Diseases of childhood, prenatal pathology. Pathology of intrauterine development. Gametopathies, blastopathy, embryopathies and fetopathy. The significance of critical periods in the pathology of intrauterine development

The frequency of congenital and hereditary pathologies in the population averages 5% of the number of newborns. Monogenic diseases occur in 5-14 children per 1000 newborns, chromosomal diseases - in 4-7, congenital malformations - in 19-20. In the structure of perinatal mortality and morbidity of children, congenital and hereditary pathologies occupy 2-3 places.

The concept of “prenatal (antenatal) pathology” includes all pathological processes and conditions of the human embryo from the moment of fertilization to the birth of the child. The human prenatal period is 280 days, or 40 weeks, after which childbirth occurs.

The antenatal period begins with the formation of the zygote and ends with the onset of labor. From an ontogenetic point of view, it is advisable to divide the antenatal period into embryonic (from the moment of formation of the zygote to 12 weeks), early fetal (from the beginning of the 12th to the 29th week of intrauterine development) and late fetal (from the 29th week to childbirth).

When the fetus is exposed to unfavorable factors in the early fetal period, a decrease in the weight of fetal organs and tissues occurs, as well as placental hypoplasia. For this period, a typical clinical manifestation of intrauterine diseases is a symmetrical form of intrauterine growth retardation (IUGR) and severe insufficiency of the uteroplacental circulation. In the late fetal period - disruption of the processes of morphofunctional maturation of the fetus. Chronic insufficiency of the uteroplacental circulation is accompanied by the development of an asymmetrical form of IUGR, chronic intrauterine fetal hypoxia, immune and infectious factors cause acute congenital diseases - hemolytic disease of the fetus and newborn, hepatitis, pneumonia, myocarditis, encephalitis, etc.

Typical manifestations of antenatal pathology are congenital malformations - gross anatomical changes in an organ and tissue (or organ system), leading to dysfunction.

Depending on the timing of the occurrence of intrauterine pathology, the following forms are distinguished: gametopathies and cymatopathies (blastopathy, embryopathy, fetopathy).

Gametopathies

The concept of “gametopathy” covers all types of damage to the male and female gametes (egg and sperm) that occur during ovo- and spermatogenesis before fertilization. Gametopathies are caused mainly by mutations. Depending on in which structures of the hereditary apparatus of the gamete the mutation occurred, the development of various mutations is possible: gene, chromosomal or genomic.

Gametes are carriers of genes inherited from their parents and from all distant ancestors. Severe damage to gametes can lead to their death, the development of infertility and spontaneous abortion. A gamete with a defect in a gene or genes can become a source of hereditary congenital malformations.

Blastopathy

The pathology of blastogenesis is limited to the first 15 days after fertilization. The main endpoints of blastopathies include:

- empty embryo sacs(they are formed as a result of aplasia or early death of the embryoblast with its subsequent resorption);

- hypoplasia and aplasia of extraembryonic organs(amnion, amniotic stalk, yolk sac);

- twin malformations(symmetrical and asymmetrical, that is, completely or partially unseparated twins);

- ectopic or ectopic pregnancy(implantation of a fertilized egg in the ovary, fallopian tube, rudimentary uterine horn and at the internal os of the uterus) or violation of the depth of implantation (superficial, unusually deep).

The cause of blastopathy is most often chromosomal aberrations in combination with environmental influences (for example, endocrine, cardiovascular diseases of the mother, hypoxia, etc.).

The pathology of the development of the entire embryo is a general disorder, in most cases incompatible with life. Most of the embryos damaged as a result of blastopathies are eliminated through spontaneous abortions, and elimination, as a rule, does not occur at the moment of damage to the embryo or even its death, but somewhat later, usually after 3-4 weeks.

Embryopathies

All types of embryo pathology (from 16 to 75 days of pregnancy) induced by exposure to damaging factors are called embryopathies. Embryopathies are characterized by disturbances in the formation of organs, which ultimately result in either the death of the embryo or congenital malformations. The term “congenital malformation” should be understood as persistent morphological changes in an organ or the entire organism that arise in utero, go beyond the limits of their possible structure and lead to dysfunction. The severity of congenital malformations varies: from minor deviations in the structure of one organ to severe changes in many organs that are incompatible with life.

Microdevelopmental anomalies (stigmas of dysmorphogenesis) are understood as morphological changes that are not accompanied by dysfunction. For example, telangiectasia, “freckles”, a gray strand above the forehead, low hair growth on the forehead or neck, deformation of the ears, Mongoloid and anti-Mongoloid eye shape, epicanthus, blue sclera, synophrysis, smoothed filter, pterygoid folds on the neck, polythelia, arachnodactyly and etc.

Often there is a combination of organ defects characteristic of the period of blastogenesis with defects in which developmental disorders are observed at the level of tissue differentiation, usually in terms corresponding to the early fetal period. Thus, blastopathies are often combined with early fetopathies. Congenital malformations are very diverse, their nosological forms number in the thousands.

Congenital defects include the following developmental disorders:

- aplasia (agenesis)- complete congenital absence of an organ or part thereof. In most cases, both terms are used as synonyms, however, to emphasize not only the absence of an organ, but also its rudiment, the term “agenesis” is used. The absence of individual parts of an organ is in some cases indicated by a term derived from the Greek word oligos (small) and the name of the affected organ (for example, “oligodactyly” - the absence of one or more fingers, “oligogyria” - the absence of individual convolutions of the brain;

- congenital hypoplasia- underdevelopment of an organ, manifested by a deficiency in the relative mass or size of the organ. A decrease in body weight of a fetus or newborn is called “congenital malnutrition (hypoplasia).” In relation to older children, the term “nanism” (dwarfism, microsomia) is used to denote reduced body size;

- congenital hypertrophy (hyperplasia)- an increase in the relative mass (or size) of an organ due to an increase in the number (hyperplasia) or volume (hypertrophy) of cells. Macrosomia (gigantism) - an increase in the length and weight of the entire body. To denote the enlargement of organs or their parts, a prefix from the Greek is used. pachis (thick) (for example, “pachygyria” - thickening of the gyrus of the brain, “pachyacria” - thickening of the phalanx of the fingers). Doubling, as well as an increase in the number of one or another organ or part of it (doubling of the uterus, double aortic arch) is designated by the term with the prefix “poly” (from the Greek poly - many) (for example, “polygyria”, “polydactyly”, “polysplenia” );

- atresia- complete absence of a channel or natural opening;

- stenosis- narrowing of the canal or opening;

The name of the defects that determine the non-separation of the limbs or their parts begins with the Greek prefix syn, sym (together), for example, “syndactyly” - non-separation of the fingers, “sympodium” - non-separation of the lower limbs;

-ectopia- displacement of an organ, that is, its location in an unusual place (for example, the location of the kidney in the pelvis, the location of the heart outside the chest;

-persistence- preservation of embryonic structures that normally disappear by a certain period of development. One of the forms of persistence is dysraphia (araphia) - non-closure of the embryonic fissure (cleft lip, palate, spine, urethra);

-heterotopia- the presence of cells, tissues or entire sections of an organ in another organ or in those areas of the same organ where they should not be (for example, sections of the pancreas in Meckel’s diverticulum, islands of cartilage in the lungs outside the bronchial wall). Such displacements of cells and tissues, as a rule, are detected only under a microscope. They are sometimes called choristia (from the Greek chorista - separating) in contrast to hamartia (from the Greek gamartus - error), which is understood as an incorrect ratio of tissues, accompanied by tumor-like growth. An example of hamartia may be the proliferation of fibrous tissue in the kidney in the form of an island, devoid of epithelial structures.

