Destructive hypoxic-ischemic brain injury in full-term infants with normothermia and hypothermia
Background. Despite the achievements of neonatology, severe asphyxia at birth and hypoxic-ischemic encephalopathy in full-term infants are still associated with high lethality, long-term neurological morbidity and disability. In the algorithm for the management of children with hypoxic-ischemic encephalopathy, it is important to use methods of additional examinations, including ultrasound examination of the brain (neurosonography), its potential for the early evaluation of the severity of the brain tissue injury using therapeutic hypothermia. Thus, the aim of the research was to determine the effect of therapeutic hypothermia on the severity of neurosonographic signs of destructive hypoxic-ischemic brain injury in full-term newborns. Materials and methods. Data were analyzed for 50 full-term neonates with severe asphyxiation and signs of destructive hypoxic-ischemic brain injury. The first group (hypothermia group 1) included 12 newborn infants who were treated with hypothermia in 2014–2016. The second group (hypothermia group 2) — 14 children with severe asphyxiation who were treated with hypothermia in 2011–2013. The third group (group of normothermia) consisted of 24 full-term babies born in 2009–2010, with no therapeutic hypothermia. Results. The share of the most severe destructive brain injuries (diffuse ischemic lesions) was 33.3 % in the first group, 35.7 % in the second group and 45.8 % in the third group. Significant differences between groups in terms of the frequency of diffuse ischemic brain injures were not found. In general, in the structure of destructive hypoxic-ischemic brain injuries in newborns after hypothermia, diffuse ischemic lesions were detected in 34.6 % of cases (non-significant differences with the group of normothermia, p = 0.385 according to Fisher’s criterion calculations). When studying the indicators of cerebral blood flow, reliable differences were found for the index of resistance of the anterior cerebral artery on the third day of life (0.53 ± 0.05 for normothermia group and 0.65 ± 0.04 for hypothermia group). Conclusions. Despite the reduction in the proportion of the most severe diffuse ischemic brain injuries among the total number of diagnosed destructive hypoxic-ischemic lesions during the introduction of hypothermia, the statistical analysis did not reveal any significant differences between the groups. After all, the development of diffuse ischemic brain injuries, first of all, is due to primary asphyxia lesions that lead to global deaths of neurons, or by these injuries, the phase of the therapeutic window in which ended up at the time of birth. But significant differences in the parameters of cerebral hemodynamics prove the fact that the potential of therapeutic hypothermia for the prevention of secondary reperfusion injury remains in these cases.
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