This document provides information on obstructive jaundice, including its definition, relevant anatomy, physiology, pathophysiology, causes, clinical presentation, and approach to patients. Obstructive jaundice is caused by cholestasis or obstruction of the biliary tree, leading to conjugated hyperbilirubinemia. The biliary tree has significant anatomical variations that surgeons must be aware of. Clinical features may include jaundice, abdominal pain, weight loss, fever, and more, depending on the underlying cause which can include gallstones, tumors, strictures, or other conditions. A thorough history and physical exam is important to evaluate obstructive jaundice.

1. OBSTRUCTIVE JAUNDICE

2. • Conjugated Hyperbilirubinemia
• Surgical jaundice
• Obstructive jaundice
DEFINATION
 Occur due to cholestasis or obstruction of
biliary tree.
SYNONYMS

3. RELEVANT SURGICAL ANATOMY

5. • Wide number of anatomical variation in extrahepatic biliary tree and in
the adjacent hepatic artery and portal vein.
• Variation are so frequent that surgeons should acquainted with their
range and should always expect unusual .

6. • Normal length 3 cm
• Normal diameter 1 – 3 mm
CYSTIC DUCT
 It joins the common hepatic duct in it’s
supraduodenal segment in 80 % cases
and form the common bile duct

8. • in some cases cystic duct is
obliterated as in cholelithiasis or
cholecystitis

9. •Normal length < 2.5 cm
•Formed by union of right and left hepatic duct
•Anatomical variation in confluence of hepatic
ducts
COMMON HEPATIC DUCT

11. • Normal length 7.5 cm
• Normal diameter3 – 7 mm
COMMON BILE DUCT

12. BLOOD SUPPLY OF THE BILIARY TREE

13. ARTERIAL ANOMALIES

15. CALOT’S TRIANGLE

16. • Blood supply runs along the sides of common bile duct
• Transaction of bile duct leads to ischemia of upper part which is
responsible for remarkable scarring and retraction of stricture in to
hilum
VASCULAR SUPPLY OF COMMON BILE
DUCT

17. • Composition of liver bile
• 97 % water
• 1-2 % bile salts
• 1 % pigments , cholesterol , fatty acids
• Bile is excreted at rate of 40 ml / hr
PHYSIOLOGY OF BILE

18. • Yellow red pigment, organic ion(c33, H36O6N 4)
METABOLISM OF BILIRUBIN

19. •Unconjugated bilirubin
•Lipid soluble
•Non polar pigment
•High affinity for albumin
•It binds with albumin and transported to liver through
hepatic or portal circulation
•Hepatic metabolism occurs in three phases

22. • Maximum renal excretion of bilirubin
220 mg / day
• Platue level of S bilirubin in obs. jaundice 25 – 30 mg /dl
• Secretion of bile is controlled by cholecystokinin secreted by duodenal
mucosa in response to food

23. •Long standing biliary obstruction can result in
alteration of both hepatic and systemic functions
•Effects on hepatic and extrahepatic biliary tree
PATHOPHYSIOLOGY OF JAUNDICE

24. •Common bile duct dilation is frequent and associated
with
•bile plugging within canaliculi
•centrilobular bile stasis
•periductular extravasation of bile with reactive
edema
•infiltration of polymorphonuclear leucocytes
•bile duct proliferation with periportal and
intralobular fibrosis leading to biliary cirrhosis

25. RENAL FAILURE
• Incidence 10 %
• Mortality rate – 32 – 100 %
SYSTEMIC EFFECTS

26. Etiology of renal failure is multifocal
• Renal ischemia
• Prostaglandin mediated alteration in renal microcirculation
• Myocardial depression
• Reduction of intravascular volume
• sepsis

27. • Invasive monitoring of patient
• Adequate hydration prior to surgery
• Control of sepsis
• Administration of mannitol
• Pre- operative biliary drainage
PREVENTION OF RENAL FAILURE

28. • Cholangitis occur in presence of infected bile
• Endotoxemia occur due to alteration in host defence mechanism
•Absence of bile from git lead to altered phagocytic
function and changes in reticuloendothelial system
•Kupffer cell activity decreases inversely with
sytemic endotoxemia
SEPSIS