Fetopathies

Fetopathies (from the Latin foetus - fetus) are a consequence of damage to the fetus from the 12th week to the moment of birth. There are early (up to 28 weeks of pregnancy) and late (from 28 weeks to childbirth) fetopathies. Fetopathies are characterized by the following features:

The rarity of congenital defects caused by exposure to teratogenic factors during the fetal period;

Any damage during this period entails the development of defects at the tissue level. In this case, either an incorrect ratio of organ tissues or a delay in their maturation may be observed.

The presence of predominantly generalized forms of infections. Characterized by multiple foci, mainly of alterative inflammation in parenchymal organs, or the presence of generalized granulomatosis (for example, with congenital listeriosis);

Infectious and toxic processes are accompanied by severe hemorrhagic diathesis (petechiae on the skin, mucous membranes, hemorrhages in internal organs);

There is a delay in involution and excessive cell proliferation in foci of extramedullary hematopoiesis;

Hypertrophy and tissue regeneration mainly due to hyperplasia of mesenchymal elements, which leads to excessive development of connective tissue (for example, in cystic fibrosis - in the pancreas, in fibroelastosis of the heart - proliferation of elastic and fibrous tissue in the endocardium).

Approved at a meeting of the Educational and Methodological Commission for the specialty “pediatrics”

Methodological support was approved at a meeting of the Department of Hospital Pediatrics, Protocol No.___ dated “__”___________20__.

Edited by the head of the Department of Hospital Pediatrics, Doctor of Medical Sciences, Professor M.A. Skachkova

Embryothepathy of newborns. Intrauterine infections of the fetus and newborn. Toolkit. - Orenburg, p.19

Competence - The ability and willingness to analyze socially significant problems and processes, to use in practice the methods of the humanities, natural sciences, biomedical and clinical sciences in various types of professional and social activities

Component – ​​analysis of socially significant problems and processes

During the discussion of patients, discussion of theoretical material, current problems of modern medicine and society are analyzed in order to form an active professional and civic position among students.

Technology is the organization of educational and independent work of students aimed at developing the moral character of a doctor: neatness, smartness, clarity, goodwill, accuracy and commitment, self-control and self-control; using as an example fiction, films, and the personal behavior of a teacher during practical classes in departments of medical organizations.

Control - individual and frontal questioning at seminars, evaluation of solutions (orally and in writing) to situational problems, checking workbooks, testing, reviewing abstracts, editing speeches.

8. Competence - the ability and willingness to carry out their activities taking into account moral and legal norms accepted in society, to comply with the rules of medical ethics, laws and regulations on working with confidential information, and to maintain medical confidentiality.

8.1.Component – ​​use in practice the fundamentals of ethics and deontology when communicating with parents of newborn children with embryofetopathies, intrauterine infections, with their relatives, and medical personnel.

8.1.2. Technology - organization of educational and independent work of students aimed at developing the moral character of a doctor: accuracy, smartness, clarity, goodwill, accuracy and commitment, self-control and self-control; using as an example fiction, films, and the personal behavior of a teacher during practical classes in departments of medical organizations.

8.1.3. Control - evaluation of solutions (orally and in writing) to situational problems, checking workbooks, testing, reviewing abstracts, editing speeches.

PC1 – capable and ready to implement the ethical and deontological aspects of medical practice in communication with colleagues, nurses and junior medical staff, with parents of newborn children with embryofetopathies or intrauterine infections.

Component - implementation of ethical and deontological aspects of medical practice in communication with colleagues, nurses and junior medical staff, with parents of newborn children.

Content - able to cultivate qualities that promote mutual understanding with a sick child, his parents and other relatives, the ability to receive moral satisfaction from his work. At each lecture and practical lesson, students’ attention is focused on the need for interaction of all parts of the treatment process to achieve the main goal - the health of the child; both positive and negative personal qualities of the doctor are analyzed; examples from practice are given.

Technology is the organization of educational and independent work of students aimed at developing the moral character of a doctor, using fiction, films, and the personal experience of the teacher as an example.

In practical classes, especially while working in the emergency department and wards, students' attention is drawn to the relationship between the doctor and the parents of children with embryofetopathies, intrauterine infections, the rules of behavior in the hospital, and the features of managing children in terminal conditions.

Control - assessment of solutions (orally and in writing) to situational problems, checking workbooks, testing, reviewing abstracts, editing speeches, assessing the behavior of students in the clinic (appearance, relationships with each other, compliance with sanitary-hygienic and medical-protective regimes).

PC-5 Is able and ready to conduct and interpret a survey, physical examination, clinical examination, the results of modern laboratory and instrumental studies, morphological analysis of biopsy, surgical and sectional material in newborns with embryofetopathy, with intrauterine infections, write a medical history of the newborn.

5.1. Component – ​​conducting a survey, physical examination of a sick child, prescribing necessary and sufficient diagnostic tests.

5.1.1. Contents - is able to collect complaints from the patient or his parents, anamnesis of life and illness, assess the general condition of the child, determine weight, height, measure body temperature, count the pulse rate and the number of respirations per minute, perform a physical examination of the patient according to the systems, make a preliminary diagnosis, prescribe the necessary studies, evaluate the examination results, make a diagnosis according to the classification

5.1.2. Technology is the organization of educational and independent work of students aimed at acquiring practical skills in collecting complaints, collecting and assessing anamnesis, as well as methods of general examination of the child, vital signs and conducting anthropometric studies, drawing up a plan for examining the patient.

5.1.3. Control - individual survey, assessment of solutions (orally and in writing) to situational problems, checking workbooks, monitoring the acquisition of practical skills.

5.2. Component – ​​filling out a medical history of the newborn.

5.2.2. Technology - organization of educational and independent work of students aimed at acquiring practical skills in working with basic medical documentation in the emergency department, in the neonatal pathology department, and in the intensive care unit.

5.2.3. Control - checking the medical records of supervised children.

PC-19 – Prescribe adequate therapeutic treatment for the most common embryofetopathies, intrauterine infections of newborns, carry out emergency treatment measures in the event of the development of life-threatening conditions.

19.1. Component – ​​Prescription of adequate treatment for embryofetopathies and intrauterine infections.

19.1.2. Technology is the organization of educational and independent work of students aimed at acquiring practical skills in working with a patient: the ability to assess the patient’s condition, make a diagnosis, prescribe treatment (choose a drug, calculate its dose for a specific patient, make notes in the medical history).

