Jaundice

 

  • Background

    Bilirubin physiology

    • (Unconjugated) bilirubin is a breakdown product of haem, created in the spleen.
    • It is then conjugated in the liver, making it water soluble and allowing it to be excreted into the GI tract at the sphincter of Oddi.
    • In the GI tract, some is converted into urobilinogen, which re-enters the circulation and is excreted by the kidneys, giving yellow colour to urine.
    • The rest is converted into stercobilinogen, giving brown colour to faeces.

    Jaundice

    Jaundice results from elevated bilirubin levels, which are visible in the sclera and skin at ≥35 μmol/L.

  • Pre-hepatic jaundice

    Pathophysiology

    Due to ↑haemolysis (haemolytic anaemia) or impaired conjugation, the latter due to UDP-glucuronosyltransferase impairment (as in Gilbert's).

    Investigations

    • Serum: ↑unconjugated bilirubin.
    • Urine: ↑urobilinogen.
  • Hepatocellular jaundice

    Pathophysiology

    Liver failure leads to impaired transport of bilirubin across hepatocyte into the bile duct.

    Causes

    Most causes of liver disease e.g. decompensated alcoholic liver disease, viral hepatitis, autoimmune, drugs.

    Signs and symptoms

    Faeces retain normal colour – as some conjugated bilirubin is still being produced – but dark pee due to elevated levels of unconjugated bilirubin being excreted.

    Investigations

    • Serum: ↑conjugated and ↑unconjugated bilirubin.
    • Urine: some urobilinogen, conjugated bilirubin.
  • Obstructive jaundice

    Aka cholestatic jaundice.

    Pathophysiology

    Obstruction in biliary tree or portal ducts leads to conjugated bilirubin not entering the GI tract, and backing up into the circulation and then kidneys.

    Causes

    Extra-hepatic:

    • Luminal: gallstones.
    • Mural: cholangiocarcinoma, biliary strictures (iatrogenic, primary sclerosing cholangitis, pancreatitis).
    • Extra-mural: pancreatic head tumour, enlarged porta hepatis lymph nodes, Mirizzi's syndrome (stones in gallbladder or cystic duct).

    Intra-hepatic:

    • Primary biliary cirrhosis, primary sclerosing cholangitis (affects both intra and extra-hepatic ducts).
    • Drugs: see drug-induced LFT changes.
    • Obstetric cholestasis.
    • Most causes of hepatocellular jaundice can also damage intrahepatic ducts, including viral hepatitis and alcoholic liver disease.

    Signs and symptoms

    • Pale poo, dark pee.
    • Itch due to build up of bile salts (not bilirubin).

    Investigations

    • Serum: LFTs show ↑conjugated bilirubin. Also check FBC, U&E, and coag.
    • Urine: ↓urobilinogen, ↑conjugated bilirubin.
    • Imaging: US, MRCP, CT.

    Management

    • Medical: IV fluids, vitamin K, antibiotics to prevent cholangitis.
    • ERCP: sphincterotomy, clearance, and stenting.
    • PTC (percutaneous transhepatic cholangiography) and surgery are alternatives to ERCP.

    Complications

    • Coagulopathy due to impaired vitamin K absorption in gut. Leads to ↑INR.
    • Hepatorenal syndrome.
    • Acute cholangitis.

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