Obstruction jaundice and pathology of jaundice and symptoms

Obstruction jaundice

3. Anatomy of the biliary tree
Physiology of bile formation
Pathophysiology of jaundice
Etiology
Clinical features
Diagnostic investigations
Treatment modalities

7. INTRAHEPATICBILE DUCTS
Anterior superior lobe duct
Anterior inferior lobe duct Anterior
segmental duct
Posterior superior duct
Posterior inferior duct Posterior
segmental duct
Right caudate lobe duct
RIGHT HEPATIC DUCT

8. Lateral superior lobe duct
Lateral inferior lobe duct Lateral
segmental duct
Medial superior lobe duct
Medial inferior lobe duct Medial
segmental duct
Left caudate lobe duct
LEFT HEPATIC DUCT

10. Common Hepatic Duct
•Formed 0.25 –2.5cm from the surface of liver
•1.5 –3.5cm long
Cystic Duct
•2 –4 cm long, 3mm diameter
•Variable cystohepatic junction

11. Fundus
Body
Infundibulum
Hartmann’s pouch
Neck

12. 5 –16 cm in Length
Four parts
•Supraduodenal
•Retroduodenal
•Pancreatic
•Intra duodenal

13. BOUNDARIES
Right-cystic duct
Left –common hepatic duct
Superiorly-inferior margin of right lobe of liver
CONTENTS
Right hepatic artery
Cystic artery
Lymph node of lund
Abberantor accessory bile duct

15. 500-1000ml per day
Secreted in 2 phases
Hepatocytes-rich in bile acids, cholesterol,
other organic constituents
Ductalepithelial cells-mainly watery solution
of sodium and bicarbonate ions.

19. Normal volume: 30-60 ml
Functions as a reservoir storing as much as
12hours of bile
Absorption of sodium by active transport
Absorption of chloride, water by secondary
diffusion
Bile is concentrated 5 –20 fold

20. LIVERBILEGALL BLADDER
BILE
WATER 97.5 g/dl 92 g/dl
BILE SALTS 1.1 g/dl 6 g/dl
BILIRUBIN 0.04 g/dl 0.3g/dl
CHOLESTEROL 0.1 g/dl 0.3 -0.9 g/dl
FATTY ACIDS 0.12 g/dl 0.3 -1.2 g/dl
LECITHIN 0.04 g/dl 0.3 g/dl
SODIUM 145.04 mEq/L 130 mEq/L
POTASSIUM 5 mEq/L 12 mEq/L
CALCIUM 5 mEq/L 23 mEq/L
CHLORIDE 100 mEq/L 25 mEq/L
BICARBONATE 28 mEq/L 10 mEq/L

23. Parenchymalsecretion-BILE ACIDS
Secretion by the ductalepithelial cells-
SECRETIN
Emptying of gall bladder-
CHOLECYSTOKININ , Vagalstimulation

24. Functions-
›Emulsification of fat particles in food and
facilitate the function of lipases
›Absorption of digested fat through the intestinal
mucosa
›Excretion of waste ( Cholesterol, Bilirubin)

26. Conjugated hyperbilirubinemiaoccurs
Levels increase by 25-45 micromol/L/day
Normal secretorypressures in the biliary tree
–15-25cm H
2O
At pressures above 35cm of H
2O the bile flow
is suppressed

27. Obstruction to outflow of bile
Increased pressure within biliary tree
Loss of hepatocyte polarity
Disruption of tight junctions between hepatocytes and
bile duct cells
Hepatocyte necrosis
Rupture of dilated biliary canaliculiinto hepatic
sinusoids
Cholangiovenousand cholangiolymphaticreflux

28. Bile Reflux
NeutrophilInfiltration
Increased Fibrinogenesis
Reticular FibreDeposition In Portal Triad
Collagen Type 1 Deposition
Hepatic Fibrosis
Obstruction Of Sinusoids
Secondary Biliary Cirrhosis
Portal Hypertension

29. BILIRUBIN LEVELS PLATEAU IN
CHRONIC CASES
Increased excretion of bile pigments other than
bilirubin by the kidney, which do not give the
diazoreaction
Increased levels of conjugated bilirubinsleads to
binding with albumin by covalent bonds forming
DELTA BILIRUBIN which is not measurable by
routine techniques

30. On CVS-
•Bile salts act on SA node-bradycardia
•Decreased cardiac contractility
•Decreased left ventricular pressures
•Decreases peripheral vascular resistance
Overall there is hypotension and
exaggerated hypotensiveresponse to blood
loss. Patient is thus more prone to shock
intraoperatively

