this is a presentation on how to approach a clinical case of obstructive jaundice, with emphasis on detailed clinical history taking, etiology, clinical examination, investigations necessary for jaundice like liver function test including varous parameters like total, indirect and direct billirubin,alkaline phosphatase ,serum proteins, coagulation profile, complete blood count, lipid profile, radiologicall investigations like ultrasound abdomen, contrast enhanced computed tomography, magnetic resonace imaging abdomen, magnetic resonance cholangio pancratogram, endoscopic cholangio pancratogram and the various treatment modalities available.
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
23. Benjamin s Classification
TYPES OF BILIARY OBSTRUCTION
Complete obstruction
Intermittent obstruction
Chronic incomplete obstruction
Segmental obstruction
24. Type 1
Complete obstruction
Primary or secondary liver tumors
Pancreatic tumors
Cholangiocarcinoma
Iatrogenic ligation of CBD
28. BILIARY OBSTRUCTION
INTRINSIC
Calculi
Acute Cholangitis
Biliary Strictures
Sclerosing Cholangitis
Parasites
Haemobilia
Benign Biliary Tumours
Cholangiocarcinoma ,Carcinoma of
ampulla of vater and Periampullary tumours
29. BILIARY OBSTRUCTION
EXTRINSIC
Mirizzi syndrome
Pancreatitis- acute and chronic
Pancreatic pseudocyst
Carcinoma of gall bladder ,pancreas
Cystic tumours of pancreas
Metastatic carcinoma
Hepatocellular carcinoma
30. 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
31. 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).
33. 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
35. 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
36. 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.
37. 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%