Congenital malformations of the fetus (CHD) are perhaps the most dangerous complication of pregnancy, leading to childhood disability and mortality.

The birth of a child with congenital developmental defects is always a great trauma for any parents. The statistics in this regard are not reassuring: in Russia, the incidence of congenital malformation reaches 5-6 cases per 1000 children.

Unfortunately, it is not possible to predict these pathologies before pregnancy. A child with congenital malformations can appear in absolutely any family, regardless of the presence or absence of bad habits, lifestyle or material wealth.

What are the developmental disorders of the fetus during pregnancy?

All abnormalities of fetal development during pregnancy can be divided for several types:

1. Hereditary

Hereditary diseases are the result of gene mutations. A mutation is a change in the hereditary properties of an organism due to rearrangements in the structures that are responsible for the storage and transmission of genetic information. These include Down syndrome, Patau syndrome, etc.

2. Congenital

Congenital anomalies are diseases acquired in the womb due to exposure to external factors (including microelements, trauma during pregnancy, etc.). They can affect almost any organ. Congenital malformations of the fetus include heart defects, underdevelopment of the brain, maxillofacial deformities, etc.

3. Multifactorial (combined factor)

The division of fetal developmental anomalies into types is quite arbitrary, because in the vast majority of cases, developmental delays are a combination of hereditary and congenital factors.

Classification of fetal malformations

The most common malformations of intrauterine development of the fetus:

• Aplasia (absence of any organ);
• Dystopia (location of an organ in an uncharacteristic place);
• Ectopia (displacement of an organ outward or into an adjacent body cavity);
• Hypotrophy, hypoplasia (decreased fetal body weight, underdevelopment);
• Hypertrophy, hyperplasia (increase in the size of any organ);
• Atresia (closure of natural openings);
• Fusion of paired organs;
• Stenosis (narrowing of the canals and openings of the fetal organs);
• Gigantism (increase in size of the body and internal organs of the fetus);
• Dyschronia (acceleration or inhibition of development of processes).

I would like to note that the severity of pathologies can be completely different. This depends on the location of the genetic defect, as well as on the duration and intensity of the toxic effect on the fetus. There is no clear relationship between them.

A woman who has been exposed to toxicity during pregnancy can give birth to a completely healthy baby. At the same time, the risk of developmental delays in the future offspring of this fetus remains, as a consequence of a genetic breakdown with the absence clinical manifestations.

Causes of fetal malformations

The issue of studying pathologies of fetal development is very diverse. This topic is dealt with by specialists of various levels and areas - geneticists, embryologists, neonatologists, and prenatal diagnostics specialists.

The cause of hereditary pathologies is a gene mutation. The appearance of congenital anomalies is caused by various adverse effects on the fetal organs during pregnancy, especially during critical periods of its development. Factors that cause congenital malformation are called teratogenic.

The most studied teratogenic factors:

• medications (taking medications prohibited during pregnancy or during a certain period of pregnancy);
• infectious (measles, chicken pox transmitted from mother to fetus);
• ionizing radiation (x-rays, radioactive radiation);
• alcohol factor (taken by a pregnant woman large quantity alcohol can lead to severe alcohol syndrome in the fetus, incompatible with life);
• nicotine factor (smoking during pregnancy can cause developmental delays in the child);
• toxic and chemical (women working in hazardous industries should avoid contact with aggressive chemicals and toxic substances several months before pregnancy and for its entire duration in order to avoid a teratogenic effect in the fetus);
• lack of vitamins and microelements (lack of folic acid and Omega-3 polyunsaturated acids, proteins, iodine, lack of a balanced diet can lead to delays in fetal development and brain dysfunction).

Often, hereditary predisposition plays a large role in the appearance of fetal congenital malformation. If the parents or close relatives of the child have congenital malformations, then the risk of giving birth to a child with the same defects increases many times.

Critical periods of fetal development

Intrauterine development of the fetus lasts on average 38-42 weeks. All this time, the fetus is well protected from external factors by the placental barrier and the mother's immune system. But there are 3 critical periods in which he is very vulnerable to harmful agents. Therefore, at this time, a pregnant woman should especially take care of herself.

The first critical period occurs approximately 7-8 days after fertilization, when the embryo undergoes the stage of implantation into the uterus. The next dangerous period is from 3 to 7 and from 9 to 12 weeks of pregnancy, when the placenta is formed. Illness, chemical or radiation exposure to a pregnant woman during these periods can lead to intrauterine malformations of the fetus.

The third critical period of pregnancy is 18-22 weeks, when the formation of neural connections in the brain occurs and the hematopoietic system begins its work. There is a delay associated with this deadline mental development fetus.

Risk factors for fetal anomalies

Risk factors for congenital malformation on the maternal side:

• age over 35 years – intrauterine growth retardation, genetic disorders;
• age under 16 years – prematurity, lack of vitamins and microelements;
• short social status– infections, fetal hypoxia, prematurity, intrauterine growth retardation;
• lack of folic acid – congenital malformations nervous system;
• consumption of alcohol, drugs and smoking – intrauterine growth retardation, sudden death syndrome, fetal alcohol syndrome;
• infections (chickenpox, rubella, herpetic infections, toxoplasmosis) - congenital malformation, intrauterine growth retardation, pneumonia, encephalopathy;
• arterial hypertension - intrauterine growth retardation, asphyxia;
• polyhydramnios – congenital malformations of the central nervous system, gastrointestinal tract and kidney pathologies;
• diseases of the thyroid gland - hypothyroidism, thyrotoxicosis, goiter;
• kidney diseases - intrauterine growth retardation, nephropathy, stillbirth;
• diseases of the lungs and heart - congenital heart defects, intrauterine growth retardation, prematurity;
• anemia - intrauterine growth retardation, stillbirth;
• bleeding – anemia, prematurity, stillbirth

Risk factors for congenital malformation from the fetus:

• anomalies of fetal presentation - hemorrhage, congenital malformations, trauma;
• multiple pregnancy – fetofetal transfusion, asphyxia, prematurity;
• intrauterine growth retardation - stillbirth, congenital malformations, asphyxia,
  Risk factors during delivery:
• premature birth is fraught with the development of asphyxia;
• late labor (delay of labor by 2 weeks or more) – possible development of asphyxia or stillbirth;
• long labor – asphyxia, stillbirth;
• prolapse of the umbilical cord - asphyxia.

Abnormalities of placenta development:

• small placenta – intrauterine growth retardation;
• large placenta – development of fetal hydrops, heart failure;
• premature placental abruption – possible large blood loss, development of anemia;
• placenta previa is fraught with blood loss and the development of anemia.

Diagnosis of fetal malformations

Prenatal diagnosis of fetal developmental anomalies and genetic pathologies is a very complex process. One of the stages of this diagnosis is screening examinations prescribed to a pregnant woman at 10-12, 20-22 and 30-32 weeks (in each trimester). This test is a blood test for biochemical serum markers of chromosomal pathology (developmental defects).

This will make it possible to obtain an assumption about the presence or absence of chromosomal abnormalities in the fetus, and ultrasound as an additional diagnostic method will show whether there are any abnormalities in the fetus. physical development fetus. Ultrasound must be performed by a highly qualified specialist and using high-quality equipment. The results of each study are assessed jointly, without breaking with each other.

Screening does not guarantee one hundred percent pathology; it only allows one to identify a high-risk group among pregnant women. This is an important and necessary measure and, despite its voluntary nature, most expectant mothers understand this. There are often cases when specialists find it difficult to answer the question about the presence of genetic defects in the fetus. Then, depending on the trimester of pregnancy, the patient is prescribed invasive research methods:

• (chorionic villus study)

It is done in the 1st trimester of pregnancy (11-12 weeks) and allows you to identify genetic abnormalities of fetal development.

• amniocentesis (examination of the anatomical fluid in which the fetus is located)

In the 1st trimester, this analysis reveals hyperplasia of the adrenal cortex, in the 2nd - CNS diseases, chromosomal pathologies.

• placentocentesis (examination of placental particles)

It is performed from 12 to 22 weeks of pregnancy to detect genetic pathologies.

• (blood collection from the fetal umbilical cord)

Allows you to identify the susceptibility of the fetus to genetic or infectious diseases.

Pregnant women are referred for mandatory consultation with a geneticist:

• whose age exceeds 35 years;
• having a child or children with genetic disorders;
• those with a history of miscarriages, undeveloped pregnancies, and stillbirths;
• whose family has relatives with Down syndrome and other chromosomal abnormalities;
• recovered from viral diseases in the 1st trimester of pregnancy;
• taking medications prohibited during pregnancy;
• exposed to radiation.

To diagnose fetal pathologies after birth, they are used the following research methods: tests of blood, urine and other biological fluids, X-rays, computed tomography and magnetic resonance imaging, ultrasound, angiography, bronchial and gastroscopy, other immune and molecular methods...

Indications for termination of pregnancy

Any detection of congenital malformation of the fetus presupposes a proposal to terminate the pregnancy for so-called medical reasons. If a woman refuses this and decides to keep the child, she is taken under special control and the pregnancy is monitored more carefully.

But to the expectant mother it should be understood that not only her feelings and experiences are important here, but also the fact that children born with serious defects and pathologies often turn out to be unviable or remain deeply disabled for life, which, of course, is very difficult for any family.