19.1.3. Control – individual survey at seminars, testing, checking medical histories of supervised children, workbooks.

19.2. Component – ​​carry out emergency treatment measures in case of development of life-threatening conditions

19.2.2. Technology is the organization of educational and independent work of students aimed at acquiring practical skills in providing emergency care and practical skills.

19.2.3. Control - individual survey at seminars, testing, checking medical histories of supervised children, workbooks.

Goal: formation and development of competencies among graduates in the specialty “Pediatrics” on the causes of occurrence, diagnostic issues and principles of complex therapy of infectious and inflammatory diseases in newborns, as well as the features of rehabilitation of children with this pathology.

Questions to consider:

Collect anamnesis from the mother of a sick child;

The student must own:

The concept of the term “embryofetopathies”. Critical periods of fetal development.

The main reasons leading to disruption of the morphological formation of the fetus.

Clinical manifestations, diagnosis and differential diagnosis of chromosomal disorders in newborns (trisomy 13,18,21). Clinical picture. Diagnostics. Differential diagnosis. Features of observation. Forecast.

Toxic causes of embryofetopathies (alcohol syndrome, drug and nicotine intoxication). Clinical picture. Diagnostics. Differential diagnosis. Treatment. Emergency and intensive care. Prevention. Outcomes.

Pathophysiological mechanisms of embryofetopathy formation in diabetes in a pregnant woman. Diabetic embryofetopathy. Pathogenesis. Clinical picture. Differential diagnosis. Treatment. Emergency care for hypoglycemia. Prevention. Outcomes.

The concept of the term “TORCH syndrome”

Etiology and pathogenesis of various intrauterine infections in newborns.

Clinical manifestations of intrauterine infections.

Diagnosis of intrauterine infections.

Differential diagnosis of various intrauterine infections.

Basic approaches to the treatment of intrauterine infections in newborns.

The main points of immunoreplacement therapy in newborns.

Pathogenetic and symptomatic therapy for intrauterine infections.

Clinical observation of newborns after discharge from hospital.

Prevention of intrauterine infection of the fetus.

Prenatal diagnosis of congenital malformations of the fetus and newborn.

Purpose and creation of the stage

Tools and visibility

Determining the purpose of the lesson, the content of each stage of the lesson

Information about the purpose of the practical lesson, the significance of the characteristics of the course of the disease depending on age

To identify the degree of preparedness of students and the survival of knowledge based on past interviews when analyzing patients

Students respond to assignments in writing; the answers received allow us to evaluate the students’ preparation

Theoretical analysis of the lesson topic

To deepen students' knowledge of embryofetopathies and intrauterine infections in newborns

Students analyze the features of the course of the disease in children

Student's folder, a manual for organizing student work at the Department of Hospital Pediatrics.

To deepen students' knowledge on issues of providing care to newborns.

Students systematize knowledge on the treatment of various forms of embryofetopathies and intrauterine infections in newborns

Joint examination of newborns with purulent-inflammatory diseases

Students report anamnesis and demonstrate the technique of examining a patient

Joint examination with the teacher

Patients, copies of medical records microtables,

Work in the X-ray room, endoscopic room, ultrasound room, specialists’ offices

Strengthen the skills of evaluating diagnostic methods.

Students systematize knowledge on the diagnosis of various forms of embryofetopathies and intrauterine infections in newborns.

Analyzes, R-grams of the chest organs, ECG, CBC, Biochemical blood test, microtables

Final control, solving situational problems.

Consolidate the knowledge gained during a theoretical analysis of the topic

Students solve non-standard problems on this topic

Sets of tests of levels II and III, situational tasks.

Evaluation of the work done

The teacher evaluates the work at each stage

Material and technical support for the lesson

Sets of blood tests, x-rays

Album of medication annotations

A set of situational tasks on this topic.

INPUT TEST CONTROL

Which route of infection is more common in the intrapartum period:

Based on the clinical picture, make an accurate diagnosis of intrauterine infection, indicating the etiological factor:

Insert correct answer

7. The diagnosis of herpetic infection in a newborn child can be clinically made if _______________ is detected

8. Thrombocytopenia in newborns can be observed with:

7.Vesicular rash with a hemorrhagic component on the skin and/or mucous membranes

Boy 6 days old. Born from 1 pregnancy, which occurred with toxicosis. Premature birth at 34 weeks. Body weight at birth 2100g. The blood type of mother and child is the same - A (II), Rh positive. On the second day of life, the child developed jaundice, the child became lethargic, adynamic, and often vomited. On the 3rd day hemorrhagic syndrome appeared. Liver +3cm, spleen +2cm, below the costal margin. Despite the therapy, the child's condition progressively worsened, severe shortness of breath appeared, tachycardia, jaundice increased, and neurological symptoms intensified: bulging of the fontanel, dehiscence of the sagittal suture, and convulsions. A lumbar puncture was performed: protein 300 mg/l, cytosis-42. Giant cells with nuclear and cytoplasmic inclusions were found in the cerebrospinal fluid. X-ray shows signs of interstitial pneumonia. Blood test: red blood cells - 4.5×10 12 /l, HB - 150g/l. color index 0.8, platelets - 130×10 9 /l, e-1%, p-12%, s-47%, l-22%, m-8%, ESR-3mm/hour, reticulocytes - 35% , indirect bilirubin - 137 µmol/l, direct - 10 µmol/l.

Neonatology. Textbook edited by N.P. Shabalov. M., 2006, volume I, II.

National guidelines for neonatology. - M.: GEOTAR-MEDIA", 2007. - Ch. 32. - 848 p.

State budgetary educational institution of higher professional education “Orenburg State Medical.

State budgetary educational institution of higher education "Bashkir State Medical University" of the Ministry.

Peculiarities of a doctor’s work in organizing monitoring of children with infectious diseases at home

The most important functions of trade union organizations (primary, district, district, etc.)

As a result of training on the topic “Epidemiology and Prevention of HIV Infection”, students should

Embryo- and fetopathy of newborns. Diagnosis, treatment and prevention

Intrauterine development, starting from the maturation of the germ cell (gamete) to the birth of a mature fetus, is divided into progenesis and cymatogenesis. Time progenesis corresponds to the maturation of gametes (egg and sperm) before fertilization, time cymatogenesis is calculated from the moment of fertilization to birth.

The intrauterine (gestational) stage of child development (cymatogenesis) lasts 280 days (40 weeks) from the moment of fertilization to the birth of the child. Since it is impossible to accurately determine the time of fertilization, in practice gestational age is calculated starting from the first day of the mother's last menstrual cycle. The intrauterine stage is divided into three periods:

1) Blastogenesis, from the moment of fertilization to the 15th day of pregnancy, when the egg is crushed, ending with the formation of embryo- and trophoblast;

2) Embryogenesis, from the 16th to the 75th day of pregnancy, when the main organogenesis occurs and the amnion and chorion are formed;

3) Fetogenesis, from the 76th to the 280th day, when the placenta has formed, differentiation and maturation of fetal tissues occur. The period of fetogenesis is divided into early fetal period(from the 76th to the 180th day), by the end of which the unripe fetus acquires viability, and late fetal period(from the 181st to the 280th day), in which the maturation of the fetus occurs with simultaneous aging of the placenta. The late fetal period turns into a short-term intrapartum period(from the time contractions appear until the umbilical cord is ligated), which lasts from 2-4 hours.

