Finishing a large cycle of topics about the structure, location and functioning of the placenta - a unique embryonic organ - one cannot 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.

FPI 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 repeatedly written 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 front, back wall or bottom. If the placenta, for one reason or another, ceases to properly 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 body.

Types of placental insufficiency

The classification of FPN is quite extensive. First of all, doctors divide it according to the form of the course. There are two forms - acute and chronic placental insufficiency. Acute, as you can already understand from the name, occurs suddenly and abruptly when the uteroplacental blood flow is disturbed. This leads to placental abruption. Basically, this option occurs directly in childbirth, but if acute FPI occurred before the onset of childbirth - for example, with an abdominal injury, this is a direct threat to the life of the fetus.

The most common form of FPI is chronic placental insufficiency, when circulatory disorders do not occur immediately, but gradually. In turn, the chronic form can be divided into two subspecies:

• Compensated form of FPI - when the fetus adapts to changes in blood supply due to the compensatory capabilities of the mother's body;
• Decompensated form of FPI - the changes are more serious, the fetus begins to experience hypoxia, its cardiac activity is disturbed, there is a developmental delay.

In separate points, doctors endure placental insufficiency with growth retardation and fetal development or without growth retardation. By the time of occurrence of FPI is divided into primary and secondary. Primary placental insufficiency occurs before 16 weeks. It is associated with a violation of the formation of the placenta. The secondary is observed on more later dates 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 - the fact that these disorders occur from 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 fetal circulatory disorders.

Symptoms and causes of FPN

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

In chronic placental insufficiency, there may be no pronounced symptoms at all, especially in its compensated form. In this case, the woman learns about the diagnosis of FPI only after an ultrasound examination. With a 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 be observed when the child moves too actively for a long time, and then calms down for a long time. A slowdown in the growth of the abdomen can hardly be noticed on its own - but the doctor will see this at the next examination and taking the necessary measurements.

There are various reasons that increase the risk of placental insufficiency:

Prevention and treatment

Of course, the best way is to prevent the occurrence of placental insufficiency. This involves 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, the rejection of bad habits, adherence to the correct diet (and its usefulness), regular walks on fresh air also play a huge role in the normal course of pregnancy.

There is no generally accepted scheme for the treatment of FPI - 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 FPI and eliminate it, and along the way, carry out therapy aimed at maintaining the blood supply to the fetus.

In the presence of compensated placental insufficiency, there is every chance for natural childbirth. In other cases, you may need cesarean section sometimes ahead of time. In this case, the child's stay in the womb will do him more harm than good. We wish you good health and hope that you will always carefully consider all doctor's prescriptions for uteroplacental insufficiency.

Placental insufficiency is a condition in which the placenta is unable to perform its functions. Why does this pathology develop during pregnancy? What threatens placental insufficiency to the fetus?

Functions of the placenta during pregnancy

The placenta (fetal place) is the organ that connects the child with the mother's body. The fetal place is formed at 14-16 weeks. On the early dates During pregnancy, all the functions of the placenta are performed by the chorion (one of the membranes of the fetal egg).

The shape of the placenta resembles a round flat disk. It is permeated with blood vessels through which the supply of nutrients to the fetus occurs. By the time the child is born, the fetal place weighs about 500 g and reaches a diameter of up to 16 cm.

Normally, the placenta is attached to one of the walls of the uterus. In some cases, the fetal site drops too low and reaches the cervix, blocking the internal os. During pregnancy, the placenta may migrate and rise higher towards the fundus of the uterus. Placenta previa is a condition in which the placenta remains at the level of the cervix after 32 weeks. In this situation, the birth of a child is possible only by caesarean section.

Functions of the placenta:

• supply of nutrients to the fetus;
• gas exchange (passage of oxygen and removal of carbon dioxide);
• protection against the penetration of hazardous substances (drugs, maternal antibodies);
• synthesis of progesterone and other hormones.

If the placenta does not perform its functions, they speak of its insufficiency. Why does this pathology develop during pregnancy?

Causes of placental insufficiency

Allocate primary and secondary placental insufficiency. The primary pathology of the fetal site is due to a violation of its structure (including the structure of the vessels). This happens with various genetic diseases, infectious processes and hormonal insufficiency of the ovaries.

Secondary placental insufficiency is associated with the following factors:

• social problems (mother's age over 30 and under 18, malnutrition, hard physical work, stress);
• bad habits of the mother (smoking, addiction to alcohol);
• mother's diseases (hypertension, diabetes mellitus and others);
• gynecological pathologies (uterine fibroids);
• complications of pregnancy (preeclampsia, infections);
• multiple pregnancy;
• taking certain medications;
• ionizing radiation.

Consequences of placental insufficiency

Under the influence of any of these factors, the blood flow in the placenta changes. The transport of nutrients from mother to fetus is disrupted, and the excretion of carbon dioxide and decay products is also slowed down. Fetal hypoxia develops - a condition characterized by a pronounced lack of oxygen. First of all, the nervous system of an unborn baby suffers from this. The consequences of hypoxia affect after birth, leading to a delay in the development of the child and other health problems.

The slowdown in the development of the baby can occur even in utero. Insufficient intake of nutrients leads to the fact that the fetus does not gain weight well. As a result, a child with low body weight and various congenital diseases is born. These children require special care in a hospital setting.

Signs of placental insufficiency

Used to diagnose a disease ultrasound procedure. During the procedure, the doctor examines the fetal area and takes certain measurements. Based on the results of the examination, the degree of maturity of the placenta is set. The prognosis and the scheme of further treatment largely depend on this parameter.

There are four degrees of placental maturity:

• 0 degree - up to 28 weeks;
• 1 degree - from 28 to 33 weeks;
• 2 degree - from 34 to 37 weeks;
• Grade 3 - after 37 weeks.

Placental insufficiency is said to be in the event that the degree of maturity of the placenta does not correspond to its term. At the end of pregnancy, the natural aging of the placenta occurs, which is manifested by the deposition of calcifications in it. This condition is normal after 37 weeks and should not occur before this period.

Simultaneously with the ultrasound examination, the doctor conducts dopplerography. This method allows you to evaluate the blood flow in the vessels of the placenta and in the umbilical cord. With placental insufficiency, a violation of the uteroplacental blood flow is very often detected.

There are three degrees of changes in blood flow in the placenta:

• I degree - a violation develops only in one of the parts of the blood flow (IA - the uteroplacental blood flow suffers; IB - the fetal-placental blood flow is disturbed);
• II degree - violations in both the uteroplacental and fetal-placental circulation;
• III degree - a critical level of blood supply to the fetus.

To assess the condition of the placenta and blood flow, an ultrasound examination is performed twice during pregnancy - at a period of 22 and 32 weeks (second and third screenings). If necessary, ultrasound and dopplerometry are repeated as often as necessary.

After 34 weeks, CTG (cardiotocography) is mandatory to assess the condition of the fetus. This method allows you to calculate the baby's heartbeat and identify possible violations. The result is measured in points. Deviation from 8 to 10 points is allowed. With CTG results of 6 and 7 points, they indicate fetal hypoxia. If according to CTG it was possible to get only 5 points or lower, an emergency caesarean section is performed. Such results indicate a critical condition of the fetus and a sharp deterioration in blood flow in the placenta.