There are other indications for termination of pregnancy:

• malignant neoplasms (pregnancy with cancer is contraindicated);
• diseases of cardio-vascular system(heart defects, deep vein thrombosis, thromboembolism);
• neurological diseases ( multiple sclerosis, myasthenia gravis);
• infectious diseases (in active form, in acute and severe stages);
• diseases of the blood and hematopoietic organs (hemoglobinopathy, aplastic anemia, leukemia);
• eye diseases (diseases of the optic nerve and retina);
• kidney disease (urolithiasis in acute form and with large stones, acute);
• diffuse connective tissue diseases;
• endocrine disorders (, thyrotoxicosis, uncompensated hypothyroidism in severe forms);
• some gynecological diseases;
• obstetric indications (unresponsive to therapy and severe, accompanied by severe vomiting, gestational trophoblastic disease, severe hereditary diseases detected during pregnancy, etc.)

Abortion for medical reasons is carried out only with the consent of the patient.

Prevention of congenital malformations of the fetus

The main measure aimed at preventing the occurrence of congenital malformations of the fetus is pregnancy planning. Not only the success of conception, but also the process of carrying a pregnancy, quick and correct delivery, and the health of the mother and child in the future may depend on high-quality preparation.

Before planning a pregnancy, it is necessary to undergo a series of examinations: take tests for (STD), HIV, hepatitis, syphilis, check blood clotting, hormonal status, sanitize the oral cavity, do an ultrasound of the pelvic organs to exclude inflammatory diseases and neoplasms, visit a therapist to identify all possible chronic diseases, ideally both parents should be genetically tested.

The key point in the prevention of congenital anomalies of the fetus is the maintenance healthy image life, giving up bad habits, balanced and nutritious nutrition, eliminating the impact on your body of any negative and harmful factors. During pregnancy, it is important to treat all possible diseases in a timely manner and follow the instructions of the obstetrician-gynecologist.

Treatment of congenital malformation of the fetus

Treatment options for congenital malformations of the fetus vary greatly depending on the nature and severity of the anomaly. Statistics on this problem, unfortunately, are not reassuring. A quarter of children with congenital anomalies die within the first year of life.

Another 25% can live quite a long time, while having intractable or difficult to treat physical and mental impairments. And only 5% of children born with congenital malformation can be treated, mostly surgically. In some cases, conservative treatment helps. Sometimes developmental defects become noticeable only as they grow older, while others are completely asymptomatic.

The concept of teragotenesis

The name of the science of teratology comes from the word “teras”, which means “monster” in Greek. Teratogenesis is literally translated as the reproduction of freaks. Currently, this term has come to be understood as various functional disorders in newborns, which also include widespread intrauterine growth retardation and subsequent behavioral changes. Until the 1950s, nothing was known about teratogenesis, and the cause of most congenital anomalies was considered to be changes in genes.

Congenital defects: classification

Depending on the frequency of their occurrence, all intrauterine anomalies are divided into three groups:

• Common defects are considered such if they occur in the population with a frequency of more than 1 case per thousand newborns;
• Moderately common (their frequency ranges from 0.1 to 0.99 cases out of a thousand newborns);
• Rare congenital malformations (less than 0.01 per thousand children).

Depending on its distribution in the child’s body, congenital malformations are distinguished:

• isolated in nature (usually one organ is affected);
• systemic (defect of the organ system);
• Multiple (several systems are affected).

birth defect According to the severity of clinical manifestations and prognosis for life, it happens:

• Lethal, which leads to the death of a child. The frequency of such congenital malformations averages about 0.5%; up to 85% of children with these anomalies do not survive to the end of the first year of life;
• Moderate-severe, in which surgical intervention is necessary to correct it (up to 2.5%);
• MAD (minor developmental anomaly), which does not require surgery and does not limit the child’s life activity (about 4%).

According to the time of exposure to a negative factor, the HF is divided into:

Pathogenesis of congenital anomalies

The pathogenetic mechanisms of the occurrence of defects are currently quite well studied. If the embryo is damaged before it is implanted into the uterine mucosa, either it dies (in the case of irreversible changes in the cells) or is restored (in the case of reversible damage). As the embryo develops further, the cell repair mechanisms cease to function, and any disturbances will lead to the formation of a defect. Genetic control of embryogenesis can be disrupted as a result of exposure to various external aggressive factors (teratogens).

The main mechanisms of teratogenesis in the fetus at the cell level will be: violations of cell division (underdevelopment of the organ occurs), their movement (the organ will be located in the wrong place) and differentiation (absence of an organ or organ system). At the tissue level, teratogenic processes will be: untimely cell death, delay in their disintegration and resorption, disruption of the gluing process, resulting in such defects as closure of the natural opening, fistula, tissue defect, etc.

What are the main risk factors for birth defect Is it much more common?

The main contributing factors are:

• Unplanned pregnancy;
• Older mother (over 35 years old);
• Insufficient medical control before conception;
• Incidence of viral infections;
• Taking medications that have a pronounced negative effect on the fetus;
• Drinking alcohol and smoking;
• Drug use;
• Poor nutrition;
• Presence of occupational hazards;
• Insufficient funding for healthcare in many countries.

The presence of which pathological conditions is an indication for prenatal prevention of congenital birth defects?

To prevent the unborn child from developing birth defects, a woman needs to prepare in advance for conception and pregnancy if the following factors are present:

• Diabetes and other diseases endocrine system and metabolism;
• Previous spontaneous miscarriages and intrauterine fetal death;
• The presence of a hereditary predisposition to developmental defects;
• The birth of previous children with intrauterine growth retardation or premature gestational age;
• The presence of various chronic diseases (arterial hypertension, epilepsy, bronchial asthma, etc.);
• Overweight and obesity;
• Using medications for a long period of time;
• Infectious diseases (especially toxoplasmosis and rubella).

How is congenital malignancy prevented?

The scheme of measures taken to prevent possible defects includes:

What do you need to know?

A geneticist from Brazil, Eduardo Castillo, formulated ten basic commandments for the prevention of congenital malformations of future children. They include the following items:

1. A woman needs to remember that if she is able to become pregnant, she can be pregnant at any time;
2. You should start your family when you are still young;
3. It is necessary to undergo prenatal control in the prescribed manner, if you need it;
4. It is advisable to get vaccinated against rubella before conception;
5. It is necessary to exclude the use of medications except those that are most necessary for you;
6. Do not drink alcohol or smoke;
7. It is also advisable to avoid smoking areas;
8. You definitely need to eat well and nutritiously, preferably vegetables and fruits;
9. Know the risks to pregnancy in your workplace;
10. When in doubt, seek answers from your doctor if you have any questions.

Photo: Alexander Anatolyevich Kryukov, orthopedist, MD.

Thus, we can conclude that most congenital anomalies in the fetus arise as a result of impaired development of the fertilized egg. This disorder can occur at any time after conception. It has been proven that the earlier a spontaneous miscarriage occurs, the more severe the change has occurred. During the first three months of gestation, about 75% of spontaneous abortions are explained by the presence of various mutations in genes and chromosomes. Folic acid has the ability to enhance the restorative properties of the embryo and protect it from damage, therefore it is recommended for all women at risk for congenital birth defects.

Congenital malformations of the fetus occupy 2-3 places in the structure of causes of perinatal death of the fetus and newborn. Early diagnosis of developmental defects is of great importance, which is necessary for a timely decision on the possibility of prolonging pregnancy, which is determined by the type of defect, compatibility with life and prognosis for postnatal development. Depending on the etiology, hereditary (genetic), exogenous and multifactorial congenital malformations of the fetus are distinguished. Hereditary include developmental defects that arise as a result of mutations, i.e. persistent changes in hereditary structures in gametes or zygotes. Depending on the level at which the mutation occurred (genes or chromosomes), monogenic syndromes and chromosomal diseases are distinguished. Exogenous defects include defects caused by the damaging effects of exogenous factors. These factors, acting during the period of gametogenesis or pregnancy, lead to the occurrence of congenital defects without disturbing the structure of the hereditary apparatus.

Defects of multifactorial origin are defects that arise under the combined influence of genetic and exogenous factors. There are also isolated (localized in one organ), systemic (within one organ system) and multiple (in organs of two or more systems) defects.

DEFECTS OF THE CENTRAL NERVOUS SYSTEM

Classification of the most common malformations of the central nervous system:

1. Hydrocephalus:

Stenosis of the cerebral aqueduct;

Open hydrocephalus;

Dandy-Walker syndrome.

2. Choroid plexus papilloma.

3. Neural tube defects:

- spina bifida;

Anencephaly;

Cephalocele.

4. Microcephaly. Hydrocephalus

Hydrocephalus- an increase in the size of the ventricles of the brain with a simultaneous increase in intracranial pressure, accompanied in most cases by an increase in the size of the head (Fig. 28).

Rice. 28. An echographic picture of severe hydrocephalus of the fetus (arrows indicate sharply dilated ventricles of the brain, the cortex of which is significantly thinned, the size of the fetal head exceeds normal values ​​for this stage of pregnancy)

Ventriculomegaly refers to an isolated increase in the size of the ventricles, not accompanied by an increase in the size of the head. Hydrocephalus occurs with a frequency of 0.1-2.5 per 1000 newborns. About 60% of fetuses with hydrocephalus are boys. Hydrocephalus can be a consequence of many diseases of various etiologies. In most cases, it develops as a result of a violation of the outflow of cerebrospinal fluid. The communicating form of hydrocephalus is caused by extraventricular

cular obstruction, while the obstructive form is an intraventricular obstruction. Occasionally, hydrocephalus is caused by increased production of cerebrospinal fluid (for example, against the background of choroid plexus papilloma) or impaired reabsorption in the subarachnoid space.

