Relevance. Every year the frequency of formation of placental insufficiency in pregnant women is steadily progressing, and women with a history of intrauterine interventions occupy a special place. To one degree or another, they have a detrimental effect not only on the endometrium, but also on the uterine vessels, which, in turn, during the onset of a desired pregnancy will lead to disruption of the trophoblast invasion, absence or insufficient gestational reconstruction of the spiral arteries and, as a consequence, a violation of the basic functions of the placenta (gas exchange, trophic, excretory, protective and intrasecretory) [1, p.23].
Violations of the morphofunctional state of the placenta are one of the main causes of the complicated course of pregnancy and childbirth, as well as perinatal morbidity and mortality. Pathological changes that occur with placental insufficiency lead to: decrease in utero-placental and fetoplacental blood flow; decrease in arterial blood supply to the placenta and fetus; restriction of gas exchange and metabolism in the fetoplacental complex; violation of the processes of maturation of the placenta; reduced synthesis and imbalance of placental hormones and their precursors of maternal and fetal origin. All these changes suppress the compensatory and adaptive capabilities of the mother-placenta-fetus system, slow down the growth and development of the fetus, and cause a complicated course of pregnancy and childbirth [2, p.51].
The pathomorphological picture of the placenta in case of placental insufficiency is characterized primarily by degenerative-dystrophic changes, a violation of the utero-placental blood flow, a change in the permeability of the stroma of the villi, signs of impaired maturation of the villi, and a number of other phenomena. Moreover, the severity of pathological changes depends on the severity and duration of the complication and the nature of the compensatory-adaptive reactions. Often the development of fetoplacental insufficiency is accompanied by a decrease in the placenta parameters (mass, volume, maternal surface area), which indicates a violation of its compensatory capabilities [3, p.75].
As a result of exposure to damaging factors and the implementation of pathogenetic mechanisms leading to placental insufficiency, fetal hypoxia develops. Most often (according to the development mechanism), arterial-hypoxemic and mixed forms of hypoxia are observed due to a decrease in the oxygen content in the mother’s blood, a decrease in the utero-placental blood flow, a violation of the transport function of the placental barrier, changes in the rheological properties of the blood, anemia, fetal malformations, and also a number of others reasons [4, p.16].
The aim of the study – was to study the incidence of fetoplacental insufficiency in women with a history of intrauterine intervention.
Materials and methods. A retrospective and prospective analysis of clinical, laboratory and instrumental examination of 50 pregnant women was carried out. Two groups of patients of 20 and 30 women, respectively, were formed. Group 1 included women with a normal pregnancy; group 2 included women who had a history of one or another intervention in the uterine cavity and fetoplacental insufficiency in a real pregnancy.
The criteria for inclusion of patients in the study were: one-pregnancy at a gestational age of 22 to 37 weeks, a confirmed diagnosis of fetoplacental insufficiency. Exclusion criteria: multiple pregnancy, extragenital pathology in the pregnant woman in the decompensation stage, diagnosed fetal malformations.
Results of the study. The average age of patients in the first group amounted to 23.2±0.08 years, in the second group – 24.4±0.08. When comparing groups of pregnant women, it was revealed that a burdened gynecological history in the form of infectious and inflammatory diseases was detected in a larger percentage of cases in group 2 of the study: vaginitis (54.4%), adnexitis and periadnexitis (62.2%).
Also in group 2 among disorders of reproductive function there are medical abortion (44%), spontaneous miscarriage (6.2%), missed pregnancy (4.4%), infertility II (16.2%), while in patients of group 1 no such violations have been identified.
Diagnostic curettage of the uterine cavity for one reason or another was in the anamnesis of 55% of women from group 2 of the study. In the group 1 of the study, no such cases were detected.
Intrauterine contraceptives for 3 years or more were used by 10% of women from group 2. Women from the group 1 did not use this method of contraception, but preferred interrupted sexual intercourse or condoms.
Complications of this pregnancy are observed to a greater extent in group 2: placental insufficiency (100%), low placentation (34.4%), fetal growth retardation syndrome (28.2%), the threat of early termination of pregnancy (52.4%), oligohydramnios (32.2%), pregnant anemia (14.2%), polyhydramnios (8.4%). Complications of this pregnancy in group 1 were represented by anemia of pregnant women (18.4%), edema of the lower extremities (8.2%), polyhydramnios (4.2%).
Analysis of the placenta showed that with an average mass of the placenta
486±0.31 g; the diameter of their terminal villi is 31.2±1.2 μm. The following picture was revealed microscopically: the predominance of mature type villi, in which non-uniform deficit of terminal branches – 100%; focal deposits of maternal fibrinoid – 74%; edge arrangement of the umbilical cord – 52%; foci calcifications – 38%. Macroscopic examination placenta there is a reduced placental-fetal coefficient. The presence of compensatory-adaptive reactions is evidenced by the presence of syncytio-capillary membranes, syncytio-capillary kidney overgrowth of maternal fibrinoid.
Conclusions. The results of the study confirm the direct effect of intrauterine interventions of various etiologies in history on the formation of placental insufficiency in subsequent pregnancy. Intrauterine interventions adversely affect the endometrium and blood vessels of the uterus.
References
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- Kramarenko, O.P. Prognosis, prophylaxis, and early therapy of fetoplacental insufficiency / O.P. Kramarenko // Lik. Sprava. – 2011. – Vol. 2. – P. 50-53.
- Salafia, C.M. Placental pathology and fetal growth restriction / C.M. Salafia // Clinical Obstetrics and Gynecology – 2012. – Vol. 40. – P. 74-79.
- Spencer, K. First-trimester biochemical markers of aneuploidy and the prediction of small-forgestational age fetuses / K. Spencer, N.J. Cowans, K. Avgidout // Ultrasound Obstetrics and Gynecology – 2011. – Vol. 3. – № 11. – P. 15-19.
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