Treatment of placental insufficiency

The goal of therapy is to restore normal blood flow in the placenta and restore its ability to perform all its functions until the very birth. For this purpose, drugs are prescribed that activate blood circulation. In most cases, actovegin and its analogues are used. The drug is administered intravenously drip. The course of treatment is from 5 to 10 days.

AT recent times to restore the functions of the placenta in obstetric practice, antiplatelet agents (pentoxifylline, dipyridamole) are actively used. These funds not only improve blood flow, but also thin the blood, preventing platelet aggregation (gluing). Such therapy is actively used in women with preeclampsia, arterial hypertension and various pathologies of the blood coagulation system.

Childbirth in women with placental insufficiency can take place through the natural birth canal. A cesarean section is performed with critical blood flow (III degree according to Doppler), as well as with an unsatisfactory condition of the fetus (CTG less than 6 points). In these situations, the operation is performed at any stage of pregnancy. In other cases, the issue is resolved individually.

Specific prevention of placental insufficiency has not been developed. Expectant mothers are encouraged to healthy lifestyle life, give up bad habits and monitor your diet. In case of exacerbation of any chronic diseases, one should not delay a visit to the doctor. Timely treatment of diseases will prevent the development of placental insufficiency during pregnancy.

Chronic placental insufficiency is a pathological change in the functions of the placenta due to the influence of any factors. The placenta is a specific organ. It is produced in the body of a pregnant woman. The placenta assumes the role of a link between the mother and her fetus. Thanks to the placenta, the unborn child receives the necessary substances for its development from the mother's body. Through the placenta, the protective, hormonal, respiratory, excretory activity of the unborn baby is carried out.

Characteristics of the pathology

Placental, or fetoplacental insufficiency, is a disease that occurs when there are abnormalities in the work of the placenta. Violations are detected in circulatory failure in the complex system mother - placenta - fetus.

This pathology develops due to the action of some factors that adversely affect the functions of the placenta. The disease interferes with the normal supply of oxygen to the fetus, which leads to the risk of delaying its development.

The disease occurs in primary and secondary form:

1. Primary placental insufficiency occurs in the first months of pregnancy (up to 16 weeks) due to negative changes in the processes of placentation and implantation.
2. Secondary placental insufficiency develops in the already existing placenta from external factors that affect both the placenta and the fetus.

Uteroplacental insufficiency is compensated and decompensated.

1. Compensated. It is characterized by changes in the placenta itself, which do not affect the mother-placenta-fetus system.
2. Decompensated. In the placental system, irreversible disorders occur that adversely affect the further successful development of pregnancy.

The disease is observed both with a delay in the development of the fetus, and without it.

Placental insufficiency in form is divided into acute and chronic:

1. Acute placental insufficiency. Happens. It is most often seen during childbirth. It is less common than the chronic form.
2. Chronic placental insufficiency. It can appear at any time of bearing a child. It often occurs in women who belong to the so-called high-risk group.

There are 3 degrees of severity in the antenatal period or intrauterine development of the fetus:

1. Grade 1: when the lag in fetometric indicators is 1 to 2 weeks compared to the gestational age or pregnancy.
2. Grade 2: the delay is 2 - 4 weeks.
3. 3 degree: the lag exceeds 4 weeks from the prescribed norm.

Signs of placental insufficiency

In the presence of compensated placental insufficiency, the pregnant woman feels good, without any negative symptoms. The disease is detected only during ultrasound.

Acute and chronic placental insufficiency have certain distinguishing features. According to normative indicators, from the 28th week of pregnancy, fetal movements should normally occur on average 10 times a day. For patients with insufficiency, the initial increased and active movements of the fetus are characteristic, but subsequently the activity is greatly reduced. In addition, there is a decrease in the size of the abdomen. The most striking symptom is spotting from the vagina; they signal about.

Reasons for the development of pathology

In medical practice, the occurrence and development of this disease is explained by the following reasons:

• poor quality and inadequate nutrition;
• women at risk: under 18 and over 35;
• endocrine diseases: thyroid dysfunction, diabetes mellitus;
• sexually transmitted infections;
• transferred abortions;
• the threat of termination of pregnancy;
• menstrual irregularities;
• chronic gynecological diseases: improperly developed uterus, fibroids, endometriosis;
• diseases during pregnancy;
• diseases of the cardiovascular system;
• anemia - lack of iron;
• constant stress;
• hereditary disorders of the fetus;
• insufficient hormonal function of the ovaries;
• bad habits: smoking, alcohol, drugs;
• incompatibility of the Rh factor, blood groups of the mother and fetus, hypercoagulability - increased blood clotting.

by the most dangerous reasons of this serious disease are considered:

1. Preeclampsia is a deterioration in the state of the vessels of the brain, kidneys, an increase blood pressure mother.
2. Extragenital pathology, when vascular damage occurs, for example, with hypertension.

Deficiency diagnosis

Since all pregnant women, and especially those with this pathology, are strictly registered with the doctor, they are diagnosed according to the following indicators:

• abdominal circumference;
• complaints of bloody discharge from the vagina;
• the number of fetal movements, the nature of his heartbeat;
• parameters of the pregnant woman (weight and height);
• tension of the muscles of the uterus and the height of its bottom.

All indicators are diagnosed by ultrasound, cardiotocography, dopplerometry.

With the help of ultrasound, the state of the placenta, its location, structure, degree of maturity, thickness are studied. If the patient has this disease, ultrasound shows symptoms such as the deposition of calcium salts in the placenta, as well as an increase or decrease in the normal thickness of the placenta. Ultrasound allows you to determine the size of the fetus and compare the dimensions of the trunk, limbs, head with the indicators laid down precisely at this stage of pregnancy. With fetal growth retardation, its size is insufficient for the diagnosed patient according to the gestational age.

According to the ultrasound data, the doctor also determines the AM index: polyhydramnios or oligohydramnios.

Based on Doppler data, the state of blood flow in the brain of the unborn child, in the uterus, in the vessels of the umbilical cord is checked. With the help of cardiotocography, listening to heart rhythms, cardiac activity of the fetus is carried out.

Treatment of the disease

Therapeutic measures for this disease are strictly individual.

The goal of treatment: maintenance of uteroplacental blood flow and fetoplacental blood supply, prevention in order to prevent delay prenatal development fetus.

Of the drugs prescribed by the attending physician, the following can be used:

1. Sedative drugs to reduce the nervous and mental arousal of the patient.
2. Tocolytics to relax the muscles of the uterus, lowering its tone.
3. Antiplatelet agents - drugs to reduce blood clotting.
4. Vasodilator drugs to enhance blood circulation, improve oxygen supply to the fetus.

Complications and consequences of the disease

Placental insufficiency has the following consequences:

1. Risk of fetal growth retardation, intrauterine cessation of development and fetal death.
2. Fetal hypoxia - insufficient oxygen supply.
3. Congenital diseases in children, in particular jaundice and pneumonia.
4. Risk of injury nervous system, changes in the structure and functioning of the fetal brain during gestation and childbirth.
5. Prematurity of the unborn child during childbirth.

Deficiency prevention

To prevent the threat of the development of the disease, it is necessary:

1. Get registered with the observant gynecologist in time.
2. Have regular check-ups with doctors.
3. Healthy food. The diet should be with enough fiber (greens, fruits, vegetables). Minimal consumption of fried, salty, hot, canned, fatty foods.
4. Sleep well.
5. Do special therapeutic exercises for pregnant women.
6. Eliminate physical activity, stressful situations.
7. Take vitamin and mineral supplements.
8. To refuse from bad habits.

