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Introduction The likelihood of adverse perinatal outcome in new coronavirus infection (NKI) COVID-19 increases with the volume of lung tissue damage and correlates with the severity of respiratory failure (DN). Nevertheless, perinatal outcomes and placenta structural changes in pregnant women with critical lung lesions during NKI COVID-19 have been insufficiently studied.The objective of this investigation was to determine perinatal outcomes and the nature of placental lesions in pregnant women with critical lung injury during novel COVID-19 coronavirus infection.Material and methods A prospective cohort comparative study was conducted, with subsequent retrospective analysis of perinatal outcomes and the results of histologic examination of the placentas in 53 pregnant women with COVID-19 NCI. Group 1 was composed of 25 women with NKI COVID-19 complicated by community-acquired pneumonia with critical lung injury (KT-4, 76% or more); Group 2 was composed of 28 pregnant women with NKI COVID-19 complicated by community-acquired pneumonia with moderate-to-severe lung injury (KT-2, 25-50%). Perinatal outcomes and the results of morphological examination of the placenta were analyzed using the provisions of the classification of placental injuries developed by the Amsterdam Placenta Workshop Group (2014).Results In the main group, there were no children born with signs of miscarriage, while in the comparison group there were 8.7% of such children. SARS-CoV-2 antigen was diagnosed in a nasopharyngeal swab immediately after birth in 1 (4.3%) live-born infant in group 2 by PCR. The child died in the postnatal period on the 33rd day of life. Antenatal fetal death in women of Group 1 was the result of marked maternal hypoxia and extremely early PP, in Group 2 - the consequence of placental lesions. A wide spectrum of placental damages, including maternal and fetal malperfusion, maternal and fetal COVID-19 complicated by critical lung injury and with moderate lung injury.Discussion The placentas of pregnant women delivered due to critical condition do not have pronounced inflammatory and distrophic disorders, being characterized by the phenomena of acute PU. On the contrary, the placentas of women who successfully completed treatment with COVID-19 NKI of moderate severity and safely delivered at late gestational age exhibit the full spectrum of inflammatory and hypoxic lesions, leading to subcompensated and decompensated PU.Conclusion Weakly pronounced dystrophic processes, lymphocytic infiltration of the decidual and fetal membranes, signs of partial maternal vascular malperfusion and fetal stromal-vascular lesions, and acute PU phenomena were recorded in the placentas of women with NCI COVID-19 and critical pulmonary lesions. The absence of marked inflammatory infiltration of villi and fetal membranes, dystrophic processes, intervillous thrombosis, and villous infarcts realized in decompensated PU in the placentas of these patients was due to the immediate delivery of pregnant women with critical pulmonary lesions in NCI COVID-19.
Introduction The likelihood of adverse perinatal outcome in new coronavirus infection (NKI) COVID-19 increases with the volume of lung tissue damage and correlates with the severity of respiratory failure (DN). Nevertheless, perinatal outcomes and placenta structural changes in pregnant women with critical lung lesions during NKI COVID-19 have been insufficiently studied.The objective of this investigation was to determine perinatal outcomes and the nature of placental lesions in pregnant women with critical lung injury during novel COVID-19 coronavirus infection.Material and methods A prospective cohort comparative study was conducted, with subsequent retrospective analysis of perinatal outcomes and the results of histologic examination of the placentas in 53 pregnant women with COVID-19 NCI. Group 1 was composed of 25 women with NKI COVID-19 complicated by community-acquired pneumonia with critical lung injury (KT-4, 76% or more); Group 2 was composed of 28 pregnant women with NKI COVID-19 complicated by community-acquired pneumonia with moderate-to-severe lung injury (KT-2, 25-50%). Perinatal outcomes and the results of morphological examination of the placenta were analyzed using the provisions of the classification of placental injuries developed by the Amsterdam Placenta Workshop Group (2014).Results In the main group, there were no children born with signs of miscarriage, while in the comparison group there were 8.7% of such children. SARS-CoV-2 antigen was diagnosed in a nasopharyngeal swab immediately after birth in 1 (4.3%) live-born infant in group 2 by PCR. The child died in the postnatal period on the 33rd day of life. Antenatal fetal death in women of Group 1 was the result of marked maternal hypoxia and extremely early PP, in Group 2 - the consequence of placental lesions. A wide spectrum of placental damages, including maternal and fetal malperfusion, maternal and fetal COVID-19 complicated by critical lung injury and with moderate lung injury.Discussion The placentas of pregnant women delivered due to critical condition do not have pronounced inflammatory and distrophic disorders, being characterized by the phenomena of acute PU. On the contrary, the placentas of women who successfully completed treatment with COVID-19 NKI of moderate severity and safely delivered at late gestational age exhibit the full spectrum of inflammatory and hypoxic lesions, leading to subcompensated and decompensated PU.Conclusion Weakly pronounced dystrophic processes, lymphocytic infiltration of the decidual and fetal membranes, signs of partial maternal vascular malperfusion and fetal stromal-vascular lesions, and acute PU phenomena were recorded in the placentas of women with NCI COVID-19 and critical pulmonary lesions. The absence of marked inflammatory infiltration of villi and fetal membranes, dystrophic processes, intervillous thrombosis, and villous infarcts realized in decompensated PU in the placentas of these patients was due to the immediate delivery of pregnant women with critical pulmonary lesions in NCI COVID-19.
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