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Approach to Obstructive
jaundice
DR Dhivya
 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 %
 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
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
 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
 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
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
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
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
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
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
ALKALINE PHOSPHATSE
 Most sensitive indicator
 Factor responsible are
 Biliary component regurgitation
 Increase in hepatic synthesis
HISTORY
 Jaundice- onset, course, itching
 Pain
 Pyrexia
 Weight loss
 Dark urine and clay coloured stools
 Travel to endemic area
 History of abdominal operation
 Drug intake ie ATT
 History of injection in preceding six
months
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
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
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.
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)
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
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
obstructive jaundice.pptx
obstructive jaundice.pptx
Benjamin s Classification
 TYPES OF BILIARY OBSTRUCTION
 Complete obstruction
 Intermittent obstruction
 Chronic incomplete obstruction
 Segmental obstruction
Type 1
 Complete obstruction
 Primary or secondary liver tumors
 Pancreatic tumors
 Cholangiocarcinoma
 Iatrogenic ligation of CBD
Type 2
 INTERMITTENT OBSTRUCTION
 CBD stones
 Periampullary tumours
 Duodenal diverticulum
 Choledochal cyst
 Biliary parasites
 hemobilia
Type 3
 CHRONIC INCOMPLETE
OBSTRUCTION
 Strictures of CBD
 Stenosis of biliary-enteric anastamosis
 Chronic pancreatitis
 Cystic fibrosis
 Sphincter of oddi stenosis
Type 4
 SEGMENTAL OBSTRUCTION
 Traumatic
 Intrahepatic stones
 Sclerosing cholangitis
 Cholangiocarcinoma
BILIARY OBSTRUCTION
INTRINSIC
 Calculi
 Acute Cholangitis
 Biliary Strictures
 Sclerosing Cholangitis
 Parasites
 Haemobilia
 Benign Biliary Tumours
 Cholangiocarcinoma ,Carcinoma of
ampulla of vater and Periampullary tumours
BILIARY OBSTRUCTION
EXTRINSIC
 Mirizzi syndrome
 Pancreatitis- acute and chronic
 Pancreatic pseudocyst
 Carcinoma of gall bladder ,pancreas
 Cystic tumours of pancreas
 Metastatic carcinoma
 Hepatocellular carcinoma
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
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).
obstructive jaundice.pptx
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
obstructive jaundice.pptx
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
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.
 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%
obstructive jaundice.pptx
obstructive jaundice.pptx
obstructive jaundice.pptx
obstructive jaundice.pptx
obstructive jaundice.pptx

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obstructive jaundice.pptx

  • 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
  • 25. Type 2  INTERMITTENT OBSTRUCTION  CBD stones  Periampullary tumours  Duodenal diverticulum  Choledochal cyst  Biliary parasites  hemobilia
  • 26. Type 3  CHRONIC INCOMPLETE OBSTRUCTION  Strictures of CBD  Stenosis of biliary-enteric anastamosis  Chronic pancreatitis  Cystic fibrosis  Sphincter of oddi stenosis
  • 27. Type 4  SEGMENTAL OBSTRUCTION  Traumatic  Intrahepatic stones  Sclerosing cholangitis  Cholangiocarcinoma
  • 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%