Extracranial anomalies in hydrocephalus occur in 63%: renal agenesis and dysplasia, ventricular septal defect, tetralogy of Fallot, meningomyelocele, cleft upper lip, soft and hard palate, atresia of the anus and rectum, gonadal dysgenesis. Hydrocephalus is mainly represented by stenosis of the cerebral aqueduct (narrowing of the Sylvian aqueduct); open hydrocephalus (enlargement of the ventricles of the brain and the subarachnoid system of the brain as a result of obstruction of the extraventricular system of the outflow tracts of cerebrospinal fluid); Dandy-Walker syndrome (a combination of hydrocephalus, a cyst of the posterior cranial fossa, defects of the cerebellar vermis, through which the cyst communicates with the cavity of the fourth ventricle). When hydrocephalus is detected, the anatomy of the brain structures, as well as the spine, should be carefully assessed to exclude spina bifida. A comprehensive examination of the fetus should include an echocardiographic examination, since hydrocephalus is often combined with congenital heart defects. In case of hydrocephalus, before the period of fetal viability, it is advisable to discuss the issue of termination of pregnancy with the parents. When prolonging pregnancy, dynamic ultrasound monitoring every 2 weeks is indicated. If hydrocephalus increases after fetal lung maturity, the question of early delivery and shunting should be raised. The effectiveness of prenatal ventricular bypass has not yet been proven and this operation is not widely used. Caesarean section is indicated only in cases of severe macrocephaly and the absence of other malformations. In the presence of gross combined anomalies that worsen the prognosis for life, the operation of choice is cephalocentesis.

Neural tube defects. This term combines anencephaly, cephalocele and spina bifida.

Spina bifida- an anomaly in the development of the spinal column, resulting from a violation of the process of closing the neural tube (Fig. 29).

The exit through a defect in the spinal cord membranes is called a meningocele. If the hernial sac contains nerve tissue, the formation

Rice. 29. Sonographic picture spina bifida in the lumbosacral spine (highlighted by an arrow)

is called meningomyelocele. Distinguish spina bifida cystica(cystic form of spina bifida with the formation of a hernial sac containing the meninges and/or brain substance) and spina bifida occulta(hidden form, which is not accompanied by the formation of a hernial protrusion). Most often, this defect is localized in the lumbar and sacral spine. Frequency of occurrence spina bifida depends on geographic region. In some areas of the UK the incidence of this defect is 4 per 1000 births. In the United States, the rate is 0.5 per 1,000, although it varies by race and geography. Spina bifida- a developmental defect that occurs due to a violation of the closure of the neural tube in the 4th week of embryonic development. This anomaly is inherited in a multifactorial manner. Spina bifid a can be formed as a result of maternal hyperthermia, if she has diabetes mellitus, exposure to teratogenic factors, and can also be part of genetic syndromes (with an isolated mutant gene) or chromosomal abnormalities (trisomy 13 and 18 pairs of chromosomes, triploidy, unbalanced translocation or ring chromosome ). Spina bifida is more common

than with 40 syndromes of multiple malformations (hydrocephalus, congenital heart defects and genitourinary system).

Prenatal examination includes karyotype determination and a thorough ultrasound examination. Particular attention should be paid to the anatomy of the head, heart, arms and legs. If a meningomyelocele is detected before fetal viability, the woman should be offered medical termination of pregnancy. When prolonging pregnancy, dynamic ultrasound examination is indicated every 2-3 weeks to assess the appearance of other signs (for example, ventriculomegaly). Parents should be provided with a consultation with a neurosurgeon to discuss the possibilities of surgical intervention after childbirth (closing the defect or shunting), as well as the prognosis for the life and health of the child. Delivery should be carried out in large perinatal centers immediately after the fetal lungs reach sufficient maturity. Empirical risk of recurrence spina bibida is 3-5%. The use of large doses of folic acid (4 mg), started 3 months before the planned pregnancy and continuing during the first half, can significantly reduce the risk of defects.

Any open neural tube defect should be closed within the first 24 hours of life. Antibiotic therapy started immediately after birth may reduce the risk of infectious complications. The prognosis for life and health depends on the level of location of the meningomyelocele, as well as on the number and nature of associated anomalies. Mental development Children who have a normal head circumference and a properly formed brain at birth do not suffer. Patients with meningomyelocele located at the L2 level or above almost always need to use a wheelchair.

Anencephaly(pseudocephaly, extracranial disencephaly) - absence of the cerebral hemispheres and most of the cranial vault, while there is a defect in the frontal bone above the supraorbital region, the temporal and part of the occipital bone are absent. Top part head is covered with a vascular membrane. The structures of the midbrain and diencephalon are partially or completely destroyed. The pituitary gland and the rhomboid fossa are mostly preserved. Typical manifestations include bulging eyes, a large tongue, and a short neck. This pathology occurs with a frequency of 1 in 1000. More often it

found in newborn girls. Akrania(exencephaly) - the absence of the cranial vault in the presence of a fragment of brain tissue. It is a rarer pathology than anencephaly. Anencephaly results from failure to close the rostral neuropore within 28 days of fertilization. Multifactorial and autosomal recessive inheritance and chromosomal abnormalities are noted. Risk factors include maternal diabetes. Experiments on animals have established the teratogenicity of radiation, salicylates, sulfonamides, and high levels of carbon dioxide. Sonographic diagnosis can be established as early as 12-13 weeks of pregnancy. Anencephaly and acrania are absolutely fatal malformations, so in both cases the woman should be offered termination of pregnancy. All newborns with anencephaly and acrania die within 2 weeks after birth. The empirical risk of recurrence of anencephaly is 3-5%. The use of large doses of folic acid (4 mg), started 3 months before the planned pregnancy and continuing during the first half, can significantly reduce the risk of defects.

Cephalocele(encephalocele, cranial or occipital meningocele, cleft skull) - protrusion of the contents of the cranium through a bone defect. The term “cranial meningocele” refers to a protrusion only through a defect in the meningeal membranes. When the brain tissue is in the hernial sac, the term "encephalocele" is used. Cephalocele is rare (1:2000 live births) and is a component of many genetic (Meckele syndromes, median facial cleft) and non-genetic (amniotic bands) syndromes. A cephalocele develops as a result of non-closure of a neural tube defect and occurs in the 4th week of development. A defect in the skull, through which the meninges and brain tissue can prolapse, is formed as a result of non-separation of the surface ectoderm and the underlying neuroectoderm. If a cephalocele is detected, the woman should be offered termination of pregnancy for medical reasons. When prolonging pregnancy, delivery tactics depend on the size and contents of the hernial sac. At large sizes defect, prolapse of a significant amount of brain tissue, as well as in the presence of microcephaly and hydrocephalus, the prognosis for life and health is extremely unfavorable.

Delivery by surgery caesarean section not shown in such observations. Decompression of the hernial sac can be recommended to create conditions for vaginal delivery. Caesarean section may be recommended if there is a small defect and if the hernial sac is small.

Microcephaly (microencephaly) is a clinical syndrome characterized by a decrease in head circumference and mental retardation. Occurs with a frequency of 1 in 1360 newborns, with combined anomalies in 1.6:1000 live births. Microcephaly is a polyetiological disease, the development of which important role genetic (chromosomal aberrations, monogenic defects) and environmental factors play a role. The prognosis depends on the presence of combined anomalies. Trisomy 13, 18, Meckel's syndrome are fatal lesions. Prenatal examination should include determination of the fetal karyotype and a thorough ultrasound examination. In the absence of accompanying anomalies, the prognosis depends on the size of the head: the smaller it is, the lower the intellectual development index. Microcephaly is an incurable disease. Obstetric tactics - termination of pregnancy before the fetus reaches viability.

ANOMALIES OF FACIAL STRUCTURES AND NECK

Facial cleft(cleft lip and palate) is a linear defect extending from the edge of the lip to the nasal opening.

A cleft palate, combined with a cleft lip, can spread through the alveolar processes and hard palate to the nasal cavity or even to the bottom of the orbit. Bilateral cleft lip is observed in 20%, cleft lip and palate - 25%. With unilateral lesions, the cleft is most often located on the left. Facial clefts account for about 13% of all malformations and are reported in 1:800 live births. Boys are more likely to have clefts than girls. Combined anomalies are found in 50% of cases with isolated cleft palate and only in 13% with cleft lip and palate. Facial structures are formed between the 4th and 10th weeks of pregnancy. Unpaired frontonasal structures merge with paired maxillary and mandibular structures.

mi tubercles. In those observations where the fusion process does not occur completely, clefts are formed. As a rule, it is possible to diagnose a facial cleft only in the second trimester of pregnancy with a screening ultrasound examination. Prenatal detection of the defect using echography is difficult, but thanks to ultrasound scanning and color Doppler mapping, the possibilities for its diagnosis are expanding. Doppler ultrasound can visualize the movement of fluid through the nose, mouth and pharynx. If there is a cleft, the nature of the fluid movement changes. Three-dimensional echography can clarify the diagnosis in those observations where, during a two-dimensional study, a cleft was suspected, but its clear visualization was not obtained. It is possible to diagnose the anomaly using fetoscopy, including embryoscopy. In the absence of associated anomalies, generally accepted obstetric tactics are used, regardless of the time of diagnosis. Taking folic acid before your next pregnancy and during the first half of your pregnancy may reduce your risk of clefts.

A cleft lip (cleft lip) does not interfere with sucking and is only cosmetic defect. With a combination of cleft upper lip, jaw and hard palate (cleft palate), functional disorders are noted: when sucking, milk flows out through the nose due to its communication with the oral cavity; milk may enter the respiratory tract. The prognosis is favorable: modern surgical methods make it possible to correct cosmetic and functional defects.

