1.
Approach to Obstructive
jaundice
DR Dhivya

2.
 Failure of normal amount of bile to
reach intestine due to mechanical
obstruction of the extra hepatic biliary
tree or within the porta hepatis
 Total serum bilirubin is 0.3-1.2 mg/dl
 With conjugated bilirubin<15 %

3.
 Total bile flow-600ml/day(500-
1000ml/day)
 Hepatocyte component is -450ml/day
 bile salt dependent due to biliary
glutathione and ductular bicarbonate
secretion
 Cholangiocyte component-150ml/day
 It depends on secretin stimulation

4.
PHYSIOLOGY OF
OBSTRUCTION
 Normal secretory pressure of bile is
15-25 cm of water
 At 35 cm of water there is suppression
of bile flow
 High pressure leads to
cholangiovenous and
cholangiolymphatic reflux of bile
 Dilatation of bile duct and intra hepatic
biliary radicals(IHBR)
 IHBR dilatation may be absent if there
is secondary hepatic fibrosis or

5.
 Increase in biliary pressure leads to
 Disruption of tight junctions between
hepatocytes and bile duct cells with
increased permeability
 Reflux of bile contents in liver sinusoids
 Neutrophil infiltration,increased
fibrinogenesis and deposition of reticulin
fiberes in portal triad

6.
 Reticulin fibers gets converted in to type 1
collagen
 Laying down of collagen fibers leads to
hepatic fibrosis obstruction of sinusoids and
secondary biliary cirrhosis and portal
hypertension
 Fibrosis can also lead to atrophy of
obstructed liver

7.
CHANGES IN LIVER BLOOD
FLOW
 Acute obstruction
 increase in hepatic arterial blood flow
 No change in portal venous blood flow
 Chronic obstruction
 Decrease in total liver blood flow ,
dilatation of sinusoids and elevation of
portal pressure

8.
CARDIOVASCULAR
EFFECTS
 Decreased cardiac contractability
 Reduced left ventricular pressure
 Impaired response to beta agonist drug
 Decreased peripheral vascular resistance
 Bradycardia due to direct effect of bile salts
on SA node.
 Hypotension and more prone to
postoperative shock

9.
COAGULATION FACTOR
DEFECTS
 Prolongation of Prothrombin time
 Loss of calcium
 Endotoxin induced damage to factor XI XII
platelets
 Low grade DIC with increased fibrin
degradation products
 Thrombocytopenia from hypersplenism
 Decreased absroption of fat solube vitamins
A,D,E,K

10.
ITCHING
 Retained bile salts
 Levels does not correlete well
 Itching disappears in terminal liver
failure but bile salt level still increased
 Other theory -Due to endogenous
opiate peptides
 Induces opiod receptor mediated
scratching activity of central origin

11.
Mechanism of
hyperbilirubinemia
 Rise by 25-43 micromol/litre/day
 Biliary venous & biliary regurgitation of
conjugated bilirubin due to disruption of
tight intracellular junction
 Trans hepatocytic regurgitation due to
reversal of the secretory polarity of
hepatocytes
 Rupture of dilated canaliculi in to sinusoids
due to necrosis of hepatocytes

12.
ALKALINE PHOSPHATSE
 Most sensitive indicator
 Factor responsible are
 Biliary component regurgitation
 Increase in hepatic synthesis

13.
HISTORY
 Jaundice- onset, course, itching
 Pain
 Pyrexia
 Weight loss
 Dark urine and clay coloured stools

14.
 Travel to endemic area
 History of abdominal operation
 Drug intake ie ATT
 History of injection in preceding six
months

15.
GENERAL EXAMINATION
 Age
 Anaemia - hemolysis, cancer , cirrhosis
 Gross weight loss-malignancy
 Hunched up position-chronic pancreatitis or
ca pancreas
 Skin changes-Bruising,purpuric
spots,spider naevi,palmar erythema,white
nails
 loss of secondary sexual characters

16.
ABDOMINAL EXAMINATION
 Dilated peri umbilical veins
 Ascitis
 Courvoisier’s Law
 Exceptions
 Double impaction of stones
 Impaction of pancreatic calculus at ampulla
of vater
 Mirizzi syndrome

17.
BIOCHEMICAL
INVESTIGATIONS
 Routine investigations
 ALP levels are elevated in nearly 100 % of
patients with extra hepatic obstruction
except in some cases of intermittent
obstruction.
 Values usually greater than 3 times the
upper limit and can exceed 5 times the
upper limit.
 An elevation less than 3 times the upper
limit is against complete extra hepatic
obstruction.

