1. Approach to a patient with
jaundice
Pr epar ed by:
Saj ad Al-Ramahy
Hawler Medical Univer sit y

2. Outlines
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Introductoin
Bilirubine Metabolism
Types of jaundice
Management

3. What is jaundice?

4. • Yellowish discoloration of skin, mucous
membrane and the sclerae due to
hyperbilirubinemia
• Jaundice is usually detectable when the
plasma bilirubin exceeds
3 mg/dl (normally <1mg/dl)

5. • Bilirubin
Metabolism

6. Jaundice can occur in four different ways:
• 1- Increased bilirubin load as in haemolysis.
2- Disturbance in the hepatic uptake & transport
of bilirubin within the hepatocytes
3- Defects in conjugation.
4- Defects in the excretion of conjugated
bilirubin across the canalicular cell
membrane or an obstruction of the large
biliary channels.

7. Types of jaundice

8. Hemolytic Jaundice
• Excess production of
bilirubin due to excess
breakdown of hemoglobin
• Indirect bilirubin
(insoluble in water since
unconjugated)
• E.g.
– Hemolytic anemia
– Malaria
– Glucose-6-phosphate
dehydrogenase deficiency

9. Hepatic Jaundice
• Inability of the liver to
transport bilirubin across the
hepatocyte into bile, due to
parenchymal liver disease.
• Increased level of conjugated
and unconjugated bilirubin
• E.g.:
– Hepatitis, cirrhosis,
hepatocellular carcinoma,
prolonged use of drugs
metabolized by liver

10. Acute or subacute hepatocellular injury
Viral hepatitis, alcohol, drugs, ischemic hepatitis, Wilson's disease,
acute fatty liver of pregnancy
Chronic hepatocellular Disease:
Viral hepatitis, alcoholic, autoimmune hepatitis, Wilson dis.,
Haemochromatosis, NASH, alpha 1 antitrypsin deficiency.
Hepatic disorders with prominent cholestasis.
* Diffuse infiltrative disorders (e.g. granulomat dise. as TB,
sarcoidosis, lymphoma, drugs) Amyloidosis, malignancy.
* Inflammation of intrahepatic bile ductules (PBC), GVHD, Drugs
(chloropromazine)
• Miscellaneous e.g. use of oestrogen & steroids, TPN, bact. Infection.
Genetic disorders:
Gilbert’s syndrome
Criggler-Neijer Syndrome

11. Obstructive Jaundice
• Caused by:
• Failure of hepatocyte to
initiates bile flow.
• Obstruction of bile flow in the
bile duct or portal tracts.
• Obstruction of bile flow in the
extrahepatic bile duct
• Bilirubin formation rate is
normal
• Conjugation is normal = direct
bilirubin

12. •
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Ex:
Tumor of the head of the pancrease
Choledocolithiasis
Parasitic infection
Traumatic biliary stricture
Pancreatitis

13. History
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Pain
Fever
Alcohol
Medications
Pruritus
Color of urine
Type of stools
Fatigue

14. Physical examination
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BP/HR/Temp.
Degree of jaundice
Presence of anemia
Abdominal tenderness
Size and character of liver
Any palpable mass e.g. gall bladder(curvoisier’s
law)
• Signs of liver failure
• Scratch marks?

15. Icterus .…………………………………. Ascites

16. Lab investigations
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Complete blood count
Liver function tests
BT/CT
PT/INR
Serum albumin

17. Other investigations
• Ultrasound:
– More sensitive than CT for gallbladder stones
– Equally sensitive for dilated ducts
– Portable, cheap, no radiation, no IV contrast
• CT:
– Better imaging of the pancreas and abdomen
• PTC- percutaneous transhepatic
cholangiogram
– Gives a picture of the intra and extrahepatic
biliary tree

18. • MRCP:
– Imaging of biliary tree comparable to ERCP
– Non invasive
• ERCP:
– Therapeutic intervention for stones
– Brushing and biopsy for malignancy
– Invasive, chances of developing pancreatitis post
procedure

19. Liver function tests
Ser.Billirubin
Indirect
0.1 – 0.3 mg/dl
Direct
0.2 – 0.7 mg/dl
SGOT (AST)
LFT
0.2-0.8 mg/dl
0-35 IU
SGPT (ALT)
0-35 IU
Alk. Phosph.
30-120 IU
Ser. Protein
5.5 – 8.5 G/dl
Alb
3.5 – 5.5 G/dl
Glob
2.0 – 3.0 G/dl

20. Enzymes
• Alkaline phosphatase
– Bone and liver
– Specific for obstructive jaundice
– Released from biliary canaliculi in case of bile duct obstruction
• Aspartate aminotransferase (AST/SGOT)
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Reflects damage to hepatic cell
Less specific
May be elevated in MI
Used with ALT to diffrentiate between heart and liver disease
• Alanine aminotransferase (ALT/SGPT)
– Produced withing the cells of the liver
– Most sensitive marker for liver cell damage

21. Clinical Findings—Hemolytic Jaundice
• Decreased hemoglobin
– Explains weakness
– Has moderate anemia
• Splenomegaly
– Increased activity of reticuloendothelial system
– Site of RBC filtration
• Liver Function Tests:
– Increased Serum bilirubin
– Increased load to the liver (increased hemolysis)
=> increased hemoglobin metabolism

22. Clinical Findings—Hepatic Jaundice
• Highly colored urine
– Increased amount of bilirubin
• Tender hepatomegaly
• Liver function tests
Seen in both
hepatocellular
jaundice and
excretioncholestatic
jaundice
– High serum bilirubin
– AST and ALT highly increased
– Alkaline phosphatase increased moderately

23. Clinical findings in obstructive jaundice
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Deep jaundice
Scratch marks on body?
High colored urine
Clay colored stools

24. How to differentiate the types of
jaundice?
• Hemolytic:
– Increased unconjugated (indirect) more than direct
(conjugated) bilirubin
– Hemoglobin level low
– Anemia
• Hepatic:
– Increased amount of both indirect and direct
– Increase in AST and ALT more than increase in ALP
• Obstructive:
– Increased amount of direct (conjugated)
– Significant increase in ALP more than AST and ALT

25. Treatment
• Treatment of pre hepatic and hepatic Jaundice
is by treating the underlying cause
• Choledocholithiasis
– Open / laparoscopic CBD exploration with stone
extraction and T tube placement.
– Endoscopic papillotomy and extraction
• Periampularry carcinoma
– Curative – whipple’s procedure
– Palliative –
- endoscopic stenting of ampulla
- bypass prcodures for

26. Whipple’s operation
• 3 structures removed
– C-loop of duodenum
– Head and neck of pancreas
– Pylorus of stomach
• 3 anastomosis are made
– Gastro-jejunostomy
– Choledocho-jejunostomy
– Pancreatico-jejunostomy

27. References
• Davidson’s Principle and Practice of Medicine
• http://www.onhealth.com/jaundice/article.htm
• http://www.emedicinehealth.com/jaundice/article_
em.htm
• http://www.nlm.nih.gov/medlineplus/jaundice.html

29. Thank you