What does placental insufficiency mean? Placental insufficiency, placental insufficiency and its consequences, intrauterine growth restriction (IUGR)

Fetoplacental insufficiency (FPI) is a condition where placental function is impaired. This usually reveals structural changes in the placenta. To one degree or another, FPN is detected in approximately every third pregnant woman, so this problem is extremely relevant.

With fetoplacental insufficiency, all functions of the placenta are disrupted. Because of this, the fetus begins to experience oxygen starvation (hypoxia), its growth and development are delayed, it becomes more susceptible to infection and harmful metabolic products. Due to disruption of the hormonal function of the placenta, the risk of premature birth and labor abnormalities is increased.

The following risk factors for FPI are identified:

Chronic diseases of the mother (heart defects, bronchial asthma, diabetes mellitus, thyroid pathology, etc.);

Infections. The condition of the placenta can be affected by foci of chronic infection in the body ( chronic diseases respiratory tract, carious teeth), sexually transmitted diseases, colds and others infectious diseases during pregnancy;

Complicated course of pregnancy (threat of miscarriage, gestosis, Rhesus conflict);

Pathology of the uterus (uterine fibroids, adenomyosis, malformations - bicornuate or saddle-shaped uterus, chronic endometritis);

Incorrect attachment of the placenta - low placentation or placenta previa, since the blood supply to the lower parts of the uterus is worse.

Abortions, spontaneous miscarriages, history of regressive pregnancies;

Unfavorable environmental factors (occupational hazards, improper or insufficient nutrition, poor ecology);

Stress and psycho-emotional tension;

Smoking during pregnancy;

Age (before 18 and after 35 years, FPN is observed more often than in others).

Normally, the blood vessels of the placenta are constantly dilated, which ensures a uniform supply of oxygen and nutrients to the fetus. With pathology, the vessels spasm and blood flow is disrupted. In addition, the state of the blood coagulation system is important. As blood clotting increases, it becomes more viscous, and microthrombi form in the blood vessels of the placenta, disrupting blood circulation in the placenta.

Naturally, with FPN the fetus begins to suffer. With fetoplacental insufficiency, the fetus often experiences hypoxia. In this case, the fetus is more susceptible to birth injuries. In newborns, the adaptation process is more difficult; subsequently, diseases of the nervous system and developmental anomalies (torticollis, hip dysplasia) are more often detected. Children born to mothers with FPN are more likely to have respiratory infections and intestinal disorders.

Classification and symptoms

There are primary and secondary placental insufficiency. In case of primary failure, a violation of the structure and function of the placenta develops already during its formation (at 16-18 weeks). IN in this case the prognosis is unfavorable, in most cases the pregnancy cannot be carried to term when the fetus is viable, spontaneous miscarriage. With secondary placental insufficiency, a normal placenta is initially formed, but more late dates its function is disrupted for some reason.

Based on the degree of impairment of the fetal condition, compensated, subcompensated and decompensated FPN are distinguished. In the compensated form of FPN, it is diagnosed by ultrasound, the fetus does not suffer, and there is no delay in fetal development. In the subcompensated form, fetal growth retardation begins. In the decompensated form, severe heartbeat disturbances, severe delay in fetal development (more than 4 weeks compared to the gestational age) are observed; in especially severe cases, fetal death fetus

While fetoplacental insufficiency is compensated, it does not manifest itself in any way and is detected only through special research methods. With severe FPN, when the fetus begins to suffer, the woman can first cancel more active fetal movements, and then a decrease in the number of movements (normally, from 28 weeks, a woman should feel movements at least 10 times a day).

When fetal development is delayed, there is a decrease in the size of the abdomen (abdominal circumference and height of the uterine fundus). They focus mainly on the height of the uterine fundus (UFH), since the abdominal circumference strongly depends on the thickness of the subcutaneous fat. Normally, IMD in cm approximately corresponds to the gestational age in weeks. In addition, the doctor evaluates the size of the abdomen over time.

Ultrasound is used to evaluate the nature of the fetal motor activity, the thickness and degree of maturity of the placenta. Normally, the thickness of the placenta in cm up to 37-38 weeks approximately corresponds to the gestational age in weeks, then the thickness of the placenta remains the same or may even decrease by 1-2 mm. A dysfunction of the placenta is indicated by a decrease or increase in its thickness by more than 5 mm compared to the normative indicators for a given period.

Normally, before 30 weeks, 0 degree of maturity is determined, from 30 to 35 weeks - I degree, at 35-38 weeks - II degree, after 38 weeks - III degree of maturity. With FPN, the placenta “ripes” earlier than it should (this is called premature aging of the placenta).

With fetoplacental insufficiency, there may be deposition of calcifications (calcium salts) in the placenta. In addition, there may be gaps in the placenta, which are called expansion of the intervillous spaces. In some cases, placental cysts are detected.

The size of the fetus must be measured and its compliance with the term assessed. If the size of the fetus does not correspond to the term, then they speak of delayed fetal development.

Sometimes with FPN the amount of water changes; there can be both polyhydramnios and oligohydramnios.

Doppler testing is mandatory - assessing the speed of blood flow in the vessels. Most often, blood flow is assessed in the vessels of the uterus, umbilical cord, and fetal brain.

Fetal hypoxia can be diagnosed using cardiotocography (CTG). At the beginning, the fetus responds to hypoxia by increasing the heart rate; as hypoxia progresses, the heart rate, on the contrary, slows down. There may be an arrhythmia. In addition, the cardiotocogram may show decelerations - areas of decreased heartbeat.

Treatment

First of all, you need to try to identify and eliminate the cause that caused the dysfunction of the placenta. It is necessary to carry out timely treatment of gestosis and the threat of miscarriage, to actively identify and treat infection in the body.

Compensated FPN does not require hospitalization. Decompensated and subcompensated FPN are treated in a hospital.

A pregnant woman needs to ensure adequate rest. Night sleep should be at least 9-10 hours, it is necessary to protect the woman from psycho-emotional stress. A balanced diet is important, with which a woman should receive a sufficient amount of protein, essential vitamins and microelements. It is advisable to use multivitamins, especially in the cold season, when there are few fresh fruits and vegetables.

There are no effective means to completely get rid of existing fetoplacental insufficiency and restore the normal morphological structure of the placenta. The means used are aimed at stabilizing the pathological process and maintaining compensatory and adaptive mechanisms.

The goals of treatment are to improve uteroplacental blood flow, improve gas exchange, correct the blood coagulation system, normalize vascular and uterine tone, and optimize metabolic processes.

To treat and prevent fetal hypoxia, oxygen cocktails can be prescribed. Currently, in pharmacies you can buy a kit for making an oxygen cocktail at home. The cocktail is usually prepared using juices or water.

The drug curantil is often used for FPN. It improves microcirculation, prevents dystrophic changes in the placenta, and eliminates hypoxia in fetal tissues. Side effects if the drug is used taking into account contraindications are extremely rare. When taken simultaneously with heparin or aspirin, the risk of bleeding is increased. Usually the drug is prescribed in courses of up to 1 month.

Another common drug is Actovegin. It is prescribed quite often, as it activates metabolic processes in tissues and improves microcirculation. The exact effect of Actovegin in FPN has not been proven, but it is assumed based on the mechanism of action of the drug. There is evidence that after taking Actovegin, a large fetus is more likely to occur, so if there is a tendency for a large fetus, they try not to prescribe it.

If treatment is carried out in a hospital, complex therapy includes droppers that improve uteroplacental blood flow (glucose-novocaine mixture, aminophylline). To relax the uterus, droppers with magnesium or ginipral are used.

In case of increased blood clotting, drugs that correct it are used, for example Heparin, Graxiparin, Clexane (antiplatelet agents).

It is impossible to list all the drugs used to treat FPN, since in each case the treatment is selected individually.

The question of the method of delivery is also decided individually. If the therapy is effective, there is no significant fetal suffering, and the cervix is ​​mature, then childbirth is carried out through the natural birth canal. If decompensated FPN is observed, therapy is ineffective, the issue of emergency delivery is resolved, most often by cesarean section.

Fetoplacental insufficiency (FPI) is a symptom complex in which various disorders occur, both from the placenta and from the fetus, due to various diseases and obstetric complications. The variety of variants of manifestation of FPN, the frequency and severity of complications for the pregnant woman and the fetus, the predominant violation of one or another function of the placenta depend on the duration of pregnancy, the strength, duration and nature of the influence of damaging factors, as well as on the stage of development of the fetus and placenta, the degree of expression of compensatory and adaptive capabilities “mother-placenta-fetus” system.

