NPP GA, even if the 2008 edition is a non-existent document of a non-existent department of a non-existent country. This document is nowhere in new Russia not registered.

The amazingness of our country is manifested in the fact that, having FAPs, we accept points from the NPP and include them in the RPP, despite the differences between the NPP and FAP. I'm not even talking about the fact that pilots are deprived of their coupons on the basis of violations of the NPP of the USSR Civil Aviation, issued by the MGA for Aeroflot.

FAP Flight operations in the Russian Air Force:

33) “decision altitude” - the altitude established for a precision approach at which the missed approach maneuver must be initiated if, before reaching this altitude, the pilot-in-command has not established the necessary visual contact with landmarks to continue the approach the landing or position of the aircraft in space, or the parameters of its movement do not ensure safe landing (hereinafter referred to as VPR);

95) “precision approach” - an instrument approach with navigation guidance in azimuth and glide path, generated using electronic means;

56) “minimum descent altitude” - the height established for a non-precision approach, below which the descent cannot be made without the necessary visual contact with landmarks (hereinafter referred to as MAF)

57) “non-precision approach” - an instrument approach without navigation guidance along a glide path generated using electronic means;

Here someone wrote about visual approach:

21) “visual approach” - an approach when the spatial position of the aircraft and its location are determined visually by the crew using the natural horizon, earthly landmarks, as well as in relation to other material objects and structures;

Visual approach according to GMP is a mixture of a hippopotamus and a crocodile, and is more similar to Circling Approach with its visual maneuvering zones established for aircraft categories.

By the way, in FAP PiVP, FINALLY, they separated “visual approach” (almost like according to Doc 4444), and “circling approach” (practically, Circling Approach)

11.5.14. A circling approach is performed:

with continuous visual contact with the runway threshold or approach lighting aids;
during the day and at dusk at airfields for which such an approach is provided.
At dusk, the approach is carried out with the runway lighting equipment turned on.
The flight crew ensures that the aircraft remains within the established visual maneuvering zone.
An approach to land from a circle at a controlled aerodrome is carried out after receiving permission from the ATS unit in accordance with the procedure developed by the operator using aeronautical information collections (based on flight instructions or an air navigation passport).
The instrument descent according to the established circling approach pattern is carried out to the altitude established at the start point of the approach along the prescribed trajectory or indicated by the ATS unit.

11.5.15. The descent of the aircraft in the visual maneuvering zone after the start of the turn onto the pre-landing straight and on the pre-landing straight is possible if there is visual contact with ground landmarks and the runway.
If visual contact with the runway is lost at any point in the visual maneuvering zone, the flight crew stops descending and performs a flight towards the runway with a climb and entering the aborted approach (missed approach) pattern using instruments.

11.5.16. The visual approach is carried out in accordance with the procedures
specified in the collection of aeronautical information or with the flight instructions (air navigation passport) of the aerodrome, or in another established manner.
A visual approach may be initiated at any point on the arrival route or at any point on an instrument approach pattern, provided that the necessary visual contact is established with landmarks and the runway.
At a controlled aerodrome, permission from the ATS unit is required to perform a visual approach.
The flight crew reports to the ATS unit that visual contact with the runway has been established.
A visual approach is carried out provided that the height of the cloud base is not lower than the minimum flight altitude at initial stage landing approach, and visibility is not less than:

5 km – at an airfield located in a flat, hilly or mountainous area with a relief height of up to 1000 m;

8 km – at an airfield located in a mountainous area with a relief height of 1000 m or more.

When two aircraft of the same type are making a simultaneous visual approach, the aircraft flying ahead, to the left or below has priority in the approach.
The flight crew of the lighter aircraft allows the heavier aircraft to land first.

A visual approach cannot be conducted unless the flight crew is familiar with the terrain and landmarks on which the approach procedure is based.

Do you feel the similarity between a visual approach according to the GMP and a “circling approach” according to the FAP PiVP?

Analysis of flight accidents has never shown that the cause of the disaster is incorrectly calculated minimums or their small values.