Before becoming pregnant, a woman must plan the birth of a child in advance.

If she suffers from various diseases, you must first cure them in order to prepare your body for motherhood.

Placental insufficiency is a syndrome caused by morphological and functional changes in the placenta, with the progression of which IGR develops, often combined with hypoxia.

SYNONYMS OF PLACENTAL INSUFFICIENCY

Fetoplacental insufficiency is a frequently used synonym, which cannot be considered successful, since it is not correct in form and essence.

PLACENTAL INSUFFICIENCY CODE ACCORDING TO ICD-10

Class XV. Pregnancy, childbirth and the puerperium (O00–O99)
Maternal care for fetal, amniotic sac and possible delivery difficulties (O30–O48)
O36. Maternal care for other identified or suspected pathological conditions fetus.
Class XVI. Certain conditions arising in the perinatal period (P00–P96)
Fetus and newborn affected by maternal conditions, complications of pregnancy, childbirth and delivery (P00-P04)
P02. Damage to the fetus and newborn due to complications from the placenta, umbilical cord and fetal membranes. Disorders related to duration of pregnancy and fetal growth (P05-P08)
P05. Slow growth and malnutrition of the fetus.
P07. Disorders associated with shortened pregnancy and low birth weight, not elsewhere classified.

EPIDEMIOLOGY OF PLACENTAL INSUFFICIENCY

Placental insufficiency is one of the most common complications of pregnancy, occurs with miscarriage in 50–77%, with preeclampsia - in 32%, with a combination of pregnancy with extragenital pathology - in 25–45%, in pregnant women who have had a viral and bacterial infection - more than in 60% of observations. PS in women who have had placental insufficiency is 10.3% among full-term newborns, and 49% among preterm ones. In 60% placental insufficiency leads to a delay in fetal development.

CLASSIFICATION OF PLACENTAL INSUFFICIENCY

A wide range of classifications of placental insufficiency has been developed. Some of them are conditional. The most common and accepted are the following classifications.

Types of placental insufficiency by time and mechanism of occurrence.
Primary - occurs before 16 weeks of pregnancy and is associated with violations of the processes of implantation and placentation.
Secondary - develops against the background of an already formed placenta (after the 16th week of pregnancy) under the influence of exogenous factors in relation to the fetus and placenta.

Types of placental insufficiency according to the clinical course:
Acute - most often associated with detachment of a normally or low-lying placenta, occurs mainly in childbirth.
· Chronic - can occur at different stages of pregnancy.
- Compensated - metabolic processes in the placenta are disturbed, there are no violations of the uteroplacental and fetal-placental circulation (according to Doppler studies in the arteries of the mother-placenta-fetus functional system).
- Decompensated - disorders of the uteroplacental and / or fetal-placental circulation are determined (according to Doppler studies in the arteries of the mother-placenta-fetus functional system).

The following degrees of geodynamic disturbances in the arteries of the functional system mother-placenta-fetus are distinguished.
Grade I - violation of uteroplacental or fetal-placental blood flow.
Grade II - violation of uteroplacental and fetal-placental blood flow.
Grade III - centralization of fetal-placental blood flow, impaired uterine blood flow.
Grade IV - critical disorders of fetal-placental blood flow (zero or reverse diastolic blood flow in the umbilical artery or aorta, impaired uterine blood flow).

Types of placental insufficiency by the presence of fetal growth retardation (FGR).
Placental insufficiency without IGR.
· Placental insufficiency with IGR.

ETIOLOGY (CAUSES) OF PLACENTAL INSUFFICIENCY

Placental insufficiency is classified as a polyetiological disease.

Causes of placental insufficiency.

Among them conditionally distinguish endo and exogenous.
endogenous causes. They call various options violations of placentation and maturation of the villi, in which vascular and enzymatic insufficiency can develop, which leads to the formation of primary placental insufficiency.
exogenous causes. These include a significant number of various factors, the action of which leads to a violation of the uteroplacental and fetal-placental circulation. As a result of their influence, secondary placental insufficiency is most often formed.

Causes of primary placental insufficiency:

· genetic factors;
· bacterial and viral infections;
endocrine factors (hormonal ovarian insufficiency, etc.);
enzymatic deficiency of decidual tissue, which acts as a nutrient medium for the developing fetal egg.

These factors lead to anatomical disorders of the structure, location, attachment of the placenta, as well as to defects in angiogenesis and vascularization, impaired differentiation of chorionic villi. The combination of pathological processes that cause the development of primary placental insufficiency is often observed in miscarriage, especially habitual, and pregnancy after infertility.

Causes of secondary placental insufficiency. It develops in obstetric diseases and complications of pregnancy.

Recent studies have proven the conditionality of dividing placental insufficiency into primary and secondary. Primary placental insufficiency in a large percentage of cases can turn into secondary, and secondary placental insufficiency is often formed against the background of subclinical pathological processes in the early stages of pregnancy. Hidden disorders of placentation can cause early onset of clinical manifestations of placental insufficiency and its severe course in the second half of pregnancy. This happens when a pregnant woman has obstetric diseases and complications of pregnancy, such as preeclampsia, threatening abortion, multiple pregnancy; extragenital diseases (hypertension, heart and kidney diseases, diabetes).

Due to the multiplicity, diversity and ambiguity of the action of etiological factors that can cause the development of placental insufficiency, there are risk factors for the development of placental insufficiency: social, obstetric-gynecological and extragenital diseases, congenital and hereditary pathology in the mother and fetus, external factors.

Risk factors for the development of placental insufficiency:

social factors: mother's age over 30 and under 18, malnutrition, heavy physical labor, psycho-emotional overload, occupational hazards, smoking, alcohol and drug use;
Extragenital diseases: diseases of the cardiovascular system, kidneys, lungs, diseases of the blood system, diabetes;
obstetric and gynecological factors:
- anamnestic (menstrual dysfunction, infertility, miscarriage, birth of premature babies);
- gynecological (anomalies of the reproductive system, uterine fibroids);
- obstetric and extragenital diseases during this pregnancy (preeclampsia, threatened miscarriage, multiple pregnancies, anomalies in the location and attachment of the placenta, infections, including urogenital infections, APS, alloimmune cytopenias);
congenital and hereditary pathology in the mother or fetus;
External factors: ionizing radiation, physical and chemical effects, including medicines.

The most significant risk factors for the development of placental insufficiency include preeclampsia and a combination of pregnancy with extragenital pathology, accompanied by vascular damage. Various etiological factors, acting at different stages of the development and functioning of the placenta, are eventually involved in a common pathogenetic mechanism leading to the development of placental insufficiency syndrome, one of the main manifestations of which is considered a violation of placental circulation - the main function of the placenta.

PATHOGENESIS OF PLACENTAL INSUFFICIENCY

The main role in the pathogenesis of placental insufficiency is assigned to a violation of uteroplacental perfusion, which leads to a decrease in the transport of oxygen and nutrients through the placenta to the fetus. The occurrence of hemodynamic disorders in the placenta is associated with violations of morphological and biochemical adaptive reactions in the placenta during physiological pregnancy. Since the development of the structures and functions of the placenta occurs in stages, the pathological changes that occur in the placenta depend on the nature and time of exposure to adverse factors.