Causes of FPN

FPN can develop under the influence various reasons. Disturbances in the formation and function of the placenta can be caused by diseases of the heart and vascular system of the pregnant woman (heart defects, circulatory failure, arterial hypertension and hypotension), pathology of the kidneys, liver, lungs, blood, chronic infection, diseases of the neuroendocrine system (diabetes mellitus, hypo- and hyperfunction of the thyroid gland, pathology of the hypothalamus and adrenal glands) and a number of other pathological conditions. FPN in anemia is caused by a decrease in the level of iron both in the maternal blood and in the placenta itself, which leads to inhibition of the activity of respiratory enzymes and the transport of iron to the fetus. In diabetes mellitus, metabolism is disrupted, hormonal disorders and changes in immune status are detected. Sclerotic vascular damage leads to a decrease in the supply of arterial blood to the placenta. An important role in the development of FPN is played by various infectious diseases, especially those occurring in an acute form or worsening during pregnancy. The placenta can be affected by bacteria, viruses, protozoa and other infectious agents.

Of no small importance in the formation of FPN is the pathology of the uterus: endometriosis, myometrial hypoplasia, malformations of the uterus (saddle-shaped, bicornuate). Uterine fibroids should be considered a risk factor for FPN. However, the risk of FPN varies among pregnant women with uterine fibroids. The high-risk group includes primigravidas aged 35 years and older with a predominantly intermuscular location of myomatous nodes large sizes, especially when the placenta is localized in the area where the tumor is located. The group with a low risk of FPN consists of young women under 30 years of age without severe extragenital diseases, with small myomatous nodes, predominantly subperitoneal, in the fundus and body of the uterus.

Among the complications of pregnancy that most often accompany FPN, the leading place is occupied by gestosis. The threat of miscarriage should be simultaneously considered both as a cause and as a consequence of FPN. Due to the different etiology of FPN when there is a threat of miscarriage, the pathogenesis of this complication has various options, and the prognosis for the fetus depends on the degree of development of protective and adaptive reactions. With a low location or placenta previa, vascularization of the subplacental zone is reduced. The thinner wall of the lower segment of the uterus does not provide the necessary conditions for sufficient vascularization of the placental bed and its normal functioning.

Relatively often, with this pathology, placental abruption occurs, accompanied by blood loss. Multiple pregnancy represents a natural model of FPN as a result of inadequate provision of the needs of two or more fetuses. The basis of FPN in isoserological incompatibility of the blood of mother and fetus most often lies in the processes of impaired maturation of the placenta. The fetus develops anemia and hypoxia, developmental delay occurs due to disturbances in protein synthesis processes and decreased enzyme activity. The functional state of the placenta is largely determined by the degree of its development in accordance with the gestational age and the preservation of protective and adaptive mechanisms. Matching the maturity of the placenta to the gestational age is one of the most important conditions for ensuring adequate development of the fetus and its protection. There is no doubt that the late age of a pregnant woman (over 35 years old) or, conversely, young age (under 17 years old), a burdened medical history (abortions, inflammatory diseases), bad habits, exposure to adverse environmental factors, poor nutrition, social vulnerability and household instability are also contribute to complicated formation of the placenta and disruption of its function.

Clinical practice and results scientific research indicate the multifactorial nature of FPN. In this regard, it is almost impossible to identify any single factor in the development of this complication. The listed pathological conditions do not equally influence the development of FPN. Most often, several etiological factors are involved in the development of this pathology, one of which may be leading. Pathological changes, which occur during FPN, lead to a decrease in uteroplacental and fetoplacental blood flow; decreased arterial blood supply to the placenta and fetus; limitation of gas exchange and metabolism in the fetoplacental complex; disruption of placental maturation processes; decreased synthesis and imbalance of placental hormones. All these changes suppress the compensatory and adaptive capabilities of the “mother-placenta-fetus” system, slow down the growth and development of the fetus, cause a complicated course of pregnancy and childbirth (threat of premature termination of pregnancy, gestosis, premature and late birth, labor anomalies, premature detachment placenta, etc.).

As a result of exposure to damaging factors and the implementation of pathogenetic mechanisms leading to FPN, fetal hypoxia naturally develops. At its initial stages, vasopressor factors are activated in the fetus, the tone of peripheral vessels increases, tachycardia is noted, the frequency of respiratory movements increases, motor activity increases, and cardiac output increases.

Further progression of hypoxia leads to the replacement of tachycardia by bradycardia, arrhythmia appears, and cardiac output decreases. The adaptive response to hypoxia is the redistribution of blood in favor of the brain, heart and adrenal glands with a simultaneous decrease in blood supply to other organs. At the same time, the motor and respiratory activity of the fetus is inhibited.

Classification of FPN

It is advisable to classify FPN taking into account the state of protective-adaptive reactions into compensated, subcompensated, decompensated.

The compensated form of FPN is characterized by the initial manifestations of the pathological process in the fetoplacental complex. Protective and adaptive mechanisms are activated and experience a certain tension, which creates conditions for the further development of the fetus and the progression of pregnancy. With adequate therapy and management of labor, the birth of a healthy child is possible.

The subcompensated form of FPN is characterized by an increase in the severity of the complication. Protective-adaptive mechanisms are under extreme stress (the capabilities of the fetoplacental complex are practically exhausted), which does not allow them to be implemented sufficiently for an adequate course of pregnancy and fetal development. The risk of complications for the fetus and newborn increases.

In the decompensated form of FPN, there is overstrain and disruption of compensatory-adaptive mechanisms, which no longer provide the necessary conditions for further normal progression of pregnancy. Irreversible morphofunctional disorders occur in the fetoplacental system. The risk of developing severe complications for the fetus and newborn (including their death) increases significantly. The clinical picture of FPN manifests itself in violations of the basic functions of the placenta.

Delay intrauterine development fetus

Changes in the respiratory function of the placenta are mainly indicated by symptoms of fetal hypoxia. In this case, the pregnant woman first pays attention to the increased (erratic) motor activity of the fetus, then to its decrease or complete absence. Most characteristic feature chronic FPN is intrauterine growth retardation. Clinical manifestation Intrauterine growth retardation is a decrease in the size of the pregnant woman's abdomen (abdominal circumference, height of the uterine fundus) compared to the normative indicators characteristic of a given period of pregnancy.

With a symmetrical form of intrauterine growth retardation, which develops with early dates pregnancy, there is a proportional lag in the length and weight of the fetus. At the same time, quantitative indicators of fetometry have lower values ​​compared to individual fluctuations characteristic of a given period of pregnancy.

The asymmetric form of intrauterine growth retardation is characterized by disproportionate development of the fetus. This form most often occurs in the second or third trimester of pregnancy and is manifested by a lag in fetal body weight with its normal length. The abdominal size is predominantly reduced and chest fetus, which is associated with delayed development of parenchymal organs (primarily the liver) and subcutaneous fatty tissue. The dimensions of the fetal head and limbs correspond to the indicators characteristic of this stage of pregnancy.

Placental dysfunction

A reflection of violations of the protective function of the placenta when the placental barrier is weakened is intrauterine infection of the fetus under the influence of pathogenic microorganisms penetrating the placenta. It is also possible for various toxic substances to penetrate the placental barrier, which also have a damaging effect on the fetus.

A change in the synthetic function of the placenta is accompanied by an imbalance in the level of hormones it produces and a decrease in protein synthesis, which is manifested by intrauterine growth retardation, hypoxia, pathology of uterine contractile activity during pregnancy and childbirth (long-term threat of premature termination of pregnancy, premature birth, anomalies of labor).

Prolonged and frequent increase in myometrial tone leads to a decrease in arterial blood flow to the placenta and causes venous stagnation. Hemodynamic disorders reduce gas exchange between the body of the mother and the fetus, which impedes the supply of oxygen and nutrients to the fetus, the removal of metabolic products, and contributes to an increase in fetal hypoxia.

Disruption of the endocrine function of the placenta can also lead to post-term pregnancy. A decrease in the hormonal activity of the placenta causes dysfunction of the vaginal epithelium, creating favorable conditions for the development of infection, exacerbation or occurrence of inflammatory diseases urogenital tract. Against the background of a disorder of the excretory function of the placenta and amniotic membranes, a pathological amount of amniotic fluid- most often oligohydramnios, and in some pathological conditions (diabetes mellitus, edematous form of hemolytic disease of the fetus, intrauterine infection, etc.) - polyhydramnios.

Diagnostics of FPN

At the initial stage of development of the FPN, the listed Clinical signs may be weakly expressed or absent. In this regard, methods of laboratory and instrumental dynamic monitoring of the state of the fetoplacental complex in a high-risk group for the development of FPN become essential. The dominant position in the clinical picture may be occupied by signs of the underlying disease or complication in which FPN developed. The severity of FPN and violations of compensatory and adaptive mechanisms are directly dependent on the severity of the underlying disease and the duration of its course. FPN acquires its most severe course when pathological signs appear during pregnancy up to 30 weeks or earlier. Thus, the most complete information about the form, nature, severity of FPN and the severity of compensatory-adaptive reactions can be obtained from complex dynamic diagnostics.

