Xr fpn what. Acute and chronic placental insufficiency during pregnancy

Fetoplacental insufficiency (abbreviated as FPI) is a condition that is characterized by circulatory disorders in the mother-placenta-fetus system, and can cause delay intrauterine development fetus

Acute and chronic fetoplacental insufficiency

Depending on how rapidly fetoplacental insufficiency developed, two forms are distinguished: acute and chronic.

For acute feto placental insufficiency the fetus experiences sudden severe oxygen starvation (hypoxia), which can lead to the most serious consequences, including its death. Acute FPN is quite rare, and the main cause of this complication is premature placental abruption.

Chronic placental insufficiency develops slowly: over weeks and even months. Thanks to this, the organisms of the pregnant woman and the fetus have time to adapt to the changes, so severe complications of chronic FPN are very rare.

Causes of fetoplacental insufficiency (FPI)

Doctors are not always able to determine why a pregnant woman developed fetoplacental insufficiency. Often this condition is found in women with a normal pregnancy.

However, the presence of the following factors increases the risk of developing chronic placental insufficiency:

• Poor quality (unbalanced) (including poor weight gain during pregnancy);
• Hypertension in pregnant women (increased blood pressure);
• Chronic diseases of the cardiovascular system in pregnant women;
• Anomalies of the uterus (bicornuate uterus, saddle uterus, etc.);
• Multiple pregnancy (twins, triplets, etc.);
• Placenta previa.

Symptoms and signs of placental insufficiency

Placental insufficiency is often asymptomatic, so most pregnant women learn about the presence of abnormalities only during an ultrasound.

However, there are some signs of placental insufficiency, if a woman notices them, she should consult with her doctor:

• Weak fetal movements or their complete absence during the day (starting from).
• Weak.
• Small belly size for the current stage of pregnancy.

It is worth noting that the last symptom of placental insufficiency is quite subjective, since the size of a pregnant woman’s abdomen can depend on many factors, and a small belly does not always mean that something is wrong with the pregnant woman or her unborn child.

Diagnosis of fetoplacental insufficiency

As a rule, the diagnosis of chronic FPN is made based on the results of ultrasound and Dopplerometry.

• Ultrasound with chronic FPN can show a delay in fetal growth, as well as a decrease in the number amniotic fluid(low water). If fetoplacental insufficiency is suspected, several ultrasound scans are usually performed at an interval of 2 weeks. Using repeated ultrasounds, the doctor determines the rate of fetal growth, which can confirm or refute the diagnosis of intrauterine growth retardation.
• Doppler is a type of ultrasound that helps evaluate blood circulation in the vessels of the placenta and fetus (in the uterine and umbilical arteries). Data obtained during Doppler measurements make it possible to determine the degree of fetoplacental insufficiency and formulate further pregnancy management tactics.

Degrees of fetoplacental insufficiency (FPI)

Depending on how severe the disturbance of blood flow is in the vessels of the uterus, umbilical cord and fetal vessels, several degrees of fetoplacental insufficiency are distinguished:

1a degree of FPN is characterized by initial changes in blood flow in the mother-placenta-fetus system, which are successfully compensated and do not affect the health of the unborn child (the size of the fetus corresponds to the gestational age).

With 1b degree of FPN blood flow disturbances intensify, and the possibilities of compensatory mechanisms are on the verge. The size of the fetus is still appropriate for the gestational age, but the risk of intrauterine growth restriction is significantly increased.

Stage 2 FPN is characterized by severe disturbances in blood flow in the mother-placenta-fetus system, which lead to a lack of oxygen and nutrients in the fetus. To provide nutrition to vital organs (brain and heart), blood circulation in the fetal body is rebuilt. This phenomenon is called centralization of fetal-placental blood flow, and its detection indicates serious disorders which may lead to intrauterine growth retardation.

Stage 3 FPN is the most severe degree of fetoplacental insufficiency. Due to severe disruption of blood flow, the fetus ceases to receive the nutrients necessary for growth, which leads to developmental delays. Doppler detects zero or reverse diastolic blood flow in the umbilical cord artery, and ultrasound reveals fetal growth restriction.