Stages of impaired uteroplacental circulation: impaired endovascular migration of the trophoblast, insufficiency of invasion of the extravillous chorion, impaired differentiation of placental villi.

· Violation of endovascular trophoblast migration in the first trimester of pregnancy leads to a delay in the formation of uteroplacental circulation with the formation of necrotic changes in the placental bed, up to its complete delimitation, and subsequent death of the embryo.

Lack of invasion of the extravillous chorion leads to incomplete transformation of the spiral arteries, which is considered one of the main mechanisms for the reduction of uteroplacental circulation with the development of placental hypoplasia and fetal hypotrophy. As a result, some of the spiral arteries do not transform throughout their entire length, while in the other part, transformations occur only in their decidual segments, without affecting myometrial ones, which preserves the ability of the vessels to respond to vasoconstrictor stimuli.

Disturbances in the differentiation of placental villi are of great importance in the pathogenesis of placental insufficiency. They are manifested by their slow development, premature aging or uneven maturation with the presence of villi of all types in the placenta. At the same time, the processes of formation of syncytiocapillary membranes are disrupted and / or the placental barrier thickens due to the accumulation of collagen and fibroblast processes in the basal layer, against which the metabolic processes through the placental membrane become more difficult.

Factors contributing to the violation of uteroplacental perfusion: obstetric and extragenital diseases of the mother, in which there is a decrease in blood flow into the intervillous space (preeclampsia, hypertension, etc.), slowing of blood flow in it against the background of difficulty in the outflow of blood and lymph (preeclampsia and cardio- vascular diseases with edematous syndrome, the threat of abortion with a long-term increased uterine tone), increased blood viscosity.

Consequences of violation of uteroplacental circulation. Violation of uteroplacental blood flow leads to ischemia, impaired microcirculation, deposition of immune complexes in the trophoblast, disruption of its structure, imbalance between branching and non-branching angiogenesis, impaired transport of oxygen and nutrients through the placenta and delivery of oxygen to the fetus.

Ischemia. A decrease in the volumetric blood flow velocity in the intervillous space leads to ischemia, under which the lipid peroxidation system is activated with the formation of free oxygen radicals, elastase is released from active neutrophils, which causes damage to the vascular endothelium. In the endothelium, there is a decrease in the synthesis of cytoprotectors and vasodilators: prostacyclin and endothelial relaxation factor (nitric oxide).

Violation of microcirculation. The release of an increased amount of tissue thromboplastin, which enhances platelet aggregation and adhesion, increases the synthesis of platelet thromboxane A2 and endothelin, which has a vasoconstrictor effect. There is a pathological increase in the thromboxane/prostacyclin index. In areas of damage to the endothelium, fibrin and lipid deposits are deposited, the number of receptors that bind vasopressor substances increases, which leads to an increase in vascular resistance, against which the uteroplacental blood flow decreases.

Deposition of immune complexes in the trophoblast. With further disruption of microcirculation processes in the tissues of the placenta, the cells of the damaged endothelium, which play the role of antigen, stimulate the production of antibodies with the deposition of immune complexes under the endothelium of the trophoblast vessels.

Violation of the structure of syncytiotrophoblast. In the future, under the influence of cytotoxic substances, the blood flow in the intervillous space slows down even more, which contributes to more pronounced damage to the endothelium. Thus, a "vicious circle" of hemodynamic disorders in the placenta is formed.

Imbalance between branching and non-branching angiogenesis. At the stage of development of the villous tree, moderate hypoxia can stimulate the proliferative ability of the cytotrophoblast, transcription of the vascular endothelial factor, angiogenesis of the branched type with the development of excessive capillarization of the villi.

At the same time, the mass of the placenta increases, due to which insufficient uteroplacental perfusion is compensated and normal vascular resistance in the placental tissue is maintained for a long time. However, in most cases, under the influence of hypoxia, placental growth factor is stimulated, which leads to a decrease in the intensity of branched-type angiogenesis, which replaces non-branching angiogenesis, with the formation of a pronounced deficiency of villus capillaries. As a result, there is no balance between branching and non-branching angiogenesis, which in the second half of pregnancy supports the normal development of the placental vasculature.

Violation of placental angiogenesis and the absence of the formation of a normal villous tree leads to circulatory disorders (occur early), which causes early development ZRP. Deficiency of the exchange surface of the placenta is formed mainly due to a decrease in the number of arterioles of the tertiary villi, both due to their insufficient formation and obliteration due to thromboembolic and vasospastic processes.

The placenta is characterized by a high level of metabolism and consumes more than half of all oxygen and more than a quarter of the total amount of glucose coming from the maternal bloodstream, therefore, with insufficient uteroplacental circulation, it is it that is damaged in the first place.

Violation of the transport of oxygen and nutrients through the placenta. The transport of oxygen and substances through the placenta is carried out through two main mechanisms: diffusion and active transport.

The ability of the placenta to transport increases with increasing gestational age, which is due to the processes of maturation and differentiation of the trophoblast. The transport function depends on the intensity of the uteroplacental and fetal-placental flow, the permeability of the placental barrier, the state of active transport systems, the level of placental metabolism, and the metabolism of the mother and fetus.

Diffusion failure. Delivery of oxygen and carbon dioxide to the fetus occurs by simple or facilitated diffusion and depends on the intensity of blood flow in the intervillous space. Decreased oxygenation of placental tissues leads to energy deficiency and, as a result, disruption of active transport systems.

Disruption of active transport. Through active transport, amino acids, proteins, peptide hormones, vitamins and other substances are transferred through the placental barrier.

As a result, the activity of synthetic processes in the placenta changes, which at the first stages is characterized by compensatory hyperproduction of most enzymes, after which it is replaced by their depletion. In most cases, the primary violation of uteroplacental perfusion and ischemia in the tissues of the placenta lead secondarily to a violation of its transport function and cell-parenchymal insufficiency, which is characterized by a change in the activity of enzymes and the state of cellular metabolism. However, in some situations, for example, in violation of the differentiation of the villi, the synthetic function of the placenta may suffer primarily.

Disruption of oxygen delivery to the fetus. Depending on the severity of the decrease in oxygen delivery to the fetus, three successive stages of this chronic pathological process are distinguished: hypoxemia, hypoxia and asphyxia.

Hypoxemia is characterized by a decrease in the oxygen content in the fetal arterial blood. Adaptive reactions are consistently developing in his body.

- Stimulation of hematopoiesis, including extramedullary, resulting in the development of polycythemia, characterized by an increase in the number of circulating red blood cells and an increase in hematocrit.

- At the initial stages, gluconeogenesis is activated in the liver, but the ability to accumulate glucose in the form of glycogen decreases. The transport of glucose to the fetus is limited, which, under conditions of energy deficiency, leads to a gradual disruption of the mechanisms of active transport in the placenta.

– With an increase in hypoxemia, cardiac output is redistributed: vital organs (brain, heart, adrenal glands) are predominantly supplied with blood.

- Decrease in the growth rate of the fetus up to its complete stop. A significant role in these processes is played by insulin deficiency in the blood of the fetus, which is responsible for the transfer of glucose through the placenta and its utilization in the skeletal muscles, liver and adipose tissue.