Taking into account the multifactorial etiology and pathogenesis of FPN, its diagnosis should be based on a comprehensive examination of the patient. To establish the diagnosis of FPN and identify the causes of this complication, significant attention should be paid to proper collection anamnesis. During the interview, the patient’s age (late or young age of a primiparous woman), the characteristics of her health, previous extragenital, neuroendocrine and gynecological diseases, surgical interventions, the presence of bad habits, find out the profession, conditions and lifestyle.

Information about the characteristics of menstrual function, the period of its formation, the number and course of previous pregnancies is of great importance. Menstrual dysfunction is a reflection of the pathology of the neuroendocrine regulation of reproductive function. It is important to assess the course of the current pregnancy, the nature of obstetric complications and, most importantly, the presence of diseases against which pregnancy develops (arterial hypertension or hypotension, pathology of the kidneys, liver, diabetes mellitus, anemia, etc.). You should pay attention to the complaints of a pregnant woman: increased or suppressed motor activity of the fetus, pain in the lower abdomen, increased tone of the uterus, the appearance of atypical discharge from the genital tract, which may be accompanied unpleasant smell and itching.

During an objective examination, the state of uterine tone is assessed by palpation. The height of the uterine fundus and abdominal circumference are measured and compared with the body weight and height of the pregnant woman, as well as the specified gestational age. Such measurements are important and at the same time the simplest indicators for diagnosing intrauterine growth retardation, oligohydramnios and polyhydramnios. During an external examination of the genital organs and when examining using mirrors, it is necessary to pay attention to the presence of signs of inflammation, the nature of discharge from the genital tract, take material from the vaginal wall, from the cervical canal and from the urethra for microbiological and cytological examination.

During an echographic examination, the size of the fetus is determined (the size of the head, torso and limbs) and compared with standard indicators characteristic of the expected gestational age. Basis ultrasound diagnostics To clarify the correspondence of fetal size to the expected gestational age and to identify intrauterine growth retardation, fetometric indicators are compared with normative data. An indispensable condition is the assessment of the anatomical structures of the fetus to identify abnormalities of its development. An echographic examination also includes placentography. In this case, the localization of the placenta, the thickness of the placenta, the distance of the placenta from the internal os, the correspondence of the degree of maturity of the placenta to the gestational age, pathological inclusions in the structure of the placenta, the location of the placenta in relation to myomatous nodes or the scar on the uterus are determined. During the study, the volume of amniotic fluid, the structure of the umbilical cord and the location of the umbilical cord loops are assessed.

Dopplerography is a highly informative, relatively simple and safe diagnostic method that can be used for comprehensive dynamic monitoring of the state of blood circulation in the “mother-placenta-fetus” system after 18-19 weeks of pregnancy, since by this time the second wave of cytotrophoblast invasion has completed . The nature of hemodynamics in the umbilical cord arteries allows us to judge the state of fetoplacental blood flow and microcirculation in the fetal part of the placenta. To diagnose disturbances in uteroplacental blood flow, studies are carried out in the uterine arteries on both sides.

An important component of a comprehensive assessment of the fetal condition is cardiotocography (CTG), which is a method of functional assessment of the fetal condition based on recording the frequency of its heartbeats and their changes depending on uterine contractions, the action of external stimuli or the activity of the fetus itself. CTG significantly expands the possibilities of antenatal diagnostics, making it possible to resolve issues of rational pregnancy management tactics.

The final tactics for managing the patient should be developed not only on the basis of an assessment of individual indicators of the state of the fetoplacental complex, but also taking into account individual characteristics specific clinical observation (term and complications of pregnancy, concomitant somatic pathology, results of an additional comprehensive examination, condition and readiness of the body for childbirth, etc.).

Treatment of pregnant women with FPN

If FPN is detected, it is advisable to hospitalize a pregnant woman in a hospital for in-depth examination and treatment. An exception may be pregnant women with a compensated form of FPN, provided that the treatment initiated has a positive effect and there are the necessary conditions for dynamic clinical and instrumental monitoring of the nature of the pregnancy and the effectiveness of the therapy. Leading place in carrying out therapeutic measures involves the treatment of the underlying disease or complication in which FPN occurred. At present, unfortunately, it is not possible to completely rid a pregnant woman of FPN using any therapeutic interventions. The therapy used can only help to stabilize the existing pathological process and maintain compensatory and adaptive mechanisms at a level that allows for the continuation of pregnancy until the possible optimal date of delivery.

The basis of treatment for placental insufficiency is measures aimed at improving uteroplacental and fetoplacental blood flow. Drugs used for this purpose dilate blood vessels, relax the muscles of the uterus, and improve the rheological properties of blood in the “mother-placenta-fetus” system.

Treatment of FPN should be aimed at improving uteroplacental and fetoplacental blood flow; intensification of gas exchange; correction of rheological and coagulation properties of blood; elimination of hypovolemia and hypoproteinemia; normalization of vascular tone and contractile activity of the uterus; strengthening antioxidant protection; optimization of metabolic and metabolic processes. A standard treatment regimen for FPN cannot exist due to the individual combination of etiological factors and pathogenetic mechanisms for the development of this complication. The selection of drugs should be carried out individually and differentiated in each specific observation, taking into account the severity and duration of the complication, etiological factors and pathogenetic mechanisms underlying this pathology. The dosage of drugs and the duration of their use require an individual approach. Attention should be paid to correcting the side effects of certain medications.

In the pathogenesis of placental insufficiency, as well as in gestosis, the main thing is endothelial dysfunction. There are three endothelial systems: mother, placenta and fetus. Therefore, the processes occurring in the vascular-platelet unit during placental insufficiency are similar to those that occur during gestosis. And this leads to metabolic disorders in the “mother-placenta-fetus” system and to fetal malnutrition.

The need for magnesium during pregnancy increases 2-3 times due to the growth and development of the fetus and placenta. Magnesium, which is involved in more than 300 enzymatic reactions, is essential for fetal growth. Magnesium ions are involved in the synthesis of DNA and RNA. 

A successful combination of magnesium with pyridoxine, which ensures protein metabolism, being a cation in more than 50 enzymatic reactions, participating in the synthesis and absorption of amino acids, promotes the formation of hemoglobin in red blood cells, which is especially important for the growing embryo and fetus. Therefore, in the presence of placental insufficiency and fetal malnutrition, it is most advisable to use magnesium preparations.

Magnesium (Magne B 6 ® forte) has a positive effect on the uteroplacental circulation, therefore its use is indicated for the treatment of placental insufficiency and fetal malnutrition. A parallelism has been established between the concentration of magnesium in the blood serum, in the myometrium, and in the placenta.

Magne B 6 ® forte also combines well with angioprotectors, angio-active agents (Trental, Curantil, Mildronate, Actovegin, etc.), with antioxidants - vitamins E, C, group B, etc.

In the treatment of threatened miscarriage and placental insufficiency, magnesium therapy can be combined with the use of vitamin E and other antioxidants, with Mildronate, Actovegin, with calcium channel blockers (verapamil), Eufillin, Papaverine, Dibazol, No-shpa, antihistamines, physiotherapeutic methods of treatment ( central electroanalgesia, inductotherapy of the perinephric region, hydroionization, etc.). Treatment of FPN begins and is carried out in the hospital for at least 4 weeks, followed by its continuation in. The total duration of treatment is at least 6-8 weeks. To assess the effectiveness of the therapy, dynamic monitoring is carried out using clinical, laboratory and instrumental research methods. An important condition for successful treatment of FPN is that the pregnant woman adheres to the appropriate regimen: proper rest for at least 10-12 hours a day, elimination of physical and emotional stress, and a rational, balanced diet.

One of the leading pathogenetic mechanisms for the development of FPN is disturbances of the uteroplacental and fetoplacental blood flow, accompanied by an increase in blood viscosity, hyperaggregation of erythrocytes and platelets, a disorder of microcirculation and vascular tone, and arterial circulatory insufficiency. Therefore, an important place in the treatment of FPN is occupied by drugs with antiplatelet and anticoagulant action, as well as drugs that normalize vascular tone.

It should be taken into account that a periodic and prolonged increase in uterine tone contributes to impaired blood circulation in the intervillous space due to a decrease in venous outflow. In this regard, in the course of therapy for FPN in patients with symptoms of threatened miscarriage, the prescription of tocolytic drugs is justified.

Thus, placental insufficiency develops during complicated pregnancy, which requires treatment and preventive measures aimed at reducing obstetric pathology. The problem of treating placental insufficiency remains not yet fully resolved, so correction of disorders should be better started before pregnancy, which can reduce the incidence of complications of pregnancy, fetus and newborn.

