Pathomorphological changes of the placenta in antenatal asphyxia of the fetus associated with the coronavirus disease (COVID-19) in pregnant women

Abstract

The objective: to determine the pathomorphological changes in the placenta by antenatal asphyxia of the fetus associated with the coronavirus disease (COVID-19) in pregnant women.Materials and methods. 21 placentas by fetal antenatal asphyxia which occurred at different terms of pregnancy in women with COVID-19 were examined. COVID-19 was diagnosed by a positive PCR test – detection of SARS-CoV-2 RNA. The study groups were defined depending on the duration of the post-covid interval (time from the diagnosis of COVID-19 to delivery). I group (n=12) included placentas of women with antenatal fetal asphyxia, in whom the postpartum interval was 1–4 weeks; II group (n=9) – placentas of women with fetal death, in whom the postpartum interval was 5–14 weeks.In the I group, antenatal asphyxia of the fetus occurred in the term from the 13th to 36th weeks of gestation, in the II group – in period from the 29th to the 41st week. Macroscopic, organometric, microscopic methods of placenta research and a statistical method were applied. Fetal-placental index (FPI) was calculatedResults. In the studied cases, antenatal fetal death occurred in different terms of pregnancy, namely, from the 14th to the 41st week of gestation (median is 32 weeks). Pregnant women had COVID-19 from the 13th to the 35th week of gestation (median is 25 weeks); when the mother was diagnosed with COVID-19 after the 35th week, there was no case of antenatal fetal death. The severity of the course of the coronavirus disease was mild in 7 pregnant women, moderate – 12 persons, and a severe course with pneumonia was diagnosed in 2 women. The severity of morphological changes in the placenta did not depend on the severity of the course of COVID-19 in the pregnant woman (chorioamnionitis, p=1.0; intervillositis, p=0.63; obliteration of arterioles, p=0.32).In the I group, a slight increase in FPI was found up to 0.19 [0.12; 0.34], in the II group – a similar indicator was 0.16 [0.13; 0.24]. However, the absolute values of the weight of the fetus and placenta in both groups were lower than those for the given gestational age.The I group of placentas there were the pronounced inflammatory changes – placentitis: chorioamnionitis – 100% (95%CI: 85.4–100) and basal deciduitis – 91.7% (95%CI: 67.1–100). In the II group the inflammatory changes of the chorioamniotic membranes and basal plate were focal and were found in 6 placentas – 66.7% (95% CI: 29.2–94.8). Intervillositis was detected in 11 placentas – 91.7% (95%CI: 67.1–100) in the I group versus 2 placentas – 22.2% (95%CI: 1.1–58.9; p=0.006) in the II group.Villositis in the I group was determined in 8 cases – 66.7% (95%CI: 35.4–91.4) and in only one placenta in the II group – 11.1% (95%CI: 0.0–43.91; p=0.034). In the placentas of both groups the fibrinoid necrosis of the arteriole wall, proliferative changes in the vessel wall and necrosis of the endothelium were detected – 100% (95%CI: 85.4–100), dyscirculatory disorders (stasis, thrombosis, hemorrhages) were found in 75% (95% CI: 44.4–95.8) of cases in the I group and in 66.7% (95% CI: 29.2–94.8) – in the II group. An increased number of syncytial nodules was observed as a manifestation of compensatory mechanisms: in the I group – 83.3% (95%CI: 54.7–98.9), in the II group – 88.9% (95%CI: 56.1–100).All studied cases in the II group were accompanied by obliteration of the lumen of the arterioles of trunk and semi-trunk villi – 100% (95%CI: 80.9–100; p=0.0006), versus the I group – 16.7% (95%CI: 1.1–45.3). At the same time, in 6 cases in the II group the morphological manifestations of restoration of the lumen (revascularization) were detected – the formation of intravascular septa – 66.7% (95% CI: 29.2–94.8), which were not found in the I group (р=0.0093). In 100% (95%CI: 80.9–100) of placentas of the II group and in 66.7% (95%CI: 35.4–91.4) of the I group the stroma fibrosis of stem and semi-stem villi, obliteration intervillous space, and hypoplasia of terminal villi were determined.Conclusions. Statistically significant differences of placentas in antenatal asphyxia of the fetus depended on the length of the postcovid interval: in the postcovid interval of 1–4 weeks (I group) the inflammatory changes prevailed – placentitis: chorioamnionitis – 100% (95%CI: 85.4–100), intervillositis – 91.7% (95% CI: 67.1–100), p=0.006; villositis – 66.7% (95%CI: 35.4–91.4), p=0.034. When the duration of the postcovid interval increased to 5–14 weeks (II group), arteriosclerosis prevailed – 100% (95% CI: 80.9–100); p=0.0006.The cause of antenatal fetal death in the women with COVID-19 in the I group is acute placental insufficiency associated with the exudative phase of inflammation (chorioamnionitis, villositis, intervillositis). In the II group, the cause of antenatal fetal asphyxia is the formation of chronic placental dysfunction caused by the proliferation phase, which was manifested by proliferative changes in the muscular layer of arterioles and their subsequent fibrosis with obliteration of the lumen of arterioles (arteriosclerosis).