Hypoxia. As a result of insufficient content of intracellular oxygen, which is necessary for aerobic metabolism and the production of a sufficient amount of energy, “hypoxic stress” develops, accompanied by the release of biologically active substances and hormones, including adrenaline and norepinephrine. This leads to an even more pronounced redistribution of blood flow towards vital organs: baro- and chemoreceptors of the aorta are activated, vasoconstriction of the abdominal aorta, mesenteric arteries and skeletal muscle vessels. As a result of increasing hypoxia, hypoglycemia, and energy deficiency, glucose metabolism switches to an anaerobic pathway, which is not able to compensate for the energy deficit. Anaerobic glycolysis products contribute to the development of metabolic acidosis.

Asphyxia. A further increase in the severity of the pathological process leads to the development of a state that is critical for the survival of the fetus. There may be a loss of mechanisms that ensure the centralization of fetal blood flow, as a result of which the blood supply to vital organs is disrupted. At the same time, the nature of the blood flow in the peripheral vessels corresponds to the blood flow in the umbilical artery - there is no translational movement of blood in the diastole phase or there is retrograde blood flow. Under these conditions, it is possible to maintain the energy balance of vital organs only for a short time, after which the cells and tissues of these organs switch to the anaerobic metabolic pathway. This process characterizes the beginning of the final phase of oxygen deficiency - asphyxia, against which irreversible changes occur in the cells of vital organs, final decompensation occurs, which leads to the death of the fetus. PI, accompanied by serious metabolic and hemodynamic disorders in the functional system mother-placenta-fetus, leads to the development of IGR - one of the main causes of perinatal morbidity and PS.

CLINICAL PICTURE (SYMPTOMS) OF PLACENTAL INSUFFICIENCY

In chronic PN, pregnant women present complaints typical of obstetric and extragenital diseases, against which chronic or acute PN develops. However, a decrease in the number of fetal movements may be noted. In acute PN during labor, clinical symptoms of PONRP may be observed.

DIAGNOSIS OF PLACENTAL INSUFFICIENCY

ANAMNESIS

When collecting an anamnesis, anamnestic data are found out that can be attributed to maternal, fetal or placental risk factors for the development of PN (see the section "Etiology"). Particular attention should be paid to the presence of clinical symptoms of threatening abortion, preeclampsia.

PHYSICAL EXAMINATION FOR PLACENTAL INSUFFICIENCY

Pregnant risk groups for the development of PN need regular clinical monitoring. During an obstetric examination, you should pay attention to the following signs:
height and weight of the pregnant woman;
Abdominal circumference, VMR (if the difference between the numerical value of the gestational age and VMR, expressed in centimeters, is more than three, we can talk about the presence of IUGR; this criterion allows us to identify about 50% of pregnancies complicated by IUGR);
uterine tone (increased with the threat of termination of pregnancy);
The presence of bloody discharge from the genital tract;
The number of fetal movements, the nature of the heartbeat during auscultation (deafness of heart tones and changes in heart rate).

LABORATORY STUDIES FOR PLACENTAL INSUFFICIENCY

They are of diagnostic value for identifying risk groups in patients who do not have fetal malnutrition compensated for PI in the third trimester of pregnancy. Laboratory research aimed at assessing the hormonal function of the placenta:

Determination of total and placental alkaline phosphatase in blood serum, followed by determination of its share in total phosphatase activity;
determination of the content of PL and oxytocinase in the blood serum;
study of urinary excretion of estriol.

In addition to the above studies, laboratory diagnostics are carried out in accordance with the algorithm for examining those obstetric and extragenital diseases, against which the PN syndrome developed.

INSTRUMENTAL STUDIES FOR PLACENTAL INSUFFICIENCY

The most commonly used instrumental methods for diagnosing PN are ultrasound and CTG. Ultrasound methods play a leading role in the diagnosis of PN and FGR. In the II and III trimesters of pregnancy, at the time of ultrasound screening (20-24 weeks and 30-34 weeks), as well as additional indications, ultrasound fetometry and Doppler blood flow in the arteries and veins of the mother-placenta-fetus functional system are performed.

When conducting ultrasound, in addition to fetometry, which allows you to establish the diagnosis of IGR, you should pay attention to the following characteristics:
Determining the location of the placenta, its thickness and structure (the degree of maturity, the presence of edema, expansion of intervillous spaces, etc.);
Identification of low or polyhydramnios (measurement of the largest vertical pocket or calculation of the AF index);
Identification of ultrasound signs of those obstetric and extragenital diseases that underlay the development of placental insufficiency;
research and assessment in points of the biophysical profile of the fetus (if the equipment is available). Perform an assessment of the so-called fetal heart rate reactivity according to CTG data (presence of a motor-cardiac reflex), respiratory rate, general motor activity, tone, volume of OV. With a normal functional state of the fetus, the total assessment of its biophysical profile is 10 points.

Doppler study of blood flow in the arteries and veins of the functional system mother-placenta-fetus is considered the main diagnostic method, the results of which characterize the state of the placental circulation and its compliance with the needs of the fetus during the II and III trimesters of pregnancy. The absence of violations of the uteroplacental and fetal-placental circulation indicates the normal functioning of the placenta.

Investigation of blood flow in the arteries. Most often, blood flow is examined in the uterine arteries, the umbilical artery, and the middle cerebral artery of the fetus.

Investigated vessels.

- Uterine arteries. Circulatory disorders are characterized by a decrease in the diastolic component on the blood flow velocity curve. The formation of pathological curves of blood flow velocity in the uterine arteries is based on incomplete invasion of the trophoblast into the spiral arteries, which leads to an increase in resistance in the pool of the uterine arteries.

- Artery of the umbilical cord. Pathological curves of blood flow velocity in the umbilical artery, the only peripheral channel of which is the vascular network of the fetal part of the placenta, consist in a decrease in the diastolic component on the blood flow velocity curve, as in the uterine artery. An increase in the vascular resistance of the placenta is due to damage to the microvessels of the villi.

- Fetal middle cerebral artery. The most studied fetal cerebral vessel is the middle cerebral artery. Its blood flow velocity curve has a form characteristic of a highly resistant vascular system. Pathological curves in the middle cerebral artery (in contrast to those in the umbilical cord and uterine arteries) are characterized by an increase in diastolic blood flow velocity (the so-called centralization).

Indicators for assessing the nature of the blood flow velocity curve. To assess the nature of the blood flow velocity curve, one of the following indicators of vascular resistance is calculated.

- Systolic-diastolic ratio.

– Index of resistance.

– Pulsation index.
It is customary to consider pathological values ​​that go beyond 90% for the gestational age.

– Cerebro-placental ratio - the value of the ratio of IR in the middle cerebral artery to IR in the umbilical artery, which under physiological conditions exceeds 1.0. A decrease in this indicator to less than 1.0 indicates a redistribution of fetal blood flow towards vital organs, primarily the brain (the phenomenon of centralization of the fetal-placental circulation).

The presence of changes in hemodynamic parameters during Doppler sonography is not identical to hypoxia. With a high probability, we can talk about hypoxia when registering the so-called critical indicators of the fetal-placental circulation (with zero and reverse diastolic blood flow in the umbilical artery, antenatal mortality is about 50%).

Investigation of blood flow in the veins. In the case of registration of critical values ​​of blood flow in the arteries of the fetal-placental circulation, the venous circulation in this system is examined. Perform Doppler studies of the vein of the umbilical cord, venous duct, inferior vena cava and jugular veins of the fetus.