Literature

1. Fedorova M.V. Placental insufficiency// Obstetrics and gynecology. 1997. No. 6. P. 40-43.
2. Serov V.N. Diagnosis and treatment of placental insufficiency // Breast cancer. 2008. pp. 35-40.
3. Kuzmin V.N., Adamyan L.V., Muzykantova V.S. Placental insufficiency in viral infections// M.: 2005. P. 103.
4. Shapovalenko S. A. Complex diagnosis and treatment of placental insufficiency in pregnant women different stages gestation // Vestnik Ros. Association of Obstetricians and Gynecologists. 2001. No. 2. P. 437.
5. Salafia C. M. Placental pathology and fetal growth restriction // Clin.Obstet.Gynecol. 2007. 40. 7409 RU.MPG.11.02.11.

V. N. Kuzmin, Doctor of Medical Sciences, Professor

MGMSU, Moscow

"Placental insufficiency"

Placental dysfunction is one of the main causes of perinatal morbidity and mortality. In recent years, it has become common to talk about placental insufficiency; this concept does not yet have clinical content, but at the same time it is included in the international statistical classification of diseases.

Placental insufficiency should be understood as a decrease in its ability to maintain adequate exchange between the organisms of the mother and fetus.

According to the classification of Fedorova and Kalashnikova /1936/, primary placental insufficiency that occurs before 16 weeks is distinguished. pregnancy, and secondary, which arose at a later date. According to these data, primary placental insufficiency occurs during the period of implantation, early embryogenesis and placentation under the influence of various factors: genetic, endocrine, infectious; acting on the gametes of the parents, the zygote, the blastocyst, the developing placenta and the female reproductive apparatus as a whole. Of great importance in the development of primary placental insufficiency is the enzymatic failure of the decidual tissue (for example, with ovarian hypofunction), which carries out trophism of the fetal egg. Primary placental insufficiency is manifested by anatomical disorders of the structure, location and attachment of the placenta, as well as defects in vascularization and disorders of chorion maturation.

Secondary placental insufficiency develops against the background of an already formed placenta under the influence of exogenous Factors. As a rule, this pathology is observed in the second half of pregnancy.

Placental insufficiency can have an acute and chronic course. Most often, acute placental insufficiency occurs as a consequence of extensive disturbances in the circulatory system, in urgent situations in obstetrics (uterine rupture, placental abruption, intraplacental thrombosis, sudden death mothers, etc.). Chronic placental insufficiency is a more common pathology, observed in approximately every 3rd pregnant woman at high risk of perinatal pathology.

Perinatal mortality with placental insufficiency reaches 60 ppm. Chronic placental insufficiency can develop relatively early (at the beginning of the second half of pregnancy) and last for a long time from several weeks to several months.

Depending on the compensatory-adaptive reserve of the placentas, this pathology is usually divided into decompensated, subcompensated and compensated forms, based on the condition of the fetus and the degree of its underdevelopment.

Etiology and pathogenesis of placental insufficiency

1. The causes of acute dysfunction of the placenta are complications of pregnancy and extragenital diseases that arise during gestation and childbirth. These primarily include late gestosis/nephropathy. preeclampsia, eclampsia/, chronic glomerulo- and pyelonephritis, diabetes mellitus, influenza, acute respiratory viral infections, etc. Often the cause of acute dysfunction of the placenta is anomalies of its location/presentation, low attachment/, as well as developmental defects/umbilical cord nodes, short umbilical cord and etc/.

The pathogenesis of acute placental insufficiency depends on its form. With acute hemorrhagic infarction of the placenta, changes occur in both the maternal and fetal parts of the placenta. It is believed that maternal circulation in the intervillous space is initially damaged as a result of changes in the spiral arteries.

Acute placental insufficiency is caused by the formation of intraplacental blood clots. Local cessation of fetal circulation in one of the catheledons is known as “nodular ischemia”.

The most dangerous thing for mother and fetus is premature abruption of a normal and low-lying placenta. In this case, in the genesis of placental apoplexy, the leading role is played by stagnation in the intervillous space.

With mechanical damage to the fetal blood flow in the umbilical cord, secondary damage occurs in the intervillous space of the placenta.

2. Chronic placental insufficiency syndrome is of a multifactorial nature. Diseases of the mother, fetus and placenta can lead to its development.

Primary placental insufficiency is formed on early stages development of the placenta as a consequence of the influence of various factors /genetic, endocrine, infectious, etc./..

Changes in the production and maturation of gametes can be caused by exposure to certain physical factors /ionizing radiation/ or chemical substances, including drugs /chronic intoxication/.

The structure and degree of development of the vascular network of the uterus, the presence of anomalies in its development and myomatous nodes, etc. are important in the formation of the placenta. Disturbances in the mother's body's adaptation to pregnancy also play a certain role.

Secondary chronic placental insufficiency develops, as a rule, against the background of an already formed placenta due to a complicated course of pregnancy, caused either by its pathology (gestosis, threat of miscarriage, etc.), or by infectious and extragenital diseases.

Despite the variety of forms of placental insufficiency, they are all, to one degree or another, accompanied by pathology of blood circulation in the uterus and placenta.

As is known, dysfunction of the peripheral arteries, which conditionally includes the uterine arteries during pregnancy, can be caused by disturbances in their vasomotility / functional expansion or narrowing /, with structural changes in the walls / arteriolosclerosis / or complete or partial blockage of the vascular lumen due to arteriolosclerosis, thrombosis or embolism. The degree of circulatory disturbance /placental insufficiency/ depends on where these changes occur, in most vessels or in individual parts of the system.

A decrease in blood flow in individual parts of the system does not necessarily lead to a significant decrease in blood circulation throughout the entire organ. As a rule, collateral inflow and outflow of blood occurs. Therefore, blood supply is almost always gradually restored. If the collateral blood flow is insufficient, then a sharp weakening of microcirculation occurs, and ischemia and degenerative processes form in the corresponding areas of the tissue.

Pathological blood circulation in the uterus and placenta can be caused by a very large number of different reasons. For example. disorder of innervation mechanisms. Neurogenic factors have a great influence on the normal functioning of the heart and the condition of the blood vessels of a pregnant woman.

Biologically active substances circulating in the blood as exogenous. and endogenous ones can change vascular tone, tissue destruction, etc. Under their influence, an increase or decrease in vascular tone may occur. Humoral transport system /in foreign. literature - mass transfer /, includes general blood circulation and fluid movement in the chain: blood-tissue-lymph-blood is functionally unified. Similar processes occur in the lymphatic system.

Therefore, the biologically active substances present in these systems, a change in their concentration or the introduction of new ones can affect the functioning conditions of the lymph and blood circulation and the formation of functional or organic damage.

Insufficiency of the uteroplacental circulation is largely determined by the nature of pregnancy complications. With different pathologies, the pathogenesis of MPC may be different.

In case of OPG-preeclampsia, the pathogenesis of circulatory damage" was presented to you in previous lectures.

In case of miscarriage, the main role is played by the central mechanisms of blood circulation regulation. In cases of habitual miscarriages, frequent instability of the cervical vascular reaction and impaired vascular reactivity of the uterus and placenta were found. Serov et al. It is believed that the leading pathogenetic mechanism of miscarriage is myometrial hypoxia as a result of hemodynamic disturbances in the uterus. If there is a threat of miscarriage, increased BMD leads to a decrease in excitability and contractile activity of the uterus.

When placental insufficiency occurs, regardless of the etiology, the same changes occur in the body of the fetus, indicating damage to humoral regulation, leading to damage to the biophysical properties of its blood. Increased viscosity is recorded in the fetal blood. In response to hypoxia in the fetus, increased amounts of norepinephrine and other amines are released from the chromoile tissues.

With Rh sensitization, primary disorders occur in the fetal body, subsequently damaging the placental and then the uteroplacental circulation. The same mechanism of damage to the BMD occurs in other fetal diseases, for example infectious, some genetically determined.

With placental insufficiency, according to Kalashnikova, widespread circulatory disorders from the maternal and fetal parts of the placenta lead to nonspecific morphological disorders: premature maturation of the strema, involutively destructive changes in the structural elements of the villous chorion and depidual tissue.

The effect of placental insufficiency on the fetus and newborn Acute placental insufficiency leads to acute fetal hypoxia and asphyxia of the newborn, the severity of which is determined by the size / size / of the affected area of ​​the placenta and the time interval from the onset of disturbance of placental blood flow to delivery. Chronic placental insufficiency can cause a terratogenic effect (cerebral palsy, heart defects), as well as fetopathy in the form of prenatal dystrophy, chronic hypoxia, their combination, and disruption of the period of adaptation to extrauterine life.

According to the WHO classification of the IX revision, 2 categories of impaired growth and development of the fetus are distinguished. “Slow growth and malnutrition of the fetus”, “Disorders associated with prolonged gestation and high birth weight.” In addition, in accordance with generally accepted criteria, all newborns, depending on intrauterine growth /gestograms/, are divided into 9 groups. The first 3 groups are full-term, premature and post-term children corresponding to the gestational age. 4,5,6 include full-term, premature and post-term infants who are too large for their gestational age. Groups 7,8,9 included full-term, premature and post-term children. small for this stage of pregnancy.

