Types of jaundice
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Types of Jaundice
Jaundice is the yellowish staining of the skin, sclera, and mucous membranes due to elevated bilirubin. It becomes clinically detectable when serum bilirubin rises above 2.5-3 mg/dL (or >35 µmol/L). It is classified into three types based on where in the bilirubin metabolism pathway the defect occurs.
Bilirubin Metabolism (Quick Overview)
- RBCs are broken down - haem is converted to unconjugated (indirect) bilirubin
- Unconjugated bilirubin is carried by albumin to the liver
- In hepatocytes, glucuronyltransferase conjugates it to glucuronic acid, forming conjugated (direct) bilirubin (water-soluble)
- Conjugated bilirubin is excreted into the bile ducts → duodenum → stercobilin (stool colour) / urobilinogen (reabsorbed, excreted in urine)
1. Pre-Hepatic Jaundice (Haemolytic)
Site of defect: Before the liver
Bilirubin type elevated: Unconjugated (indirect)
Bilirubin type elevated: Unconjugated (indirect)
The liver's conjugation capacity is overwhelmed by excessive breakdown of red blood cells or other haem-containing compounds.
Causes
| Category | Examples |
|---|---|
| Inherited haemolytic anaemias | Sickle cell disease, G6PD deficiency, hereditary spherocytosis, thalassaemia |
| Acquired immune-mediated | Autoimmune haemolytic anaemia, drug-induced haemolysis (direct Coombs positive) |
| Acquired non-immune | Microangiopathic haemolytic anaemia (TTP, HUS), mechanical haemolysis (prosthetic valves), malaria, drugs/toxins (Coombs negative) |
| Protein loss | Hypoalbuminaemia (burns, malnutrition) - impairs bilirubin transport to liver |
Features
- Urine: normal colour (unconjugated bilirubin is not water-soluble, cannot be filtered)
- Stools: dark (excess urobilinogen)
- No bilirubinuria
- Elevated LDH, low haptoglobin, reticulocytosis
2. Hepatic (Intrahepatic) Jaundice
Site of defect: Within the liver
Bilirubin type elevated: Both unconjugated and conjugated (mixed)
Bilirubin type elevated: Both unconjugated and conjugated (mixed)
This category covers conditions affecting hepatocyte conjugation, excretion, or hepatic blood flow.
A. Defects in Conjugation (Unconjugated hyperbilirubinaemia)
| Condition | Notes |
|---|---|
| Gilbert's Syndrome | Most common. Reduced glucuronyltransferase activity (~4-7% of population). Benign; triggered by fasting, stress, illness. Mild, transient, unconjugated rise |
| Crigler-Najjar Syndrome | Rare, severe enzyme deficiency in neonates. Type I (absent enzyme) - fatal without treatment; Type II (reduced enzyme) - manageable |
| Neonatal jaundice | Immature hepatic conjugation in newborns |
B. Defects in Excretion (Conjugated hyperbilirubinaemia)
| Condition | Notes |
|---|---|
| Dubin-Johnson Syndrome | Impaired transport of conjugated bilirubin from hepatocyte into bile. Benign, conjugated hyperbilirubinaemia. Liver appears black on gross pathology |
| Rotor's Syndrome | Similar to Dubin-Johnson but without liver pigmentation. Benign |
C. Acquired Hepatocellular Disease (Mixed)
| Category | Examples |
|---|---|
| Viral hepatitis | Hepatitis A, B, C, D, E; EBV, CMV |
| Alcoholic hepatitis | Direct hepatocyte toxicity |
| Autoimmune hepatitis | Immune-mediated hepatocyte destruction |
| Drug-induced | Paracetamol (acetaminophen) toxicity, oral contraceptive pills, anabolic steroids |
| Ischaemic/hypoxic hepatitis | Shock liver, cardiac failure |
| Intrahepatic cholestasis | Primary biliary cholangitis (PBC), primary sclerosing cholangitis (PSC), vanishing bile duct syndrome |
| Cirrhosis (decompensated) | End-stage liver disease - jaundice indicates decompensation, median survival ~1.6 years |
| Sepsis | Inflammatory disruption of bilirubin transport |
Features
- Urine: dark (bilirubinuria with conjugated type)
- Stools: pale (if excretion impaired)
- Elevated ALT/AST, deranged clotting, hypoalbuminaemia
- Signs of liver failure: encephalopathy, ascites, coagulopathy
3. Post-Hepatic (Obstructive / Extrahepatic) Jaundice
Site of defect: After the liver, in the biliary system
Bilirubin type elevated: Conjugated (direct)
Bilirubin type elevated: Conjugated (direct)
Obstruction prevents conjugated bilirubin from flowing into the duodenum. Bile backs up into the bloodstream.
Causes - Intrinsic (Within the bile duct)
| Cause | Notes |
|---|---|
| Choledocholithiasis | Most common benign cause - stones in common bile duct |
| Cholangiocarcinoma | Malignant stricture of bile duct |
| Biliary strictures | Post-surgical, post-inflammatory |
| Primary sclerosing cholangitis (PSC) | Chronic fibro-inflammatory stricturing |
| Cholangitis | Infection (Charcot's triad: fever, RUQ pain, jaundice) |
| Papillary/ampullary disorders | Ampullary carcinoma, sphincter of Oddi dysfunction |
Causes - Extrinsic (Compression from outside)
| Cause | Notes |
|---|---|
| Carcinoma of pancreatic head | Most common malignant cause - "painless jaundice" |
| Pancreatitis / pseudocyst | Compresses common bile duct |
| Lymphadenopathy | Porta hepatis nodes |
| Surgical complications | Misplaced clips, retained stones, biliary ischaemia |
Features
- Urine: dark (conjugated bilirubin is water-soluble, excreted by kidney)
- Stools: pale/clay-coloured (no stercobilin reaching gut)
- Pruritus (very prominent - due to bile salt deposition in skin)
- Raised ALP and GGT (> ALT/AST)
- Courvoisier's sign: palpable non-tender gallbladder (suggests malignant obstruction)
Summary Comparison Table
| Feature | Pre-Hepatic | Hepatic (Intrahepatic) | Post-Hepatic |
|---|---|---|---|
| Bilirubin type | Unconjugated | Mixed | Conjugated |
| Urine colour | Normal | Dark (if conjugated) | Dark |
| Stool colour | Dark | Pale (cholestasis) | Pale/Clay |
| Bilirubinuria | Absent | Present (if conjugated) | Present |
| Urobilinogen in urine | Increased | Decreased | Absent |
| Pruritus | Absent | Variable | Prominent |
| ALP/GGT | Normal | Mildly raised | Markedly raised |
| ALT/AST | Normal | Markedly raised | Mildly raised |
| Key example | Haemolytic anaemia | Viral hepatitis | Gallstone / pancreatic cancer |
Special Categories Worth Knowing
- Neonatal (Physiological) Jaundice - immature conjugation, appears day 2-3, resolves by day 10. Pathological if appears <24 hrs (haemolytic) or persists >2 weeks.
- Intrahepatic cholestasis of pregnancy (ICP) - hormonally-mediated impaired bile secretion; associated with fetal risk.
- Familial / hereditary syndromes - Gilbert's, Crigler-Najjar (unconjugated), Dubin-Johnson, Rotor's (conjugated).
Sources:
- Schwartz's Principles of Surgery, 11th Edition, pp. 1381-1382
- Goldman-Cecil Medicine, International Edition
- Sleisenger and Fordtran's Gastrointestinal and Liver Disease
- Pye's Surgical Handicraft, 22nd Edition
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