A. If your blood glucose level is below 2.6 mmol/L (45 mg/dL) but above 1.1 mmol/L (25 mg/dL)

1. Put the baby to the breast more often. If the baby cannot be breastfed, it is necessary to give expressed breast milk using an alternative method (cup, spoon, syringe, gastric tube).

2. Determine blood glucose levels after 6 hours:

If your blood glucose level is still below 2.6 mmol/L (45 mg/dL) but not below 1.1 mmol/L (25 mg/dL), you should increase the frequency of breastfeeding and/or the volume of expressed breast milk. If blood glucose levels have not reached normal levels, consider prescribing an intravenous glucose infusion;

If blood glucose levels are below 1.1 mmol/L (25 mg/dL), treat as described below.

B. Blood glucose level is below 1.1 mmol/L (25 mg/dL)

1. Provide intravenous access if this has not already been done. Intravenously, slowly, over 5 minutes, inject a 10% glucose solution at the rate of 2 ml/kg body weight.

2. If an intravenous catheter cannot be placed quickly, administer a 10% glucose solution orally at a rate of 2 ml/kg body weight (via a gastric tube if the child cannot suck).

3. Continue intravenous administration of a 10% glucose solution in a volume corresponding to the age-related daily needs of the child (on average 90 ml/kg/day).

4. Determine blood glucose levels 3 hours after the start of treatment;

If the blood glucose level remains below 1.1 mmol/L (25 mg/dL), repeat the glucose infusion as described above and continue the infusion;

If the blood glucose level is above 1.1 mmol/L (25 mg/dL) but below 2.6 mmol/L (45 mg/dL) at each test, continue the continuous infusion and test the blood glucose level every 6 hours until it reaches 2.6 mmol/L (45 mg/dL) or more in two consecutive tests;

5. Put the baby to the breast more often. If the baby cannot be breastfed, give expressed breast milk or formula using an alternative feeding method (cup, spoon, syringe, tube).

6. With improvement of enteral feeding, reduce the volume of intravenously administered glucose slowly (over 3 days), while simultaneously increasing oral food intake.

Do not abruptly interrupt the glucose infusion.

Prognosis for DF.Perinatal mortality of children with DF is approximately 2-5 times higher than the regional average. In the group of children from mothers with diabetes complicated by proliferative retinopathy and diabetic cardiopathy, it reaches 6-10%. Although it is believed that in children with DF who survived the neonatal period and do not have congenital defects, by 2-3 months there is a complete reverse development of all signs of fetopathy, nevertheless, in 1/3-1/4 children, cerebral dysfunctions are subsequently detected (in including 2-3% - cerebral palsy, epilepsy or convulsive syndrome), approximately half - functional abnormalities of the cardiovascular system, 1/3 - carbohydrate metabolism disorders. The risk of juvenile DM in children with DF is 2% (with DM in the father - 6%).

Children from mothers with thyroid diseases. It is believed that about 0.5-1.0% of pregnant women have diseases of the thyroid gland, however, only in some of them (diffuse toxic goiter, autoimmune thyroiditis with a high titer of antibodies during pregnancy) has an increased frequency of embryo- and fetopathies, especially hypoplasia, been proven or aplasia of the thyroid gland (congenital hypothyroidism is diagnosed in 12-15% of newborns from mothers with diffuse toxic goiter) and transient dysfunction of the thyroid gland (transient neonatal thyrotoxicosis - in 1.0-1.5%).

Thyrotoxic embryopathy may develop in the case of diffuse toxic goiter in the first trimester of pregnancy, especially with the initial prescription of Mercazolil: intrauterine growth retardation of the dysplastic type and often congenital malformations - heart, kidney, microcephaly, hydrocephalus and other lesions of the central nervous system (their frequency is 5-7 times higher than in children from healthy mothers). Therefore, diffuse toxic goiter in the first trimester of pregnancy is an indication for its termination. A pregnancy that is relatively safe for the fetus is possible no earlier than 2 years after successful conservative or surgical treatment of the mother and provided that autoantibodies in her thyroid gland disappear.

Alcoholic embryofetopathy develops in 30-50% of children born to mothers suffering from chronic alcoholism. However, even conception while intoxicated is dangerous for the unborn child. Such children have a significantly lower IQ at school age, neuroses, enuresis, visual and hearing abnormalities, and increased aggressiveness are more often observed. Considering that alcohol, when consumed systematically, can cause degenerative and dystrophic changes in the germ cells before fertilization, father's alcoholism, although it does not cause alcoholic fetopathy, can be the cause of encephalopathy, manifested by the symptoms described above.

When the mother drinks alcohol in the first weeks of pregnancy, the embryotoxic effect of ethanol and acetaldehyde is revealed (the embryo lacks alcohol dehydrogenase and the activity of acetaldehydrogenase is sharply reduced) - inhibition of the synthesis of DNA and proteins (including enzymes), primarily in the rudiment of the brain. Among the pathogenetic factors of the damaging effect of alcohol on the human fetus, there are also deficiencies of folic acid and zinc, prostaglandin E, activation of free radical lipid peroxidation, impaired placental circulation and hence fetal hypoxia. In addition, with alcoholism, people usually have a number of concomitant diseases, eating disorders, and other bad habits (smoking).

Clinical manifestations of alcoholic embryofetopathy: 1) intrauterine growth retardation (IUGR) of the dysplastic (less often hypotrophic) type and the birth of a child in asphyxia;

2) craniofacial dysmorphism in 80-90% of children (microcephaly; microphthalmia with shortening of the length of the palpebral fissure in full-term and premature infants with a gestation period of more than 32 weeks - less than 14 mm, and with long periods of prematurity - less than 13 mm; flat wide root of hypoplastic nose, low forehead, high palate, flattening of the occiput; less common are epicanthus, strabismus, blepharophimosis, prognathia, a large mouth with a thin upper lip and an elongated philtrum - labial, subnasal philtrum - “fish mouth”, bevel of the upper helix and low location of the auricles, midface hypoplasia);

3) congenital malformations in 30-50% of children (heart - most often septal defects; genitals - hypospadias, hypoplastic labia in girls, vaginal duplication; anus - its closure by a septum, displacement; limbs - abnormal arrangement of fingers, hypoplasia of nails, syndactyly , clinodactyly, hip dysplasia, incomplete extension of the elbow joints; hemangiomas; excess hair, especially on the forehead; abnormal lines on the palms and other dermatoglyphics);

4) cerebral insufficiency and mental retardation with subsequent oligophrenia, hyperreactivity and aggressiveness, muscle hypotonia.

Most children with alcoholic embryofetopathy are girls. Male embryos probably die at the earliest stages of development (embryotoxic effect of ethanol).