Treatment of fetoplacental insufficiency (FPI)

There is still no generally accepted treatment regimen for chronic placental insufficiency. The management of pregnancy in this condition depends on the degree of FPN, as well as data obtained during examination of the fetus using CTG (cardiotocography).

Possibilities drug treatment fetoplacental insufficiency are limited, since known drugs have not yet proven their effectiveness in scientific experiments.

The tactic of prescribing bed rest for pregnant women with chronic FPN has also not shown its effectiveness. Currently, experts recommend that pregnant women with FPN maintain at least a minimal degree of physical activity, as this stimulates blood flow and has a beneficial effect on the well-being of the expectant mother and her unborn child.

Recommendations for placental insufficiency, which have proven their effectiveness, boil down to changing some of the habits of the pregnant woman. First of all, a pregnant woman should give up smoking (including passive smoking), and secondly, establish high-quality balanced diet, including all essential vitamins and minerals. There is also evidence that magnesium supplements reduce the risk of fetal growth retardation.

Do I need to go to the hospital for chronic fetoplacental insufficiency (FPI)?

For fetoplacental insufficiency of degrees 1a, 1b and 2, hospitalization, as a rule, is not required, since the prescribed treatment can be received at home. Your doctor will likely schedule more frequent visits and follow-up examinations to monitor the condition and well-being of your unborn baby.

In case of stage 3 FPN with intrauterine growth retardation, hospitalization may be required, during which doctors will closely monitor the well-being of the unborn child.

Premature birth with fetoplacental insufficiency

In the event that the life of the unborn child is at risk, and further stay in the womb may adversely affect his health, the pregnant woman may be recommended to have a premature birth.

Depending on the stage of pregnancy and the results of CTG, doctors decide whether it is safe or required. A few days before planned delivery, a course of treatment with corticosteroid hormones is carried out, which accelerates the maturation of the fetal lungs and reduces the risk of complications after birth.

Delivery at term with fetoplacental insufficiency

If throughout pregnancy the condition of the fetus does not cause concern, it is recommended to wait until labor begins on its own. It is currently not recommended to induce labor unless absolutely necessary if the pregnancy is less than 39 weeks.

As a rule, the diagnosis of placental insufficiency is not an indication for cesarean section in a full-term pregnancy. However, the planned C-section may be recommended if FPN is combined with breech, short umbilical cord, tight entanglement and some other conditions.

FPN during pregnancy is the most common pathology, during the development and formation of which the embryo does not receive enough nutrition and oxygen due to impaired functioning of the placenta. The severity of complications largely depends on the reasons that caused fetoplacental insufficiency, so it is important to conduct a thorough diagnosis.

Reasons for the formation of FPI (fetoplacental insufficiency)

FPN during pregnancy is a functional insufficiency of the placenta, hypoxia occurs, the fetus lacks oxygen, which causes varying degrees of developmental delay and other pathological processes in the embryo.

Formation occurs under the influence of many factors that influence the compensatory possibility between the mother, placenta and fetus. Diseases contribute to the development of placental insufficiency internal organs, chronic inflammation or pathologies of the reproductive system. A high risk of a pathological condition of the placenta always remains with women who are diagnosed with gestosis in the later stages of pregnancy.

The risk group also includes the following categories of pregnant women:

• women under 18 years of age or after 35 years of age;
• at antisocial way life (tobacco smoking, alcoholism, drug addiction);
• difficult working conditions;
• the presence of endocrine diseases;
• deviations associated with violation monthly cycle and constant failure to bear a child, fibroids and others;
• after infections on early stage gestational period;
• if there are any systemic diseases – diabetes, pulmonary or renal failure, high blood pressure;
• associated hereditary or congenital factors.

The causes of fetoplacental insufficiency are associated with various pathologies and abnormal structure of the uterus (bicornuate, saddle-shaped) or with its functional features as a result of damage to the endometrium due to previous curettages and abortions. Often the cause of FPI is anemia, when the blood is significantly deficient in iron, an element that performs the transport function of delivering oxygen to intrauterine development.

