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Chapter: Paediatrics: Gastroenterology and nutrition

Paediatrics: Jaundice

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

Jaundice

 

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. 

Causes

 

   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.

 

Causes

 

Infectious

 

·  Viral hepatitis, including chronic hepatitis.

 

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

   Toxoplasma gondii.

 

Toxic

 

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

   Fungi (Amanita phalloides).

 

Metabolic

 

   Galactosaemia, hereditary fructose intolerance.

   Tyrosinaemia type 1.

   Wilson’s disease.

   A1-antitrypsin deficiency.

   Hypothyroidism.

   Peroxisomal disorders, e.g. Zellweger syndrome.

   Dubin–Johnson syndrome, Rotor syndrome.

 

Biliary hypoplasia

 

   Non-syndromic.

   Syndromic, e.g. Alagille syndrome.

 

Cardiovascular

 

   Budd–Chiari syndrome.

   Right heart failure.

 

Autoimmune hepatitis 

Autoimmune hepatitis.

Cholestatic (obstructive) jaundice

 

Conjugated hyperbilirubinaemia is due to bile tract obstruction.

 

Causes

 

Biliary atresia.

 

Choledochal cyst.

 

Caroli’s disease.

 

Primary sclerosing cholangitis (commonly associated with IBD).

 

Cholelithiasis (may be secondary to chronic haemolysis).

 

Cholecystitis.

 

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).

 

Examination 

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

 

Investigations

 

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.

 

Treatment

 

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.

 

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Paediatrics: Gastroenterology and nutrition : Paediatrics: Jaundice |


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