ASSESSMENT OF PSYCHOMOTOR DEVELOPMENT IN INFANTS WITH BILIRUBIN-INDUCED NEUROLOGICAL DYSFUNCTION.

Pathological jaundice in newborns is the leading cause of neonatal morbidity and mortality worldwide. The pathological course of neonatal jaundice remains an urgent problem in the world today. [1] The nature of accumulation of the main amount of bilirubin in the deep roots of the brain in hyperbilirubinemia has not yet been fully determined. As a result of the neurological disorders caused by the toxic effect of bilirubin, it leads to bilirubin encephalopathy. As a result of the accumulation of bilirubin, the basal ganglia, hypothalamus, nuclei of the brain stem (e.g., oculomotor, cochlear, vestibular and olivary nuclei) and brain are damaged.[2]. The aim of the study was to study the features of the neurological status in premature and full-term children with pathological neonatal jaundice in order to expand and improve treatment and prevention programs. [1,2]. The object of the study were 54 newborns with pathological neonatal jaundice: the 1st group - premature newborns (20 children), the 2nd group - full-term newborns (34 children). Analysis of the study showed that when assessing the reaction of children on the AVPU scale, it can be concluded that the vast majority of full-term sick children have reaction A - active wakefulness. Premature babies have lower response scores on the scale. So, they have a significantly higher (p<0.01) reaction to pain "B". And only premature babies have the lowest score of O (coma). Coma is noted only in premature infants with hemolytic jaundice, which is associated with high indirect hyperbilirubinemia. [1,9]

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