Degrees of fetoplacental insufficiency

Classification of FPN at the gestation stage is made according to severity, duration and time of formation. Depending on the gestation period, a distinction is made between primary (incorrectly implanted membrane) and secondary pathology (with a normally formed placenta, insufficient functioning is observed under the influence of negative factors).

Clinical development involves two types of pathology:

1. Acute placental insufficiency - the membrane begins to detach at any stage of gestation. The cause is mainly thrombosis and impaired gas exchange function.
2. Chronic FPN is diagnosed more often and occurs in mid-pregnancy. The pathology is characterized by placental aging ahead of time and, in turn, is divided into the following forms:

• compensated - considered the most favorable, with impaired metabolic processes, but with preserved blood circulation between the uterus and the fetus;
• decompensated - blood flow is disrupted either between the baby and the placenta, or between the uterine cavity and the placental membrane;
• subcompensated chronic fetoplacental insufficiency is caused by a significant decrease in the functional abilities of the placenta, and a significant delay in fetal development is observed.

Additionally, there are criteria for distinguishing by the degree of FPN. 1st degree is subdivided depending on the location of the deficiency:

• FPN grade 1a – there is a lack of hemodynamics of blood flow between the uterine cavity and the placenta;
• FPN degree 1b - is caused by poor blood flow between the fetus and the membrane.

Signs of fetoplacental insufficiency of the 2nd degree are characterized by impaired blood circulation at all levels, but at the same time, the indicators do not reach a critical level, unlike pathology of the 3rd degree, a threat to the baby’s life arises.

Treatment of fetoplacental insufficiency

The treatment protocol for FPN includes, first of all, therapy for the initial pathological factors. If the child does not feel discomfort, then prophylaxis and gradual stabilization of blood circulation are prescribed.

Treatment of placental insufficiency in pregnant women with a threat to the life of the child involves the use of medications in a hospital setting. During therapy, drugs are used that improve the quality of blood circulation and activate metabolic processes (Curantil, Eufillin, Troxevasin and others). To reduce the tone of the uterus, Magnesia, Ginipral or No-Shpa are prescribed.

Clinical recommendations consist of constant dynamic monitoring when diagnosing FPN using ultrasound, CTG and Doppler sonography. A woman needs to maintain absolute peace and avoid stressful situations so as not to cause an increase in the tone of the uterus. In order to prevent and improve blood flow, the diet should consist of many fruits and vegetables so that the fetus receives maximum amount vitamins and microelements.

Concluding a large series of topics about the structure, location and functioning of the placenta - a unique embryonic organ - one cannot help but talk about placental insufficiency, better known as fetoplacental insufficiency or FPI. A large number of women hear this expression from a doctor, but often not everyone is able to understand what kind of disease it is, how it threatens the fetus, and whether it can be cured.

FPN can hardly be called a disease, since it would be more correct to define it as a circulatory disorder in the “mother-placenta-fetus” system. We have already written more than once that the placenta has two sides, one of which belongs to the fetus - it is connected to it by its umbilical cord, and the second surface is attached to the uterus - the anterior one. back wall or the bottom. If the placenta, for one reason or another, ceases to adequately perform its many functions, we are talking about the occurrence of placental insufficiency. That is, in the literal sense – about the insufficient functioning of the organ.

Types of placental insufficiency

The classification of FPN is quite extensive. First of all, doctors divide it according to the form of its flow. There are two forms - acute and chronic placental insufficiency. Acute, as can be understood from the name, occurs suddenly and sharply when the uteroplacental blood flow is disrupted. This leads to placental abruption. Basically, this option occurs directly during childbirth, but if acute FPN occurs before the onset of labor - for example, due to an abdominal injury, this is a direct threat to the life of the fetus.