In order to differentiate the assessment of the correspondence of the weight and length of the child’s body to the gestational age, percentile tables and Dementieva curves are used. The average norm is located between the 25.50 and 75 percentiles. Values ​​below the 25th percentile or above the 75th percentile are considered deviations from the norm.

Of the various forms of impaired physical development of newborns with placental insufficiency, growth retardation (low weight in relation to gestational age, or small children for term) and fetal malnutrition (intrauterine or congenital malnutrition) are most often observed. The distinction between these forms, with the exception of congenital metabolic disorders, is extremely difficult.

Depending on the lag in anthropometric data, 3 degrees of delayed fetal development are distinguished. At grade 1, the data are located between the 25th and 2nd percentiles. and the delay from gestational age is about 2 weeks. Developmental delay of degrees 2 and 3 is characterized by a simultaneous decrease in the weight and length of the newborn’s body. At grade 2, body weight is between the 10th and 4th percentiles, at grade 3 - at the 3rd percentile and below.

In addition, the weight-height coefficient is used: with normal anthropometric data, this parameter varies above 60, with 1st degree malnutrition - from 60 to 55, with 2nd degree malnutrition - 55 - 50, and 3rd degree - below 50.

We analyzed the course of pregnancy in 255 patients /from the general population/, whose children were born with signs of intrauterine malnutrition of 1st degree /75.5%/, 2nd degree /17.6%/, and 3rd degree /6.7%/. Of these, young primiparas /under 19 years old/ accounted for 8.6%, women in labor over 35 years old - 6.7%, 13.7% of women were short in stature /below 155 cm/. Thus, it was proven that symmetrical malnutrition is genetically caused and not a pathology.

Chronic fetal hypoxia, resulting from a violation of transplacental gas exchange, does not develop in every pregnant woman with placental insufficiency and depends on the stage of development and the nature of changes in the placenta. Chronic hypoxia often leads to the birth of children with asphyxia and ante- or intranatal fetal death, but in some cases it does not significantly affect the general condition of the child at birth.

As studies carried out at our department have shown, oxygen deficiency leads to characteristic changes in metabolism, hemodynamics and microcirculation, well known to you, at birth in every second child and disrupts adaptation processes in the first days of life in 50-75% of children.

Studies of metabolism in the mother-water-fetus system and newborns indicate a nonspecific response of the fetus to acute and chronic hypoxia.

Clinic of placental insufficiency.

Placental insufficiency has some general and local manifestations, despite extremely mild clinical symptoms. As a rule, pregnant women do not complain. However, some pregnant women do not experience physiological weight gain. Metabolic and hormonal imbalances are possible. Local manifestations of placental insufficiency include changes in the body of the fetus and placenta. There are disturbances in the growth and development of the fetus, its condition suffers, which is expressed in changes in its motor activity and cardiac activity. Changes in the placenta /structural and functional/ can only be determined using objective research methods.

A comprehensive examination carried out for the purpose of diagnosing placental insufficiency should include: 1/.assessment of the growth and development of the fetus by carefully measuring the height of the uterine fundus, taking into account the abdominal circumference and body weight of the pregnant woman, ultrasound biometry of the blanket, 2/.assessment of the condition of the fetus by studying its motor function activity and cardiac activity, 3/.ultrasound assessment of the condition of the placenta, 4/.study of placental circulation, blood flow in the vessels of the umbilical cord and large vessels of the fetus, 5/.determination of the level of hormones in the blood and specific proteins of pregnancy, 6/.assessment of the state of metabolism and hemostasis in the body of a pregnant woman.

Growth and development of the fetus. The growth and development of the fetus during pregnancy is determined using external obstetric examination (measurement and palpation) and ultrasound scanning. Each of these methods has its own advantages and disadvantages. A screening test is to measure the height of the uterine fundus above the womb and compare it with the abdominal circumference, body weight and height of the pregnant woman. UMR before 30 weeks is 0.7-1.9 cm/week, between 30-36 - 0.6-1.2 cm/week and after 36 weeks -0.1-0.4 cm/week. When verifying data on this indicator with the weight of newborns, it was found that the difference can only be detected between healthy fetuses, fetuses with severe malnutrition (below the 10th percentile) and large fetuses (above the 90th percentile).

Establishing fetal growth using clinical methods presents certain difficulties; in these situations, ultrasound provides invaluable assistance.

In the early stages of pregnancy, the size of the ovum is measured, and the outer and inner diameter of the ovum is measured. The error in this case is up to 1 week of development.

When establishing the gestational age and fetal weight after the 1st trimester, measuring the biparietal size of the head, or fetal cephalometry, remains the most common method. In addition to the BPR, the heads use such parameters as the area and circumference of the head and the fronto-occipital diameter. Up to 30 weeks pregnancy, BPD increases by 3 mm/week, at 30-34 weeks - by 1.3 mm/week, and after 34 weeks - by 1 mm/week_

In recent years, in addition to BPD, determination of fetal femur length has been used to determine the gestational age of the fetus. The growth rate of the femur up to 24 weeks is 3 mm/week, from 25 to 35 weeks. is 2.2 mm/week, after 35 weeks - 1.8 mm/week.

In our country, measurement of two fetal sizes has become widespread: the average diameter of the fetal chest at the level of the leaflet valves of the heart and the abdomen at the origin of the umbilical cord.

In addition, it was proposed to measure the volumes of the fetus and uterus and other anatomical formations of the fetus and uterus. There are many different nomograms, and this is not our topic. The ultrasound will be read separately.

Condition of the fetus. The condition of the fetus with placental insufficiency depends on the degree of preservation of the compensatory mechanisms of the placenta. Information about disorders in the fetal body during pregnancy can be obtained by assessing its cardiac activity, hemodynamics and motor activity, including respiratory movements, studying the composition of amniotic fluid and some parameters of maternal homeostasis. Cardiovascular monitoring allows us to identify initial signs of intrauterine hypoxia or metabolic disorders.

The state of fetal cardiac activity during placental insufficiency mainly reflects the nature of changes in the placenta and is less dependent on pregnancy complications. Chronic fetal hypoxia is detected during a non-stress test; most often, monotony of the rhythm, lack of acceleration in response to fetal movements, or the occurrence of decelerations, often turning into bradycardia, are observed.

With intrauterine growth retardation, in addition to the signs listed above, peak-shaped decelerations of type deep 0 are often recorded. Particular attention should be paid to the reaction of the fetal cardiac activity in response to its movements. Krause identifies five types of responses, three of which reflect the good state of the fetus with the appearance of accelerations, a volley of high oscillations, and a saltatory rhythm. the reaction is considered doubtful when peak-shaped decelerations of type deep 0 occur. The absence of any reaction to fetal movement is a bad sign. Spontaneous abnormalities in fetal cardiac activity (score 6 or lower on the Fisher scale) detected during cardiac monitoring are an unfavorable sign for the fetus. If placental insufficiency is suspected, it is advisable to take into account the motor activity of the fetus. The counting of movements is carried out by the pregnant woman herself within 30 minutes. Normally, the average frequency of fetal movements is about 3 in 10 minutes. Their increase in frequency and intensification, as well as a sharp decrease in the frequency of motor activity, indicates the occurrence of fetal pathology.

Valuable information about the condition of the fetus during ultrasound examination can be obtained by assessing the respiratory movements of the fetus. Assessment of this biophysical parameter can provide, albeit indirect, fairly accurate information about the state of the central nervous system of the fetus. Normally, the fetal respiratory rate reaches 50 per minute at the age of 35-40 weeks. They are not constant and are combined with periods of apnea. for which time intervals of 6 seconds or more should be taken. The absence or change in fetal respiratory movements at the end of pregnancy is a poor prognostic sign, especially the type of shortness of breath. A decrease in respiratory activity has been established when the fetus is delayed in development.

The use of ultrasound in widespread practice makes it possible to determine the biophysical profile of the fetus. Most authors include five parameters in this concept: the results of a non-stress test conducted during cardiac monitoring, and four indicators determined by echography (respiratory rate, physical activity, muscle tone fetal volume of amniotic fluid. Vinceleus also takes into account the degree of maturity of the placenta. The maximum score is 12 points, with 6-7. scores, a repeat study is necessary. With a score of 6-4 points, there is significant fetal suffering, and pregnancy management tactics depend on the degree of fetal maturity and the preparedness of the birth canal for childbirth.

The cordocentesis currently used is worthy of attention - puncture of the umbilical cord vessels and determination of acid-base balance of fetal blood and other studies of microdoses of fetal blood.