18.
ALT/AST
 hepato cellular damage.
 ALT found primarily in the liver, where as
AST also found in heart ,kidney, skeletal
muscle and brain
 AST is less specific for liver function
 ALT can confirm the hepatic origin of the
less specific but more sensitive AST.
 In extra hepatic obstruction usually AST
levels are not elevated(< 10 times the upper
reference limit)

19.
GGTP
 Correlates with ALP level
 Most sensitive indicator of biliary tract
disease
 Better indicator of obstruction in children –
levels are independent of age
 Helpful in the diagnosis of acute biliary tract
obstruction in contrast to ALP because ALP
lags behind the onset of obstruction

20.
5- NUCLEOTIDASE
 The principal value is to confirm the hepatic
origin of an elevated ALP
 This is particularly helpful in children,
pregnant women and patients who may
have bone disease resulting in rise of ALP
 It is more useful than ALP/GGTP in
detecting hepatic metastasis

21.
Benjamin s Classification
 TYPES OF BILIARY OBSTRUCTION
 Complete obstruction
 Intermittent obstruction
 Chronic incomplete obstruction
 Segmental obstruction

22.
Type 1
 Complete obstruction
 Primary or secondary liver tumors
 Pancreatic tumors
 Cholangiocarcinoma
 Iatrogenic ligation of CBD

23.
Type 2
 INTERMITTENT OBSTRUCTION
 CBD stones
 Periampullary tumours
 Duodenal diverticulum
 Choledochal cyst
 Biliary parasites
 hemobilia

24.
Type 3
 CHRONIC INCOMPLETE
OBSTRUCTION
 Strictures of CBD
 Stenosis of biliary-enteric anastamosis
 Chronic pancreatitis
 Cystic fibrosis
 Sphincter of oddi stenosis

25.
Type 4
 SEGMENTAL OBSTRUCTION
 Traumatic
 Intrahepatic stones
 Sclerosing cholangitis
 Cholangiocarcinoma

26.
BILIARY OBSTRUCTION
INTRINSIC
 Calculi
 Acute Cholangitis
 Biliary Strictures
 Sclerosing Cholangitis
 Parasites
 Haemobilia
 Benign Biliary Tumours
 Cholangiocarcinoma ,Carcinoma of
ampulla of vater and Periampullary tumours

27.
BILIARY OBSTRUCTION
EXTRINSIC
 Mirizzi syndrome
 Pancreatitis- acute and chronic
 Pancreatic pseudocyst
 Carcinoma of gall bladder ,pancreas
 Cystic tumours of pancreas
 Metastatic carcinoma
 Hepatocellular carcinoma

28.
CONGENITAL AND GENETIC
DISORDERS
 Biliary atresia
 Choledocal cyst
 Caroli’s disease
 Progressive familial intra hepatic
cholestasis
 Primary biliary cirrhosis
 Alpha 1 antitrypsin defeciency
 Tyrosinemia
 Neonatal hepatitis
 Wilson disease
 dyskinesia of sphincter of odi

29.
IMAGING
 GOALS
 To confirm the presence of an extrahepatic
obstruction
 To determine the level of the obstruction, to
identify the specific cause of the obstruction
 To provide additional information relating to
the underlying diagnosis (eg., Staging in
case of malignancy).

30.
Ultrasound
 initial screening test
 high specificity (>98%) and sensitivity
(>95%) for the diagnosis of
cholelithiasis
 Dilation of the extrahepatic (>10 mm)
or intrahepatic (>4 mm) bile ducts
suggests biliary obstruction

31.
MRCP
 Fluid found in the biliary tree is hyper
intense on T2-weighted images
 determine the extent and type of
tumor
 detect malignant hilar and perihilar
obstruction
 Absolute contraindications

32.
EUS
 Higher-frequency ultrasonic waves
compared to traditional US (3.5 mhz vs 20
mhz)
 98% diagnostic accuracy in obstructive
jaundice
 sensitivity of EUS for focal mass lesions in
pancreas has been reported to be superior
to that of CT particularly for tumors smaller
than 3 cm in diameter.

33.
 Compared to MRCP for the diagnosis of
biliary stricture, EUS is more specific (100%
vs 76%) and has a greater positive
predictive value (100% vs 25%) although
the two have equal sensitivity (67%)
 The positive yield of eus-fna for cytology in
malignant obstruction has been reported to
be as high as 96%