Cystic hygroma(lymphangioma or consequences of obstruction of the jugular lymphatic trunk) is an encysted accumulation of fluid (Fig. 30). It is characterized by the presence of single or multiple soft tissue cysts in the neck area, formed as a result of disorders in the lymphatic system. Cystic hygromas occur with a frequency of 1:200 spontaneous miscarriages (coccygeal-parietal fetal size more than 30 mm). Cystic hygroma is often combined with chromosomal aberrations (Turner syndrome, trisomy 13, 18, 21 pairs of chromosomes, mosaicism). As an isolated anomaly, it is inherited in an autosomal recessive manner. Prognosis: in most cases, the fetus dies in the first two trimesters of pregnancy. About 90% require surgical treatment, 31% develop swallowing disorders and respiratory obstruction

Rice. thirty. An echographic picture of a cystic hygroma of the fetal neck during a 16-week pregnancy (a large liquid formation is visualized in the area of ​​the fetal neck - indicated by an arrow)

ways. Facial nerve paresis due to surgical treatment occurs in 24% of patients.

Obstetric tactics consist in terminating pregnancy with early diagnosis of cystic hygroma of the fetal neck; in case of full-term pregnancy, childbirth is carried out through the natural birth canal.

CONGENITAL HEART DEFECTS

The incidence of congenital heart defects (CHD) ranges from 1-2 to 8-9 per 1000 live births. The most common CHDs are atrial and ventricular septal defects, patent ductus arteriosus, pulmonary artery stenosis, hypoplastic left heart syndrome, single ventricle, etc. In 90% of cases, CHDs are the result of multifactorial damage (genetic predisposition and environmental factors). The risk of recurrence of the defect is 2-5% after the birth of one and 10-15% after the birth of two sick children. Monogenic inheritance

The condition is observed in 1-2% of children with congenital heart disease. 5% of children have chromosomal abnormalities, of which trisomy is the main one. In 1-2% of newborns, there is a combined effect of various teratogens. Echocardiographic examination of the fetus is the most informative method for prenatal diagnosis of congenital heart disease. Indications for prenatal diagnosis are determined by the condition of the mother and fetus.

1. Indications due to the mother’s condition:

Presence of congenital heart disease in family members;

Diabetes;

Taking medications by a pregnant woman during organogenesis;

Alcoholism;

Systemic lupus erythematosus;

Phenylketonuria.

2. Indications due to the condition of the fetus:

Polyhydramnios;

Non-immune dropsy;

Heart rhythm disturbances;

Extracardiac defects;

Chromosomal abnormalities;

Symmetrical form of intrauterine growth restriction. The prognosis depends on the type of defect, the presence of concomitant anomalies and chromosomal abnormalities.

Obstetric tactics include the following: after a thorough echocardiographic examination, cordo or amniocentesis is performed to obtain material for chromosomal analysis. If congenital heart disease is detected in a non-viable fetus, termination of pregnancy is indicated. In case of full-term pregnancy, it is better to carry out delivery in specialized perinatal centers. In case of combined defects and genetic abnormalities, termination of pregnancy is necessary at any stage.

single ventricle of the heart. This is a severe congenital defect in which the ventricles of the heart are represented by a single chamber or a large dominant ventricle in combination with a common atrioventricular junction containing two atrioventricular valves. The frequency of occurrence of the defect is not precisely determined. A single ventricle is easily diagnosed using a standard four-chamber section of the fetal heart. The only one

the ventricle can be morphologically either right or left. The overall survival rate for all types of single ventricle of the heart in patients without surgical treatment is 30%. A single ventricle is often combined with chromosomal abnormalities, gene disorders (Holt-Oram syndrome), asplenia/polysplenia syndrome, and is often formed due to certain maternal diseases, as well as against the background of the teratogenic effects of retinoic acid. Prenatal examination when a single ventricle is detected should include determination of the karyotype and a detailed examination of the ultrasound anatomy of the fetus. The clinical course of the disease and management tactics in the neonatal period are determined by the state of the pulmonary and systemic blood flow.

Atrial septal defect(ASD) (Fig. 31). Represents a deficiency of the septum separating the atria. It is observed in 17% of all congenital heart defects and is its most common structural anomaly. Often combined with other intracardiac anomalies, as well as non-immune hydrops fetalis. Possible combination with chromosomal abnormalities. Most small ASDs are not detected during prenatal ultrasound examination of the fetus. Diagnosis can only be made using multiple sections and color Doppler imaging. Prenatal examination when an ASD is detected should include

Rice. 31. Sonographic picture of an extensive atrial septal defect (indicated by an arrow)

begin determining the karyotype and detailed study of the ultrasound anatomy of the fetus. Detection of an isolated ASD in the prenatal period does not require changes in the management of pregnancy and childbirth. IN late dates During pregnancy, a dynamic assessment of the fetal condition should be carried out.

Ventricular septal defect(VSD). Represents a deficiency of the septum separating the ventricles. Based on localization, defects of the upper part of the septum (at the level of the mitral and tricuspid valves), the muscular part and the outlet part of the septum (subaortic, subpulmonary) are distinguished. By size, VSDs are divided into small (up to 4 mm) and large. VSD can be isolated or combined with other anomalies, chromosomal defects and hereditary syndromes. In the general structure of congenital heart defects, about 20% are isolated VSD, which is the most frequently diagnosed defect. The incidence of minor, hemodynamically insignificant muscle defects reaches 53:1000 live births. About 90% of such defects close spontaneously by 10 months of life and do not affect the prognosis for life and health.

Most small VSDs are not detected during prenatal ultrasound examination of the fetus. Diagnosis can only be made using multiple sections and color Doppler imaging. Most often, VSD is isolated, but can be combined with chromosomal abnormalities, gene disorders, and multiple malformation syndromes. Prenatal examination when a VSD is detected should include determination of the karyotype and a detailed study of the ultrasound anatomy of the fetus. Detection of isolated VSD in the prenatal period does not require changes in the management of pregnancy and childbirth. In late pregnancy, dynamic assessment of the fetal condition should be carried out. If a VSD is suspected, parents must be provided with complete information about the prognosis for the life and health of the unborn child and notify the pediatrician to ensure adequate monitoring of the newborn. Even with large VSDs, the disease can sometimes be asymptomatic for up to 2-8 weeks. In 50% of cases, minor defects close spontaneously before the age of 5 years, and of the remaining 80% disappear in adolescence. Most patients with uncomplicated VSD have a good prognosis for life and health. If the course is favorable

The disease does not require significant restrictions on physical activity.

Ebstein's anomaly- a congenital heart defect characterized by abnormal development and location of the tricuspid valve leaflets. With Ebstein's anomaly, the septal and posterior sails of the tricuspid valve develop directly from the endocardium of the right ventricle of the heart, which leads to displacement of the anomalous valve deep into the right ventricle and division of the ventricle into two sections: distal (subvalvular) - active and proximal (supravalvular or atrialized) - passive. The supravalvular section, connecting to the right atrium, forms a single functional formation. Ebstein's anomaly accounts for 0.5% of all congenital heart defects. Ebstein's anomaly can be easily diagnosed by examining a standard four-chamber fetal heart because it is almost always accompanied by cardiomegaly. Prenatal diagnosis of the defect is based on the detection of significantly enlarged right chambers of the heart at the expense of the right atrium. The key to diagnosing Ebstein's anomaly is the visualization of a displaced tricuspid valve in the presence of a dilated right atrium and normal right ventricular myocardium. The detection of tricuspid regurgitation during Doppler echocardiographic examination of the fetus is of important prognostic significance for Ebstein's anomaly. The earliest prenatal ultrasound diagnosis of Ebstein's anomaly was carried out at 18-19 weeks of pregnancy. The prognosis for life with Ebstein's anomaly is usually favorable in cases where children survive without surgical treatment during the first year of life. Ebstein's anomaly is not often combined with chromosomal aberrations and multiple congenital malformation syndromes. Extracardiac anomalies are observed in 25%. The outcome in the neonatal period depends on the severity of changes in the tricuspid valve. In children with severe tricuspid valve insufficiency, a high percentage of deaths is observed. Clinically, tricuspid valve insufficiency is manifested by increased cyanosis, acidosis and signs of heart failure. Surgical treatment is indicated in patients with severe symptoms of the disease that prevent normal life child. The operation involves closing the septal

defect, plastic surgery of the tricuspid valve and its relocation to a typical location. Hospital mortality is 6.3%.

Tetralogy of Fallot- a complex defect, including several anomalies of the heart structure: ventricular septal defect, aortic dextraposition, obstruction of the pulmonary artery outlet and right ventricular hypertrophy. In the general structure of congenital heart defects in live births, tetralogy of Fallot accounts for 4-11%. It is very difficult to diagnose tetralogy of Fallot when studying the four-chambered fetal heart. When using sections through the exit sections of the main arteries, a typical subaortic VSD and dextraposition of the aorta can be detected. An important additional criterion is the expansion and displacement of the aortic root. Tetralogy of Fallot is a blue type defect, i.e. in newborns, pronounced cyanosis is detected at the age of 6 weeks to 6 months. Tetralogy of Fallot is a difficult-to-diagnose heart defect that often goes undetected during screening. ultrasound examination up to 22 weeks of pregnancy. Most often, this defect is diagnosed in the third trimester of pregnancy or after birth. Tetralogy of Fallot does not require specific management tactics. When this pathology is detected, a comprehensive examination and prenatal counseling are necessary. Almost 30% of live births with tetralogy of Fallot have associated extracardiac anomalies. Currently, more than 30 syndromes of multiple developmental defects have been described, the structure of which includes tetralogy of Fallot. Prenatal examination when tetralogy of Fallot is detected should include determination of the karyotype and a detailed study of the ultrasound anatomy of the fetus. The prognosis for life with tetralogy of Fallot largely depends on the degree of obstruction of the right ventricular outflow tract. More than 90% of patients who have undergone complete correction of tetralogy of Fallot survive to adulthood. In the long-term period, 80% of patients feel satisfactory and have normal functional indicators.