In addition to the listed methods, the biochemical composition of amniotic fluid is examined during amniocentesis. They contain an increased content of acidic metabolic products, a decrease in pH, a change in the ratio of biologically active substances, and the activity of a number of enzymes.

Assessment of the condition of the placenta and placental circulation.

Ultrasound imaging for placental insufficiency allows one to detect some pathological changes in the placenta (cysts, calcification, fibrinoid necrosis, areas of abruption, etc.). There are 4 degrees of placental maturity. The combination of disturbances in the placenta with its premature aging may indicate placental insufficiency and the need for delivery. Placentometry provides valuable information about the condition of the placenta. those. determination of its thickness, area and volume. A decrease in the area and volume of the placenta indicates the presence of placental insufficiency.

In order to assess blood circulation in the placenta, methods are used that allow one to get an idea of ​​the uterine, utero-placental. fetal-placental and fetal blood flow. Rheography and radioisotope placentoscintigraphy have been used for a relatively long time, while Doppler ultrasound began to be used only in recent years.

Based on the results of reogray of the abdominal organs, you can get a rough idea of ​​the blood supply to the uterus. The method has not yet been fully developed and can be used as a screening method.

More accurate data on blood circulation in the intervillous space of the placenta can be obtained using radioisotope placentoscintigraphy. This method is based on visualization of the organ, obtaining from its shielded areas the dynamic characteristics of the intake and distribution of radiopharmaceuticals administered to the mother.

The results of placentoscintigraphy in a patient are shown. Slide. Studies conducted by us and other authors have shown that normally OC in the intervillous space of the placenta fluctuates within 100 ml/min per 100 g of placental tissue. In pathology, there is a significant decrease of 30% or more from the norm, and various parameters of the activity-time curves also change.

With the introduction of Doppler ultrasound into obstetric practice, it became possible to study blood flow in the arcuate arteries, which at the end of pregnancy represent cords with a diameter of about 3 mm. The state of diastolic and systolic blood flow in the arcuate arteries of the uterus in the last trimester of a physiological pregnancy ranges between 62 and 70%. A decrease in this ratio to 52% and below indicates a significant decrease in blood flow in the uterine arteries, and consequently in the intervillous space of the placenta.

The study of fetal blood flow in the umbilical cord has great diagnostic significance. Blood flow in the umbilical cord vein normally fluctuates within 100 ml/min. It is customary to study blood flow in the umbilical cord arteries using pulsogram analysis. as in the arcuate arteries. During the physiological course of pregnancy, the ratio of diastolic and systolic blood flows is about 60-70%, the resistance of the umbilical vessels does not exceed 2. Pi, according to our data, ranges from 0.9 to 1.5. With a pathological course of pregnancy, Pi reaches 3.

Hormonal imbalances. An important diagnostic criterion for placental insufficiency is the level of hormones in the blood of a pregnant woman. In the early stages of pregnancy, the most informative indicator is the concentration of hCG-chorian gonadotropin, a decrease in which, as a rule, is accompanied by a delay or arrest of embryo development. At a later stage, in the second half of pregnancy, the concentration of placental lactogen is of great importance. With placental insufficiency, the concentration of PL in the blood decreases by 50%, and with fetal hypoxia by almost 2 times. The role of progesterone determination is controversial. To a large extent, the function of the fetoplacental system is characterized by the concentration of estriol. since when the fetus suffers due to placental insufficiency, the production of this hormone by the liver decreases. A decrease in the level of estriol in the blood of pregnant women by more than 50% is an indicator of a threatening condition of the fetus. Oncofetoproteins, such as alpha-fetoprotein, alpha-2-fertility microglobulin, PAPP, etc., are of great diagnostic significance in determining placental insufficiency. In cases of fetal development disorders, prenatal damage and placental insufficiency, the level of these substances varies significantly from control data.

Indicators of hemostasis and metabolism. Placental insufficiency of any etiology is based on disturbances in placental circulation, including microcirculation and metabolic processes, which are closely related. They are accompanied by changes in blood flow not only in the placenta, but also in the body of the mother and fetus.

It should be noted that micropiriculation disorders are detected early, even before the appearance of clinical symptoms of gestosis and placental insufficiency. The criteria for placental insufficiency are an increase in erythrocyte aggregation against the background of hyperfibrinogenemia, a decrease in the number of platelets and an increase in their aggregation. In the diagnosis of placental insufficiency, an increase in platelet aggregation on collagen is of great importance. With satisfactory placental function, the activity of thermostable alkaline sosphotase accounts for more than 50% of the total phosphatase activity. If TAP activity is less than 25%, this indicates severe placental insufficiency and a poor prognosis for the fetus.

In amniotic fluid with placental insufficiency, the concentration of non-essential amino acids increases and the concentration of essential amino acids decreases. The concentration of urea and potassium increases, acidic metabolic products accumulate, the activity of histidine catabolism enzymes increases, etc.

TREATMENT OF PLACENTAL INSUFFICIENCY

Abroad, when identifying placental insufficiency and BMD deficiency. as a rule, after 28 weeks of gestation they resort to early delivery, since thanks to intensive therapy, newborns often even with a low weight (up to 1000 g) survive in 95% of cases. When giving birth, the overwhelming number of obstetricians take into account the gestational age, fetal weight and the severity of the condition of the mother or placental insufficiency. This is due to the fact that to date, the second leading cause of PS in the vast majority of countries in the world is the mortality of premature infants. In 1948 At the 1st World Health Assembly of the League of Nations, it was proposed that all children born with a body weight of less than 2500 g be considered premature. In fact, many newborns weighing less than 2500 g show signs of sufficient maturity and should not be considered preterm. On the other hand, some newborns (a typical example are children of mothers with diabetes), despite their large body weight, may not be mature enough in their development.

Placental insufficiency is a consequence of the alarming mortality rate of babies shortly before birth, as well as in the first week after birth. Despite the enormous developments in the field of reproductive medicine, the question of this pathology is still open, and its research is a priority for domestic and foreign scientists. Next, we’ll look at how to treat placental insufficiency during pregnancy.

Placental insufficiency is confirmed in approximately 3.5% of healthy expectant mothers and in 4.5% of pregnant women suffering from any other concomitant illness. As a result of this serious defect, about 50% of newborns die in the first days of life, and the surviving children subsequently suffer from damage to the central nervous system and lag behind their peers in terms of psychomotor and physical development.

Placental insufficiency: the essence of pathology

The organ that is formed exclusively during pregnancy and is a kind of bridge between the mother and the fetus is called the placenta, or the baby's place. Thanks to the placenta, the fetus is surrounded by a reliable immune barrier and receives required amount nutrients, hormones and oxygen, and in return gives off carbon dioxide and decay products. Fencing little man from the toxic effects of harmful substances and the influence of pathogenic microorganisms, a child’s place gives him the opportunity to fully develop and grow.

Placental insufficiency is based on a disorder of microcirculation and compensatory mechanism, due to which the placenta becomes functionally defective. The fetus also suffers due to impaired gas exchange, damage to the central nervous system, endocrine and immune systems.

Causes of placental insufficiency during pregnancy

There are a lot of factors that provoke the development of placental insufficiency. They are conventionally divided into 4 large groups:

1. Features of an obstetric and gynecological nature: the presence of genetic abnormalities and various developmental defects in the first child, violation monthly cycle, serious gynecological diseases and surgical operations in the reproductive system before pregnancy, spontaneous abortions and established recurrent miscarriage, previous premature births, primary infertility, complications during pregnancy and childbirth of previous children.
2. Features of the current pregnancy. The lion's share of cases of placental insufficiency occurs due to infection of the mother and fetus with viral and bacterial infections (for example, chlamydia). Also included in this group are late toxicosis, threat of miscarriage, Rh incompatibility, multiple births, improper attachment of the placenta, pathological immaturity of the genital organs.
3. Somatic pathologies in the expectant mother. The risk of developing placental insufficiency is increased by diseases of the endocrine (diabetes mellitus), cardiovascular (arterial hypertension), hematopoietic, respiratory and genitourinary (pyelonephritis) systems.
4. Social and everyday factors: expectant mother under 18 or over 30 years old, bad habits, poor nutrition, stress, harmful production factors (for example, the influence of radiation or chemicals).

Often placental insufficiency develops as a result of a complex of several factors belonging to different groups risk.

Forms of placental insufficiency during pregnancy

Depending on the nature and location of the pathological process in the placenta, insufficiency is classified into several forms:

• hemodynamic - blood flow slows down in the uteroplacental and fetal-placental circulatory system;
• placental-membrane - the properties of the placental membrane for transporting metabolic products are disrupted;
• cellular-parenchymal - the performance of trophoblastic cells of the placenta decreases.

The listed structures are closely related to each other, so most often placental insufficiency is the result of complex disorders.