Unfavorable signs of impaired venous circulation (pathological curves of blood flow velocity)

- Vein of the umbilical cord. Preservation of its pulsation after the 16th week of pregnancy. The symptom indicates cardiovascular decompensation in the fetus.

- Venous duct. The absence of orthograde blood flow in all phases of the cardiac cycle, which indicates a violation
oxygenation of vital organs.

- Inferior vena cava of the fetus. Violation of the outflow of blood from the lower half of the body of the fetus.

- Fetal jugular veins. Violation of the outflow of blood from the upper half of the body of the fetus.

Cardiotocography

Diagnostic criteria have been developed for pregnancy of 32 weeks or more (see the chapter "Instrumental non-invasive research methods").

The most significant diagnostic criteria for violation of the functional state of the fetus during pregnancy:

Decreased amplitude of the motor-cardiac (myocardial) reflex and/or
- Decreased amplitude of heart rate oscillations.

It must be remembered that a decrease in the amplitude can be observed not only in violation of the functional state of the fetus, but also in connection with the recording during the calm state of the fetus in the activity-rest cycle, pathological immaturity of the fetal CNS against the background of placental insufficiency, and taking medications by a pregnant woman.

The main diagnostic sign of a violation of the functional state of the fetus during childbirth is the nature of the reaction of the fetal heart rate to the contraction.

· Study of the cyclic organization of functional states (formation of the "activity-rest" cycle). Under physiological conditions, the "activity-rest" cycle is formed by 34-35 weeks of pregnancy. The delay or absence of the formation of the cycle indicates a violation of the functional state of the fetal central nervous system (delay in the maturation of its coordinating and integrating function) against the background of placental insufficiency.

SCREENING

Ultrasound diagnostics during pregnancy must be performed 3 times at 11–14, 20–24 and 32–34 weeks.

INDICATIONS FOR CONSULTATION OF OTHER SPECIALISTS

The need for consultations depends on obstetric and extragenital pathology, against which placental insufficiency develops.

EXAMPLE FORMULATION OF THE DIAGNOSIS FOR PLACENTAL INSUFFICIENCY

PONRP. Acute placental insufficiency. Fetal hypoxia.
Chronic compensated placental insufficiency.
Chronic compensated placental insufficiency. ZRP.
Chronic decompensated placental insufficiency. I degree of hemodynamic disturbances.
Chronic decompensated placental insufficiency. Critical disorders of the fetus-placental
blood flow. ZRP.

TREATMENT OF PLACENTAL INSUFFICIENCY

GOALS OF TREATMENT

The development of placental insufficiency is associated with morphological changes in the placenta, against which, first of all, hemodynamic disorders occur, therefore it is impossible to achieve a cure for these processes. The main goal of treatment is to prolong pregnancy and timely delivery.

Prolongation of pregnancy is carried out by optimizing blood circulation and correcting metabolic disorders in the placenta in the presence of significant immaturity of the fetus (up to 34 weeks of pregnancy) and the inability to provide him with adequate neonatal care after childbirth.

Timely choice of the term and method of delivery when the fetus reaches a period viable for extrauterine existence (usually after 34 weeks of pregnancy). This requires an adequate diagnosis of the degree of placental dysfunction.

INDICATIONS FOR HOSPITALIZATION FOR PLACENTAL INSUFFICIENCY

Indications for hospitalization in an obstetric hospital are determined individually, taking into account concomitant pathology.

Allocate indications during pregnancy and before delivery.

Indications during pregnancy:
- decompensation (according to Doppler) of the placental circulation, regardless of its degree;
- violation of the functional state of the fetus, identified by other diagnostic methods;
- the presence of SRP.

MEDICAL TREATMENT OF PLACENTAL INSUFFICIENCY

Therapy of placental insufficiency is largely determined by the need to eliminate the causes of circulatory disorders in the placenta. In patients with threatened interruption, an important component of the treatment of placental insufficiency is to reduce the tone of the uterine muscles; with gestosis - elimination of angiospasm and improvement of micro and macrohemodynamics. It is also important to carry out pathogenetically substantiated therapy for such diseases as hypertension, DM, APS, etc.

Complex pathogenetic therapy of placental insufficiency

The complex pathogenetic therapy of placental insufficiency includes, first of all, drugs with a vasoactive effect. In order to improve the fetal-placental circulation, it is advisable to use a combination of actovegin with b-adrenergic agonists. Actovegin © is prescribed as an intravenous infusion: 80–160 mg (2–4 ml) of Actovegin © in 200 ml of 5% glucose solution. The number of infusions depends on the dynamics of Doppler parameters in the fetal-placental circulation (up to 10 infusions). Subsequently, it is possible to use actovegin © and hexoprenaline orally: actovegin © in the form of a long-acting dragee (200 mg), 1 tablet per day, hexoprenaline 0.5 mg, 1/4–1/2 tablets, two to six times a day.

AT last years widespread use in obstetric practice for the prevention of diseases that cause the development of placental insufficiency and its treatment, antiplatelet agents are used: dipyridamole, pentoxifylline. The following requirements are imposed on antiplatelet agents used in obstetrics:

absence of teratogenic and embryotoxic action;
· normalization of the ratio of PG by increasing the synthesis of PG P-I2;
improvement of microcirculation and placental blood flow;
no risk of bleeding and weakening of the hypotensive effect of drugs used to treat preeclampsia.

Indications for taking antiplatelet agents:

diseases of the cardiovascular system (heart defects, hypertension, varicose veins lower extremities);
chronic diseases of the kidneys and liver;
Thrombophlebitis and thrombosis of venous vessels;
Endocrine diseases (DM, etc.);
APS;
DIC syndrome.

The safest antiplatelet agent and angioprotector is dipyridamole. It can be used at any stage of pregnancy and combined with antihypertensive drugs, acetylsalicylic acid, heparin. It improves microcirculation in the placenta by increasing the intensity of collateral blood flow, increasing the synthesis of P-I2, reducing platelet activation and aggregation. The drug as a means of preventing and treating placental insufficiency in pregnant women with preeclampsia is prescribed in doses of 75-225 mg / day. Its maximum daily dose is 450 mg. When taking dipyridamole, there is no risk of overdose and bleeding, so the drug can be used until delivery, and if necessary, starting from the first days after childbirth.

When pregnancy is combined with severe forms of insulin-dependent diabetes mellitus, as well as in women in whom APS is the cause of adverse pregnancy outcomes, low molecular weight heparins and heparinoids (fraxiparin, sulodexide) are effective means for the prevention and treatment of placental insufficiency. The timing and duration of therapy with these drugs in each case should be selected individually. In addition, in APS, in addition to antiplatelet agents and low molecular weight heparins, intravenous immunoglobulins are used as the main means, and fish oil and Wobenzym © are recommended as additional therapy.

Recently, preference has been given to drugs of a combined vasoactive and metabolic type.

For example, in case of hemodynamic disturbances in the functional system mother-placenta-fetus, 5.0 ml of a 10% solution of trimethylhydrazinium propionate in 200 ml of 0.9% pra NaCl or 5% glucose solution is administered intravenously, preferably in combination with the introduction of 5.0 ml of 5% ascorbic acid. The drug has a neuroprotective effect, does not have the effect of "robbing"; its action is reversible.

