Pathological features of the placenta in intrapartum fetal death

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Introduction. It is not a secret that intrapartum fetal death is 8 times higher than maternal mortality [1]. The etiology and pathogenesis of stillbirth remain unknown to present obstetrics. Studies of the morphological structure of the placenta can provide basic information about the peculiarities of pregnancy and fetal development. In this regard, the need for a full-fledged morphological examination of the placenta becomes relevant.

The aim of this study is to analyze the morphological structure of the placenta during pregnancy complicated by intrapartum fetal death.

Materials and methods. A retrospective analysis of 136 cases of antenatal fetal death in patients treated at obstetric and gynecological hospitals in the Kursk region for the period 2021-2022 was carried out. The patients were divided into groups according to gestation periods: 22-28 weeks (n=29), 29-33 weeks (n=43), 34-36 weeks (n=27), 37-42 weeks (n=37). In the postpartum period we performed a morphological examination of the placenta with an assessment of the structure of the placental tree, types of villi, the severity of compensatory and adaptive reactions, the presence of inflammatory and dystrophic changes in the placenta. Statistical correlation was performed by using the Spearman coefficient in the SPSS Statistics program. The results were statistically significant at p<0.05.

Results. We found that placental mass decreased significantly with stillbirth. At 22-28 weeks, signs of primary placental insufficiency were detected in 91% of the drugs. Vascular lesions were represented by placental infarctions in 50% of the drugs, acute inflammatory immune disorders represented by deciduitis, chorioamnionitis were detected in 45% of the drugs.

At 29-33.6 weeks, compensatory mechanisms corresponded to the gestation period of 40% of the drugs. Vascular lesions of the placenta were detected in 55%, acute inflammatory immune processes (intervillusitis, chorioamnionitis) – in 40%, chronic inflammatory immune processes – in 9%. The morphological structure of the placenta at  34-37 weeks was characterized by vascular lesions of the placenta in 30%, acute inflammatory and immune processes in 11%. Compensatory mechanisms are moderately expressed in 56% of drugs.

At 37-42 weeks, moderately pronounced compensatory mechanisms of the placenta were noted in 70%, vascular lesions, including umbilical cord vascular thrombosis, in 30%, acute inflammatory and immune processes in 5% of drugs.

Regression statistical analysis showed that the time of fetal death depends on severity of changes in the placenta. Thus, earlier fetal death was associated with less pronounced compensatory reactions of the placenta and the presence of acute placental insufficiency. It was also revealed that infectious genesis (r=0.96), complications of maternal somatic pathology (r=0.7), along with chronic endometritis (r=0.7), a history of reproductive losses (r=0.53) and late childbearing age (r=0.6) (p<0.05) led to placental insufficiency.

Conclusion. To sum up, significant information about the etiology of stillbirth can be collected by examining the morphological structure of the placenta, and can be used to determine the cause of fetal death. Moreover, it can help to develop measures for the management and to prevent  pregnancy with  stillbirth in the future.

About the authors

Alina Sergeevna Rubtsova

Kursk state medical university

Email: alina55.rubtsova@yandex.ru
ORCID iD: 0009-0003-8990-9666
SPIN-code: 2652-0366

Student

Russian Federation, 3 K. Marx Street, Kursk, Kursk region, 305041, Russian Federation

Oxana Yurievna Ivanova

Kursk State Medical University

Author for correspondence.
Email: ivanovanv@kursksmu.net
ORCID iD: 0000-0003-2350-1740
SPIN-code: 5064-5808

Head of the Department of Obstetrics and Gynecology, Kursk State Government Medical University Ministry of Health of Russia, MD.

Russian Federation, 3 K. Marx Street, Kursk, Kursk region, 305041, Russian Federation

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