Jaundice

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What is Jaundice?

Yellow discolouration of the sclera and skin due to hyperbilirubinaemia (> 50 umol/L)

What is the pathophysiology?

Jaundice is the breakdown product from the catabolism of haem = Made when RBCs are destroyed.

Normally, bilirubin conjugates in the liver making it water soluble so it can be excreted in bile and further broken down to urobilinogen and then stercobilin (colours the stool brown).

When this pathway is disrupted, Jaundice occurs

There are 3 different types:

1. Pre-hepatic

Excessive RBC breakdown overwhelms the liver's ability to conjugate bilirubin

Unconjugated hyperbilirubinaemia

Causes include

Haemolytic anaemia

Gilbert's syndrome

Mild liver disorder affecting bilirubin metabolism due to faulty enzyme

Crigler-Najjar Syndrome

Rare inherited disorder affecting bilirubin metabolism causing non-haemolytic jaundice and brain damage (kernicterus) in infants

2. Intrahepatic / Hepatocellular

Hepatic cell dysfunction means liver loses ability to conjugate bilirubin

Cirrhosis leads to compression of intrahepatic portions of biliary tree to cause obstruction.

Unconjugated / conjugated (mixed) hyperbilirubinaemia

Causes include

Alcoholic liver disease

Viral hepatitis

Iatrogenic (e.g. medication)

Hereditary haemochromatosis

Autoimmune hepatitis

Primary biliary cirrhosis / Primary sclerosing cholangitis

Hepatocellular carcinoma

3. Post-hepatic

Obstruction of biliary drainage

Conjugated hyperbilirubinaemia

Causes included

Intra-luminal (e.g. gallstones)

Mural causes

Cholangiocarcinoma

Strictures

Drug-induced cholestasis

Extra-mural

Pancreatic cancer

Abdominal masses (e.g. lymphomas)

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Bilirubinuria

Conjugated bilirubin is water soluble so excreted in urine and gives it it's colour.

In conjugated / mixed hyperbilirubinaemias there is dark (coca-cola) urine

Pale stool due to reduced stercobilin

Unconjugated bilirubin isn't water soluble so isn't excreted in urine.

Normal urine seen

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Investigations

Blood tests

LFT's

Bilirubin = Quantifies degree of jaundice

Albumin = Marker of liver synthesising function

Reduced in liver failure

AST & ALT = Markers of hepatocellular injury (intrahepatic)

AST:ALT > 2 = Alcoholic liver disease likely

AST:ALT around 1 = Viral hepatitis more likely

ALP = Raised in biliary obstruction (post-hepatic problems)

Also raised in pregnancy , bone disease & certain malignancies

Gamma-GT

More specific for biliary obstruction than ALP.

Coagulation studies

Prothrombin can be used as marker for liver synthesis function

FBC

Anaemia + Raised MCV = Megaloblastic anaemia

Thrombocytopenia

U&E's

Specialist blood tests (e.g. Viral serology & Non-infective markers)

Imaging

USS Abdo (1st line)

To identify obstructive pathology or gross liver pathology

MRCP

2nd line when USS Abdo was inconclusive / limited

Also used as work up to surgical intervention

Liver biopsy

When diagnosis not yet made

Liver Screen

Can be done when there is not initial cause for liver dysfunction.

Acute liver injury

Viral serology

Hep A, B, C, D, E

CMV & EBV

Non-infective markers

Paracetamol levels

Caeruloplasmin

ANA & IgG subtypes

Chronic liver injury

Viral serology

Hep B & C

Non-infective markers

Caeruloplasmin

Ferritin & Transferrin saturation

Tissue Transglutaminase antibody

Alpha-1 antitrypsin

Autoantibodies

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Management

Treat the underlying cause

Obstructive causes may require:

Endoscopic Retrograde Cholangiopancreatography (ERCP)

To remove blockage or stent the common bile duct.

Cholestyramine

Increases biliary drainage

Relieves itching

Anti-histamines

Relieve itching

Monitor for coagulopathy

Treat promptly if any evidence of bleeding or rapid coagulopathy

Vitamin K or Fresh frozen plasma (FFP)

Treat hypoglycaemia orally if possible

If not 5% dextrose is needed

Monitor for hepatic encephalopathy

Confusion due to decompensating chronic liver disease

Treat with laxatives (lactulose/senna) +/- neomycin or rifaximin

Reduces no. of ammonia producing bacteria in bowel