TERMS AND METHODS OF DELIVERY

The main cause of acute and chronic fetal hypoxia, as well as the birth of children with neurological disorders, is placental insufficiency, therefore, the choice of the optimal timing and method of delivery for women with this pathology can significantly reduce perinatal losses.

If symptoms of a violation of the functional state of the fetus are detected according to clinical, laboratory and instrumental data before the onset of labor, the issue of the timing and method of delivery is decided individually, taking into account, first of all, the severity of the identified violations, the readiness of the birth canal for childbirth and the totality of obstetric and extragenital diseases of the pregnant woman.

Indications for early termination of pregnancy (with a gestational age of more than 30–32 weeks):

Critical disorders of fetal-placental blood flow;

III degree of disturbances in the functional system mother-placenta-fetus.

Perinatal outcomes with earlier delivery are uncertain. The method of choice for delivery in the interests of the fetus is caesarean section. When a symmetrical form of IGR is detected, first of all, an error in determining the gestational age should be excluded, and then the presence of a chromosomal pathology in the fetus should be excluded. In the presence of placental insufficiency with hemodynamic disturbances of the I-II degree, it is not advisable to prolong the pregnancy for more than 37 weeks.

Indications for early termination of pregnancy if prolongation of pregnancy is ineffective (up to the 37th week of pregnancy):

· the absence of positive dynamics of indicators of fetometry and/or dopplerometry after a 10-day course of treatment of placental insufficiency;

fetal hypotrophy.

In the absence of biological readiness of the soft birth canal for childbirth, the presence of IUGR with signs of a violation of the functional state of the fetus in older primiparas with a burdened obstetric and gynecological history, the method of choice for delivery is a caesarean section.

Indications for vaginal delivery: a favorable obstetric situation and satisfactory indicators of the fetal condition (according to ultrasound, CTG, dopplerometry, functional stress tests).

In this case, the main attention should be paid to the timely preparation of the birth canal (kelp, dinoprostone), monitoring of the fetus, adequate pain relief.

If it is planned to conduct labor through the natural birth canal, labor induction is carried out with early amniotomy under constant monitoring of the functional state of the fetus using direct CTG. If necessary in childbirth, it is advisable to conduct a Zaling test.

EVALUATION OF THE EFFICACY OF THE TREATMENT OF PLACENTAL INSUFFICIENCY

Fetometric indicators are determined once every two weeks.
· The frequency of Doppler studies of the vessels of the functional system mother-placenta-fetus depends on the degree of hemodynamic disturbances.
· Dynamic monitoring of the functional state of the fetus by CTG is carried out at least once a week.

PREVENTION OF PLACENTAL INSUFFICIENCY

It includes a wide range of drug and non-drug interventions.
Treatment of obstetric and extragenital diseases predisposing to the development of placental insufficiency.
· Regulation of tissue metabolism and redox processes in pregnant risk groups for the development of placental insufficiency. For this purpose, antioxidants are prescribed (a-tocopherol acetate, ascorbic acid), hepatoprotectors (Essentiale©, artichoke leaf extract [hofitol©]).
· Normalization of the processes of excitation and inhibition in the central nervous system in pregnant women with asthenic constitution and increased level of anxiety. For this, nootropics (piracetam) are used; glycine, which has a significant anti-stress effect.
· With vegetovascular dystonia of the hypotonic type, adaptogens (tincture of magnolia vine, eleutorococcus, ginseng, aralia) have a good effect.
To normalize sleep, complex herbal preparations containing extracts of valerian, hawthorn, lemon balm, hops, peppermint and lemon mint are used: novo-passit ©, medicinal rhizomes with roots tincture + lemon balm medicinal herb extract + peppermint, valerian officinalis rhizomes with roots tincture + hops cones extract.

Therapeutic and preventive measures should include diet therapy, vitamin therapy, foods and nutritional supplements that stimulate bowel function (sour-milk products, wholemeal bread, laminolact).

INFORMATION FOR THE PATIENT

Placental insufficiency is a formidable complication of pregnancy, leading to high morbidity and mortality of the fetus and newborn. Since the causes of its development are maternal diseases (cardiovascular diseases, kidney diseases, diabetes mellitus), in the development mechanism of which vascular disorders, it is advisable to conduct an examination and treatment of this pathology when planning a pregnancy. Significantly increases the risk of developing placental insufficiency in smokers, patients who use alcohol and drugs.

PREDICTION OF PLACENTAL INSUFFICIENCY

Favorable for mild hemodynamic disorders in the functional system mother-placenta-fetus.

Doubtful with severe malnutrition and severe hemodynamic disorders.

before birth. Intrauterine growth retardation may be associated with an abnormality of the fetus or the inability of the placenta to nourish it with the necessary substances. Identification of developmental delay is based primarily on the measurement of the height of the uterus and on ultrasound of the 3rd trimester, during which measurements of the abdominal cavity and head of the unborn child are made. During the first two trimesters, fetal growth is usually normal and delay is rare.

Additional tests (uterine Doppler and umbilical cord Doppler) can detect the causes of developmental delay and prescribe treatment depending on the results.

After birth. A newborn with a small weight is weaker than others. Doctors should look after him, as he may have some metabolic abnormalities. The number of feedings is increased (7 or 8 per day) due to the danger of glycemia; sometimes a food probe is needed to ensure a constant intake of food. To prevent possible hypocalcemia (calcium content in the blood is below normal), the child is given vitamin D. Finally, if the temperature of the newborn is too low, he is placed in an incubator.

This is a consequence of intrauterine growth retardation, or malnutrition.

First of all, the problem of placental insufficiency affects smokers. The symbolism is absolutely eloquent and straightforward, the mother does not give her child proper life support. In this regard, smoking, and knowledge of these relationships has long been known, almost always represents a half-deliberate attack on the unborn child. The fetus reacts to each cigarette as a painful blow much more sensitively than the mother, or about the same as the mother during the smoking of the first cigarette. Newborn children of smokers suffer from withdrawal and lack of adaptability, which can be expressed in the form of frequent cries, lack of appetite and sleep disturbances.

You should not, however, "pounce" on smokers and accuse them of all mortal sins. It would be much better to understand that they are consciously suffering from addiction, and they are helpless after it, and they do not need anything as urgently as help.

In our country, placental insufficiency occurs not only in smokers, but also in alcoholics and drug addicts, primarily heroin addicts. In third world countries, placental insufficiency is also often the result of malnutrition of the expectant mother. And although these women did not have a good basis for pregnancy, they still conceived. Internal denial of pregnancy is generally less common in underdeveloped Third World countries than among modern women. We have this picture disease most often affects unconscious, internally unstable women who do not have immune barriers - including those against unwanted children.

Placental insufficiency is a symptom of many types of pregnancy complications; it is not an independent disease, but a manifestation of disturbances in the structure and function of the fetus's nutrition and the correctness of its development.

According to the time of occurrence, primary, secondary and mixed forms of placental insufficiency are distinguished. Primary placental insufficiency develops before 16 weeks of pregnancy, under the influence of implantation disorders, early embryogenesis under the influence of genetic defects in the embryo; immunological incompatibility of the blood of the mother and fetus by blood group or by the Rh blood affiliation; endocrine inferiority of the ovaries, and again we return to the problem of STIs that disrupt the connection of the fetal egg with the uterine wall. Placental insufficiency is manifested by changes in its structure, poverty of vascular blood supply, incorrect attachment (lower segment, placenta previa), and a violation of the time of chorion formation. This form is often combined with a stop in the development of pregnancy (missed pregnancy), malformations of the fetus.