31. Decreased cardiac function
Hypovolemia
Bile salts causing increased PGE2 levels
Endotoxemia
Renal vasoconstriction
Shunting of blood from renal cortex
Complement activation in glomeruli
RENAL FAILURE

32. COAGULATION ABNORMALITIES
•Increased prothrombintime
•Decreased absorption of fat soluble vitamins A, D, E,
K
•Endotoxininduced alteration in coagulation factors XI,
XII, platelets

33. ITCHING
•Due to increased bile salts, but levels poorly correlate
•May be due to endogenous opiate peptides which
cause central opioidmediated scatchingactivity
POOR WOUND HEALING
•Due to decreased propylhydroxylaseenzyme in skin
leading to formation of defective collagen
•Increased risk of wound dehiscence

35. Type 1 ( complete
obstruction)
•Primary or secondary liver
tumors
•Iatrogenic ligation of CBD
•Pancreatic tumors,
cholangiocarcinoma
Type 2 ( intermittent
obstruction)
•Choledocholithiasis
•Periampullarytumor
•Choledochalcyst
•Bile duct papilloma
•Hemobilia
•Duodenal diverticula
Type 3 ( chronic
complete obstruction)
•Bile duct stricture
•Biliary atresia
•Post radiotherapy
•Chronic pancreatitis
•Cystic fibrosis
Type 4 ( segmental
obstruction)
•Sclerosingcholangitis
•Traumatic
•Hepatolithisis

36. INTRINSIC PATHOLOGY
Choledocholithiasis
Acute Cholangitis
Biliary Strictures
Primary SclerosingCholangitis
Parasites
Haemobilia
Intra ductalpapillomas
Cholangiocarcinoma
Periampullarytumours

37. EXTRINSIC PATHOLOGY
Mirizzisyndrome
Pancreatitis ( acute and chronic)
Pancreatic pseudocyst
Carcinoma of gall bladder
Carcinoma of pancreas
Cystic tumours of pancreas
Metastatic carcinoma
Hepatocellularcarcinoma

38. CONGENITAL AND GENETIC DISORDERS
Biliary atresia
Choledochalcyst
Caroli’sdisease
Primary biliary cirrhosis
Alpha 1 antitrypsin deficiency
Tyrosinemia
Neonatal hepatitis
Wilson disease
Dyskinesiaof sphincter of Oddi

40. Icterus
Pruritus
Pale, acholicstools
Steatorrhoea
High colouredurine
Fever
Loss of weight
Loss of appetite
Pain in right
hypochondrium
Palpable gall bladder
Charcotstriad
Lump in abdomen

42. Routine blood investigations
Serum bilirubin
Serum albumin
Albumin: globulin ( A:G) ratio
Prothrombintime
Serum Alkaline Phosphatase(ALP)
SGOT/ AST
SGPT/ ALT
Gamma GlutamylTransferase(GGT)
5’-Nucleotidase

43. Normal levels-44 to 147 IU/L
Raised in all cases of biliary obstruction
except in intermittent obstruction
Raise by atleast3 times the upper limit is
diagnostic of biliary obstruction

44. Normal levels AST 5-40 IU/L
Normal level of ALT 7-56IU/L
Elevated levels are indicative of hepatocellulardamage.
AST is less specific but more sensitive for liver function.ALT
can confirm the hepatic origin of AST.
In extra hepatic obstruction usually AST levels are not
elevated(< 10 times the upper reference limit)

45. Most sensitive indicator of biliary tract
disease especially in children.
Helpful in the diagnosis of acute biliary tract
obstruction.
Correlates with ALP level but ALP levels take
longer duration to increase.

46. This is particularly helpful in children,
pregnant women and patients who may have
bone disease resulting in rise of ALP
Confirms the hepatic origin of ALP
It is more useful than ALP/GGTin detecting
hepatic metastasis

47. When suspecting malignancy
CA 19-9
Stool for occult blood

49. Most calculi in biliary tract are radioluscent
Seagull/ Benz sign may be seen
occasionally
Helps to exclude other causes of RUQpain

50. Sensitive, inexpensive, but operator dependent
Able to identify calculousdisease accurately
Finding of dilated bile duct (>8mm) in setting of
jaundice suggests obstruction to the biliary tract
Also malignant lesions such as carcinoma GB,
cholangiocarcinomamay be identified