Transposition of the great arteries- a heart defect in which the aorta or most of it comes out of the right ventricle, and the pulmonary artery comes out of the left ventricle. Accounts for 5-7% of all congenital heart defects. Usually not diagnosed in the prenatal period during a screening examination, since the study of the fetal heart is limited to the study

only a four-chamber slice. To identify a defect, visualization of the great vessels is necessary with the study of their location relative to each other. Normally, the main arteries cross, and during transposition they leave the ventricles in parallel: the aorta - from the right ventricle, the pulmonary artery - from the left. Transposition of the great arteries with intact interventricular and interatrial septa is not compatible with life. About 8% of live births with transposition of the main arteries have associated extracardiac anomalies. Prenatal examination should include determination of the karyotype and a detailed examination of the ultrasound anatomy of the fetus. Most newborns with transposition of the main arteries and an intact interventricular septum experience severe cyanosis from the first days of life. Surgical correction should be performed immediately after detection of inadequate mixing of blood flows. The mortality rate of newborns with this type of surgical treatment is less than 5-10%.

DEFECTS OF THE CHEST ORGANS

Congenital diaphragmatic hernia- a defect that occurs as a result of a slowdown in the process of closing the pleuroperitoneal canal. With this defect, there is usually insufficient development of the posterolateral portion of the left half of the diaphragm. The lack of separation between the abdominal cavity and the chest leads to the displacement of the stomach, spleen, intestines and even the liver into the chest cavity, which can be accompanied by a shift in the mediastinum and cause compression of the lungs. As a result, bilateral pulmonary hypoplasia often develops. varying degrees gravity. Underdevelopment of the lungs leads to abnormal formation of their vascular system and secondary pulmonary hypertension. Congenital diaphragmatic hernia occurs in approximately 1 in 2,400 newborns.

There are four main types of defect: posterolateral (Bochdalek's hernia), anterolateral, sternal and Morgagni hernia. Bilateral diaphragmatic hernias account for 1% of all types of defects. The movement of the heart to the right half of the chest in combination with an echo-negative structure (stomach) in its left half is most often diagnosed with a left-sided diaphragmatic hernia.

In right-sided hernias, the heart is usually displaced to the left. The intestines and liver may also be visualized in the chest. With this defect, polyhydramnios is often noted. Combined anomalies are observed in 23% of fetuses. Among them, congenital heart defects prevail, accounting for 16%. Diagnosis of the defect can be made as early as 14 weeks of pregnancy. Mortality in congenital diaphragmatic hernia correlates with the time of detection of the defect: only 33% of newborns with the defect survive in cases where the diagnosis was made before 25 weeks, and 67% - if the hernia was detected at a later date. Diaphragmatic defects usually have a multifactorial genesis, but 12% of cases are combined with other malformations or are part of chromosomal and non-chromosomal syndromes. Prenatal examination must necessarily include determination of the fetal karyotype and detailed ultrasound examination. If combined anomalies are detected, differential diagnosis can be carried out only during a consultation with the involvement of geneticists, syndromologists, and pediatricians. Parents should be recommended to consult a pediatric surgeon to discuss the specifics of treatment tactics in the neonatal period, prognosis for life and health. The course of the neonatal period depends on the severity of pulmonary hypoplasia and the severity of hypertension. The size of the hernial formation and the volume of functioning lung tissue also have a significant impact on the outcome in the neonatal period. Abnormal lung development can be predicted in the presence of polyhydramnios, gastric dilatation, and movement of the fetal liver into the chest cavity. According to the literature, only 22% of children who were diagnosed prenatally survived. Even with an isolated congenital diaphragmatic hernia, only 40% survive. Neonatal death usually occurs as a result of pulmonary hypertension and/or respiratory failure.

ANOMALIES OF FORMATION OF THE ABDOMINAL CAVITY WALLS AND DEVELOPMENTAL MALFORMATIONS OF THE GASTROINTESTINAL TRACT

Omphalocele (umbilical hernia)(Fig. 32). Occurs as a result of non-return of organs abdominal cavity from the amniotic cavity through the umbilical ring. An omphalocele may include any

Rice. 32. Sonographic picture of an omphalocele (a hernial sac containing intestinal loops and liver is visualized)

visceral organs. The size of the hernial formation is determined by its contents.

It is covered with an amnioperitoneal membrane, along the lateral surface of which the umbilical cord vessels pass. The incidence of omphalocele is 1 in 3000-6000 newborns. There are isolated and combined forms of omphalocele. This pathology is accompanied by trisomy in 35-58%, congenital heart defects in 47%, developmental defects of the genitourinary system in 40%, and neural tube defects in 39%. Delay intrauterine growth detected in 20% of observations.

Prenatal ultrasound diagnosis is based on the detection of a round or oval-shaped formation filled with abdominal organs and adjacent directly to the anterior abdominal wall. Most often, the hernial contents include intestinal loops and liver. The umbilical cord is attached directly to the hernial sac. In some cases, prenatal diagnosis can be made at the end of the first trimester of pregnancy, although in most cases, omphalocele is detected in the second trimester. The prognosis depends on the accompanying anomalies. Perinatal losses are more often associated with congenital heart disease, chromosomal

aberrations and prematurity. The largest defect is eliminated by a one-stage operation; for large ones, multi-stage operations are performed to close the hole in the anterior abdominal wall with a silicone or Teflon membrane. Obstetric tactics are determined by the timing of detection of the defect, the presence of combined anomalies and chromosomal disorders. If a defect is detected in early dates the pregnancy should be terminated. If concomitant anomalies incompatible with life are detected, it is necessary to terminate the pregnancy at any stage. The method of delivery depends on the viability of the fetus, since during the birth process with large omphaloceles, rupture of the hernial sac and infection of the internal organs of the fetus can occur.

Gastroschisis- defect of the anterior abdominal wall in the peri-umbilical region with eventeration of intestinal loops covered with inflammatory exudate. The defect is usually located to the right of the navel; hernial organs do not have a membrane. The incidence of gastroschisis is 0.94:10,000 newborns. The frequency of the defect in pregnant women under 20 years of age is higher and amounts to 7 per 10,000 newborns.

Since the late 70s. XX century In Europe and the USA, there continues to be a trend towards an increase in the frequency of births of children with gastroschisis. There are isolated and combined forms. Isolated gastroschisis is more common and accounts for an average of 79%. The combined form is detected in 10-30% of cases and most often represents a combination of gastroschisis with atresia or intestinal stenosis. Among other anomalies, congenital heart defects and urinary system defects, syndrome prune-belly hydrocephalus, low and polyhydramnios.

The anomaly occurs sporadically, but there have been cases of familial disease with an autosomal dominant mode of inheritance.

The earliest prenatal ultrasound diagnosis using transvaginal echography was carried out at 12 weeks of pregnancy. In most cases, the diagnosis is made in the second trimester of pregnancy, since in the early stages (10-13 weeks) a false-positive diagnosis is possible due to the presence of a physiological intestinal hernia in the fetus. Prenatal ultrasound diagnosis of gastroschisis is usually based on visualization of intestinal loops in the amniotic fluid near the fetal anterior abdominal wall. Sometimes, except for intestinal loops, beyond the

Other organs may also be located within the abdominal cavity. The accuracy of ultrasound diagnosis of gastroschisis in the second and third trimesters of pregnancy varies from 70 to 95% and depends on the gestational age, fetal position, size of the defect and the number of organs located outside the anterior abdominal wall.

The overall prognosis for newborns with isolated gastroschisis is favorable: more than 90% of children survive. When prolonging pregnancy, management tactics in the second trimester have no special features. Due to the low frequency of combination of isolated gastroschisis with chromosomal abnormalities, prenatal karyotyping can be avoided. In the third trimester of pregnancy, it is necessary to conduct a dynamic assessment of the functional state of the fetus, since the frequency of distress during gastroschisis is quite high and in 23-50% of cases intrauterine growth retardation occurs.

If gastroschisis is detected before the period of fetal viability, pregnancy should be terminated. In full-term pregnancies, the birth takes place in a facility where surgical care can be provided.

Duodenal atresia- the most common cause of small intestinal obstruction. The frequency of the anomaly is 1:10,000 live births. Etiology unknown. The defect may occur under the influence of teratogenic factors. Family observations of pyloroduodenal atresia with an autosomal recessive type of inheritance are described. In 30-52% of patients, the anomaly is isolated, and in 37%, malformations of the skeletal system are detected: an abnormal number of ribs, agenesis of the sacrum, cauda equina, bilateral cervical ribs, bilateral absence of the first fingers, etc. In 2%, combined anomalies of the gastrointestinal tract are diagnosed: incomplete rotation of the stomach, atresia of the esophagus, ileum and anus, transposition of the liver. In 8-20% of patients, congenital heart defects are detected; in approximately 1/3 of cases, duodenal atresia is combined with trisomy 21 pairs of chromosomes. The main prenatal echographic findings in duodenal atresia are polyhydramnios and the classic sign "double bubble" in the abdominal cavity of the fetus. The “double bubble” image appears as a result of the dilation of part of the duodenum and stomach. The constriction between these formations is formed by the pyloric part of the stomach.

ka and is of great importance for accurate prenatal diagnosis of this defect. In the vast majority of cases, duodenal atresia is diagnosed in the second and third trimesters of pregnancy. In earlier stages, diagnosing this defect presents significant difficulties. The earliest diagnosis of duodenal atresia was made at 14 weeks.

