Obstructive Jaundice
M K Alam
MS; FRCS Ed
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Objectives
• Definition
• Anatomy of the hepatobiliary tree
• Biochemistry of bilirubin
• Types of Jaundice
• Causes of OBSTRUCTIVE Jaundice.
• Clinical presentation
• Laboratory investigations
• Radiological investigations
• Treatment options
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Definition of Jaundice
• Yellowish pigmentation of the skin and
other tissues (sclera, mucous membrane, deep tissue…)
due to deposition of bile pigment(bilirubin)
when serum level exceed 3mg/dl (50 µmol/L)
• Normal Total serum bilirubin is 0.3-1.9 mg/dl
Direct bilirubin < 0.4 mg/dl
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Anatomy of the hepatobiliary tree
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Bilirubin Biochemistry
• 80% of bilirubin is formed by the degradation
of Heme from RBC.
• The reminder Heme containing enzymes
(cytochromes, catalase, peroxidase..)
• Potentially toxic
• Remains harmless by binding to albumin
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Unconjugated Bilirubin
(indirect bilirubin)
• Insoluble in water
• Tightly complex to albumin
• Not filtered through renal glomeruli
• Not excreted in urine
• Toxic substance
• The main form of bilirubin in the blood
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Conjugated Bilirubin
(Direct bilirubin)
• Bilirubin conjugated in the liver before its excretion
into bile
• Conjugated with glucuronic acid
• Changes bilirubin into water soluble
• Can be filtered through renal glomeruli
• Present in low concentration in the blood
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Con’t
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Types of Jaundice
A. Pre-hepatic
B. Hepatic
C. Post-hepatic (Obstructive)
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Pre-hepatic
• Excess extra-hepatic production of
bilirubin raising unconjugated form.
Haemolytic anemias: congenital spherocytosis,
sickle cell disease
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Hepatic jaundice
Disability of liver to uptake/ conjugate bilirubin (hepatocellular),
or excrete bile from the liver (cholestatic)
Acute :
• Viral hepatitis A, B, C..
• Other viruses: EBV,
CMV
• Drugs
– Dose-dependant e.g.
paracetamol
– Idiosyncratic
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•
•
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Toxins
Autoimmune hepatitis
Alcoholic hepatitis
Tumours
Chronic :
• Viral hepatitis B, C
• Chronic AI hepatitis
• Genetic (Crigler–Najjar,
Gilbert syndroms)
• End-stage liver disease (of
any cause)
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–
–
–
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Alcoholic
Hepatitis B, C
Autoimmune
Haemochromatosis
Wilson’s disease
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Cholestatic jaundice
• Cholestasis denotes a pathologic condition of
impaired bile formation and or bile flow.
– Intrahepatic cholestasis (Intrahepatic biliary tree
diseases or hepatocellular secretory failure
– Extrahepatic cholestasis (biliary obstruction)
frequently is amenable to surgical correction.
