepatolithiasis,
Biliary-enteric Anastomotic, and
Biliary tract infections with Clonorchis or in chronic
typhoid carriers.
 Features common to most risk factors include biliary
stasis, bile duct stones, and infection.
12/13/24 T.A 103
Pathology
 Over 95% are Adenocarcinomas, Adenosquamous
and squamous cell .
 Morphologically they are divided into
Nodular (the most common type),
Scirrhous ,
Diffusely infiltrating
Papillary.

 Anatomically they are divided into distal, proximal, or

perihilar tumors.
 ‘Klatskin tumors’ involving the confluence of hepatic
duct
12/13/24 T.A 104
Spread by
 Direct invasion of the portal vein to liver
 Lymphatic spread

12/13/24 T.A 105

 Clinical Manifestations and
Diagnosis
 Painless jaundice is the most common presentation.
Pruritus, mild right upper quadrant pain, anorexia, fatigue,
and weight loss.
 Cholangitis in about 10% of patients.
 Silvery stool
 Except for jaundice, P/E is usually normal.
 GB may be palpable
 U/S or CT scan.
 PTC defines the proximal extent of the tumor, ERC for
evaluation of distal bile duct tumors. Celiac angiography &
MRI.
12/13/24 T.A 106
Treatment & Prognosis
 Surgical excision the only potentially curative Tx
 Nonoperative biliary decompression is for patients with
unrespectable disease.
 Percutaneous metal stents drainage for proximal tumors
& endoscopic placement for distal tumors. There is a
significant risk of cholangitis .
 Surgical bypass offers improved patency and
fewer episodes of cholangitis.
 No proven role for adjuvant chemo radiotherapy.
 A median survival between 5 and 8 months.
12/13/24 T.A 107
4. Pancreatic Ca
 70% are adenocarcinoma
 70% at the head and the reaming 30% at the tail and body
 Causes include
 Tropical pancreatitis ----can be multifocal
 Hemochromatosis
 Diabetics
 Alcohol and smoking
 Westernization---- in food and feeding
 Industrial carcinogen
 Diet

12/13/24 T.A 108

 …..
 Periampullary tumor contains
 Lower part of CBD-------10%
 Duodenum----10%
 Ampulla of Vater----20-40%
 Head of pancreas--- 40-60%
 Microscopic types of PCa include
 Mucous
 Nonmucous
 Anaplastic
 Cystadenocarcinoma
12/13/24 T.A 109
 Clinical features

 Pancreatic duct obstruction or involvement of

retroperitonial nerve produce persistant pain that
radiate to the back
 WL
 Constitute symptoms
 Jaundice if the site is at the head
 Vommiting suggests duodenal obstruction
 Signs of anemia
 Trousseau’s sign ----thrombophlebitis migran’s
 Abdomenal mass
 Evidence of metastasis
12/13/24 T.A 110
…
 Pain is due to
 Involvement of retroperitoneal nerve by malignant cells
 Pancreatic duct obstruction leading to stasis and
stretching
 Gall blader can be palpable in 30% of pancreatic
cancer and 50% of periampullary tumors

12/13/24 T.A 111

Difference b/n PCa and Gca

12/13/24 T.A 112

Chief symptoms

T.A 113
Ivx and Rx

IVx
 US
 Contrast enema
 CA19.9

Rx
 Periampullary---whipple’s operation
 Total pancreticoectomy
 Palliative radio therapy

12/13/24 T.A 114

4. Cystic neoplasm of pancreas

T.A 115
 Comparison of cystic neoplasm
from psuedocyst

12/13/24 T.A 116

….

12/13/24 T.A 117

…….

12/13/24 T.A 118

……

12/13/24 T.A 119

Treatment of psuedocyst
 If < 6 cm in size observe
 If > 6cm in size drain
 Internally as
 Cystoduodunotomy
 Cystogastrotomy
 Cystojejunostomy ---the preferred procudrer
 Externally to the out side environment
 Cystoectomy is not possible b/c it can aggravate the pancreatic
enzyme release and severe

12/13/24 T.A 120

6. Cystic fibrosis

12/13/24 T.A 121

…..

12/13/24 T.A 122

123
Pancreatic ascites
 Accumulation of enzyme rich pancreatic exudate w/c
is non infected protein reach > 25g/l in the peritoneal
cavity
 Cause include
 Acute pancreatitis
 Chronic pancreatitis
 Trauma
 Rupture psuedocyst

12/13/24 T.A 124

Pathology
Disruption of ductal system followed by spread of
enzyme rich fluid
Anteriorly -----ascites
Posteriorly-----plural effusion
Gross abdomenal distension
Shifting dullness
Breathlessness due to plural effusion
Dxed by CT US and ERCG
Serial tapping with parenteral nutrition and albumin
administration b/c of associated with
Hypoalbuminemia
12/13/24 T.A 125
8. Stricture of the CBD
 80% are post operative stricture for GS and 20%
inflamatory
 Slowly progressive painless jaundice acount1-2 % of
OBJ
 Can be
 Post traumatic
 Types
 Type 1---- low CBD stump> 2 cm
 Type 2-----middle CBD <2 cm
 Type 3-----hailer confluent R and L intact
 Type 4---- R and left duct separated
 Type 5----- involvement of the intrahepatic duct
 Post inflamatory
 Malignant stricture
12/13/24 T.A 126
……..

T.A 127
Clinical feature
 Slowly progressive painless jaundice
 Hx of previous surgery
 Hepatomegaly due to back pressure
 Recurrent cholangitis due to bile stasis

 IVX
 USG
 T-tube
 ERCG
 MRCG

 Treatment
 Choledochojejnostomy
 Hepatojejnostomy
12/13/24 T.A 128
9 . Sclerosing cholangitis
 Multiple stricture and dilatation of the CBD with the feature of fibrous
ticking of CBD
 Primary
 Unknown cause
 Secondary
 Stone injury
 May complicated to biliary cirrhoses obstruction or Cholangicarcinoma
 ERCG is the best treatment in acute case b/c of pain and it is also used
to
 Place stent
 Remove stone
 Sphincteroectomy

12/13/24 T.A 129

 10. Choledochal cyst
 Congenital cyst occuring in the CBD due to partial
or complete weakness of the wall of the CBD

12/13/24 T.A 130

…..

12/13/24 T.A 131

12/13/24 T.A 132
12/13/24 T.A 133
11. Infectious cause
 Ascaris ----cause pnemobilli so should be removed
rather than drug b/c the dead parasite blocks the CBD
 Cloches

12/13/24 T.A 134

12. Mizzi syndrome
 The presence of stone in the cystic
duct or GB neck causes inflammation
and obstruction of CBD.

12/13/24 T.A 135

Pre-op preparation
 Ryle’s tube gastric decompression
 Administration of vit A 10mg sc/IM for 5-days before
surgery.
 Serum electrolyte should be determine
 Blood should be prepared.
 Keep NPO overnight
 Anti acid and antiemetic's should be given
 Catheterization
 Ab prophylaxis before 30 minute of operation
because this is a clean contaminated wound.
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Postoperative care
 Vital sign every 15 minute for the 1st two hrs.
 Follow anyearly sign of complication.
 Monitor the urine out put.
 Analgesics
 Mentainance fluid till the pt take PO

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 Thank you!!!

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