In the neonatal period, hyperexcitability syndrome is typical; difficulties in sucking, swallowing, motor coordination, and hypoglycemia are common. Sometimes in the first hours of life, hyperexcitability is so pronounced that, along with shortness of breath, tremors, restless screaming, convulsions appear, which disappear after giving the child 0.5 g of alcohol; The child is diagnosed with alcohol withdrawal syndrome.

Subsequently, children with alcoholic fetopathy experience delayed physical development (microcephaly becomes more pronounced), dementia and other neuropsychiatric diseases, endocrine disorders. Frequent diseases of the respiratory tract in such children are caused by a defect in secretory immunity and cilia of the ciliated epithelium of the respiratory tract, and disorders of mucociliary transport.

Even in the absence of signs of alcoholic embryofetopathy at birth, children from families of alcoholics often have a low IQ, aggressiveness, speech disorders, neuroses, enuresis, epilepsy, mental retardation, visual and hearing abnormalities, i.e. prenatal alcohol exposure has a “behavioral” teratogenic effect.

At autopsies of children born with alcoholic embryofetopathy, severe malformations of the brain are found: underdevelopment of the cerebral cortex, choroid plexuses of the ventricles and cerebellum, gliosis, atypical arrangement of cell layers.

It should be noted that there is no “safe” level of alcohol consumption during pregnancy and the prohibition of its use by pregnant and lactating women is absolute.

Fetal tobacco syndrome is possible not only in active smokers (consuming more than 5 cigarettes per day), but also in passive ones.

In women, the frequency of miscarriages, gestosis, prematurity, placenta previa and abruption, and bleeding during childbirth increases; in a child - IUGR of the hypotrophic type due to intrauterine hypoxia, hypovitaminosis (in particular deficiency of folic acid, folicobalamin), accumulation of toxic substances in the fetal blood (carboxyhemoglobin, nicotine, thiocyanate), cleft lip and palate, birth with asphyxia, perinatal morbidity and mortality, including the development of sudden death syndrome.

Difficulty in adapting newborns to extrauterine life - polycythaemic syndrome, activation of the sympathetic-adrenal system with hyperexcitability syndrome, slow recovery of transient weight loss and jaundice, more active and prolonged synthesis of fetal hemoglobin and 2,3-diphosphoglycerate - signs of persistent tissue hypoxia.

In addition, the child, both in the neonatal period and in the future, increases the risk of breathing disorders during sleep (noisy, wheezing, snoring), pulmonary pathology (ARVI, bronchitis), delayed psychomotor and physical development, sudden death syndrome during the first 8 months life.

It is also believed that the consequence of antenatal exposure to tobacco may be a decrease in intellectual abilities and an early tendency to smoke. There are studies that have established that the birth of children with congenital malformations that affect the fate of the child is 2 times more common among fathers who are heavy smokers.

Smoking can also reduce a mother's milk supply, and nicotine, a product of cigarette smoke, can be found in a mother's milk.

Children of mothers with substance abuse and drug addictions. In modern cities, 2-3% of children are born to mothers who are drug addicts or substance abusers. As a rule, substance abusers and drug addicts use more than one substance, they abuse a variety of medications, and, in addition, smoke, drink alcohol, have concomitant diseases (anemia, cardiopathy, liver disease, kidney disease, nervous system, mental disorders), diseases transmitted sexually.

Women drug addicts, as a rule, are dystrophic and often live in poor living and social conditions. Pregnant drug addicts usually turn to medical institutions late or do not register with the antenatal clinic at all.

Of course, each of the substances listed above has specific features that determine the characteristics of maternal pathology, damage to the embryo and fetus, but there are also general effects that occur with high frequency:

1) miscarriage, miscarriages and stillbirths;

2) gestosis, eclampsia, abnormal fetal positions, placental pathology (previa, abruption, placental insufficiency, and hence chronic fetal hypoxia);

3) IUGR of the fetus of the hypoplastic or hypotrophic and even dysplastic type;

4) abnormal labor (premature rupture of water, weakness of labor, chorioamnionitis);

5) antenatal encephalopathies in the fetus (primarily anomalies of brain development - both visible, obvious congenital defects and defects revealed only with additional studies), congenital defects of a variety of organs and systems (heart, genitourinary system), often combined, or an abundance of stigmas of disembryogenesis;

6) birth of children in asphyxia with aspiration of meconium;

7) intracranial hemorrhages in children;

8) pulmonary pathology in the early neonatal period;

9) perinatal infections in a child, including those due to perinatally acquired immunodeficiency;

10) maternal and perinatal mortality, sudden death syndrome in a child both in the neonatal period and later.

Of course, a particular child, as a rule, does not have all of the listed pathologies. For example, it is believed that the main problem for children of cocaine-using mothers is prematurity.

The most typical problem for a neonatologist when working with children of mothers who are drug addicts and substance abusers is the development of abstinence in them - drug deprivation syndrome.

Withdrawal syndrome can develop in newborn mothers who are drug addicts and substance abusers, as well as alcoholics or those who were treated shortly before birth with barbiturates, tranquilizers, antidepressants, diphenhydramine and other histamine blockers. The clinical picture of withdrawal syndrome is characterized by profuse sweating, increased neuro-reflex excitability with a “piercing” unemotional cry, chaotic motor activity with “freezing” in pretentious poses, hyperesthesia and hyperacusis (the child reacts by crying to swaddling, an attempt to be picked up, a sharp sound, a sharp light), tremors, increased tendon reflexes, “convulsive readiness” or convulsions; sleep disorders, persistent finger and hand sucking, but poor sucking from the breast or bottle, regurgitation, “choking” (children “choking”), vomiting, diarrhea, abdominal distension, nasal congestion, sneezing, tachycardia or bradycardia, tachypnea or shortness of breath, seizures apnea for more than 10 seconds, various types of periodic breathing, muscle hypertension, clonus, nystagmus, rapid cooling or overheating, vegetative-vascular disorders (“marbling” of the skin and its increased vulnerability, Harlequin symptom), subfebrile and sometimes febrile body temperature, severe transient jaundice .

The diagnosis is based on a thorough medical history of the mother, conversations with her relatives and people around her, analysis of the clinical picture of the mother and child, data from a drug test of the urine of the mother and child, and sometimes their blood.

The diagnosis of withdrawal syndrome is made on the basis of a total score on the L. Finnegan scale - 9 points or more.

System for assessing neonatal abstinence syndrome (according to L. Finnegan, modified by J. Yoon)

Typically, abstinence syndrome clinically occurs immediately after birth, most often in the first 72 hours of a newborn’s life, but its delayed appearance is possible and even in the 2-3rd week of life. The duration of acute manifestations is usually from several days to a week, although longer cases have been described - even up to several weeks.

Treatment is carried out according to the following scheme. It is advisable to place mother and child in the same room and have constant contact (kangaroo type). The child must be fed more often - 8-10 times a day; hypercaloric formulas are useful for artificial feeding. A protective regimen and minimization of injections are indicated. Among medications for very strong agitation of a child, convulsions, the first choice is phenobarbital: the first day at a “loading” daily dose of 20 mg/kg, divided into 3 doses, and then 4.5 mg/kg per day once.

