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 fetoplacental blood circulation. Against this background, the development of compensatory-adaptive mechanisms in the placenta is usually enhanced, 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 a breakdown 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, often symmetrical.

It is currently generally recognized that one of the most oxygen-dependent and, therefore, most sensitive to the damaging effects of hypoxia is nervous tissue, which becomes the initial target of the pathological effects of oxygen deficiency.

Hypoxia delays the maturation of the structures of the brain stem in the embryo from 6-11 weeks of development, causes the occurrence of vascular dysplasia, slows down the maturation of the blood-brain barrier, the imperfection of which and increased permeability, in turn, are key to the occurrence of organic pathology of the central nervous system. In the postnatal period, neurological disorders of hypoxic genesis vary widely: from functional disorders of the central nervous system to severe syndromes of mental development disorders.

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

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

Based on morphological changes that lead to universal reactions in the body of the mother and fetus and, therefore, are not isolated, three forms of placental insufficiency are distinguished:

1. Hemodynamic, caused by disturbances in the uteroplacental and fetal-placental basins.
2. Placental-membrane, characterized by a decrease in the ability of the placental membrane to transport metabolites.
3. Cellular-parenchymatous, associated with disturbances in the cellular activity of the trophoblast and placenta.

For practical medicine, it is more important to differentiate placental insufficiency into primary (up to 16 weeks), which is caused by vascular and enzymatic insufficiency due to disruption of the hormonal function of the ovaries, changes in the endo- and myometrium, somatic diseases of the woman, and harmful environmental factors. Secondary placental insufficiency is a consequence of disruption of uterine blood flow as a result of hypo- or hypertension in the mother, infarctions, detachment of part of the placenta, changes in the rheological properties of the blood, as well as inflammatory reactions due to the presence of an infectious agent in the mother's body at later stages.

In habitual miscarriage, placental insufficiency is always primary. This is due to the polyetiology of habitual miscarriage (ovarian hypofunction, failure of the uterine receptor apparatus due to frequent previous curettage or genital infantilism, the presence of inflammatory reactions in the myometrium, as well as coagulopathic changes in autoimmune processes). In addition, primary placental insufficiency occurs due to anatomical disruption of the structure, location and attachment of the placenta, as well as vascularization defects and disruptions in the maturation of the chorion.

A distinction is made between acute and chronic placental insufficiency. In the pathogenesis of acute insufficiency, a major role is played by acute decidual perfusion disorder, which develops into circular damage to the placenta. This type of placental insufficiency occurs as a consequence of extensive placental infarctions and premature detachment with its normal location (PND) with the formation of a retroplacental hematoma, which results in relatively rapid fetal death and termination of pregnancy. The leading role in the pathogenesis of PND is played by disorders of the implantation and placentation process. A certain role is given to hormonal factors, mental and mechanical trauma.

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

Chronic placental insufficiency is characterized by a clinical picture of a long-term threat of termination of pregnancy and delayed fetal development in the second and, more often, third trimesters. The development of chronic placental insufficiency against the background of disturbances in compensatory reactions of microcirculation can lead to absolute placental insufficiency and intrauterine death of the fetus. Preservation of compensatory processes indicates relative placental insufficiency. In these cases, pregnancy usually ends with timely delivery, but the development of ante- or intranatal hypoxia and/or fetal hypotrophy of varying severity is possible. Some authors (Radzinsky V.E., 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 developing chronic placental insufficiency can be clearly identified:

• A violation of the nutritional function or trophic insufficiency, in which the absorption and assimilation of nutrients, as well as the synthesis of the fetus's own metabolic products, are disrupted;
• Respiratory failure consisting of a disruption in the transport of oxygen and carbon dioxide.

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

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