The most common other form of FPN is chronic placental insufficiency, when circulatory impairment does not occur immediately, but gradually. In turn, the chronic form can be divided into two subtypes:

• Compensated form of FPN – when the fetus adapts to changes in blood supply due to the compensatory capabilities of the mother’s body;
• Decompensated form of FPN - the changes are more serious, the fetus begins to experience hypoxia, its cardiac activity is disrupted, and developmental delays are observed.

In some cases, doctors rule out placental insufficiency with or without growth retardation of the fetus. According to the period of occurrence, FPN is divided into primary and secondary. Primary placental insufficiency occurs before 16 weeks. It is associated with impaired formation of the placenta. Secondary is observed at later stages, when the already formed placenta does not receive sufficient blood supply.

Uteroplacental insufficiency means that disturbances in the blood supply occur in the mother-placenta system. Fetal-placental – that these disorders occur on the part of the placenta and the fetus. There is a high risk that without appropriate treatment the fetus will be in critical condition. Thus, the first degree - uteroplacental insufficiency - already requires medical intervention in order to prevent the occurrence of disturbances in the blood supply to the fetus.

Symptoms and causes of FPN

The most threatening symptom of acute FPN is the occurrence of bleeding, which may indicate that partial or complete placental abruption has occurred. That is why doctors always warn pregnant women about the need to quickly contact a doctor if any bleeding occurs.

With chronic placental insufficiency, there may be no obvious symptoms at all, especially in its compensated form. In this case, the woman learns about the diagnosis of FPN only after an ultrasound examination. In the decompensated form, a woman may notice a decrease in the number of fetal movements. After 28 weeks, the number of movements should not be less than 10 per day. Another option may occur when the child moves too actively for a long time, and then calms down for a long time. A slowdown in the growth rate of the abdomen can hardly be noticed on your own - but the doctor will see it during the next examination and take the necessary measurements.

Exist various reasons, which increase the risk of placental insufficiency:

Prevention and treatment

Undoubtedly, the best way is the prevention of placental insufficiency. This implies careful planning of pregnancy and finding out the characteristics of your health. For example, if the presence of any infection is confirmed, you can eliminate this factor in advance. In addition, refusal bad habits, compliance correct mode nutrition (and its completeness), regular walks on fresh air also play a huge role in the normal course of pregnancy.

There is no generally accepted treatment regimen for FPN - if it has a compensated form, then it is enough for a woman to undergo outpatient treatment, in other cases hospitalization is necessary. First of all, doctors will identify the cause of FPN and eliminate it, and at the same time carry out therapy aimed at maintaining blood supply to the fetus.

In the case of compensated placental insufficiency, there is every chance of natural childbirth . In other cases, a caesarean section may be required, sometimes prematurely. In this case, the child's presence in the womb will cause him more harm than good. We wish you good health and hope that you will always pay attention to all doctor’s prescriptions for uteroplacental insufficiency.

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, disruption of the monthly cycle, serious gynecological diseases and surgical operations in the reproductive system before pregnancy, spontaneous abortions and established recurrent miscarriage, previous premature birth, 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). This group also includes late toxicosis, threat of miscarriage, Rh incompatibility, multiple births, improper attachment of the placenta, and pathological immaturity of the genital organs.
3. Somatic pathologies in the expectant mother. The risk of developing placental insufficiency is increased by 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. Clinical picture pathology includes a violation of trophic function, which entails hormonal and gas exchange abnormalities in 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 has important during advanced 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 an IV.

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.

Doctors resort to surgical delivery of a patient via cesarean section 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.

Fetoplacental insufficiency (FPN) accounts for more than 20% of the causes of perinatal mortality. Long-term observations of many authors over the development of children born to mothers diagnosed with FPN have led to the conclusion that this pathology causes not only a sharp increase in perinatal mortality, but also numerous changes in the child’s body, which during the first years of life cause disturbances in his physical health. And mental development, as well as increased somatic and infectious morbidity (N. L. Garmasheva, N. N. Konstantinova, 1978; E. M. Vikhlyaeva, 1983; I. P. Ivanov, 1983; V. E. Radzinsky, 1992).