Loading doses of phenobarbital are not prescribed if the child has respiratory distress syndrome, especially if breathing with continuous positive airway pressure (positive expiratory pressure) is used. The drug of second choice is diazepam (Seduxen, Sibazon). We must remember that the maximum clinical severity of withdrawal syndrome is the 3rd-5th days of life, and then its intensity decreases. The duration of pharmacotherapy is usually at least 7-10 days. Other therapy is symptomatic; for example, for asphyxia, the administration of nalorphine (0.01 mg/kg) is indicated.

In follow-up, such children are often diagnosed with delayed psychomotor and physical development, hearing deficits, low IQ, abnormalities of sexual development and behavior.

Industrial fetal syndrome is a recently identified and not yet clearly defined syndrome, characterized by prematurity or IUGR of all types, difficulty adapting to extrauterine life, pronounced transient jaundice, the child’s tendency to increased bleeding due to vitamin K deficiency, infections, large losses of initial body weight and its slow recovery, neurological disorders.

The syndrome is identified due to environmental hazards, environmental pollution with products of incomplete combustion of oil, dioxidine, lead, silicon, herbicides and other industrial emissions. The accumulation of the mentioned and other products in the placenta leads to disruption of its barrier and other functions, intrauterine hypoxia and trophic disorders in the fetus, primarily to disruption of the functional state of the liver and brain. It is clear that such children have an increased incidence of birth with asphyxia and neurological disorders both in the neonatal period and in the future.

The teratogenic effect of the following xenobiotics has been established: gasoline vapors, dioxins, isocyanates, carbon monoxide, pesticides (hexachlorocyclohexane, diphenylchloroethane, chlorophos), polychlorinated hydrocarbons, mercury, lead, toluene.

It is believed that an increased frequency of this syndrome is observed in women living near gas stations, intersections of major roads, in large environmentally unfavorable cities, working as drivers, at gas stations, chemical industry enterprises, and with pesticides in agriculture. Of course, in each specific case it is necessary to carefully evaluate the mother’s medical history, age and state of health, working conditions, placenta, and only then make a judgment. Each chemical causes specific damage. For example, with massive contact of a pregnant woman with methylated mercury, in 60% of cases the fetus develops microcephaly, and then delayed psychomotor development, blindness, deafness, spasticity, convulsions, and eye abnormalities are detected; with lead – increased incidence of stillbirths and miscarriages, brain malformations.

Radiation embryopathy. It is believed that it occurs when a pregnant woman is exposed to radiation in the early stages, but does not have a specific picture: IUGR of the hypoplastic type with microcephaly and sometimes nephropathy, and later, to varying degrees, pronounced defects in psychomotor development. In later life, there is an increased incidence of leukemia, malignant tumors, and infertility. The most sensitive indicator of possible radiation embryopathy is an increased frequency of a complex of cytogenetic abnormalities in peripheral blood cells. Such anomalies were found in 39% of persons 20 years of age exposed to radiation in the womb at a dose of about 100 rad or more (2% in the control group).

Drug embryofetopathies. Currently, about 5 million drugs and xentobiotics are known that humans have contact with, but only 1600 of them have been studied in experiments on pregnant animals. At the same time, the risk of side effects of drugs on the fetus in humans is quite difficult to assess, because in this case it is necessary to take into account the mother’s diseases, both recognized and unrecognized, complications of pregnancy, the nutrition of the pregnant woman and her existing hypovitaminosis, genotype, age of the mother and father, their occupational hazards, the frequency of spontaneous defects, the environmental situation and, probably, some unknown factors.

There are embryotoxic, teratogenic and specific and nonspecific pharmacological effects of drugs and xentobiotics (foreign chemicals for humans) on the fetus.

Embryotoxic effect xenobiotics is the negative effect of the substance on the zygote and blastocyst located in the lumen of the fallopian tubes or in the uterine cavity. The consequence of embryotoxicity can be termination of pregnancy, the formation of twins, and developmental defects with disruption of the embryonic axis.

Teratogenic effect – the ability to disrupt the normal development of the embryo and cause the appearance of various congenital defects and anomalies. The most dangerous periods in this regard are the days of intrauterine life.

Specific and non-specific pharmacological effect of drugs on the fetus used to treat the intrauterine patient (for example, with cardiac arrhythmias in the fetus), but it can also lead to complications developing as in the fetus (drug fetotoxicity), and manifests itself only in a newborn.

There is a group of drugs whose embryotoxic, teratogenic effects have been established or there are serious reasons to assume their embryotoxicity (class D): androgens, their derivatives (including danazol, retabolil, etc.) and antiandrogens, estrogens, antiestrogens, progestogens, antithyroid and oral antidiabetic drugs , oral contraceptives (taken during pregnancy), anticancer drugs, antimetabolites, antiepileptic drugs (especially diphenin), antimalarial drugs, D-penicillamine, oral anticoagulants - vitamin K antagonists, inhalational anesthetics (for department staff), streptomycin, tetracycline, thalidomide . These drugs should not be prescribed to pregnant women unless there are life-threatening conditions in the mother for which they need to be used (for example, lymphogranulomatosis or other tumor diseases, epilepsy with recurrent seizures).

The second group includes drugs whose embryotoxic effect is controversial (class C): corticosteroids, tranquilizers, antidepressants, antipsychotics, thyroid hormones, antiemetics, antituberculosis and anti-inflammatory drugs (salicylates), sulfonamides, barbiturates, diuretics, antihistamines. These drugs should not be widely prescribed to pregnant women in maximum doses and, if possible, prescribed in short courses; they should be avoided in the first two months of pregnancy. Since the mid-80s in England, acetylsalicylic acid (aspirin), prescribed in a dose of 1-2 mg/kg/day, has become widespread in the treatment of gestosis. At this dose, aspirin, while inhibiting the synthesis of thromboxane A2, does not change the synthesis of prostacyclin and other prostaglandins that vasodilate and inhibit platelet aggregation, which leads to an improvement in the rheological properties of blood, blood flow in the placenta, and sharply reduces the severity of uteroplacental insufficiency and fetal hypoxia. Aspirin is given for a long time - several months, without any complications in the fetus. However, aspirin should be stopped 2 weeks before birth. Treatment with acetylsalicylic acid is contraindicated for women with hemorrhagic diathesis, in particular with hereditary thrombocytopathies.

Mothers with hereditary thrombocytopathies (approximately 5% of all women) may experience bleeding of varying severity, which they can transmit to the child, not only when treated with aspirin, but also under the influence of several platelet inhibitors prescribed simultaneously.

Drug fetotoxicity can cause various pathological syndromes in newborns.

Hemorrhagic disease of newborns is promoted by anticonvulsants (suxilep), salicylates, indirect anticoagulants, carbenicillin, antidiabetic sulfonylurea derivatives, hypothiazide, and furosemide prescribed to mothers shortly before birth.