51. Assesmentof distal bile duct and the
ampulla
Assesmentof vascular invasion by the
tumors
Radial echoendoscope-for tomographic
evaluation
Linear echoendoscopefor guiding
interventions

52. Triple phase CT is especially useful
Provides superior anatomical detail on the
biliary tree as well as other abdominal
organs
Important especially in preoperative planning

53. Invasive test
Useful in imaging the biliary and pancreatic
ducts
Diagnostic and therapeutic in most benign
biliary conditions
Able to provide tissue samples in malignant
condtions
Complication rate upto10%
oCholangitis
oPancreatitis
oDuodenal injury of perforation
oSphincter stenosis

54. Non invasive modality to image biliary and pancreatic
ducts.
Technique uses the fluid present in the biliary and
pancreatic ducts as a contrast agent highlighting them in
heavily T2 weighted sequences.
Provides multiplanar3D reconstructions.
Only diagnostic.
Indicated in cases where ERCPis not feasible.

55. Biliary scintigraphy
Radioisotope such as Tc
99
labelledHIDA,
PIPIDA, BRIDAare used
These are actively taken up by hepatocytes
and also secreted into the biliary canaliculi
Failure to fill the gall bladder within 2hrs of
administration indicates obstruction in the
tract
CCKenhanced emptying of gall bladder may
also be demonstrated

57. INDICATIONS
Abnormal LFT
Anomalous biliary anatomy
Inability to perform ERCP
Dilated biliary tree
Pre operative suspicion of CBDstones

58. PERCUTANEOUS TRANSHEPATIC
CHOLANGIOGRAPHY
Indications-
Failure of ERCP
High biliary strictures
Klatskintumor
Can be used in severe obstructive jaundice to
also decompress the dilated biliary tree

60. Correction of fluid and electrolyte imbalance
InjvitK, fresh frozen plasma
Lactulose, oral neomycin
Mannitol
Broad spectrum antibiotics
Decompression of biliary tree
Management of the cause of obstruction

61. Inflammatory obliteration of intrahepaticand
extrahepaticbiliary ducts
Associated with splenicabnormalities, absent IVC,
intestinal malformation.
ETIOLOGY
•Immune mediated inflammatory reaction
•Viral insult
•HLA-B12 association
•CFC1 gene mutation

63. CLINICAL FEATURES
Jaundice-persisting
beyond 14days age
Pale stools
Dark urine
Failure to thrive
Hepatomegaly
Ascitis
INVESTIGATIONS
Liver function tests
TORCH screening
Ultrasound
HIDAscan
MRCP
ERCP
LIVER BIOPSY

66. Roux -en-y hepato-
portoenterostomy
Does not cure
Delays need for a liver
transplant by atleast10yrs

68. Cystic dilatation of biliary tract
Associated with –intestinal atresia, imperforate
anus, pancreatic AVM, pancreatic divisum
2 theories-Pancreatobiliaryreflux
-Functional obstruction to CBD
Clinical features-palpable RUQmass, jaundice,
pain, fever, nausea and vomiting

70. Complications-cholangitis, pancreatitis, cyst
rupture, biliary peritonitis
Premalignant condition
Investigations-
•Ultrasound
•HIDA
•CECT
•ERCP/ MRCP

73. Treatment-
•Excision of cyst
•Reconstruction with roux-en-y
hepaticojejunostomy
•Enucleationof cyst

74. Supersaturationof secreted bile(lithogenicbile)
Concentration of bile in GB
Crystal nucleation
Gall bladder dysmotility
Stone formation

75. Types of stones
Pure cholesterol stones (cholesterol solitaire)-
usually single, rare (6%)
Pigment stones-green or black coloured, usually
multiple, tiny, seen in hemolytic conditions
Mixed-90% of the gall bladder stones, multiple,
composed of cholesterol, calcium phosphates,
carbonates, palmitates. Characteristically multi-
faceted.

76. CBDstones ( CHOLEDOCHOLITHIASIS )
TYPES-
PRIMARY-formed de novo in the bile duct.
Brown stones are common and usually
multiple
SECONDARY-stones formed in the gall
bladder and pass into the bile ducts

77. Asymptomatic
Biliary colic
Obstructive jaundice
Acute/ chronic cholecystitis, cholangitis
CharcotsTriad
Reynold’sPentad
COMPLICATIONS
•Empyemagall bladder
•Mucocele/ limey gall bladder
•Perforation, biliary peritonitis
•Carcinoma gall bladder

78. USG-dilated bile duct >8mm in setting of
jaundice
ERCP-
›Cholangitis
›Biliary pancreatitis
›Limited expertise with CBDexploration
›Morbid patient
MRCP-