Secondary placental insufficiency develops after 16 weeks, occurs under the influence of external influences and internal negative factors of the pregnant woman's body. Secondary placental insufficiency is associated with complications of pregnancy and manifests itself in impaired blood flow in the vessels of the uterus and placenta, which worsens the supply of oxygen and nutrients to the fetus, and there is a simultaneous oxygen starvation of the fetus (hr. Hypoxia) and a delay in its intrauterine development. Often, primary placental insufficiency becomes secondary.

Along the course, acute and chronic forms of placental insufficiency are distinguished. Acute insufficiency of uteroplacental blood flow occurs when placental abruption, normally located or presenting, with rupture of the marginal sinus of the placenta, rupture of the uterus and other acute conditions in obstetrics. With a delay in professional assistance, the death of the fetus quickly occurs, and there is a threat to the woman's life. Chronic placental insufficiency occurs within a few weeks, develops at the beginning of the second half of pregnancy. It is associated with disease internal organs a pregnant woman, exacerbation of chronic diseases during pregnancy, their development and decompensation, which is precisely what causes dysfunction of the placenta (see below).

According to the state of the possibility of compensation, absolute and relative placental insufficiency are distinguished. With a relative form of placental insufficiency, compensatory mechanisms in the placenta are still preserved, this form is treatable.

In an unfavorable situation in childbirth - persistent weakness of labor activity, prolonged stimulation of labor activity or prolonged labor induction - fetal hypoxia occurs - a violation of its oxygen supply.

With absolute insufficiency of the placenta, the ability to compensate is depleted, a chronic form of oxygen deficiency, hypoxia occurs, and this results in intrauterine growth retardation, lagging the size of the fetus from the standards of height-weight correspondence to the gestational age. Chronic hypoxia can bring the fetus to death.

Modern diagnostics makes it possible to distinguish decompensated, subcompensated and compensated forms of placental insufficiency. The presence of one form or another of compensation for placental insufficiency is determined by the degree of lag of the fetus in size from the standards this period pregnancy, the severity of chronic intrauterine hypoxia, the depth of vascular insufficiency of the placental-uterine and fetal-placental blood flow, the hormone-forming function of the placenta and the effectiveness of the treatment.

Placental insufficiency most often develops in diseases of the internal organs of a pregnant woman - hypertension, diseases of the kidneys and urinary tract, chronic anemia (anemia), a combined form of diseases of internal organs, such as rheumatoid diseases, where joints and heart valves are affected, connective tissue throughout the body.

In second place are the reasons for the complications of pregnancy itself: a long-term threat of abortion, anemia in pregnant women, preeclampsia.

Diagnosis of placental insufficiency is based on the determination of the hormonal function of the placenta. A decrease in the levels of hormones synthesized in the placenta by 30-50% indicates placental insufficiency. But ultrasound is the most informative. In this case, the location, thickness and degree of structure of the placenta are evaluated. The third degree of placental maturity in terms up to 36-37 weeks of pregnancy indicates its early aging - a violation of functional mechanisms, placental insufficiency. In some cases, cysts in the placenta are determined - traces of catastrophic circulatory disorders - placental infarctions. Sometimes even many small cysts do not disturb the condition of the fetus. But large cysts lead to the death of part of the placental tissue and chronic fetal hypoxia. Excessive thinning of the placenta with the threat of miscarriage, with gestosis of pregnant women or thickening of the placenta with diabetes mellitus and hemolytic conflict between the blood of the mother and fetus by more than 0.5 cm indicate placental insufficiency, require the appointment of complex treatment and repeated ultrasound. Doppler study allows to clarify the nature of the violation of blood flow in the uterine arteries and fetal vessels.

Sometimes, and one might say - most often, placental insufficiency is diagnosed only on the basis of signs of IUGR of the fetus - intrauterine growth retardation. This is called fetal malnutrition (insufficient fatness, lack of nutrition).

There are symmetric and asymmetric fetal growth retardation.

Symmetric malnutrition - a proportional decrease in all sizes of the fetus according to ultrasound. This is observed in 10-35% of cases. This form of fetal growth retardation develops in the second trimester of pregnancy. If this is diagnosed at the border of the I and II trimesters, at 13-15 weeks of pregnancy, then there is a suspicion of missed genetic defects and chromosomal abnormalities (trisomy of the 18th pair of chromosomes, Down syndrome or Shereshevsky-Turner syndrome).

Diagnosis must be made by comparing carefully determined gestational age, fetal size measurements over time (every 2 weeks) and previous pregnancies (if any) to identify a trend towards low birth weight babies. For the development of this form of growth retardation, in addition to the above, smoking of the expectant mother and / or her alcoholism, malnutrition of the pregnant woman (hypovitaminosis) are important. Also characteristic forms of carriage of viral infections - rubella, herpes, cytomegalovirus; venereal diseases - syphilis; toxoplasmosis.

Sometimes developmental defects such as microcephaly (a sharp decrease in the size of the brain, its underdevelopment), congenital heart defects, anomalies of the umbilical cord vessels (a single artery), Potter's syndrome (hereditary anomalies of almost all internal organs, spine, facial skull, absence or underdevelopment of the kidneys) are detected. , genital organs), the fetus dies in the first hours of life. If such defects are detected, the woman is offered to terminate the pregnancy.

In connection with the foregoing, it seems logical to perform amnio- or cordocentesis for genetic and chromosomal analysis of the fetus.

Asymmetric fetal hypotrophy is a condition when the dimensions of the fetal head and long bones of the limbs correspond to the calendar period of pregnancy, and the dimensions of the chest and abdominal cavities (circumferences, average diameters) are 2 weeks behind (I degree), 3-4 weeks (II degree) and more than weeks (grade III). Placentometry is also carried out - examination of the placenta, determination of the degree of maturity, thickness, identification of cysts, sclerosis, fossils. Are evaluated and amniotic fluid, their number, suspension.

Diagnosis is not difficult and is possible with the first ultrasound. Additional diagnostics - an assessment of the state of the fetoplacental complex and the compensatory capabilities of the fetus should include dopplerometry, a study of the degree of disturbance of the uteroplacental and fetal-placental blood flow. And cardiotocography is necessary - a study of the fetal heartbeat, where a number of characteristics are conclusion about the condition of the fetus.

The choice of the term and method of delivery is determined by the gestational age, when diseases or defects of the fetus and placenta are established, the presence of hypoxia (poverty in oxygen supply), the degree of fetal malnutrition, growth retardation, the effectiveness of treatment of a form of placental insufficiency and the nature of the state of the whole body of the pregnant woman, the presence of chronic diseases or anomalies in the genital area.

Treatment of placental insufficiency is carried out under the control of ultrasound, dopplerometry, cardiotocography. Ultrasound is repeated after 2 weeks, CTG - every 2 days, doppler study- every 3-4 days.

In a critical state of blood flow and a gestational age lower than 32-34 weeks, studies are carried out daily. With critical blood flow after 34 weeks, delivery should be carried out in the next 3-4 hours. If the effect of treatment is present, the pregnancy is prolonged to 36-37 weeks against the background of ongoing treatment. In the absence of the effect of treatment or a deterioration in the condition of the fetus, early delivery is performed.