Hyperbilirubinemia can be caused by sulfonamides, chloramphenicol, barbiturates, amidopyrine, phenacetin, antipyrine, PAS, novobiocin, and glucocorticoid hormones prescribed in the last stages of pregnancy.

Asphyxia at birth , The delay in the appearance of the first breath is caused by narcotic drugs and general anesthetics.

Swelling of the nasal mucosa and hence obstruction of the nasal passages in newborns can be caused by antihypertensive drugs taken by the mother shortly before birth (reserpine and others). These same drugs can lead to fetal bradycardia and paralytic ileus.

Low birth weight can be caused by a course of chloramphenicol prescribed to the mother before childbirth (in addition, “gray syndrome”, bloating, collapse and anemia), aminoglycosides (along with deafness), and beta blockers.

Respiratory distress syndrome may be facilitated by the use of ethanol to suppress preterm labor.

Heart failure in a newborn can be provoked by the mother's prescription of salicylates and indomethacin during pregnancy, because they, by inhibiting the synthesis of prostaglandins, cause spasm of the fetal ductus arteriosus.

Fetoplacental insufficiency, or fetal distress, is the most universal symptom complex reflecting the unfavorable state of the fetus, which can be briefly described as follows:

Symmetrical (hypoplastic) or asymmetrical (hypotrophic) forms of intrauterine growth retardation (IUGR).

Disturbances of fetal cardiac activity (episodes of accelerated pulse to beats per minute, extrasystoles, episodes of slowed pulse with a frequency of less than 110 beats per minute).

Changes in the frequency of fetal respiratory movements (FRM): increase - more than 60 per 1 minute, decrease - less than 45 per 1 minute, shortening of the duration of FRM to less than 30 seconds, absence of FRM.

Changes in the motor activity of the fetus (one or two episodes of generalized movements, isolated movements of only the limbs, erratic motor activity of the fetus, absence of movements).

Changes in the tone of the fetus (the torso does not straighten, only extension movements of the limbs are recorded, the extended position of the fetus, the absence of return during movements to the initial position of flexion).

Abnormalities of the placenta (according to ultrasound data) - signs of a lag or advance in the degree of maturity of the placenta (state of the placenta that does not correspond to the gestational age), abnormal location, pathological inclusions in the placenta, placental edema.

Changes in the volume of amniotic fluid (polyhydramnios, oligohydramnios).

The most clear data for recording fetoplacental insufficiency in the fetus is obtained by assessing the “biophysical profile” of the fetus and Doppler measurements (assessment of blood flow in the umbilical cord arteries, aorta and middle cerebral artery). The most common manifestations of fetoplacental insufficiency in a newborn are: birth in a state of asphyxia or respiratory depression, signs of IUGR, impaired adaptation to extrauterine life conditions, and increased infectious morbidity.

Multiple pregnancy. The incidence of twin births is approximately 1:80 births, with variations in different countries - from 1:500 births in Asia to 1:20 births in Africa. Monozygotic pairs account for approximately 30% and dizygotic pairs for 70% of all twins. In twins, the incidence of IUGR and congenital malformations is increased, especially in monochorionic monozygotic twins. Approximately 10% of twins have feto-fetal transfusion with polycythemia in one and anemia in the other. If this occurs in the early fetal period, the consequences can be very severe for both fetuses.

With a frequency of 1:35,000 births, reverse arterial perfusion syndrome occurs with acardia or acephaly in one of the twins and provision of blood flow at the expense of the other. There are also conjoined twins - thoracopagus (common chest), xyphopagus (common anterior abdominal wall - from the xiphoid process to the navel), picopagus (common gluteal region, buttocks), craniopagus (common head).

A twin born second has a 2-4 times higher risk of developing asphyxia, SDS syndrome, while infectious complications are more common in the first twin.

In the last decades of the 20th century, a fundamentally new direction in medicine arose - fetal therapy. When diagnosing hemolytic disease (erythroblastosis) in a fetus, replacement blood transfusions are performed; for anemia, red blood cell transfusions are performed through the umbilical cord vessels, and recombinant erythropoietin is administered.

If hypothyroidism is detected in the fetus, thyroxine is injected into the amniotic fluid, adrenogenital syndrome - dexamethasone is prescribed to the pregnant woman, severe cardiac arrhythmias and other cardiac disorders - β-blockers, calcium channel inhibitors, cardiac glycosides, etc.

If congenital malformation is detected in the fetus, the obstetrician, pediatric surgeon and pediatrician collegiately discuss the tactics of labor management, management and treatment of the child immediately after birth. According to the literature, consultation with a surgeon is necessary in approximately 5% of pregnant women. Currently, many successful intrauterine surgical interventions in the fetus have been described - the application of a nephrostomy or the creation of a vesico-amniotic shunt for obstructive nephropathies and fetal hydronephrosis, thoracentesis for hydrothorax, removal of embryonic tumors, etc.

For ante- and perinatal pathology, prevention is complex and begins even before pregnancy; it must be of a state nature and be primary and secondary.

How conditioned gametopathies?

Gametopathies include a wide range of pathological conditions that arise as a result of mutations in the germ cells of the child’s parents (sporadic mutations) or in distant ancestors (inherited mutations), as well as due to damage to gametes during the formation, formation and maturation of germ cells.

How conditioned blastopathy?

Blastopathy- a broader concept that includes disorders of gametogenesis, as well as all pathological processes in a free or fixed blastocyst and during its implantation through the uterine epithelium into the endometrium, i.e. during the first 1 2-1 5 days after fertilization. They develop under the influence of damaging factors (alcohol, chemicals, radiation, pregnancy complications, extragenital and infectious diseases of the mother).

Classification of blastopathy:

1) Blastopathies that led to early elimination of the embryo (in the first weeks of pregnancy).

1. Anomalies in the development of the blastocyst, amniotic cavity and yolk sac.

2. Empty embryo sac due to aplasia or embryoblast resorption (without amnion, amniotic stalk and yolk sac).

3. Hypoplasia of the amniotic cavity with partial or complete extra-amniotic location of the embryo in the coelom.

4. Aplasia, hypoplasia or calcification of the yolk sac.

5. Twin defects: thoracopagus, ischiopagus, etc.

6. Unspecified early blastopathies: abnormal blastocyst, complete topographic inversion of the embryoblast.

2) Blastopathies that caused severe disturbances in the embryo and fetus in the first months of pregnancy.

1. Pathology of blastocyst implantation - ectopic development of pregnancy (ovarian, tubal and intraperitoneal).

2. Intrauterine ectopia: implantation of a blastocyst in the uterine horn, at the internal os of the cervical canal - low attachment and placenta previa, in the cervical canal - cervical pregnancy.

3) Blastopathy with delayed clinical effect.

1. Violations of the depth of implantation - superficial implantation - hypoplasia and disturbances in the shape of the placenta.