There are two main parameters in the minimums: VPR (MVS) and L-view.

This safe altitude takes into account obstacles in areas whose size and configuration are related to the precision characteristics of a particular landing system and the speed category of the aircraft.

All existing methods for determining VPR(MVS) are based on OCA/H, which is published in the AIP.

Therefore, the cause of accidents during landing is not the low values ​​of the minimums (no matter which of the existing methods they are calculated), but their violation.

It is necessary to propose measures to ensure that under no circumstances does the crew descend below the VTOL/MVS without reliable visual contact and full confidence in the safety of the landing.

If, upon reaching the VPR/MVS or MAPt point, the PIC has not established reliable visual contact with ground reference points, or has established, but the position of the aircraft in space, or the parameters of its movement do not guarantee a safe landing, then a missed approach maneuver must be performed.

Landing minimums

Factors influencing the calculation and determination of minimums:

• radio guidance equipment: guidance accuracy, location relative to the runway;
• lighting equipment for approach and runway;
• accuracy of onboard guidance and control systems;
• rules and methods for constructing an obstacle registration zone (definition of OSA/N);
• the value of the height and location of the obstacle falling within the obstacle registration zone;
• aircraft category;
• the value of the minimums published in the Aircraft Flight Manual;
• methodology for determining minimums.

Which technique is better?

A methodology for determining aerodrome minima for takeoff and landing can be considered good when it contains:

• all existing guidance aids at the final stage of landing, all types and modes of approach;
• all the variety of lighting equipment, taking into account their possible failures;
• all on-board equipment options, including HUD, HUDLS, EVS;
• requirements and recommendations for preparing pilots for landing approaches at certain minimums;
• recommendations to operators on establishing operating minima.

Based on these criteria, we will consider existing methods.

Existing methods for determining minimums

Russia:

• Order of the DVT of the Ministry of Transport of the Russian Federation No. DV-123/38 dated September 20, 1993 “On implementation in practice civil aviation visual approaches to landing aircraft of 1-3 classes";
• Directive of the DVT of the Ministry of Transport of the Russian Federation dated December 14, 1994 No. 172/i “On establishing minimums for takeoff and landing of aircraft of the B-757, B-737 type”;
• Order of the DVT of the Ministry of Transport of the Russian Federation dated December 28, 1993 No. DV-160 “On the establishment of categories for Russian civil aviation aircraft in accordance with ICAO rules and on the introduction of a methodology for determining aerodrome minima for visual approach”;
• FSVT Order No. DV-86 dated 08.08.1994 “On the implementation of the “Guidelines for constructing airfield layouts and determining safe obstacle clearance heights”;
• Order of the Ministry of Defense of the Russian Federation and the Ministry of Transport of the Russian Federation dated December 15, 1994 No. 270/DV-123 “On the implementation of the Unified Methodology for Determining Minimum Aerodromes for Takeoff and Landing of Aircraft” (hereinafter referred to as EM);
• Letter of the FAS Russia dated 07/09/1997 No. 53/i “On the publication of minimums for take-off and landing of aircraft at foreign airfields in aeronautical information documents.”

ICAO. All Weather Operations Manual, Doc 9365, 1991 edition.

USA. Order 8260.3, U.S. Standard for Terminal Instrument Procedures (TERPS), 25th amendment dated 03/09/2012.

Jeppesen Explanation of Common Minimum Specification (ECOM). Based on TERPS.

States EU. EU OPS Subpart E - All Weather Operations, Appendix 1 (New) to OPS 1.430 New. Aerodrome Operating Minima. Applicable from 07/16/2011

Brief comparative analysis of methods

Unified methodology:

1. ILS precision approach - no definition of Category III minima;
2. non-precision approach is limited for use by the RTS set;
3. training minimums apply;
4. there is no procedure for determining the minimum when:
   • application of area navigation;
   • performing a continuous descent during a non-precision approach;
   • application of HUD, HUDLS;
5. the MBC-RVR/VIS ratio is conservative;
6. approach lighting equipment is not divided according to the length of the approach lights;
7. the value of recalculated meteorological visibility in RVR/CMV is not used;
8. no minimums are established for alternate airfields.