Depending on the nature of the hemodynamic disorder in pathology, the following forms are distinguished:

• stage 1a placental insufficiency during pregnancy - disturbances occur only in the bloodstream of the uterus;
• 1b degree - the blood flow in the child’s vascular system changes;
• 2 degrees - both uterine and fetal blood circulation is disrupted, but in general the situation remains not critical;
• 3 degrees - there is a critical disruption of blood flow in the umbilical artery, there is a threat to the life of the fetus. The patient is indicated for early delivery.

According to the clinical picture, two forms of pathology are distinguished - acute and chronic.

Acute placental insufficiency during pregnancy

The acute form of insufficiency is associated with disorders such as placental infarction and premature detachment, which entails retroplacental hemorrhage and hematoma formation. The acute course of the pathological process usually leads to fetal fading and forced termination of pregnancy.

Chronic placental insufficiency during pregnancy

This form of pathology is more common than acute, and is diagnosed in every third expectant mother, who is at risk for women with perinatal abnormalities. Chronic failure placenta develops in the first half of gestation or from the beginning of the second half and lasts from several weeks to several months. The clinical picture of the pathology includes a violation of the trophic function, which entails hormonal and gas exchange abnormalities in the placental function.

Symptoms of placental insufficiency during pregnancy

The following signs usually serve as the reason for a thorough examination of the expectant mother for placental insufficiency:

• slow increase in size of the uterus. The fetus receives insufficient oxygen and nutrients, so its development is suspended. As a result, the growth of the uterus significantly lags behind the normative indicators. In a healthy pregnancy, the fundus of the uterus reaches the symphysis pubis by the 12th week of gestation. With the onset of the 13th week of pregnancy, the uterus can already be felt through the abdominal wall. The height of its fundus in centimeters is equal to the week of pregnancy;
• decreased fetal motor activity. A decrease in the quantitative indicator of movements occurs due to hypoxia. If the fetus “goes quiet” suddenly, the pregnant woman herself may notice this symptom;

• increased blood pressure and peripheral edema. This indicator is important during long periods of pregnancy. When signs of hypertension are combined with peripheral edema or the presence of protein in the urine, the expectant mother is likely to develop preeclampsia. In this condition, the pregnant woman should immediately seek medical help;
• painful sensations in the lower abdominal segment. In the diagnosis of placental insufficiency, such ailment is considered indirect sign pathology. The pain may be caused by another abnormality that provokes the development of placental insufficiency. Typically, pain in the lower abdomen is one of the symptoms of uterine artery thrombosis, premature placental abruption, uterine hypertonicity, tubal and uterine infections. All these diseases are potential factors for the development of placental insufficiency;

• discharge of blood from the vagina. Throughout the entire 9 months of pregnancy, such a symptom does not bode well for a woman. If we talk about the placenta, the appearance of blood indicates its detachment, incorrect location with damage, injury to the placenta or uterus itself. Any of these disorders may form the basis of placental insufficiency.

Let us clarify that the symptoms listed above cannot be called direct evidence of the presence of placental insufficiency in a pregnant woman. In most cases, they may not exist at all. Placental insufficiency tends to hidden development. While the fetus suffers due to the small volume of metabolic processes, the mother usually does not experience any discomfort. The only correct tactics for timely detection of pathology and its treatment are regular check-ups with a doctor.

Consequences of placental insufficiency during pregnancy

Pathology can radically affect the course of pregnancy and lead to subsequent complications:

• placental abruption;
• post-term pregnancy;
• high probability of fetal death in the womb.

What is the danger of placental insufficiency during pregnancy for the baby:

• fetal malnutrition or low birth weight of a child;
• pathologies of cerebral circulation in an infant;
• pneumonia;
• mental retardation;
• neurological abnormalities;
• disturbances in the functional activity of the intestines;
• frequent colds;
• various developmental defects.

Diagnosis of placental insufficiency during pregnancy

There are several ways to detect pathology:

1. A physical examination of the expectant mother, during which they give an accurate assessment of the size, tone of the uterus, abdominal circumference and compare these indicators with the established norm. Deviations in the number of fetal movements and heart rate can also be detected.
2. Ultrasound. The method allows you to accurately determine the size of the child, the volume of amniotic fluid and the size of the placenta. Using Doppler, blood flow in the vessels of the uterus is assessed, children's place, umbilical artery and vein.
3. Research in the laboratory. As part of this diagnosis, the hormonal parameters of the placenta are studied.

Treatment of placental insufficiency during pregnancy

Treatment tactics depend on the stage of pregnancy:

• up to 34 weeks - the immaturity of the fetus is still very pronounced, and therefore it is impossible to provide assistance after its birth, so they try to maintain and prolong the pregnancy;
• after 34 weeks, the fetus is already quite viable, so doctors choose a method of delivery and set a due date.

To maintain the pregnancy until 34 weeks, the expectant mother is hospitalized in the obstetrics and gynecology department. There she is prescribed complex treatment to normalize blood circulation and microcirculation, as well as to prevent or correct metabolic processes.

The woman is shown complete rest. In order for the patient to relax and fully rest, she will benefit from procedures such as ion therapy, physiotherapy for the adrenal glands, and electrical relaxation of the uterus.

Of course, drug therapy is of great importance in correcting insufficient child space. The development of this pathology, as well as excessive miscarriage and damage to the walls of blood vessels, contributes to a large number of amino acid homocysteine ​​in the blood of a pregnant woman. To reduce the level of this substance, the drug Angiovit is used, which contains B vitamins and folic acid. For the expectant mother It is recommended to take it for 1 month.

Pentoxifylline is another mandatory pharmaceutical drug. The drug has a pronounced vasodilator and angioprotective effect, improves microcirculation and reduces vascular resistance. It is prescribed at 400 - 800 mg per day or through a drip.

As vasoactive agents, a combination of Actovegin solution (up to 10 droppers) and hexoprenaline tablets (0.25 - 1.5 mg per day) is prescribed.

The drugs Pentoxifylline and Dipyridamole have recently been used not only for treatment. According to doctors, these antiplatelet agents and angioprotectors help prevent the development of placental insufficiency during pregnancy. Dipyridamole is approved for use at any stage of gestation. It is used in combination with anticoagulants and drugs intended to normalize blood pressure.

Childbirth with placental insufficiency and methods of preventing the development of pathology

Successful completion of pregnancy due to placental insufficiency consists of prompt diagnosis of any functional abnormalities in the development of the baby, professional risk assessment and timely preparation of the birth canal for the birth of the child.

Natural childbirth with placental insufficiency is possible. The main thing is that the condition of the birth canal of the woman, the woman in labor and the fetus is satisfactory. The degree of readiness of the baby for birth is determined using Doppler ultrasound, cardiotocography and various functional stress tests.

To the surgical delivery of the patient using the method caesarean section doctors resort to it in case of visible irregularities in the patient’s obstetric and gynecological medical history, as well as in the presence of deviations in the intrauterine development of the child.

To prevent placental insufficiency during pregnancy, timely normalization or complete elimination of factors that provoke pathology is important. The pregnant woman will also be given advice on healthy eating, will prescribe complexes of essential vitamins and minerals, sedatives, and, if necessary, medications.

While carrying a long-awaited baby, women are often forced to face various kinds of problems. In some situations, there is no danger for either the mother or her baby. However, if you have any ailments, you should consult a doctor.

If a woman is diagnosed with placental insufficiency during pregnancy, this is not a death sentence. This disease represents a whole complex of changes in the area where the growing fetus is located. In some cases, such a pathology can lead to disruptions in the functioning of the baby’s organs that are just beginning to develop. Therefore, it is worth considering in more detail what uteroplacental insufficiency is. If you clarify the symptoms of the disease, you can avoid serious complications.

General information

Placental insufficiency is a special syndrome that leads to disruptions in the functioning of this important component. This occurs against the backdrop of the fact that the fetus begins to react to the ailments from which the woman herself suffers.

If we talk about the manifestation of this disease, then it is usually expressed in the fact that the placenta at some point ceases to respond to the needs of the baby. In this case, quite serious molecular changes occur, affecting cells and neighboring tissues. This affects the speed and quality of development internal organs fetus

If we talk about statistics, placental insufficiency during pregnancy occurs in 30% of cases. Most often, this is caused by diseases of the cardiovascular system, hormonal imbalances, and inflammatory processes occurring in the woman’s genitourinary system. In some situations, with a complex degree of pathology, it can lead to fetal death.

Those women who have previously experienced a miscarriage or suffered from a number of complications, including the so-called frozen pregnancy, are most susceptible to placental insufficiency. During this disease, the fetus may begin to be delayed in development. This phenomenon is commonly called feto-placental insufficiency.

Varieties

In medical practice, primary placental insufficiency is distinguished. It develops during the first 16 weeks of pregnancy. During this period of time, the necessary nutrient medium for the fetus is formed and the fertilized egg is directly fixed on one of the walls of the uterus. At the secondary stage of development of the disease, blood flow disturbances occur.