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Consequences of Cholestasis
Retention of bile salt in liver
• Decreased hepatocyte function
• Decreased Kupffer cell activity
• Decreased albumin & clotting factors synthesis
• Decreased collagen synthesis, impaired wound healing
Retention of bile constituents in serum
• Jaundice, dark urine and pruritis
• CVS depression
• Nephrotoxicity
• Hypercholesterolemia, atheroma, Xanthoma
Consequences of Cholestasis
Absence of bile in Intestine
• Escape of endotoxins into portal blood
• Mal-absorption of fats and Vitamin A, D, E & K
• Clay colored stools
Intrahepatic cholestasis
• Cholestatic phase of AVH
• Alcoholic Hepatitis
• Drug induced liver disease
• Primary biliary cirrhosis
• Primary sclerosing cholangitis
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•
•
•
TPN
Cholestasis of pregnancy
Sepsis
Benign postoperative Cholestasis
Drugs that lead to Cholestasis
Jaundice
• Estrogen
• Tamoxifen
• Anabolic steroid
• Azathioprine
• Chlorpromazine
• Carbamazepine
• Antibiotics- Erythromycin, Rifampicin
Post hepatic
(Obstructive Jaundice)
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Benign
• Choledocholithiasis*
• Primary sclerosing cholangitis
• Post-surgical stricture
• Pancreatitis
• Parasitic infections
Malignant
• Carcinoma gall bladder
• Periampullary carcinoma
• Cholangiocarcinoma
• Carcinoma of the head of pancreas
• Obstruction due to metastatic LN
History
- Age, gender
- Pain / painless ,onset , duration
- Fever ,fatty dyspepsia
- Jaundice, dark urine, pale stool
- Alcohol, blood transfusion
- Medication , drug abuse
- Surgery(post op complication)
- Hemolytic disorders
- Weight loss, loss of appetite
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Clinical presentation
• RUQ pain/painless, nausea, vomiting, fever,
jaundice, dark urine , pale stool, pruritus
• Charcot triad: pain, jaundice, fever
• Reynold’s pentad: triad+ confusion, shock
• Skin xanthomas
• Symptoms of intestinal mal-absorption
• Deficiency of fat soluble vitamins
• Calculous obstruction: Younger patient,
intermittent abdominal pain, fatty dyspepsia,
fluctuant jaundice, dark urine, pale stool, pruritus
(bile salt deposits)
• Neoplasia: Older age, painless/ mild discomfort,
weight loss, progressive jaundice, dark urine, pale
stool, pruritus, Courvoisier sign, hepatomegaly
• Hepatocellular: Stigmata of CLD- liver palm, spider
naevi, gynecomastia, signs of PH (splenomegaly,
ascitis, caput medusae), hepatomegaly
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Courvoisier’s law/sign
If the CBD is obst. due to
calculus , the GB is usually
not distended owing to
previous inflammatory
fibrosis.
If CBD is obstr. due to
malignant growth, the GB
becomes distended in order
to reduce the press. in the
biliary system.
Laboratory Investigations
• Blood test (Hemoglobin, WBC, Platelets)?
• Coagulation Profile
• Hepatic profile
• Hepatitis profile
• Tumour marker
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Laboratory Investigations
Hepatic Profile:
AST
(10-40)
ALT
(10-40)
Alkaline phosphatase
(40-100 U/L)
Albumin
(35-50 g/L)
Total bilirubin
(5-20 umol/L)
Direct bilirubin
(<5 umol/L)
Indirect bilirubin
(<12 umol/L)
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Alkaline Phosphatase
• Liver, bone, placenta and intestine
Used mainly as indicator of ductal causes: partial
obstruction of bile ducts, primary biliary cirrhosis,
sclerosing cholangitis
• Elevated in all extra hepatic obstruction with values
greater 3-5 times the normal
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GGT
• Very sensitive for hepatobiliary diseases.
• Mainly it increases in ductal injury
• In case of increase in alkaline phosphatase GGT is a
good test to exclude the bone source of ALP
High Alkaline Phosph. Normal GGT  Bone source likely
High Alkaline Phosph . High GGT  Hepatic source likely
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AST & ALT
• AST (aspartate aminotransferase) : liver, cardiac
muscle, skeletal muscles, kidneys, brain, pancreas
• ALT (alanine aminotransferase) liver, skeletal muscle
• Used as indicator of liver cell injury
• ALT is more specific
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Haemolytic jaundice
• High unconjugated (indirect) serum bilirubin
• No bilirubin in urine
• Normal liver enzymes
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Obstructive jaundice
• Serum conjugated bilirubin
> 50% of total: more suggestive of post hepatic
than hepatic jaundice
• ALP 
• Transaminases: normal/ moderately
elevated
• Fecal urobilinogen:  -incomplete obstruction ,
absent - complete obstruction
• Urobilinogen in urine: absent in complete
obstructive jaundice with  bilirubinuria.
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Case Scenario
82-yr old, male
Presents with:
Progressive jaundice
Itching
Loss of weight .