Doc 9365 :

1. Approach minimum is not considered:
   • according to ILS for Category IIIC;
   • area navigation method;
2. there is no mention of helicopters;
3. not considered:
   • use of light visual glide path;
   • setting a minimum with AVP;
   • minimum for alternate airfields.

TERPS- largely harmonized with EU OPS, but there are differences:

1. considered:
   • establishing a minimum for Category I, II, III;
   • use of 4 types (lengthwise) of travel lights;
   • approach using area navigation: LPV, LNAV/VNAV, Baro VNAV (difference);
   • trajectories for glide path angles 3° - 6.4° (difference);
   • minimums for military aviation (difference);
   • minimums for helicopters (difference);
   • visibility value when using HUD;
2. the use of a light visual glide path is not considered;
3. The main difference is that obstacle registration zones and the definition of OSN are considered.

EU O.P.S.

Differences from TERPS:

1. application considered:
   • HUD, HUDLS, EVS;
   • CDFA (continued descent on final approach);
   • conversion of meteorological visibility to RVR/CMV;
   • RNAV/LNAV (horizontal area navigation);
   • VDF direction finder;
   • Categories I, II and IIIA, IIIB.
2. There are no minimums for helicopters.

Unified methodology

All Weather Flying Guide,Doc 9365 - to operators and aerodrome States to have an understanding of the methodology for developing aerodrome operating minima.

Commercial transport aircraft (multi-engine aircraft).

EU OPS- on the operators.

TERPS- to airfields and operators.

Data taken into account when determining landing minima

Approach systems used

Comparison of approach lights

Comparison of approach lights in the Russian Federation data as of 01/01/12

Definition of OCH

For an ILS approach, the OCH is determined the same way in all methods.
In the USA, for non-precision approaches, OCH is determined according to TERPS.
EU OPS uses Doc 8168 Vol. 2.
In Russia, the Guidelines for constructing airfield schemes and determining safe obstacle clearance heights (hereinafter referred to as the Guidelines) are used.

The guidance considers the definition of DOS for:

• OSB excluding additional zone;
• VOR without taking into account the additional area in the missed approach phase;
• PRL without taking into account the additional zone;
• KRM, but the minimum is not published;
• RNAV10 for the initial segment and RNAV4 for the final segment.

Comparison of methods according to the ratio VIS/RVR - VPR/MVS

Takeoff Minima

USA. Minimums less than standard

In FAP 128, in the section Aerodrome Operating Minima, there is no information at which points the RVR value for takeoff should be presented.

Publication of minimums by region by ICAO states as of 03/01/2012.

Appendix 6. Part I, paragraph 4.2.8 Aerodrome operating minima

Note. This Standard does not require the State in whose territory the aerodrome is located to establish aerodrome operating minima.

Status and publication of minimums in Russia

• In the Russian AIP, minimums for takeoff and landing are not published, but OCA/N for landing approaches are indicated.
• Conclusion: in Russia state minimums are not established.
• In the IPP, minimums are calculated by the airport using EM and then published in the CAI on-board collections.
• Reasons for publishing the minimums: Order of the Ministry of Transport of Russia dated January 31, 2011 No. 29 “On approval of standard instructions for flight operations in the area of ​​an air hub, aerodrome (heliport) and standard diagrams of the aeronautical passport of an aerodrome (heliport), landing site.”

Clause of the order of the Ministry of Transport of Russia No. 29

• 2.3. Minimums for airfields and air hub heliports.
• Minimums of airfields and air hub heliports for takeoff and landing according to instrument flight rules. Minimums for failures of individual means of radio technical support for flights, aviation telecommunications, lighting and meteorological equipment.

FAP 128 is defined in clause 5.17. The operator shall establish operating minima for each aerodrome used based on the methods set out in the Operating Procedures.