There are primary FPN, associated with chorion pathology in the early stages, which leads to spontaneous abortions and IUGR, and secondary (acute - premature placental abruption and chronic - changes in feto-placental homeostasis, IUGR, fetal death).

ETIOLOGY AND PATHOGENESIS

All types of extragenital diseases and obstetric pathologies lead to the development of chronic FPN. Depending on the degree of severity and the relationship between changes at all levels, the following phases of FPN have been established (V. E. Radzinsky, 1992):

1. compensated - characterized by stimulation of all types of adaptive-homeostatic reactions that ensure the functioning of the placenta in the phase of stable hyperfunction, which is noted in PN caused by prolonged pregnancy, mild forms of short-term gestosis, lipid metabolism disorders, chronic pyelonephritis;

2. subcompensated -characterized by a decrease in the level of adaptive reactions compared to the norm, a distortion in the set of ribosomes, activation of glycolytic processes, increased lipid levels, and a decrease in hormonal function. These changes are noted during postterm pregnancy, long-term mild forms of late gestosis, stage I-II hypertension, and rheumatic heart defects with signs of circulatory disorders;

3. decompensated (within 1-2 days) - characterized by a predominance of dysregulatory processes, a breakdown of hierarchical regulation, the appearance of multiple feedbacks between the molecular, cellular and tissue components of homeostasis, but without their subsequent implementation, which leads to a breakdown of compensation. This phase develops rapidly with weakness labor activity, combined gestosis.

Factors, predisposing to FPN and aggravating it are: maternal age (less than 18 and more than 32 years), smoking, alcohol consumption, taking various medications, a burdened obstetric history, i.e. those factors, the combination of which is the basis for including women in that or another group at increased risk of the occurrence and development of perinatal pathology during pregnancy and childbirth.

Research by I.M. Ordiyants (1989) has established that in multiparous women, starting from the seventh birth, in all cases, regardless of the presence or absence of extragenital and obstetric pathology, FPN is diagnosed. The prognosis for the outcome of pregnancy and childbirth with diagnosed FPN depends on the state of adaptation - homeostatic reactions of the placenta. Relative insufficiency of the placenta with weakly expressed compensatory and adaptive reactions is accompanied by retardation of intrauterine development of the fetus. Hypoxic conditions leading to impaired microcirculation and metabolism in the fetoplacental complex, determine the development of FPN, which in turn forms a vicious circle of mutual pathological influences in the mother-placenta-fetus system. Despite the fact that FPN established in the second half of pregnancy is secondary in most cases, its role in maintaining and aggravating the pathological state of the fetoplacental complex is extremely large. The severity of compensatory-adaptive reactions largely depends on the underlying pathological process that led to FPN. Naturally, with extragenital diseases preceding pregnancy, the nature of the adaptive-homeostatic reactions of the placenta will differ from that with PN, caused by purely obstetric pathology or a combination of these pathological processes (V. E. Radzinsky, 1987).

DIAGNOSTICS

Development modern methods studies of the state of the fetoplacental complex in the dynamics of pregnancy and childbirth made it possible to timely diagnose and treat the main clinical forms of fetal suffering - intrauterine growth retardation (hypotrophy) and/or its chronic hypoxia.

Prenatal diagnosis specified states:

Echography (“biophysical profile” according to Manning or as modified by Vintzileos, fetometry, study of the placenta, in particular determination of the degree of maturity according to Grannum),

Cardiotocography (Fisher, Krebs, Savelyeva scoring systems or computer evaluation of data according to Demidov, Redman & Dowes)

Doppler flowmetry in the vessels of the “mother-placenta-fetus” system.

Cytology,

Amnioscopy,

Hormonal methods.

Hormonal studies of placental function. At least 20% of pregnant women need hormonal monitoring. These include pregnant women with hypertensive disorders during pregnancy, including late gestosis, with a burdened obstetric and gynecological history (premature birth, spontaneous miscarriages, menstrual dysfunction, infertility) who have low body weight and a slight increase during pregnancy, who have suffered severe early toxicosis, chronic threat of miscarriage, with abruption and abnormal location of the placenta, tumors of the uterus, malformations and other risk factors.