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History of presenting illness
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Gradually progressive jaundice
Recurrent episodes of itching
White stools for 2 months
Dark yellow urine
Generalized weakness & fatigability- 6 months
Weight loss - 1 year
Reduced appetite
No fever
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Past illness
– No h/o DM, HT, TB,
– No past Surgical history
• Personal History
– Smoker – 25 yrs
– Non-alcoholic
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Physical Examination
– Pulse 88/min, BP 110/70 mmHg, afebrile
– Anemia +, Jaundice ++
– No lymphadenopathy
– Scratch marks
• Abdomen
– Soft non-tender–
– Palpable gall bladder
– No free fluid
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Investigations
• Hb. 11.7, Hct. 35
• WBC: 6000, Platelet: 350,000
• Serum creatinine: 1.2 mg
• Total bilirubin: 20 mg; (unconj. 2 mg, conj. 18 mg)
• Alkaline phosphatase: 990 U/L
• Total protein: 6.5 grams;
• CA 19-9: 350 units/ml
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Imaging studies
To determine:
• Extrahepatic obstruction
• Level of obstruction
• Cause of obstruction
• Staging
• Best therapeutic approach
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ULTRASOUND
– Best imaging for biliary tree,
non-invasive, cheap, high
accuracy esp. in gallstones
and biliary dilatation.
– Disadvantage: distal bile
duct may be obscured by
bowel gas
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ENDOSCOPIC ULTRASOUND
(EUS)
• 98%diagnostic accuracy in obstructive jaundice
• It allows diagnostic tissue sampling (EUS-FNA)
• High sensitivity for identification of focal
pancreatic mass, superior to CT.
• More specific to biliary stricture compared to
MRCP.
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Imaging/ ERCP
• CT :
– Main role in malignancies for primary and
metastatic tumors
• MRCP:
– Non invasive to visualize the hepato biliary tree.
• ERCP:
– invasive, therapeutic (biopsy, brush cytology, Stone
extraction or stenting)
– Complications: Pancreatitis, Cholangitis, Hge, Sepsis
– limitations: Unfavorable anatomy
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ERCP
MRCP
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• PTC indications:
– when ERCP either is inappropriate or has failed.
– Drainage of biliary obstructions.
• Oral Cholecystography (OCG):
• useful with symptomatic patients with negative US
• HIDA Scan: useful in acute cholecystitis
• Diagnostic Laparoscopy
• Angiography: Rule out abnormal vascular anatomy
• Tumor markers- CA19-9 , CEA
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Scenario case (cont.)
• USG- solid mass in distal CBD, dilated CBD,
Intrahepatic Biliary distension and distended GB
• CT abdomen show grossly dilated intra and
extra hepatic biliary channels with distended gall
bladder. Possibility of periampullary mass.
• Advised ERCP.
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Treatment options for obstructive jaundice
• Antibiotic therapy (if indicated for infection)
• Intravenous fluids
• Pain medications, nutritional support
• ERCP: biopsy, stone removal ,dilatation, stent placement
• Surgery: Curative resection, palliative by-pass
• Adjuvant therapy for cancer: chemotherapy, or radiotherapy
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ERCP (Stone CBD, Periampullary carcinoma)
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CBD stone extraction
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Surgical Procedures for
Obstructive Jaundice
Preoperative preparation
• Oral H2 antagonist
• Vit. K or FFP
• Perioperative broad spectrum antibiotics
• Rehydration and adequate diuresis
• Furosemide/ Manitol
• Catheterization & CVP monitoring
Carcinoma gallbladder: Radical
Cholecystectomy with wedge
resection & CBD excision
Cholediocholithiasis: ERCP
removal, CBD exploration
Cholangio Ca: Liver resection,
Whipple operation,
Stenting by ERCP or PTC- palliative
Biliary Stricture:
Hepatico-jejenostomy/
Periampullary Ca:
Whipple’s operation
Carcinoma head
pancreas: Whipple op.
Bilio-enteric bypass
(palliative)
Whipple’s Procedure
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Postoperative management
- Correct Fluid & Electrolyte imbalance
- Correct hypothermia
- Achieve CVS stability
- Adequate analgesia & chest physiotherapy
- Antibiotics + H2 receptor antagonist
- Maintain urine output
- Replace blood and blood products
Thank you!
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