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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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