Appendix 6. Part I. International commercial air transport. Aircraft.

4.2.8 Aerodrome operating minima

4.2.8.1 The State of the Operator requires the operator to establish operating minima for each aerodrome used for operations and approves methods for determining such minima. ...

Different minimums

• The minimum determined by the operator and the airport may be different.
• Therefore, the status of the minimums in the IPP and in the CAI collections is not clear, because CAI collections are not a document approved by the authority in the field of civil aviation. The CAI collections are a commercial product the same as the JEPPESEN collection.
• The aviation community is divided on whether an airport should define and publish minimums? But clearly, his task is to calculate and publish OCA/N for each landing system and provide information about lighting equipment.
• To monitor compliance with minimums by ATS authorities, operators can be invited to submit their minimums to interested structures based at the airport.

The operator decides, and the Federal Air Transport Agency agrees on the methodology.

The conditions for agreeing on the methodology are:

1. VPR/MVS values ​​are not lower than safe heights in accordance with Doc 8168 PANS OPS;
2. it is possible to establish minimums for all used landing aids and methods on specific types of aircraft, taking into account various combinations of technical and visual guidance aids;
3. contains rules for the preparation and admission of crews for landing approaches in adverse weather conditions.

What methods should be used to determine minimums?

• EM corresponded to the equipment of the generation of aircraft created in the 70-80s. She showed her worth. You can express your gratitude to the creators of EM: Belogorodsky S.L., Muzalev A.A., Roizenzon A.L. and other authors and continue to use it for this aircraft fleet.
• The emergence of aircraft with greater navigation capabilities suggests that it is necessary to use modern methods for determining operating minima.
• EU OPS is acceptable for airplanes, but there are no rules for determining minimums for helicopters. TERPS contains such rules.
• In this regard, it is advisable to have a methodology in Russia that would include all the best that exists today.

A comment

On March 23, 2012, a meeting was held at the Federal Air Transport Agency on the topic:
Prevention of violations of meteorological weather minimums, prevention of aviation accidents due to collisions of aircraft with the earth's surface and obstacles in controlled flight, issues of ensuring flight safety in civil aviation of the Russian Federation (CFIT).
The meeting was attended by: specialists from the central office, Interregional Territorial Air Transport Directorates of the FAVT, representatives of the Department of State Policy in the Field of Civil Aviation of the Ministry of Transport of Russia, FSUE GosNII GA, State Institution Flight Safety in Air Transport, flight directors (deputies for FRA) , heads of flight safety inspections of Russian airlines, specialists from the FSUE State ATM Corporation.

In his speech, S.N. Pogrebnoy, Director for ATM and IVP of the FSUE State ATM Corporation. spoke about the inappropriateness of the proposal: “In order to monitor compliance with the minimums by ATS authorities, it is possible to invite operators to submit their minimums to interested structures based at the airport.”

Air traffic controllers monitor minimums large quantity airlines flying to airports in the Moscow air zone is not possible.

The author agrees with the opinion of Pogrebny S.N. and, as an alternative, proposes to use ICAO provisions regarding compliance with minima. They are presented in two documents: the Manual of Radiotelephone Communications (Doc 9432) and the Procedures for Air Navigation Services. Air Traffic Management (Doc 4444).

Extract from Doc 9432, paragraph 7.6 Surveillance Radar Approach:

Excerpt from Doc 4444, paragraph 12.3 ATC phraseology:

It is clear from Doc 9432 and Doc 4444 that the Approach Controller only reminds the pilot to check his minimum.

PRAPI - 98 contains Appendix 1. “List of events subject to investigation in operation.” According to paragraph 16 of this Appendix, violation of minimum weather conditions during takeoff and landing is subject to investigation. In case of violation of the minimum, the flight director is obliged to send a TLG ALR (initial message about an aviation accident, incident, serious incident, as well as any information about a threat to the safety of the aircraft, crew and passengers) to the addresses established in TS-95 and report to the inspection.

