Features of the recovery period of hypoxic lesion to the central nervous system in children of the first year of life with congenital heart disease

Автор: Zhelev V.A., Pogudina A.S., Mikhalev E.V., Okorokov A.O., Krivonogova T.S., Nagaeva T.A., Ponomareva D.A.

Журнал: Сибирский журнал клинической и экспериментальной медицины @cardiotomsk

Рубрика: Клинические исследования

Статья в выпуске: 3 т.35, 2020 года.

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Aim. To study the features of recovery period of hypoxic lesion to the central nervous system (CNS) in children of the first year of life in the presence of congenital heart disease (CHD).Material and Methods. The study involved 80 children born full-term and premature with gestational status of 35-37 weeks with hypoxic damage to the CNS. The main observation group comprised 50 children with CHD (interventricular and atrial septal defects, open ductus arteriosus). All children underwent a comprehensive health assessment, standard echocardiography, and neurosonography at ages of five to seven days and one, three, and six months. Biochemical analysis included assessment of serum neurospecific enolase (NSE), succinate dehydrogenase (SDG), and α-glycerophosphate dehydrogenase (α-GPDH). The control group included 20 full-term newborns without CHD and CNS lesions.Results. The main manifestations in newborns with CHD and hypoxic damage to the CNS were the suppression syndrome, agitation, and hypertension-hydrocephalic syndrome. At the age of six months, a delay in motor development indicators persisted in 35% of children in the main group. The high NSE level in newborns with concomitant septal heart defects was associated with a decrease in the quantitative indicators of neuropsychic development (g = -0.6, p function show_eabstract() { $('#eabstract1').hide(); $('#eabstract2').show(); $('#eabstract_expand').hide(); }

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Hypoxic perinatal lesion, congenital heart disease, children, succinate dehydrogenase, α-glycerophosphate dehydrogenase

Короткий адрес: https://sciup.org/149125359

IDR: 149125359   |   DOI: 10.29001/2073-8552-2020-35-3-53-58

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