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

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 < 0.05). The children with CHD and hypoxic damage to the CNS in the first year of life were significantly more often (p < 0.05) deficient in weight and height. A decrease in the resistance level in the first year of life was observed in 40% of children from the main group, which significantly differed compared with group of children without CHD (p < 0.001). The newborns with hypoxic CNS and CHD lesions had a decrease in the activity of α-GPDH and SDG at the age of five to seven days; the low activity of SDG persisted at the ages of one and six months; the enzyme activity in children of the comparison group was normal (p < 0.05).

Conclusion. Children with CHD had the features of clinical course of perinatal damage to the CNS in the acute and recovery periods, a slowdown in the rate of physical and neuropsychic development, a decrease in the resistance level, and impaired functional state of the body. The decreases in the activities of SDG and α-GPDH in children with hypoxic lesions to the CNS in the presence of CHD implied the disturbances in cellular bioenergetics and resulted in inadequate response to external factors.

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