The question arises: what is the minimum violation? After all, the air traffic controller does not know the operating minimum value of the landing crew. He is guided by the minimum published in the IPP, but it has nothing to do with the aircraft approaching to land.

Perhaps it would be worthwhile in the Russian Federation to legislate a rule on informing the air traffic controller about the crew minimum when approaching an aerodrome in conditions close to the operational crew minimum, not only by landing radar, but also by other approach systems.

It can be proposed to make additions to FAP 128 with the following content after paragraph 3.89 (shown in fill).

3.89. If the reported meteorological visibility or reference RVR is below the operational minimum for landing, the IFR approach shall not continue below the documented aeronautical information altitude for the start of the final approach.

The PIC informs the ATS unit controller about the value of the crew operating minimum for landing.

Add clause 3.50. Before takeoff:

The PIC informs the air traffic controller about the value of the crew operating minimum for takeoff. meaning

*m) MINIMUM [RUNWAY VISUAL RANGE (or RVR) or VISIBILITY (meaning) (unitsmeasurements)]

*y) OPERATING MINIMA

Perhaps the aviation community will have different opinions on this matter, but in order to prevent the reduction of aviation accidents due to an aircraft colliding with the ground and obstacles in a controlled flight due to violation of the minimums, it is advisable to inform the air traffic controller about the value of the crew operating minimum. Such a report will allow the flight crew to create an additional psychological barrier about not violating the minimum, and the ATS unit will have a clear understanding of the value of the minimum declared by the PIC.

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 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. C-section indicated only in cases of severe macrocephaly and the absence of other developmental defects. 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. The upper part of the head is covered with a vascular membrane. The structures of the midbrain and diencephalon are partially or completely destroyed. The pituitary gland and rhomboid fossa are largely preserved. Typical appearances include bulging eyes, a large tongue, and a short neck. This pathology occurs with a frequency of 1 in 1000. More often than not,

found in newborn girls. Akrania(exencephaly) - 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. An echographic 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 brain tissue is found 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 cesarean section is not indicated in such observations. Decompression of the hernial sac can be recommended to create conditions for vaginal delivery. A 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, in the development of which genetic (chromosomal aberrations, monogenic defects) and environmental factors play an important 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 a 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;

Reception of a pregnant woman medicines 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, a 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.

The only 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. Cumulative survival 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, small 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. Children with severe tricuspid valve insufficiency have a high percentage of deaths. 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 interfere with the child’s normal life. 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 remains undetected by screening ultrasound before 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 of varying severity often develops. 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. Moving the heart to the right side 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 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%. Intrauterine growth retardation is detected in 20% of cases.

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 associated abnormalities. 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 defects, 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 can occur internal organs fetus

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. With normal values ​​of blood flow in the ductus venosus, fetuses with ascites in most cases have a favorable perinatal outcome. 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 frequency 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 echoten and bladder, as well as severe 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 of 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 fatal in the neonatal period to asymptomatic, 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.

Pyeelectasia. 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 based on 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 pyeloectasia 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 of 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 insufficiency 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 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 will 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 exercise. 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.

When we discovered dilation of the fetal renal pelvis during the second planned ultrasound at 22 weeks, I didn’t know where to run and who to turn to for help, I looked through the entire Internet and found very little information on this issue. I decided to describe my problem here, in case someone like me is looking for support and information.

So, at the second planned ultrasound at 22 weeks, the fetus was found to have dilated the pelvis of the left kidney to 7 mm. The doctor suggested that the baby had not peed and that perhaps everything would return to normal. The second kidney was of normal size. But in conclusion he wrote: CA marker: pyeelectasis of the left fetal kidney. Genetic consultation. I was terribly scared and went to the planning center for expert ultrasound, where they scared me even more: supposedly if I decide to leave the child, it will take a long time to get him on his feet and perhaps he will be disabled. In the worst case, all this threatens to remove the kidney. In conclusion, he made a diagnosis: hydronephrotic transformation of the left kidney. The geneticist completely stunned me: she talked to me as if I was already planning to terminate the pregnancy, explained where to go and who to contact so that I could be terminated without persuasion, then explained for a long time that she didn’t really want to see our sick children, so that we would only They brought healthy people. And in conclusion, she offered me amniocentesis, but for 14 thousand rubles at the health center on Krasnaya, since they did not have reagents. This proposal was due to the fact that pyeloectasia of the fetal kidneys is a marker of chromosomal abnormalities, in particular Down syndrome. My husband and I left her in great shock, but held on.

