Jaundice

The liver of a newborn baby may not be capable of conjugating all of the bilirubin presented to it. The consequence is neonatal jaundice, and many babies become jaundiced during the first week of life. In full-term babies this usually resolves rapidly, but in premature babies it may persist. As a general rule, jaundice during the first 24 hours after birth is always pathological, and often indicates increased unconjugated bilirubin resulting from red blood cell destruction (haemolysis) due to blood group incompatibility or infection. Similarly, jaundice that lasts more than 10 days after birth should always be investigated. It may indicate a variety of clinical conditions, including galactosaemia, congenital hypothyroidism, cystic fibrosis or glucose-6-phosphate dehydrogenase deficiency.

Persistent jaundice due to unconjugated hyperbilirubinaemia should not be ignored. Unconjugated bilirubin is lipophilic and can cross the blood–brain barrier and bind to proteins in the brain where it is neurotoxic. This happens when albumin (the normal carrier of unconjugated bilirubin) becomes saturated. The clinical syndrome of bilirubin-encephalopathy is called kernicterus (Fig 79.1) and may result in death or severe mental handicap. Where the excess bilirubin is found to be conjugated, the pathology is different, and kernicterus is not a feature, since conjugated bilirubin is water-soluble rather than lipophilic. Causes include neonatal hepatitis, possibly contracted from the mother at birth; biliary atresia, resulting in severely impaired biliary drainage; and inherited deficiency of alpha-1-antitrypsin, a powerful protease, the absence of which is associated with liver and lung damage.

Hypoglycaemia

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