There is also:

• Acute placental insufficiency. In this case, a sharp disruption of blood flow in the uterus occurs. This is explained by the detachment of the placenta itself and the appearance of hematomas. This stage is very dangerous because it can develop within a few hours. During this time, the fetus becomes hypoxic and dies.
• Chronic placental insufficiency. In this case, the disruption of blood flow occurs gradually. When the nutrient medium loses its ability to adapt to changed conditions, it undergoes degeneration. In addition, other changes may be caused.

Chronic placental insufficiency is less dangerous than an acute attack. However, this type of illness requires immediate medical intervention.

Degree of severity of the disease

Based on this indicator, the following are distinguished:

• Compensated placental insufficiency. In this case, minor disturbances in biochemical processes occur in the body of the expectant mother. For example, too much protein is produced. In this case, the placenta remains normal level blood flow, but there is still a possibility of fetal hypoxia.
• Decompensated failure. In this case, during the formation of the placenta, quite serious disturbances occur, which negatively affect the functions of the nutritional material necessary for the baby. In addition, at this stage there is a deterioration in blood flow in the uterus, which leads to serious oxygen starvation of the fetus.

Three phases of disease development

This pathology develops according to a certain pattern. In the first phase, the placenta begins to react sharply to any changes occurring in the woman’s body. She works with increased strength, if a representative of the fair sex is diagnosed with prolonged pregnancy. Also, a similar disease develops against the background of mild gestosis and with an increase in cholesterol levels in the body of the expectant mother.

During the second phase, the placenta loses its previous activity. At the same time, her indicators are outside the normal range. During this period, an increase in lipids is observed, and the activity of hormones, on the contrary, decreases. Such changes are caused by mild gestosis, hypertension, heart defects and other diseases.

In the third phase, a complete failure of the placenta occurs. As a result, the fetus's blood circulation is seriously impaired. This phase of placental insufficiency leads to serious delays in the process of intrauterine development of the fetus. This can lead to hypoxia and death.

It is also worth considering why such a disease often appears in women carrying a baby.

Placental insufficiency of the 1st degree: causes of occurrence

This type of pathology manifests itself primarily due to genetic disorders associated with the fetus itself. This happens in rare cases when the genetic material of the parents contains certain errors. Trisomy may be detected in the fetus. This means that it has three identical types of chromosomes. Deletion and other things can also be diagnosed.

Another reason for the development of stage 1 uteroplacental insufficiency is that the mother could suffer from serious infectious diseases during the first 16 weeks of bearing the baby. In this case, viruses or bacteria in her body could have caused similar fetal abnormalities.

Also, insufficient ovarian activity often leads to this stage of development of the disease. For example, if the female body produces insufficient amounts of progesterone, which is necessary for a full pregnancy.

Placental insufficiency 2nd degree: why it develops

In this case, the most common reason is that the woman has certain biological characteristics that lead to such troubles. It is also worth considering the age of the expectant mother. If she is under 18 years old or over 30, then the body may not be able to fully cope with bearing a baby. In the first case, he is not yet fully prepared for such shocks, and in the second, he may turn out to be too “worn out” for such events.

Also, the cause of placental pregnancy can be the lifestyle of the expectant mother. If a woman eats poorly, continues to smoke, drink or use drugs, then all this will have a detrimental effect on the developing fetus.

Particular caution should be exercised by those who, as part of their work, are forced to come into contact with aggressive chemicals or poisons. Also, fetal abnormalities and disruption of the formation of the placenta can be caused by the fact that a woman, due to her profession, is forced to constantly work with X-ray equipment or in conditions of extremely high or low temperatures. Excessive physical activity, which is strictly contraindicated for pregnant women, can also have a negative impact.

Also, speaking about the causes of placental insufficiency, it is worth paying attention to whether the woman suffers from chronic ailments. For example, if she was previously diagnosed with kidney disease, cardiovascular disease, high blood sugar or hormonal disorders, then all this can lead to unpleasant consequences for the fetus, in particular in the process of proper formation of the placenta. Those who suffer from thyroid pathologies and blood diseases should also be careful.

It is also worth carefully studying the medical history of the expectant mother. Very often, women who have undergone infertility treatment or experienced a miscarriage experience placental insufficiency. Any complications that were recorded during a previous pregnancy can result in consequences that affect the proper functioning of internal organs and the formation of the placenta necessary for the development of the baby.

If a woman had an abortion or had a malformation of the uterus, this may also affect the process of bearing the fetus.

Risk factors

Those women who lead wrong image life, suffer from obesity and constant stress and depression.

Gynecological illnesses suffered in the past can also lead to serious problems in the present. For example, if a woman suffered from endometrial lesions. As a rule, this is caused by an incorrectly performed procedure to terminate a pregnancy. Representatives of the fair sex who have previously been diagnosed with uterine fibroids should also undergo a doctor's examination and undergo tests more often. The same applies to those who were treated for infections such as chlamydia and other gynecological diseases of the pelvis.

However, if there were no problems earlier, this does not mean that you can relax. During the current pregnancy, a wide variety of complications can also develop that can provoke placental insufficiency. For example, if a woman suffers from bleeding during the second trimester of bearing a baby. The same applies to those who are diagnosed with oligohydramnios or polyhydramnios.

Representatives of the fair sex with negative Rh factor you need to be doubly careful. This indicator is very dangerous. In some situations, pregnancy is completely contraindicated for women.

Symptoms

If we talk about the manifestations of placental insufficiency, then its presence is almost impossible to determine independently. As a rule, when the first serious symptoms, the fetus already receives quite serious damage incompatible with life. To diagnose the first manifestations of this disease, a comprehensive examination is necessary. Based on the data obtained, the specialist will be able to see the main manifestations of placental insufficiency. These include:

• Partial restructuring of arterial vessels. However, in 56% of cases, such a clinical picture is typical for normal pregnancy. Therefore, the doctor also pays attention to the size of fibroids, if they are detected. If the nodes are quite large, then there is a possibility that the uteroplacental arteries have been deformed.
• Also, with the development of placental insufficiency, you can see dead areas.
• Signal about possible problem It could also be that the muscular membrane is too thin, which is located between the fibroid and the fertilized egg itself.

Treatment

If we talk about therapeutic measures, then first of all doctors try to improve blood flow in the uterus. Also, in the process of treating placental insufficiency, preventive measures are taken to eliminate the possibility of delayed fetal development. This takes into account the size and condition of the baby.

Also at this stage, doctors try to choose best time for childbirth and its type. In some situations, the birth of a baby naturally becomes impossible, then a caesarean section is performed.

One of the main stages of treatment is careful monitoring of any changes in the condition of the fetus. For this purpose, a weekly ultrasound is required. It is also necessary to measure the speed of blood flow in the uterus and its main vessels. Such checks are carried out every 3-5 days.

Cardiotocography is also performed. This procedure is a recording of how synchronously contractions of the fetal heart muscle occur. This activity must be performed daily.

Treatment also includes taking medications. First of all, the doctor prescribes medications that can significantly improve blood flow. Angioprotectors are also used, whose activity is aimed at protecting blood vessels from possible damage. In some situations, it is necessary to reduce muscle tension directly in the uterus itself. For this, the doctor prescribes tocolytics.

Since a woman is already experiencing enormous stress during this period, an additional stressful state can only aggravate the situation. Therefore, representatives of the fair sex are recommended to take mild sedatives. The doctor also prescribes a course of general restoratives that can stabilize the mother’s condition and improve the functioning of the immune system.

If a woman has been diagnosed with decompensated insufficiency, then in this case there is a serious delay in the development of the fertilized egg. In such situations, urgent hospitalization is required.

Possible complications

As mentioned earlier, such a pathology can lead to hypoxia and delayed fetal development. All these negative phenomena can lead to his intrauterine death.

If the baby is nevertheless carried to term and born, then the development of pneumonia, pathological jaundice and other skin ailments is possible.

Placental insufficiency of the fetus can lead to prematurity, even if the birth took place at the prescribed time. In this case, the baby’s weight can barely reach 2000 g, provided that the child was born at 38-40 weeks.

Also, such a disease can provoke quite serious perinatal damage to the fetal nervous system. In this case, the child’s brain functioning will be impaired.

Prevention

In order to avoid such problems, it is necessary to take a responsible approach to planning and preparing for pregnancy. If a woman has certain chronic diseases, then it is necessary to cure them in a timely manner and only after that start thinking about conceiving a baby.

The expectant mother must get a good night's sleep and spend time fresh air as much time as possible. In this case, you must register with the antenatal clinic. The doctor must conduct a comprehensive examination and monitor the health of the expectant mother at all stages of bearing the baby.

You also need to monitor your diet and be sure to give up all bad habits. You need to include as many fruits, vegetables and greens in your diet.