Currently, to identify the functional ability of the placenta, estriol (E 3 ) in the blood is determined radioimmunological method. However, due to the biosynthesis of steroid hormones associated with fetal endocrine secretion, their diagnostic information is specific to more late dates pregnancy.

About the conditions of fetal development in early dates pregnancy is more informed by the protein hormones of the placenta - human chorionic gonadotropin (CG) and placental lactogen (PL), since they are produced by trophoblast and syncytiotrophoblast ovum.

Postpartum diagnostics the state of the placenta is carried out mainly using morphometric and morphological methods. By examining the content of hormones of the fetoplacental complex in biological fluids, the doctor has the opportunity to diagnose disorders of the fetus in various complications of pregnancy or extragenital pathology. In this case, there is usually no specificity of endocrine indicators. Changes in the content of hormones in the blood or urine do not correspond to the disease of the pregnant woman. The severity of the patient’s condition to a certain extent correlates with the amount of secreted hormones, since most often severe pathology (nephropathy II-III stage, hypertension stage II, cardiovascular disorders) causes fetal hypoxia. Hormonal test data have special meaning after 30 weeks of pregnancy. It has been established that the lower the excretion of estriol in the urine, the more pronounced the hypoxic changes in the fetal body, the more often its cardiac activity changes. It is especially important that the levels of estriol and hCG excretion decrease before clinical signs of fetal hypoxia appear.

Amnioscopy for various disorders of the fetus, it allows us to identify changes in the amount of amniotic fluid, as well as changes in their transparency and color. Despite the contradictory opinions about the role of “meconium” waters, it should be considered that greenish waters during pregnancy are a sign of fetal hypoxia (T. D. Travyanko et al., 1989).

When examining amniotic fluid obtained by amniocentesis , the most important indicators for diagnosing fetal hypoxia are pH (below 7.02), PCO 2 (over 7.33 kPa), RO 2 (below 10.66 kPa), potassium concentration (over 5.5 mmol/l), urea (over 7.5 mmol/l), chlorides (over 110 mmol/l), glucose (decrease from 1.2 to 0, 8 mmol/l for severe fetal hypoxia) (G.P. Maksimov, 1989). A reliable sign of fetal hypoxia is an increase of 2.5 times or more in the content in the amniotic fluid. b -glucuronidase. M. Hagamani and co-authors (1979) found that the concentration of estrogens and human chorionic mammotropin in amniotic fluid during hypoxia and fetal malnutrition is significantly reduced.

IN last years an indispensable diagnostic method pathological conditions the fetus is his ultrasonography And biometry of the placenta . Its thinning (up to 2 cm) or thickening (over 5 cm) in last month, pregnancy indicates developing placental insufficiency (L. S. Persianinov, V. N. Demidov, 1982). Echography also makes it possible to diagnose a number of pathological conditions of the placenta. The definition of the so-called biophysical profile fetus , which includes a comprehensive assessment of 5 parameters:

Breathing movements of the fetus

Physical activity fruit,

Muscle tone fruit,

The amount of amniotic fluid,

Non-stress test (NST) for cardiotocography.

In the modification of Vintzileos (1987), a 6th parameter was added - the degree of maturity of the placenta according to Grannum. According to many researchers, a comprehensive assessment of the “biophysical profile” of the fetus allows one to obtain the most objective information about its vital functions. It has been established that the prognostic value positive result when determining the “biophysical profile” of the fetus is 90%. F. Manning et al. (1981) developed a special scoring system for assessing this indicator (similar to the Apgar scale). According to R. Richter (1984), the frequency of adverse pregnancy outcomes for the fetus with a score of 10 points is 6%, 8 points - 13%, 6 points - 30%, 4 points - 75%, 2 points - 100%. According to A. M. Vintzileos et al. (1987), the main errors in the interpretation of data from the “biophysical profile” of the fetus, leading to incorrect pregnancy management tactics, are:

The choice of pregnancy management tactics, based only on scoring without taking into account clinical data in each specific case;

Making a decision on pregnancy management tactics without taking into account data from a previous study of the “biophysical profile” of the fetus and how long ago it was carried out;

Assessment of the fetal condition only on the basis of ultrasound results without using NST data;

Insufficient qualifications of the researcher.