To determine obstetric tactics, a detailed ultrasound assessment of the anatomy of the internal organs of the fetus and its karyotyping are performed. Before the period of fetal viability, termination of pregnancy is indicated. If an isolated anomaly is detected in the third trimester, it is possible to prolong pregnancy with subsequent delivery in a regional perinatal center and surgical correction of the malformation.

Isolated ascites. Ascites is the accumulation of fluid in the peritoneal cavity. The frequency has not been precisely established. During ultrasound examination of the fetus, ascites is manifested by the presence of an echo-negative space 5 mm or more thick in the abdominal cavity. In the prenatal period, ascites can be isolated or be one of the signs of hydrops of non-immune origin. In addition to ascites, fetal hydrops is characterized by the presence of subcutaneous edema, pleural and pericardial effusions, as well as an increase in the thickness of the placenta more than 6 cm, polyhydramnios and hydrocele.

Ascites can be combined with various structural abnormalities, so a thorough examination of all internal organs of the fetus is indicated. Among the causes of isolated ascites, meconium peritonitis and congenital hepatitis should be highlighted.

Until now, there have been no publications in the literature about the detection of isolated ascites in the first trimester of pregnancy. Most observations of early diagnosis of ascites occur at the beginning of the second trimester of pregnancy. One of the most common causes of non-immune hydrops is chromosomal abnormalities. In isolated ascites, chromosomal defects are detected less frequently, but they must be taken into account as a possible background for the development of this pathology. When ascites is detected in the fetus, it is first necessary to exclude combined anomalies and intrauterine infections. The course of fetal ascites depends on its etiology. Idiopathic isolated ascites has a favorable prognosis. In more than 50% of cases, its spontaneous disappearance is noted. The most common cause of isolated ascites is intrauterine infection.

parvovirus B19. When prolonging pregnancy, it is necessary to carry out dynamic echographic monitoring, including Doppler assessment of blood flow in the venous duct. At normal values blood flow in the venous duct in fetuses with ascites, in most cases a favorable perinatal outcome is noted. When ascites increases, some authors recommend performing a therapeutic puncture, especially in cases where the process progresses in late pregnancy. The main purpose of puncture is to prevent discoordinated labor and respiratory distress in the neonatal period. If isolated ascites is detected in the prenatal period and a concomitant pathology incompatible with life is excluded, after birth the child needs careful dynamic monitoring and symptomatic therapy.

DEVELOPMENTAL DISORDERS OF THE KIDNEY AND URINARY TRACT

Renal agenesis- complete absence of both kidneys. The occurrence of the defect is due to a disruption in the sequential chain of processes of normal embryogenesis from pronephros to metanephros. The incidence averages 1:4500 newborns. It is noted that it is found twice as often in boys. The pathognomonic triad of echographic signs of renal agenesis in the fetus is represented by the absence of their echoshadow and Bladder, as well as pronounced oligohydramnios. Oligohydramnios is a late manifestation and can be detected after the 16-18th week of pregnancy. Typically, bilateral renal agenesis is accompanied by a symmetrical form of fetal growth restriction syndrome. Renal agenesis is most often sporadic, but can be combined with various anomalies of internal organs. The direct consequences of oligohydramnios are pulmonary hypoplasia, skeletal and facial deformities, and fetal growth restriction syndrome. Renal agenesis has been described in more than 140 syndromes of multiple congenital malformations, chromosomal abnormalities, and teratogens. Once the diagnosis is made, karyotyping should be performed prenatally or after birth to exclude chromosomal abnormalities. In all observations of renal agenesis, a complete pathological examination is necessary. An echographic examination is indicated

kidney examinations in close relatives. If a defect is detected prenatally, termination of pregnancy at any stage should be recommended. If the family decides to prolong the pregnancy, conservative obstetric tactics are indicated.

Autosomal recessive polycystic kidney disease (infantile form). It manifests itself as a bilateral symmetrical enlargement of the kidneys as a result of the replacement of the parenchyma with secondarily expanded collecting ducts without proliferation of connective tissue. Varies from the classic lethal variant to infantile, juvenile and even adult forms. In the infantile form, secondary dilatation and hyperplasia of normally formed collecting ducts of the kidneys are noted. The kidneys are affected symmetrically, with cystic formations measuring 1-2 mm in size. The frequency is 1.3-5.9:1000 newborns. The main echographic criteria for the defect are enlarged hyperechoic kidneys, absence of bladder echoshadow and oligohydramnios. The increase in the size of the kidneys is sometimes so significant that they occupy most of the cross-section of the fetal abdomen. The typical echographic picture may not appear until the third trimester of pregnancy. The prognosis is unfavorable. Death occurs from renal failure. Obstetric tactics include terminating pregnancy at any stage.

Adult-type polycystic kidney disease(autosomal dominant disease, hepatorenal polycystic disease of adult type, Potter syndrome type III) is characterized by the replacement of the renal parenchyma by numerous cysts different sizes, which are formed due to the expansion of the collecting ducts and other tubular segments of the nephron. The kidneys are affected on both sides and are enlarged, but a unilateral process may be the first manifestation of the disease. The liver is also involved in the pathological process - periportal fibrosis develops, which is focal in nature. The etiology of the disease is unknown, but the type of inheritance causes a 50% risk of developing the disease, and its genetic focus is located on the 16th pair of chromosomes. One in 1,000 people carries the mutant gene. Penetration of the gene occurs in 100% of cases, however, the course of the disease can vary from severe forms with a fatal outcome in the neonatal period to asymptomatic ones, detected only at autopsy.

Polycystic kidney disease(multycystic disease, cystic kidney disease, Potter syndrome type II, dysplastic kidney disease) is characterized by cystic degeneration of the renal parenchyma due to primary dilation of the renal tubules. In multicystic renal dysplasia, the ureter and pelvis are most often atretic or absent. The process can be bilateral, unilateral and segmental. With multicystic dysplasia, the kidney is usually significantly increased in size; the usual shape and normal tissue are absent. The kidney is represented by multiple cysts with anechoic contents (Fig. 33).

Rice. 33. Echogram of bilateral fetal polycystic kidneys (sharply enlarged kidneys containing multiple cysts of different diameters - indicated by an arrow)

The sizes of cysts vary over a fairly wide range and depend on the stage of pregnancy. Closer to full term, the diameter of the cysts can reach 3.5-4 cm. The bladder is usually visualized with a unilateral process and is not visualized with a bilateral process. With a bilateral process, oligohydramnios is usually observed. The disease occurs mainly sporadically and can be secondary in combination with other syndromes. Obstetrics

The tactic for a bilateral process diagnosed in the early stages, due to an unfavorable prognosis, is to terminate the pregnancy. In case of a unilateral process and a normal karyotype without associated anomalies, normal delivery is indicated, followed by consultation of the child with a specialist.

Dilatation of the urinary tract. Anomalies of the genitourinary system in the fetus, accompanied by dilatation of the urinary tract, can be caused by various reasons, including vesicoureteral reflux, idiopathic pyelectasia, obstructive disorders, etc. From a clinical point of view, in the prenatal period it is advisable to distinguish pyelectasia and obstructive uropathy.

Pyelectasis. Pyeelectasis is characterized by excessive fluid accumulation and dilation of the fetal renal pelvis.

Pyeelectasis is the most common finding on fetal ultrasound. The frequency of its development has not been established, since this pathology is a sporadic phenomenon. After birth, it is diagnosed 5 times more often in boys. In 27% of children with hydronephrosis, vesicoureteral reflux, bilateral duplication of the ureters, bilateral obstructive megaureter, non-functioning contralateral kidney and its agenesis are detected, and in 19% - developmental anomalies of various organs. For prenatal ultrasound diagnosis of pyeloectasia, the fetal kidneys should be examined using both transverse and longitudinal scanning. Dilatation of the renal pelvis is judged on the basis of its anteroposterior size on a transverse scan of the kidney. Most researchers consider pyeloectasia to be an expansion of the renal pelvis in the second trimester of pregnancy of more than 5 mm, and in the third trimester of more than 8 mm. When the fetal renal pelvis dilates beyond 10 mm, it is customary to speak of hydronephrosis. The most common classification of hydronephrosis in the fetus is:

Grade I (physiological dilatation):

Renal pelvis: anteroposterior size<1 см;

Cortical layer: not changed.

Grade II:

Renal pelvis: 1.0-1.5 cm;

Calyxes: not visualized;

Cortical layer: not changed.

Grade III:

Renal pelvis: anteroposterior size >1.5 cm;

Calyx: slightly widened;

Cortical layer: not changed.

Grade IV:

Renal pelvis: anteroposterior size >1.5 cm;

Calyxes: moderately dilated;

Cortical layer: slightly changed.

Grade V:

Renal pelvis: anteroposterior size >1.5 cm;

Calyxes: significantly expanded;

Cortical layer: atrophy.

