Pathogenesis of placental insufficiency

The primary links in the pathogenesis of placental insufficiency are a decrease in uteroplacental blood flow, a lag in the formation of cotyledons and placental placental circulation. Against this background, the development of compensatory-adaptive mechanisms in the placenta is usually strengthened, especially in the early stages of pregnancy. As a result of excessive stimulation of compensatory mechanisms premature maturation of the placenta occurs, which leads to disruption of adaptive reactions and the emergence of a threat of interruption at any stage of gestation. The fetus develops under conditions of chronic hypoxia, which leads to the birth of a child with pronounced signs of intrauterine growth retardation, more often of a symmetrical nature.

It is now generally recognized that one of the most oxygen-dependent and, therefore, the most sensitive to the damaging effect of hypoxia, is the neural tissue, which becomes the initial object of the pathological effect of oxygen deficiency.

Hypoxia delays the maturation of brain stem structures in the embryo as early as 6-11 weeks of development, causes vascular dysplasia, slows the maturation of the blood-brain barrier, whose imperfection and increased permeability, in turn, are key to the onset of organic pathology of the central nervous system. In the postnatal period, neurologic disorders of hypoxic genesis vary in a wide range: from functional disorders of the central nervous system to severe syndromes of mental development disorders.

The high level of perinatal abnormalities in pregnancy, complicated by placental insufficiency and miscarriage, dictates the need for further, more in-depth study of this problem.

The generally accepted classification of placental insufficiency due to its multifactorial nature, the possibility of occurrence at different times, varying degrees of clinical manifestations has not been developed at present.

Based on the morphological changes that lead to universal reactions in the maternal and fetal body and, thus, are not isolated, it identifies three forms of placental insufficiency:

1. Hemodynamic, caused by abnormalities in the utero-placental and fertile-placental basins.
2. Placental-membrane, characterized by a decrease in the ability of the placental membrane to transport metabolites.
3. Cell-parenchymal, associated with violations of the cellular activity of trophoblast and placenta.

For practical medicine, it is more important to distinguish between placental insufficiency and primary (up to 16 weeks), which is caused by vascular and enzymatic insufficiency due to a violation of the hormonal function of the ovaries, changes in endometrium and myometrium, women's physical illnesses and environmental hazards. Secondary placental insufficiency is a consequence of a violation of uterine blood flow as a result of hypo- or hypertension in the mother, heart attacks, placental abruption, changes in the rheological properties of the blood, and inflammatory reactions due to the presence of an infectious agent in the mother's body at a later date.

With habitual miscarriage, placental insufficiency is always primary. This is due to the polyethiologic nature of habitual miscarriage (hypofunction of the ovaries, failure of the receptor apparatus of the uterus due to frequent previous curettage or genital infantilism, the presence of inflammatory reactions in myometrium, and coagulopathic changes in autoimmune processes). In addition, the primary placental insufficiency arises from anatomical disruption in the structure, location and attachment of the placenta, as well as defects in vascularization and disturbances in the ripening of the chorion.

Distinguish between acute and chronic placental insufficiency. In the pathogenesis of acute insufficiency, an important role is played by acute violation of decidual perfusion, which translates into circular damage to the placenta. This type of placental insufficiency arises as a result of extensive placenta infarcts and premature detachment at its normal location (PONRP) with the formation of a retrocopental hematoma, as a result of which the fetal death and termination of pregnancy occur relatively quickly. The leading role in the pathogenesis of PONPR is played by violations of the implantation and placentation process. A certain role in this is given to hormonal factors, mental and mechanical trauma.

Chronic placental insufficiency) is observed in every third woman from the group of high perinatal risk. It manifests itself first by a violation of the nutritional function, and then by hormonal disorders. Later, there may be signs of impaired respiratory function of the placenta. In the pathogenesis of this type of pathology, chronic disorder of decidual perfusion with violation of placentation and placental regulation is of primary importance. Perinatal mortality in chronic placental insufficiency is 60%.

Chronic placental insufficiency is characterized by a clinical picture of a prolonged threat of abortion and a delay in the development of the fetus in II and more often in the III trimesters. The development of chronic placental insufficiency against the background of disorders of compensatory reactions of microcirculation can lead to absolute placental insufficiency and intrauterine fetal death. The preservation of compensatory processes indicates a relative placental insufficiency. In these cases, pregnancy usually ends with timely delivery, but it is possible to develop ante- or intranatal hypoxia and / or fetal hypotrophy of varying severity. Some authors (Radzinsky VE, 1985) distinguish compensated, subcompensated and decompensated forms of placental insufficiency.

Despite the multifactorial nature of placental insufficiency, there are certain patterns in the development of this syndrome. As a rule, two main ways of formation of chronic placental insufficiency can be clearly distinguished:

• Violation of nutritional function or trophic insufficiency, in which the absorption and assimilation of nutritious products is disrupted, as well as the synthesis of the own metabolic products of the fetus;
• Respiratory failure, consisting in violation of oxygen and carbon dioxide transport.

It should be noted that the occurrence of placental insufficiency in the first type occurs at the earliest stages of pregnancy and more often leads to a delay in the intrauterine development of the fetus. Both named ways of development of a disturbance of function of a placenta can exist independently or be combined with each other. They underlie the pathogenesis of both primary and secondary placental insufficiency.

[1], [2], [3], [4], [5], [6], [7], [8], [9], [10], [11]