Manning et al. (1981) propose the following obstetric tactics depending on the score when determining the “biophysical profile” of the fetus. A score of 8-10 points indicates the normal condition of the fetus. Repeated examination of the fetus should be carried out only in pregnant women at high risk of perinatal pathology after 1-2 weeks. With a score of 4-6 points, obstetric tactics are determined taking into account signs of fetal maturity and preparedness of the birth canal.

In cases of insufficient fetal maturity and lack of preparedness of the birth canal, the study is repeated after 24 hours. If a repeated unfavorable result is obtained, corticosteroid therapy is necessary, followed by delivery after 48 hours. If there are signs of fetal maturity, early delivery is indicated.

A score of 0-2 points is an extremely unfavorable sign and serves as an indication for quick, careful delivery. In the absence of signs of fetal maturity, delivery should be carried out after 48 hours of preparation with corticosteroids.

Cardiotocography (CTG) allows you to objectively assess the nature of the fetal cardiac activity and contractile activity of the uterus. At the same time, many studies have proven that incorrect interpretation of data obtained from CTG leads to overdiagnosis of hypoxic conditions, which, in turn, leads to an unjustified increase in the frequency of surgical delivery by cesarean section. To eliminate the subjectivity inherent in the visual assessment of cardiotocograms, even when using special scoring systems, in recent years, automated computer systems for assessing cardiotocograms have been developed and put into practice.

Method Doppler ultrasound , with the help of which direct measurements of blood flow in various vascular zones of the mother-placenta-fetus system are carried out in dynamics, allows one to assess the state of uteroplacental blood flow and therefore has important diagnostic and prognostic significance in the group of pregnant women at high perinatal risk. Numerous studies have proven that a comprehensive assessment of blood circulation in the mother-placenta-fetus system allows for improved diagnosis and selection of optimal obstetric tactics for FPN. A classification of disorders of uteroplacental and fetal placental blood flow was developed, based on the assessment of blood flow velocity curves in the uterine arteries and umbilical cord arteries (Strizhakov A.N. et al. 1989). According to this classification, there are three degrees of severity of hemodynamic disorders:

I degree:

A - disruption of uteroplacental blood flow with intact fetal-placental blood flow.

B - disruption of fetal-placental blood flow with intact uteroplacental blood flow.

II degree: simultaneous disturbance of the uteroplacental and fetal placental blood flow, which does not reach critical changes (end-diastolic blood flow is preserved).

III degree: critical disturbances of fetal-placental blood flow (lack of blood flow or reverse diastolic blood flow) with intact or impaired uteroplacental blood flow.

A directly proportional relationship with a high correlation coefficient was noted between the degree of hemodynamic disturbances in the mother-placenta-fetus system and the incidence of fetal growth retardation, intrauterine hypoxia, surgical delivery by cesarean section, severe condition of the newborn and perinatal losses. It should be noted that during dynamic observation there was no normalization or improvement of hemodynamic parameters in grades IA, II and III of disturbance of the uteroplacental-fetal blood flow. Normalization of fetal-placental blood flow was noted only in grade I B, usually in pregnant women with a threat of miscarriage.

Currently, there are no sufficient grounds and convincing data to consider the use of Doppler ultrasound as a screening method in obstetric practice justified. However, it is undeniable that Doppler examination of uteroplacental and fetal blood flow has important diagnostic and prognostic value in the group of pregnant women at high perinatal risk. Most attention Researchers are interested in assessing fetal hemodynamics and uteroplacental blood flow during FPN. This is due, firstly, to the fact that FPN is one of the main causes of perinatal morbidity and mortality, and secondly, in the pathogenesis of the pathology under consideration, the leading role is played by hemodynamic disorders of the uteroplacental and fetal placental blood flow. Although hemodynamic disturbances that can be detected by Doppler examination are noted in the vast majority of cases of FPN, not all forms of FPN are accompanied by significant changes in uteroplacental and fetal placental blood flow. This appears to be the reason for the majority of false negative Doppler results in this pathology. Therefore, it is necessary to once again emphasize the need for comprehensive consideration of data from three main complementary research methods in the obstetric clinic: echography, CTG and Doppler. (Medvedev M.V. Clinical guide to ultrasound, Volume II, 1996).