We decided that we would fight for our baby and at 24 weeks we went for a control ultrasound. Conclusion: dilation of the pelvis of the left kidney of the fetus up to 8 mm. There was no talk of a congenital malformation, but the doctor still placed a marker. I reassured myself that the second kidney was healthy and that means we had a chance to live, and the second one could be cured, especially since this was confirmed by a pediatric urologist at the Regional Children’s Hospital. Filatova.

I calmed down, we began to slowly acquire the necessary things for the baby, we bought a crib and a stroller. And then there was a scheduled ultrasound at 31 weeks. The doctor amazed me with his negligence; he only measured the size of the fetus and water. He had to insist that he look at the baby’s kidneys. As a result: pyeloectasia of the left fetal kidney of 20 mm, expansion of the calyx up to 14 mm. Of course he places the HA marker.

I am terrified. The pediatric urologist said that up to 20 mm the kidneys are not operated on, but only observed. And we are already 20 mm and there are still 10 weeks until the end of pregnancy, they can still grow! And such expansion actually speaks of hydronephrosis, especially since the calyces are also dilated. There is nothing to do except wait for the birth of the child to accurately determine the diagnosis. Our baby is very large, at 35 weeks he is the size of his head and tummy. Again I try to hold on and hope for the best; people’s children do not survive with such a diagnosis. But the doctor at the residential complex just blew my mind during the last visit: I asked her about the kidneys, but she doesn’t care about them, she’s worried about the marker for Down syndrome! Although I read that kidney pyeloectasia alone without other developmental disorders is not a marker of CA. Now all that remains is to wait for the baby to be born. I try to be less nervous, persuade him to get better and hope for the best. I will gradually unsubscribe about the further course of the problem, if anyone is interested.

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 may give birth absolutely healthy child. At the same time, the risk of developmental delays in the future offspring of this fetus remains, as a consequence of genetic damage with the absence of 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, 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 (drinking a large amount of alcohol by a pregnant woman 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 balanced nutrition 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 during which it 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. This period is associated with delayed mental development of the fetus.

Risk factors for fetal abnormalities

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;
• low social status – infections, fetal hypoxia, prematurity, intrauterine growth retardation;
• lack of folic acid – congenital malformations of the nervous system;
• consumption of alcohol, drugs and smoking – intrauterine growth retardation, sudden death syndrome, fetal alcohol syndrome;
• infections (chicken pox, 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 placental 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 (week 11-12) 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 - diseases of the central nervous system, chromosomal pathologies.

• placentocentesis (examination of placental particles)

Performed from 12 to 22 weeks of pregnancy to identify 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 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 the cardiovascular 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 diseases ( urolithiasis disease 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 (refractory to therapy and severe, accompanied by severe vomiting, gestational trophoblastic disease, severe hereditary diseases identified 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 malformation 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 can depend on high-quality preparation.

Before planning a pregnancy, you need to undergo a number of examinations: take tests for (STDs), HIV, hepatitis, syphilis, check blood clotting, hormonal status, sanitation of 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 undergo genetic testing.

The key point in the prevention of congenital anomalies of the fetus is maintaining healthy image life, giving up bad habits, balanced and nutritious nutrition, eliminating the impact of any negative and harmful factors on your body. During pregnancy, it is important to promptly treat all possible diseases 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 are treatable, mostly surgically. In some cases, conservative treatment helps. Sometimes developmental defects become noticeable only as they grow older, while others are completely asymptomatic.