29. • E coli and Kleibsella
• Pseudomonas and enterobacter
• Bacteroides and clostridium
• Streptococcal viridans
COMMON ORGANISMS IN
CHOLANGITIS

30. • Pre opertative administration of sodium deoxycholate
• Antibiotics according to culture
PREVENTION & TREATMENT OF
SEPSIS

32. • Bleeding may result from hepatocellular dysfunction and vit k
deficiency
• Severe liver dysfunction leads to reduced synthesis of factor 2 , 7 , 9
,10 and hypoprothombinemia
BLEEDING

33. • Preop exogeneous vit k reverses coagulopathy partially
• Transfusion of FFP may be required
TREATMENT

34. CAUSES OF OBSTRUCTIVE JAUNDICE
OBS. JAUNDICE
WITHOUT MECH. OBSTRUCTION WITH MECH. OBSTRUCTION
ACUTE CHRONIC EXTRA-HEPATIC INTRA-HEPATIC
CHLORPROMAZIN
E
CHLORPROPRAMI
DE
VIRAL
CHOLESTASIS
PREGNANCY
CHOLESTASIS
PRIMARY BILIARY
CIRRHOSIS
PRIMARY
CHOLANGIOCARCI
NOMA
INTRA-HEPATIC
STONE

35. EXTRA - HEPATIC
IN LUMEN OUTSIDE WALL
IN WALL
CBD STONE
PRIMARY
CHOLANGIOCARCIN
OMA
PARASITES
STRICTURE
SCLEROSING
CHOLANGITIS
CHOLEDOCHAL CYST
BILIARY ATRESIA
AMPULLARY
STENOSIS
PERIAMPULLARY
CARCINOMA
CHRONIC
PANCREATITIS
LARGE PSEUDOCYST
LYMPH NODE

37. APPROACH TO PATIENT
AGE
CHILDREN ELDERLY
ADULT
CHOLEDOCHAL
CYST
BILIARY
ATRESIA
CBD STONE
CHRONIC
PANCREATITIS
PSEUDOCYST
PERIAMPULLAR
Y CARCINOMA
GB CARCINOMA
BILE DUCT
CARCINOMA

38. APPROACH TO PATIENT
SEX
MALE FEMALE
CBD STONE
CHOLEDOCHAL
CYST
CARCINOMA GB
PERIAMPULLARY
CARCINOMA
SCLEROSING
CHOLANGITIS
HEPATOMA

39. • In CBD stone – biliary colic
• In carcinoma – dull aching pain
• In chronic pancreatitis – boring type of continuous pain
• In sclerosing cholangitis – painless jaundice
• In biliary stricture – painless jaundice
ABDOMINAL PAIN

41. •Fluctuating course
• bile duct stone
• periampullary carcinoma
•Progressive jaundice
• biliary stricture
• sclerosing cholangitis
JAUNDICE

42. •Stool
• Acholic stool
• Occult blood may be present in stool
• Diarrhoea or steatorrhoea may be present
•Dark coloured urine
STOOL & URINE

43. •Biliary colic
•Chronic pancreatitis
•Cholecystitis
•Duodenal obstruction
NAUSEA & VOMITTING
 Carcinoma
 Chronic pancreatitis
ANOREXIA & WEIGHT LOSS

44. • Cholangitis
• Charcot’s Triad
• Raynaud’s Pentad
FEVER
LUMP IN ABDOMEN
 Courvoisier’s law

45. • Past history of obstructive jaundice in case of gallstone or CBD
stone
• P/H/O previous surgery
PAST HISTORY

46. • G B stone
• Ca pancreas
FAMILY HISTORY
 Chronic smoker
 Alcoholic
PERSONAL HISTORY

47. • Altered sensorium
• Malnutrition and wasting
• Vital signs
Temperature
Pulse
BP
GENERAL EXAMINATION

48. • Lump may be liver gall baldder or pancreas
• Xanthoma present in chronic biliary obstruction and in biliary cirrhosis
• Palpation
Murphy’s sign
Abdominal lump
• Per rectal examination
PER ABDOMINAL EXAMINATION