2. Deep implantation: placenta circumvallata, fenestrata, marginata, membranacea, accreta, placenta accreta (Fig. 13.3).

3. Lateral and marginal orientation - shell or marginal attachment of the umbilical cord.

4. Blastopathy during artificial insemination. What such embryopathies?

Embryopathies include pathological changes in the differentiation of cells and tissues of the embryo, developing in the period from the 20th day to 1-2 weeks after fertilization, leading to the occurrence of fetal malformations, delay or death of the embryo.

Classification of embryopathy:

1) Defects of the initial histogenesis of the embryo (from the 13th to the 19th day of gestation).

1. Anomalies of the axial complex in the embryo of 6-8 presometic stages.

2. Hypo- and aplasia of the notochord and neural plate.

2) Defects of the initial organogenesis of the embryo (from the 20th to the 34th day).

1. Panorganodysplasia with anomalies in the external shape of the embryo at 9-1 2 and 1 3-1 5 post-somitic stages.

2. Unaccounted for anomalies in early miscarriages.

3) Pathology of late organogenesis of the embryo (from the 35th to the 70th day).

1. Congenital cystic cervical lymphangiomas.

2. Single and multiple malformations of organs and systems.

3. Non-developing pregnancy.

What such fetopathy?*,

Fetopathies- these are diseases and functional disorders that occur in the fetus under the influence of exogenous influences during the period from the 13th week of pregnancy to birth.

Which exist kinds fetopathy?

Depending on the pathogenesis and etiological factor, infectious and non-infectious fetopathies are distinguished.

What include To infectious fetopathies?

Infectious include fetopathy that occurs under the influence of an infectious agent and tends to generalize, accompanied by specific changes in the fetus (congenital syphilis, tuberculosis, infections classified as the TORCH complex).

"Obstetrics in Questions and Answers"

What include To non-infectious fetopathies?

Non-infectious fetopathies include diseases of the fetus that develop as a result of placental insufficiency and metabolic disorders in the fetus during pregnancy complications and extragenital diseases (hypoxia, fetal malnutrition; hemolytic disease of the fetus; congenital generalized arterial calcification; myocardial fibroelastosis; diabetic, thyrotoxic, alcoholic fetopathy).

What such critical period?

Critical period- this is a period of development characterized by increased sensitivity of the embryo and embryo to the damaging effects of various factors.

Which exist critical periods?

The first critical period occurs at the end of the first and the entire second week of gestation. The effect of the damaging factor is realized, as a rule, in the form of the death of the embryo.

The second critical period occurs at 3-6 weeks of gestation. For antenatal damage, the most dangerous period in general is the first trimester, when the mother-placenta-fetus system is just emerging and the connections between its individual components are still fragile.

The third critical period is the last month of pregnancy, which is characterized by a significant dissociation between the cessation of placental weight gain and the rapid increase in fetal weight.

The cause of embryopathy can be hereditary genetic disorders, infectious diseases, intoxication with poisons, lack of oxygen, radiation and other pathogenic influences transmitted from the mother to the embryo. Embryopathies lead to disruption of the formation of embryonic organs and are the cause of malformations of organs and body parts, spontaneous abortions.

To prevent embryopathy, it is important to protect the woman’s health in the first months of pregnancy (see Antenatal fetal care).

Embryopathies (from the Greek embryon - uterine fetus, embryo and pathos - suffering, disease) are diseases of the embryo that arise during the period of embryogenesis - the main primitive formation of the most important organs.

Embryogenesis begins from the middle of the first month and ends with the third month of intrauterine life (Fig.).

Pathology of the prenatal period according to Gertler (scheme): I - pathology of progenis; II-V - pathology of the embryo (days 1-280): II - pathology of the period of blastogenesis (days 1-15); III - pathology of the embryogenesis period (16-75th day); IV-pathology of the fetal period (day 76-280); V - pathology of placenta development (15-280th day). 1-ovary; 2 - testicle; 3 - embryoblast; 4 - trophoblast; 5- amnion; 6 - embryo; 7 - chorion; 8 - fruit; 9 - placenta.

Any damaging effect on the embryo causes either its death or a disruption of the formation processes, called a developmental defect. Consequently, embryopathies manifest themselves in the form of malformations of organs or parts of the body of the embryo. In addition to morphologically expressed developmental defects, functional disorders of organs and systems (of an enzymatic and metabolic nature) are also observed. Such functional embryopathies may be identified later in the individual's life.

Using embryological data, it is possible to judge, to a certain extent accurately, the time of onset of embryopathy, since the organ is most sensitive at the moment of the highest mitotic activity of the tissue primordia that form it. The main determining point in the occurrence of a particular developmental defect is the time when the harmful agent had its effect on the embryo; for example, different agents (radiation energy, maternal diabetes) can lead to the same malformation (anencephaly) if their influence took place in the 3rd week of embryonic life. However, the role of the characteristics of the harmful agent itself cannot be excluded, since the tropism of this agent to certain tissues of the embryo is of undoubted importance (for example, the rubella virus primarily affects the tissue lining of the lens, milk teeth, inner ear, heart; the epidemic hepatitis virus affects the lining of the liver and gall bladder moves).

The causes of embryopathy can be endogenous (genotypic) and exogenous (various influences from the mother’s body). The teratogenic effect of various exogenous influences depends on the genetic characteristics of a particular subject. Thus, in experiments on animals of genetically different strains, the number of developmental defects obtained under the influence of exogenous influences is not the same.

Very little is yet known about particular forms of human embryopathies. Among embryopathies of viral origin, the most fully studied is rubeolar embryopathy, which, depending on the duration of the mother’s illness with rubella, is expressed in malformations of the eye, inner ear, heart, and tooth buds. It is believed that influenza, epidemic hepatitis, polio, Coxsackie, and cytomegaly viruses also have a teratogenic effect.

Diabetic embryopathy is observed in 3-12% of cases in children whose mothers suffer from diabetes; in this case, intestinal atresia, heart defects, malformations of the limbs, skull and anencephaly occur.

Human radiation embryopathies have been little studied. Residents of Hiroshima and Nagasaki who suffered from the atomic bomb suffered miscarriages, the birth of premature fetuses or fetuses with functional impairments; There was no noticeable increase in developmental defects.

Drug-induced embryopathies have been widely studied experimentally. The teratogenic effect of sulfonamides, some antibiotics (tetracycline, terramycin, auromycin), hormones (corticosteroids, insulin), cytostatics (aminopterin), and vitamins has been established. Thalidomide embryopathy, which occurred in West Germany after the use of thalidomide to pregnant women, became famous. At the same time, children were born with malformations of the limbs. Some researchers point to the teratogenic effect of quinine (malformations of the neural tube, limbs). There is still little reliable information regarding other drug-induced human embryopathies.

The prognosis of embryopathy of the most important organs is unfavorable for life. In some cases, surgery is possible. Prevention is of decisive importance - protecting a pregnant woman (especially in the first weeks of pregnancy) from all kinds of harmful influences, including the use of active drug therapy. It must be borne in mind that embryopathy can be combined with fetopathy (see). In these cases, active therapy of the newborn is required, if possible, of a specific nature. See also Defects, development.