Nuclear jaundice
Last reviewed: 23.04.2024
All iLive content is medically reviewed or fact checked to ensure as much factual accuracy as possible.
We have strict sourcing guidelines and only link to reputable media sites, academic research institutions and, whenever possible, medically peer reviewed studies. Note that the numbers in parentheses ([1], [2], etc.) are clickable links to these studies.
If you feel that any of our content is inaccurate, out-of-date, or otherwise questionable, please select it and press Ctrl + Enter.
Nuclear jaundice (bilirubin encephalopathy) is a brain damage caused by the deposition of bilirubin in the basal ganglia and the nuclei of the brainstem.
Normally, bilirubin bound to albumin remains in the intravascular space. However, bilirubin can penetrate the blood-brain barrier and cause bilirubin encephalopathy at significantly increased bilirubin concentrations; a significant decrease in the concentration of albumin in the blood serum (for example, in premature infants); when bilirubin is displaced from the compound with albumin by competing substances (for example, sulfisoxazole, ceftriaxone, aspirin, free fatty acids and hydrogen ions in fasting, sepsis or acidosis).
[Symptoms of nuclear jaundice
A premature baby does not always have classic signs when developing bilirubin encephalopathy. The first symptoms of nuclear jaundice in term infants are retardation, decreased appetite, vomiting. Further, opisthotonus, convulsions and death may develop. Nuclear jaundice can lead to a delay in mental development, choreoathetoid cerebral palsy, non-irosensory hearing loss, paralysis of the gaze upward. It is not known whether mild degrees of bilirubin encephalopathy can cause less severe neurological impairment (eg, perceptual-motor disorders and learning disabilities).
Treatment of nuclear jaundice
Treatment of already developed bilirubin encephalopathy does not exist. Nuclear jaundice is prevented by the treatment of hyperbilirubinemia.