Ultrastructure of placenta in antenatal fetal death

The current obstetrical protocols and the improved perinatal services have led to a significant decrease in the intrapartum and neonatal mortality; however, the rate of antenatal fetal death remains high. In a search for a mechanism of this abnormality, we conducted a comprehensive morphological study of the placental ultrastructure in women with antenatal fetal death. Aim: to determine the ultrastructural characteristics of the placenta in these women. Materials and methods. We analyzed 60 cases of antenatal fetal death and conducted an electron microscopic study of placental terminal chorionic villi. The placenta samples were fixed in 2.5% glutaraldehyde, then processed in alcohol at increasing concentration and acetone for dehydration, and finally polymerized in araldite resin. Ultrathin sections were obtained using an ultra-microtome and then examined with an electron microscope. Results. In 53 (88.3%) women, antenatal fetal death occurred in the early gestation period and in 7 (11.7%) women – at a period of 38-41 weeks. In the main group, the age of women ranged from 18 years to 42 years, and in the comparison group – from 22 to 37 years. In the main group, 16 (26.6%) women were in the late reproductive period (36 years and older). Among the women with antenatal fetal death, the most common diagnoses were: chronic fetoplacental insufficiency (CFPI) – 23 (39%), fetal development retardation syndrome (FDRS) – 16 (27%), and premature detachment of a normally situated placenta (PDNSP) – 10 (17%). Changes in the syncytiotrophoblast structure were detected in patients of both groups; in these changes, signs of vacuolization and destruction were most common. In women of the main group, sclerotic stroma and infiltration by mononuclears were found, whereas loosening and swelling of the stroma were detected in both groups. Changes in the vascular bed were revealed in 100% of cases with antenatal fetal death and in 40% in comparison group. Conclusion. In antenatal fetal death, the most common causes were: CFPI, FDRS, and PDNSP. In the morphological terms, there were destructive changes in the syncytiotrophoblast, edematous-destructive, sclerotic and necrotic changes in the stromal terminal chorionic villi, vascular changes (hypovascularization, stroma obliteration, stasis and erythrocyte sludging, formation of erythrocyte thrombi in the lumens of blood vessels), dysfunctional changes in endotheliocytes, and inflammatory changes.

Antenatal fetal death, placenta, chronic fetoplacental insufficiency, endothelial dysfunction