Home | | Paediatrics | Paediatrics: Jaundice

Chapter: Paediatrics: Gastroenterology and nutrition

Paediatrics: Jaundice

Jaundice occurs when serum bilirubin >25–30mmol/L. It is rare outside neonatal period.



Jaundice occurs when serum bilirubin >25–30mmol/L. It is rare outside neonatal period. First determine the SBR and conjugated (direct) fraction. Unconjugated jaundice is rarely due to liver disease. Conjugated jaundice (>20mmol/L) is due to liver disease and requires investigation.


Unconjugated jaundice


Due to excess bilirubin production, impaired liver uptake, or conjugation. 



   Haemolysis (spherocytosis, G6PD deficiency, sickle cell anaemia, thalassaemia, HUS).

   Defective bilirubin conjugation (Gilbert syndrome, Crigler–Najjar syndrome).


Intrahepatic cholestasis


Here, jaundice is due to hepatocyte damage +/– cholestasis. There is un-conjugated +/– conjugated hyperbilirubinaemia.






·  Viral hepatitis, including chronic hepatitis.


   Bacterial hepatitis (leptospirosis [Weil’s disease], septicaemia, Mycoplasma, liver abscess).

   Toxoplasma gondii.




   Drugs or poisons, e.g. paracetamol overdose, sodium valproate, anti-TB drugs, cytotoxic drugs.

   Fungi (Amanita phalloides).




   Galactosaemia, hereditary fructose intolerance.

   Tyrosinaemia type 1.

   Wilson’s disease.

   A1-antitrypsin deficiency.


   Peroxisomal disorders, e.g. Zellweger syndrome.

   Dubin–Johnson syndrome, Rotor syndrome.


Biliary hypoplasia



   Syndromic, e.g. Alagille syndrome.




   Budd–Chiari syndrome.

   Right heart failure.


Autoimmune hepatitis 

Autoimmune hepatitis.

Cholestatic (obstructive) jaundice


Conjugated hyperbilirubinaemia is due to bile tract obstruction.




Biliary atresia.


Choledochal cyst.


Caroli’s disease.


Primary sclerosing cholangitis (commonly associated with IBD).


Cholelithiasis (may be secondary to chronic haemolysis).




Cystic fibrosis.


Obstructive tumours or cysts.


Management of jaundice


Full history 

e.g. medications, family history, overseas travel, past blood transfusions, jaundice contacts, pale stools, or dark urine (cholestasis).



Vital signs; conscious level (hepatic coma); hepatic stigmata (= chronic liver disease); pallor (haemolysis); hepatomegaly; splenomegaly; ascites; peripheral oedema.




Depending on which of the above pattern presents these may include:

FBC, blood film, reticulocyte count.

Coagulation studies.

U&E, SBR (total and conjugated), LFT, albumin, total protein, TFT.

Viral serology (hepatitis A, B, C, EBV, CMV), blood culture, leptospira and toxoplasma antibody titres.

IEM screen, ammonia, copper studies (serum copper i, d, or n, serum caeruloplasmin ‘fall’ in Wilson’s disease), blood glucose, A1-antitrypsin level, galactose-1-uridyl-phosphatase level.

Immunoglobulins, anti-nuclear antibody, smooth muscle and liver/ kidney antibodies (autoimmune hepatitis);

Abdominal US, abdominal CT/MRI, biliary scintigraphy, e.g. hepatoiminodiacetic acid [HIDA] scan).

Liver biopsy.




Remove or treat underlying cause.


Correct blood glucose if it is low.


Correct any clotting abnormalities.



Phototherapy may be helpful only if jaundice has a significant unconjugated component, e.g. Crigler–Najjar syndrome


Treat any associated anaemia if due to haemolysis.


Treat liver failure as appropriate.


Study Material, Lecturing Notes, Assignment, Reference, Wiki description explanation, brief detail
Paediatrics: Gastroenterology and nutrition : Paediatrics: Jaundice |

Privacy Policy, Terms and Conditions, DMCA Policy and Compliant

Copyright © 2018-2023 BrainKart.com; All Rights Reserved. Developed by Therithal info, Chennai.