An equally valuable diagnostic method for pathological conditions of the fetus is determination of acid-base status fetal blood taken from the vessels of the skin of the presenting head (sample Zalinga). In the first stage of labor, a decrease in pH to 7.2 is regarded as subcompensated acidosis, below 7.2 is decompensated acidosis, which indicates fetal hypoxia. The state of decompensated acidosis in combination with changes in heart rate is a reliable sign of fetal hypoxia, which requires immediate delivery (L. B. Markin, 1989).

A comprehensive study makes it possible to reliably determine the degree of fetal suffering and timely treatment of FPN.

TREATMENT

Treatment of FPN includes therapy for the underlying disease, as well as a set of measures aimed at improving uteroplacental circulation and metabolic processes in the fetoplacental complex.

Compensated forms of FPN do not require specific therapy. It is enough to carry out the usual antihypoxic measures and ensure cellular processes plastic and energetic material (glucose, ascorbic acid, galascorbine, sigetin, estrogens, amino acids).

Subcompensated forms of FPN are subject to intensive therapy, including drugs that stimulate the synthesis of cyclic adenosine monophosphate: methylxanthines (theophylline, aminophylline, trental, papaverine, no-spa), as well as b - adrenomimetics (alupent, partusisten), stimulants of protein biosynthesis (tocopherol acetate, essentiale, phenobarbital, zixorin); means of protecting biomembranes (polyunsaturated fatty acids - Essentiale, Linetol; steroid hormones - estradiol dipropionate) against the background of selective improvement of uteroplacental circulation (sigetin, Premarin).

It is unacceptable to administer large quantities at the same time. medicines. It is necessary to choose drugs that affect several parts of adaptive reactions at once, and limit the use of drugs that disrupt the bioenergetics of the placenta, in particular mitochondrial respiratory activity (oxytocin, predion).

V. E. Radzinsky (1982) proposed the following treatment regimen for chronic FPN:

Glucose - 1000 ml 5% solution IV drip daily or every other day.

Trental - 5 ml or aminophylline 10 ml 2.4% solution intravenously in glucose solution daily.

Essentiale - 5 ml IV drip daily or Linetol 20 ml 3 times a day.

Tocopherol acetate (vitamin E) - 1 ml of 30% solution IM 1 time per day.

Bricanil or orciprenaline sulfate (alupent) -0.5 mg in 500 ml of 5% glucose solution IV slowly, at a rate of 5-7 drops per minute.

Amino acid solutions (alvesin, aminon) intravenously and/or protein enpit, 1 tablespoon 3 times a day.

Cytochrome C (Cyto-Mack) 30 mg IV.

Actovegin 80 mg IV.

Treatment is carried out for 10-12 days under the control of the state of the fetoplacental complex. 2-3 weeks before birth, it is necessary to begin daily intravenous or intramuscular administration of 4-6 ml of 1% solution of sigetin, and 7-10 days before birth - 1-2 ml of 0.1% solution of estradiol dipropionate or folliculin at the rate of 300 IU/ kg body weight. In parallel with estrogen preparations, other means of comprehensive prenatal preparation are prescribed.

Chronic decompensated FPN, even amenable to complex therapy, in the presence of a viable fetus, is an indication for cesarean section. It should only be noted that cesarean section for chronic FPN should be performed only in those hospitals where there are all the conditions for caring for newborns (appropriate equipment, round-the-clock duty of a neonatologist and resuscitator). IN otherwise morbidity and mortality of newborns with surgical delivery are not much different from those with vaginal delivery, and the risk of surgery becomes unjustified.