Kernicterus refers to the advanced stage of brain damage in newborns secondary to the accumulation of bilirubin.
Free bilirubin, that is to say unconjugated, if it is too high (above 250 to 300 µmol/L (approximately 14.5 to 17.5 mg/dL) in full-term children) binds to the central gray nuclei resulting in irreversible brain damage and damage to the cranial nerves (VIII in particular) at this stage. This increase in bilirubin is linked to hyper-haemolysis on the one hand, and/or to the delay (prematurity) or absence of the initiation of the hepatic enzymes necessary for the glucuronidation of bilirubin. This glucuronidation was useless in utero, the bilirubin being eliminated via the placenta.
In vitro, free bilirubin alters the number of dendrites, axons and synapses of neurons and acts on glial cells. At the biochemical level, this molecule would stimulate oxidative stress, favoring the oxidation of proteins and the peroxidation of lipids, inhibiting the anti-oxidative defenses of the cell.
The maximum values allowed range from 0.8 to 1.2. Beyond that, the risk of kernicterus is major. This report can be used in the indication of exchange transfusion.