79. ERCP-sphincterotomy
Laparoscopic CBDexploration
Open CBDexploration
›Transduodenalsphincteroplasty
›Choledochoduodenostomy
›Roux en y choledochojejunostomy
Percutaneousdrainage and stone extraction

80. Compression of Common hepatic or common
bile duct by a stone impacted in the cystic
duct or hartmanspouch leading to formation
of cholecysto-choledochalfistula.
Often a large cholesterol solitaire
Classification ( csendes)

81. Type 1-extrinsic compression of CBD
Type 2-stone eroding through less than
1/3
rd
the circumference of CBD
Type 3-Fistula involving upto2/3
rd
the
circumference of CBD
Type 4-Cholecystocholedochalfistula with
destruction of the CBD

82. Usually diagnosed on CT or intraoperatively
Cholecystectomy( partial or complete) with
intra operative cholangiogram, and T-tube
insertion.
Reconstruction with hepaticojejunostomy
may be required in type 4

84. Autoimmune process involving intra and extra
hepatic biliary tree
Associated with riedlesthyroiditis, ulcerative
colitis
Inflammation, scarring of bile ducts causing
progressive cholestasis
Elevated ALP, p ANCA
ERCP-diffuse multifocal dilatations and
stricturresof the biliary tree
Biopsy-onion skin concentric periductalfibrosis

85. Cholereticagents-USDA
Antifibrogenicagents-colchicine
Balloon dilatation of dominant strictures
Biliary reconstruction
Orthotopicliver transplantation

86. Post operative
Inflammatory
›CBDstones
›Parasites
›PSC
Malignant

88. Intra operative cholangiogram
ERCP-Balloon dilatation and stenting
Choledochoduodenostomy/ jejunostomy
Roux en y heapaticojejunostomy

89. Risk factors-
PSC
Choledochalcyst
Hepatolithiasis
Hepatitis B and C
Lynch sydromeII
Clonorchissinensisinfestation
Multiple biliary papillomatosis
Thorotrast, nitrosamines, dioxin
Previous biliary enteric anastomosis

90. Based on location of tumor
Proximal lesions-perihilar(klatskintumor),
intrahepatic
Lesions in the middle third
Distal lesions-periampullarycarcinoma
Based on pathologic subtypes
Sclerosing
Nodular
Papillary

95. INVESTIGATIONS
Triple phase CT-assesmentof resectability,
preoperative planning, metastases.
Cholangiography-to determine the proximal
extent of resection
Tissue diagnosis-only important in patients
with unresectabledisease

96. R0 resection is the only strategy that affords
possibility of cure
Contraindications for resection
Bilobarintrahepaticmetastases
Extrahepaticdisease
Encasement of the portal vein
Bilateral hepatic lobar artery involvement
Lobar atrophy with contralateralportal vein or
biliary radical involvement

97. Distal lesions-pancreatico-duodenectomy
Proximal lesions-en bloc resection of common
bile duct with hepatic parenchyma and regional
nodal tissue
Type 1-common duct resection , cholecystectomy, 5-
10mm margin
Type 2-partial hepatic resection including the
caudate lobe
Types 3 and 4-complex resection up to secondary
biliary radicals, and reconstruction of hepatic artery,
portal vein
Biliary drainage is provided by Roux en Y
hepaticojejunostomy, transanastomoticstenting

98. Endoscopic or percutaneousdrainage
according to site of lesion
Analgesia
IV narcotics
Percutaneousablation of celiac plexus
Endoscopic duodenal stenting

99. RISK FACTORS-
Chronic inflammatory conditions
Gall stones larger than 3cm
Choledochalcyst
PSC
Porcelain gall bladder
Gall bladder polyp larger than 10mm

101. USG-irregularly thickened gall bladder wall ,
polyp >10mm size, heterogenousmass in
gall bladder
TriphasicCT-to delineate hepatic artery and
portal venous involvement

102. Pre operative suspicion-
Extended liver resections, including segments IV, V,
VIII
Right trisegmentectomy
Following cholecystectomy
›T1b lesion-extended cholecystectomyincluding
draining nodal basins, cystic duct, excision of CBD
with Roux en y reconstruction
›T2 lesions-radical cholecystectomy

103. Carcinoma head of pancreas or
periampullary-Whipplesoperation, ERCP
stenting
Parasites-Endoscopic removal
Intra ductalpapillomas-wide local excision
and reconstruction