Enlargement of the fetal renal pelvis can be observed with various chromosomal abnormalities. The frequency of chromosomal defects in fetuses with pyeloectasia averages 8%. In most fetuses with chromosomal abnormalities, a combination of pyeelectasia and other developmental anomalies is detected. Moderately severe pyelectasis has a good prognosis and the need for surgical treatment after childbirth is quite rare. In most cases, spontaneous resolution of moderately severe pyelectasis is noted after the birth of the child.

Obstetric tactics depend on the time of occurrence and duration of the pathological process, as well as the degree of renal dysfunction. Early delivery is justified in case of oligohydramnios. In the postnatal period, dynamic observation and consultation with a pediatric urologist are indicated.

Obstructive uropathy. Obstruction of the urinary tract in the fetus can be observed at any level: high obstruction, obstruction at the level of the ureteropelvic junction (UPJ), obstruction at the middle level (ureter), obstruction at the level of the vesicoureteral junction (UPJ), low obstruction (urethra). OLMS is the most common cause obstructive uropathy in the fetus and accounts for an average of 50% of all congenital urological anomalies. The main echographic features of OLMS include dilatation of the renal pelvis with or without dilatation of the calyces; the ureters are not visualized; the bladder may be of normal size or in some cases not visualized. Tactics for OLMS should be wait-and-see. Installation of a vesico-amniotic shunt is not indicated. To ultrasonic cri-

The symptoms of APMS in the fetus include dilatation of the ureter and pyelectasis. The bladder is usually of normal size. Management tactics are similar to those for OLMS. The most common cause of low obstruction is the posterior urethral valves. With severe obstruction, oligohydramnios is observed, leading to hypoplasia of the lungs, deformities of the facial structures and limbs, fibrosis and dysplasia of the renal parenchyma. The echographic picture is characterized by the presence of a dilated urethra proximal to the site of obstruction and pronounced dilatation of the bladder. Prenatal tactics for low obstruction depend on the duration of pregnancy, the presence of oligohydramnios and associated anomalies, as well as the functional state of the kidneys. For moderately severe and non-progressive pyelectasis, conservative tactics should be followed. With the progression of obstructive disorders, delivery with possible surgical correction of the defect is justified to prevent severe renal impairment in the fetus. In case of premature pregnancy in fetuses with severe obstructive uropathy, intrauterine surgical correction of the defect can be performed.

DEVELOPMENTAL DISORDERS OF THE BONE SYSTEM

Among congenital malformations of the skeletal system, the most common are amelia (aplasia of all extremities); phocomelia (underdevelopment of the proximal limbs, with the hands and feet connected directly to the body); aplasia of one of the bones of the leg or forearm; polydactyly (increase in the number of fingers on a limb); syndactyly (reduction in the number of fingers due to fusion of soft tissue or bone tissue of adjacent fingers); abnormal placement of feet; osteochondrodysplasia, characterized by abnormalities in the growth and development of cartilage and/or bones (achondrogenesis, achondroplasia, thanatoform dysplasia, osteogenesis imperfecta, hypophosphatasia, etc.).

The most important thing is to diagnose defects that are incompatible with life. Many forms of skeletal dysplasia are combined with pulmonary hypoplasia, caused by the small size of the chest due to underdevelopment of the ribs. The development of pulmonary failure in this case can be the cause of death of children in the first hours of extrauterine life.

Achondroplasia is one of the most common non-lethal skeletal dysplasias and is caused by a new mutation in 90% of cases. Achondroplasia is an osteochondroplasia with defects in the long bones and/or axial skeleton. Frequency - 0.24-5:10,000 births. The ratio of male to female fruits is 1:1. Bone shortening due to achondroplasia may not become apparent in the fetus until 24 weeks of gestation. The classic sonographic appearance includes short limbs (less than 5th percentile), small chest size, macrocephaly, and a saddle nose. Life expectancy with achondroplasia depends primarily on the time when small chest sizes do not cause serious respiratory problems. Intellectual development with the defect is normal, but there is a high risk of neurological disorders, in particular compression of the spinal cord at the level of the foramen magnum, which can limit physical activity. Macrocephaly may be the result of moderate hydrocephalus due to the small size of the foramen magnum. Achondroplasia is a well-studied and common type of congenital dwarfism in newborns. Central and obstructive apnea may be serious problems for them. At the age of 6-7 years of life, chronic recurrent middle ear infections are often observed. In the early childhood curvature of the lower extremities is also often observed, which, in severe conditions, requires surgical correction. Typically, the height of adults with achondroplasia varies from 106 to 142 cm.

At all times, one or another intrauterine malformation of a child has occurred. The seemingly smaller percentage of developmental anomalies in children during the time of our grandmothers is due to the fact that now, thanks to a qualitatively new level of examination and management of pregnant women, it is possible to carry out a pregnancy that, without outside intervention, would have been interrupted at a short period in previous times. The main reason spontaneous abortions in short periods, various genetically determined anomalies of deformity appear. Thus, we can say that at this stage the first natural selection in the life of an individual occurs.

Causes of fetal malformations

There are many reasons for the development of anomalies in children during intrauterine development. In the first place, of course, are all kinds of genetic defects, both hereditary and acquired as a result of various disorders of embryogenesis. Changes at the genetic level occur under the influence of unfavorable environmental factors: ionizing radiation, exposure to toxic chemicals, including some medications. A genetic defect can be passed on to a child from one of the parents, or it can be a “personal acquisition” - the mutation occurs after the combination of high-quality genetic information of a man and a woman. Unfortunately, methods for effectively preventing such situations have not yet been invented. Most embryos carrying a genetic mutation are not viable and their development stops almost immediately after fertilization, at the very beginning of the formation of the embryo. This situation is called fetal development arrest and requires a thorough clarification of the reasons for its development. In addition to the genetic defects described above, maternal diseases can lead to pregnancy failure: infectious (including sexually transmitted infections), endocrine, and disorders of the immune system.

What are the types of congenital malformations of the fetus?

The severity of pathology in fetal development may vary. This depends on the location of the genetic breakdown, and on the strength and duration of the toxic effect, if any. It should be noted that there is no clear relationship between the intensity of external influence and the severity of a particular developmental defect. A woman exposed to toxicity during pregnancy can give birth to a healthy baby. However, there remains a risk that a fetal malformation will appear in the grandchildren or even great-grandchildren of this woman, as a consequence of genetic damage that occurred in her child during the prenatal period, but did not have clinical manifestations.
The most common congenital malformations of the fetus:
– complete or partial absence, deformation of one or another organ or part of the body (limbs, brain, internal organs);
– anatomical defects of the face and neck (cleft lip and palate, other anomalies of the facial skeleton);
– spina bifida – cleft of the spinal canal expressed to varying degrees;
– congenital heart defects;
The most common chromosomal abnormalities: Down syndrome and Edwards syndrome accompany multiple intrauterine malformations of the fetus.

Diagnosis of fetal malformations

Prenatal diagnosis of fetal malformations and chromosomal pathology is a very complex process. One of the stages of such diagnostics is the so-called screening studies - a set of examinations that are prescribed to a woman at 12, 20 and 30 weeks of pregnancy. This complex includes a blood test for biochemical serum markers of chromosomal pathology (tests for fetal malformations).

In the first trimester (double test):
– free β-subunit of human chorionic gonadotropin;
– PAPP-A (pregnancy associated plasma protein A): plasma protein A associated with pregnancy.
In the second trimester (triple test):
– total hCG or free β-subunit of hCG;
– α-fetoprotein (AFP);
– free (unconjugated) estriol.
Depending on the laboratory's capabilities, the latter analysis is sometimes not performed. An obligatory addition to such a study is an ultrasound of the uterus and fetus.

The result of each study cannot be assessed in isolation from other data - that is, the assessment of the result must be comprehensive and carried out only by a specialist.
Such an examination does not provide a 100% guarantee, but only allows us to identify a high-risk group among pregnant women who need invasive diagnostic methods - chorionic biopsy, cordocentesis to determine the karyotype of the fetus and exclude its chromosomal pathology.
Chorionic biopsy in the first trimester and placentocentesis or cordocentesis in the second trimester can with 100% accuracy exclude or confirm only chromosomal pathology in the fetus, but not defects! Congenital malformations of the fetus (CHD) can be excluded only with the help of fetal ultrasound and, most often, at 20-22 weeks of pregnancy. Moreover, ultrasound diagnostic doctors performing fetal ultrasound must have extensive experience in fetal ultrasound and have specialization in prenatal diagnosis of congenital malformation. Unfortunately, not all ultrasound diagnostic doctors know the anatomical features of the fetus well, which is why they miss congenital birth defects. For the same reason, signs characteristic of genetic diseases can sometimes be seen (shape of the skull, features of skin folds, characteristic ratios of the size of the facial/cerebral skull, head size/body length, etc.). Another reason for errors in the prenatal diagnosis of congenital malformations is the low quality of the equipment used for the study. With the low resolution of an ultrasound machine, even a highly qualified diagnostician can leave “behind the scenes” what is obvious to a medical student, provided the quality of the device is high. As a rule, in regional centers and large cities there are medical genetic centers where women are required to be examined and consulted at least once during pregnancy.

Pregnant women must be referred for medical and genetic counseling:
– over 35 years old;
– having a child with Down syndrome or other genetically determined pathology;
– with cases of miscarriages, stillbirths, undeveloped pregnancies;
– if in the family of one of the parents there are patients with Down syndrome and other chromosomal pathologies;
– those who have had viral diseases during early stages of pregnancy;
– when taking certain medications;
– if there was exposure to radiation.

