Nuclear jaundice, also called “bilirubin encephalopathy”, is a brain damage caused by the deposition of bilirubin in the basal ganglia and brainstem nuclei. Bilirubin is tightly bound to serum albumin and cannot freely cross the blood-brain barrier. As long as there is a bilirubin binding site on the albumin, it will not cause jaundice. Significantly elevated serum bilirubin, low serum albumin concentration or the presence of substances in the serum that compete with bilirubin for albumin binding sites, certain drugs including sulfonamides, cephalosporins and aspirin, may increase the risk of jaundice. Premature infants are at risk for jaundice due to low serum albumin concentrations. Competing molecules may be elevated in the serum of newborns with starvation, sepsis, respiratory distress, or metabolic acidosis, conditions that put newborns at any serum bilirubin level at an increased risk of jaundice. Once bilirubin infiltrates the central nervous system, it can lead to toxic damage to neuronal cells. Bilirubin encephalopathy is one of the high-risk factors for cerebral palsy. The early symptoms in full-term infants are lethargy, poor milk intake and vomiting, followed by keratoconus, ocular gaze, convulsions and death. In preterm infants, jaundice may not present with recognizable clinical signs. It is not clear whether reducing the degree of bilirubin encephalopathy reduces the neurological damage (e.g., perceptual-motor impairment and learning difficulties). There is no reliable test to determine the risk of kernicterus in a given neonate, and the diagnosis is confirmed by autopsy. Clinical manifestations of bilirubin encephalopathy: Bilirubin encephalopathy usually occurs 2-7 days after birth, mainly in children with high unspliced bilirubinemia, and is more common in premature infants. Neurological symptoms often appear gradually with increasing nuclear jaundice, and a handful of progressive appearances are divided into 4 stages.