Jaundice Classification
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Direct answer
Jaundice (icterus) is the yellow discolouration of skin, sclerae and mucosae by bilirubin, usually visible when serum bilirubin exceeds about 2 to 3 mg/dL. Clinico-pathological classification rests on which fraction is raised: unconjugated (pre-hepatic or haemolytic, plus conjugation defects) or conjugated (hepatic and post-hepatic or obstructive) — a conjugated fraction above twenty per cent of the total defines conjugated jaundice.
What you must remember
- Bilirubin pathway: haem from aged red cells is broken to biliverdin and bilirubin in macrophages; albumin carries insoluble unconjugated bilirubin to the liver, where UDP-glucuronyl transferase conjugates it for excretion in bile, and gut bacteria reduce it to urobilinogen and stercobilin.
- Pre-hepatic (haemolytic): unconjugated bilirubin raised, absent from urine (acholuric jaundice) because it is albumin-bound; urine urobilinogen is increased, stool is normally coloured, and splenomegaly with anaemia accompanies — causes include hereditary spherocytosis, G6PD deficiency, thalassaemia and haemolytic disease of the newborn.
- Hepatocellular: both fractions raised, bilirubin appears in urine, transaminases are high, and stigmata of liver disease point to viral hepatitis, alcoholic hepatitis or cirrhosis, drug injury and leptospirosis.
- Post-hepatic (obstructive) cholestasis: conjugated bilirubin raised with dark urine (bilirubinuria), pale or clay-coloured stools, pruritus from retained bile salts, and a raised alkaline phosphatase and GGT — causes are choledocholithiasis, carcinoma of the head of pancreas, cholangiocarcinoma and strictures.
- Inherited hyperbilirubinaemias: Gilbert syndrome (mild unconjugated, benign), Crigler-Najjar syndrome (severe unconjugated, kernicterus risk in type I), and Dubin-Johnson and Rotor syndromes (conjugated, benign; Dubin-Johnson with a black liver from pigment).
- Neonatal jaundice: physiological immaturity of glucuronidation is common; pathological haemolysis (ABO or Rh incompatibility) risks kernicterus — unconjugated bilirubin depositing in basal ganglia.
- Clinical pearl — Courvoisier law: painless obstructive jaundice with a palpable, non-tender gallbladder is unlikely to be from gallstones and points to malignancy of the pancreatic head.
Common confusion
Urine findings are the perennial muddle. Haemolytic jaundice has no bilirubin in urine (unconjugated bilirubin is albumin-bound and not filtered) but excess urobilinogen; obstructive jaundice has dark urine from conjugated bilirubin with absent urobilinogen, since bile never reaches the gut. Fix this one contrast and most MCQs on jaundice fall instantly.
Exam-focused takeaway
Theory answers should classify jaundice, give two or three causes per class, and contrast urine and stool findings plus the enzyme pattern of each. Viva examiners ask about Courvoisier law, kernicterus and the inherited syndromes. MCQs test the Gilbert, Crigler-Najjar and Dubin-Johnson pairings, the twenty per cent conjugated fraction rule, and urine urobilinogen patterns.
Frequently asked questions
At what bilirubin level does jaundice become visible?
Scleral icterus usually appears when total serum bilirubin exceeds about 2 to 3 mg/dL; sclerae stain first because of their high elastin content.
Why is urine dark in obstructive but not haemolytic jaundice?
Conjugated bilirubin is water-soluble and filtered into urine; unconjugated bilirubin travels bound to albumin and cannot cross the glomerulus.
What is Courvoisier law?
A distended, painless gallbladder with obstructive jaundice suggests malignancy at the head of the pancreas rather than gallstones, because stones cause fibrosis and scarring.
What is kernicterus?
Deposition of unconjugated bilirubin in the basal ganglia and brainstem of neonates, causing encephalopathy, choreoathetosis and deafness.
Which inherited syndromes cause conjugated hyperbilirubinaemia?
Dubin-Johnson syndrome, with a black pigmented liver due to MRP2 transport defect, and Rotor syndrome — both benign.