So, to identify genetic defects in the fetus, it is necessary, first of all, to conduct screening blood tests. This will give a presumptive answer about the presence or absence of chromosomal abnormalities in the child. After an ultrasound, it becomes clear whether there are physical malformations or not. If specialists find it difficult to resolve the issue of genetic defects, chorionic villus biopsy or cordocentesis is prescribed (depending on the stage of pregnancy).
Any case of detection of congenital malformation becomes a reason to offer the woman termination of pregnancy for medical reasons. If a woman decides to keep the child, she should be monitored especially closely, preferably by specialists from a medical genetic center.
Malformations of a child, in most cases, significantly limit his ability to live. The causes of fetal malformations must be established to determine the degree of risk in subsequent pregnancies.

16769 0

Congenital malformations of the fetus occupy 2-3 places in the structure of causes of perinatal mortality, and their frequency is last years has increased significantly. In this regard, early diagnosis of malformations is of particular relevance, facilitating timely resolution of the issue of the possibility of further prolongation of pregnancy, which, in turn, is determined by the type of anomaly, compatibility with life and prognosis for postnatal development.

The classification of common malformations of the central nervous system (CNS) can be presented as follows:

1. Hydrocephalus:

a) stenosis of the cerebral aqueduct;

b) open hydrocephalus;

c) Dandy-Walker syndrome.

2. Choroid plexus papilloma.

3. Neural tube defects:

a) spina bifida;

b) anencephaly;

c) cephalocele.

4. Microcephaly.

Hydrocephalus occurs with a frequency of 0.3-0.8 per 1000 live births. In most cases, congenital hydrocephalus is caused by obstruction in one of the sections of the cerebrospinal fluid (CSF) circulation path. Hydrocephalus is often combined with other anomalies: in 37% of cases it is accompanied by other intracranial pathology - hypoplasia of the corpus callosum, cephalocele, arteriovenous anomalies, arachnoid cysts; extracranial anomalies - in 63%. Among the latter, malformations of the kidneys (unilateral and bilateral agenesis and dysplasia), heart defects (ventricular septal defect, tetralogy of Fallot), meningomyelocele, splitting of the upper lip, hard and soft palate, agenesis of the anus and colon, gonadal dysgenesis, Meckele syndrome should be noted. . Chromosomal abnormalities are found in 11% of fetuses - trisomy 21 pairs, balanced translocations, mosaicism.

Hydrocephalus comes in three main forms:

• stenosis of the cerebral aqueduct;
• open hydrocephalus;
• Dandy-Walker syndrome.

Cerebral aqueductal stenosis(SVM) is a form of obstructive hydrocephalus caused by narrowing of the Sylvian aqueduct. The specific frequency of SVM reaches 43%, the ratio of male and female children is 1:8. The anomaly has a polyetiological character: genetic, infectious, teratogenic and tumor factors, among which infectious (50%) predominate. In experimental studies, the role of toxoplasmosis, syphilis, cytomegalovirus infection, mumps and influenza has been confirmed.

In a certain part of the observations, the cause of stenosis of the cerebral aqueduct is a genetic pathology that can be inherited in a recessive type linked to the X chromosome. Sex-linked inheritance is considered to be a rare cause of WMS, as it occurs with a frequency of 1 case per 200 siblings of probands with hydrocephalus. However, it is possible that this type of inheritance is 25% among male children. It is assumed that glioma, meningioma, neurofibromatosis and tuberous sclerosis lead to stenosis of the aqueduct due to the compression mechanism, and open hydrocephalus - as a result of white matter edema and external compression. Combined anomalies occur in 16% of children.

Diagnosis of this form of hydrocephalus is based on the detection by ultrasound of the expansion of the lateral and III ventricles with unchanged dimensions of the IV ventricle. It is necessary to conduct a thorough scan of the fetal spine to exclude sex-associated anomalies (Fig. 1).

Rice. 1. Pregnancy 21 weeks. Obstructive hydrocephalus

Forecast: childhood mortality ranges from 11-30%; intellectual development may be normal.

Obstetric tactics: before the fetus reaches viability, termination of pregnancy is indicated; when establishing a diagnosis in the later stages, the method of delivery is determined solely by obstetric indications.

Open hydrocephalus(OG) - expansion of the ventricles of the brain and its subarachnoid system as a result of obstruction of the extraventricular system of the outflow tracts of cerebrospinal fluid.

Open hydrocephalus is the second most common, accounting for 38% of all hydrocephalus cases. The etiology of OH is not specified. OH is detected in children with spinal defects and obliteration of the anterior sagittal sinus, subarachnoid hemorrhages, choroid plexus papilloma and the absence of Paccioni granulations. Subarachnoid hemorrhage is the most common cause of open hydrocephalus in newborns; in the prenatal period it is extremely rare. It is also rarely inherited, although the frequency of repetition reaches 1-2%, which is significantly higher than in the general population.

Pathogenesis: mechanical obstruction of the extraventricular system of the brain and impaired reabsorption of CSF lead to expansion of the subarachnoid space, and then the cerebral ventricles; internal hydrocephalus develops against the background of obstruction of the cerebral aqueduct due to increased intracranial pressure.

Prenatal diagnosis of OH is carried out using dynamic ultrasound scanning. In this case, a pathognomonic sign is the expansion of the subarachnoid cistern.

Forecast: The mortality rate reaches 11%. Most surviving children retain normal intelligence. When OH is combined with neural tube defects or choroid plexus papilloma, the prognosis is more unfavorable.

Obstetric tactics: in the early stages of detection of OH, termination of pregnancy is indicated; in full-term pregnancy, childbirth is carried out through the natural birth canal.

For Dandy-Walker syndrome Typically a combination of the following anomalies:

1) hydrocephalus of varying degrees;

2) cysts of the posterior cranial fossa;

3) defects of the cerebellar vermis, through which the cyst communicates with the cavity of the fourth ventricle.

The syndrome occurs in 12% of children with congenital hydrocephalus. Etiology unknown. This syndrome can be one of the manifestations of genetic diseases (Meckel and Warburg syndromes), and can also be detected with chromosomal aberrations (Turner syndrome, 6p-, 9gh+, trisomy 9, triploidy). In rare cases, autosomal recessive inheritance is possible with a risk of recurrence of up to 25%.

Pathoembryogenesis. According to the Dandy-Walker theory, atresia of the foramina of Luschka and Magendie usually leads to dilation of the ventricular system. The syndrome is a complex anomaly of the development of the midline structures of the brain in the region of the rhomboid fossa. Hypoplasia of the cerebellar vermis and cysts of the postcranial fossa occur secondaryly, due to compression of it by the sharply dilated fourth ventricle. There is also an imbalance in the production of cerebrospinal fluid in the lateral, third and fourth ventricles. The brain worm defect varies from complete aplasia to slight clefting. Despite the fact that hydrocephalus is the main diagnostic sign of Dandy-Walker syndrome, in most children it is absent at the time of birth; however, it manifests itself in the first months of the child’s life.

The syndrome is often (in more than 50% of cases) combined with other malformations of the central nervous system (agenesis of the corpus callosum, encephalocele), kidney defects (polycystic disease) and heart defects (ventricular septal defect).

Diagnostics: this anomaly is indicated by the detection of cystic formations in the posterior cranial fossa during echography; The pathognomonic acoustic sign of the syndrome is a defect in the vermis of the brain, through which the cyst communicates with the fourth ventricle.

Forecast unfavorable: mortality reaches 50%, 50-60% of surviving children have delayed intellectual development.

Obstetric tactics: termination of pregnancy is carried out at any stage.

Choroid plexus papilloma(PSS). Intracranial neoplasm occurs with a frequency of 0.6% of all brain tumors detected in adults and 3% in children. Papilloma can be localized in any part of the ventricular system, but is more often found at the level of the vestibule of the lateral ventricles. Unilateral localization of the tumor is typical, although a bilateral process cannot be ruled out. Most often, PSS is represented by villous tissue, histologically similar to the tissue of the intact choroid plexus, and is benign in nature. However, malignancy of the tumor with germination into adjacent nervous tissue is possible. Choroid plexus papilloma is usually combined with hydrocephalus.

Etiology unknown. In world practice, there are isolated observations of PSS in patients with Aicardi syndrome (this disease is linked to the X chromosome and is characterized by agenesis of the corpus callosum, chorioretinal lacunae, spinal abnormalities, epilepsy and mental retardation).

PSS is diagnosed in children with hydrocephalus during neurosonography or x-ray examination. In childhood, contrast computed tomography should be considered the method of choice. As a method of prenatal diagnosis, the most informative is ultrasound scanning. Echographic criteria for PSS are the asymmetry of the shape and size of the contralateral ventricles, visualization of weakly echogenic formations adjacent to the normal choroid plexus in the vestibule of the lateral ventricles. Prenatally, PSS of the third and fourth ventricles is not detected.

The method of choice for PSS therapy is surgical removal of the tumor. If the process is benign surgical treatment may have a favorable outcome, but the operation is technically difficult and is accompanied by large blood loss. In case of malignant lesions (in more than 20% of cases), the prognosis is unfavorable. The mortality rate for PSS reaches 35%, and 72% of surviving children have mental and mental development defects of varying severity.

Obstetric tactics: childbirth is carried out through the natural birth canal; the use of vaginal delivery operations is contraindicated. Delivery in large perinatal centers is recommended, where emergency neonatological and pediatric neurosurgical care can be provided. Questioning the use of caesarean section to reduce risk birth trauma with intracranial hemorrhage has not been completely resolved.

Selected lectures on obstetrics and gynecology

Ed. A.N. Strizhakova, A.I. Davydova, L.D. Belotserkovtseva