Parchment fruit. Classification of deformities, single deformities, multiple deformities - malformations of animals

The exact causes of intrauterine death of one of the children during multiple pregnancy are not known for sure, but experts can identify a number of factors that lead to such situations:

• genetic abnormalities in the development of one of the fetuses;
• severe circulatory disorders in the placenta;
• disturbance of blood circulation in the vessels of the umbilical cord in the fetus, for example, during the formation of a node;
• trauma to the mother's abdomen, resulting in placental abruption of one of the fetuses.

Signs of fetal fading in twins

The clinical picture when one of the children of twins freezes largely depends on the gestation period at which this occurred. If the fetus dies before the 12th week of gestation, the woman may not notice the development of a particular clinical picture; the most common signs are aching pain in the lower abdomen and possible blood discharge from the vagina. If one of the fetuses dies before 10 weeks, doctors talk about the phenomenon of a “disappearing” fetus.

If the death of one of the children occurs after the 10th week of gestation, then the so-called “paper fetus” is formed - a condition that represents the weeping and subsequent mummification of the dead fetus and its membranes. As a result of its death, the embryo is compressed by the growing amniotic sac of the second baby, and partial absorption of the components of the amnion of the dead embryo is observed. A woman may have no clinical picture; she will only learn about the fading of one of the fetuses through an ultrasound scan.

Diagnosis of antenatal death of one fetus in multiple pregnancy

The most important tool for diagnosing freezing of one of the fetuses in twins is the ultrasound method. On the monitor screen, the doctor clearly sees the absence of a heartbeat in one of the babies, and can even tell the woman exactly at what time the death occurred.

How common is it that one of the fetuses fails during twins?

When carrying two babies, according to statistics, the death of one of them occurs in 2% of cases or 1 time among a thousand multiple pregnancies. Most often, freezing of one of the embryos is observed when the fetuses have one common placenta (monochorionic multiple pregnancy).

The danger of intrauterine death of one of the children for the mother and the second embryo

If one of the children freezes in the uterus up to 10 weeks of gestation, then in most cases this does not pose a danger to the life and further development of the second child and to the body of the expectant mother herself.

When one of the embryos freezes from 10 to 13 weeks most often a “paper” fetus is formed, and the second child continues to develop in the uterus. There are, of course, risks of anomalies, but they are not significant.

If one of the children dies in later stages intrauterine development, the threat appears primarily to the life of the child remaining in the uterus. As a result of cardiac arrest in one baby, there is a risk of exsanguination of the living child, since through the blood vessels of the placenta, the blood of the living fetus begins to be actively pumped into the vessels of the dead fetus, turning its body into a kind of blood reservoir. As a result of such bleeding, a living baby is at risk of developing the following conditions:

• severe hypovolemia of a living fetus;
• severe damage to the nervous system and heart of a living fetus;
• development of acute oxygen starvation of the child in the uterus.

The presence of a dead fetus in the mother’s body late in pregnancy creates the preconditions for the development of severe circulatory disorders and the formation of thrombosis, which can pose a threat to her life.

What to do if one of the twins dies?

The actions of specialists in the event of the death of one of the twin babies largely depends on the period at which the death of the child inside occurred. When one of the twin embryos freezes up to 10-12 weeks Pregnancies in 90% of cases end successfully for the mother and the surviving baby.

Death of one of the children in the second trimester increases the risk for the mother and living child, to save which the best option is considered to be intrauterine infusion of blood plasma and cessation of contact between the circulatory systems of children in the uterine cavity. The survival rate of the second baby with timely detection and measures taken is about 60%.

If the death of one of the children occurs in the last months of pregnancy, then the woman is urgently given birth, and the baby is placed in the intensive care ward for further nursing.

Irina Levchenko, obstetrician-gynecologist, especially for the site website

The duration of pregnancy depends on the number of fetuses. The average gestation length for twins is 260 days (37 weeks) and for triplets it is 247 days (35 weeks). The course of multiple pregnancy is more unfavorable with monochorionic (especially when combined with monoamniotic) type of placentation compared to bichorionic.

During multiple pregnancy, increased demands are placed on the woman’s body. All organs and systems function under great stress. Various complications are much more common.

Hemodynamic, volemic and other disorders develop earlier. BCC during a multiple pregnancy increases by 50-60%, while during a singleton pregnancy it increases by 40-50%. Due to the displacement of the diaphragm by a significantly enlarged uterus, the activity of the heart becomes difficult - shortness of breath, fatigue, and tachycardia occur.

Enlargement of the uterus, especially towards the end of pregnancy, leads to compression of the internal organs, which is manifested by impaired intestinal function, frequent urination, and heartburn.

The inferior vena cava is partially compressed. As a result, varicose veins of the extremities, vulva, and rectal veins often occur.

Almost 4-5 times more often, gestosis is observed, which is characterized by an earlier onset, a protracted and more severe clinical course, and is often combined with acute pyelonephritis in pregnant women.

Due to the increased need and utilization of iron and the reduced ability to absorb folic acid, pregnant women often develop iron deficiency and megaloblastic anemia. Characteristic of multiple pregnancy is a pronounced decrease in serum iron content and an increase in the production of transferrin and ceruloplasmin.

The presence of a large flattened placenta or several placentas is often the cause of low location and placenta previa.

Much more often than with a singleton pregnancy, complications such as bleeding during pregnancy and childbirth and labor anomalies are observed.

Often during multiple pregnancies, abnormal positions of the fetuses occur: breech presentation (24-30%), transverse position (5-6%).

One of the most common complications during multiple pregnancy is its premature termination. Premature birth is observed in 25-50% of cases, depending on the number of fetuses. This is due to significant overextension of the uterus, insufficiency of the uteroplacental circulation, gestosis, the more common immunological incompatibility of the ABO system and other complications.

During a multiple pregnancy, the uterus reaches a large size not only due to the large number of fetuses, but also due to frequent polyhydramnios.

Rice. 12.4. Types of conjoined twins, a - thoracopagus; b - craniopagus.

Rice. 12.4. Continuation.

B - pygopagus; d - incomplete divergence of twins.

The development of twins born at term is normal in most cases. However, their body weight is usually less (10% or more) than in a singleton pregnancy. In case of twins, the birth weight of children less than 2500 g is observed in 40-60%.

The low weight of twins in this case is most often due to insufficiency of the uteroplacental complex, which is not able to sufficiently provide adequate conditions for optimal growth and development of the twins. The consequence of this is IUGR of the fetus, which is common in multiple pregnancies. The weight of twins accordingly decreases in proportion to their number (triplets, quadruplets, etc.).

The difference in body weight between twins can reach 200-300 g, and sometimes more.

Uneven (dissociated) development of twins is associated with unequal supply of nutrients from the single placental circulation.

In multiple pregnancies, fetal malformations are 2 times (up to 18.8%) higher than their frequency in women with singleton pregnancies and are most typical for monozygotic fetuses.

Conjoined twins are the most typical example of defects observed only in the monoamniotic type of multiple pregnancy. 75% of conjoined twins are girls.

Among the different types of twin fusion, the following are distinguished (Fig. 12.4):

Thoracopagi (fusion in the chest area) - 18-74%;

Omphalopagus and xyphopagus (fusion in the navel and xiphoid cartilage) - 0.5-10%;

Thoracomphalopagus - 28%;

Craniopagus (fusion of homologous parts of the skull) - 1-6%;

Incomplete divergence: bifurcation in only one part or area of ​​the body - 10%;

Pygopagus and ischiopagus (connection of the lateral and lower sections of the coccyx and sacrum) are 18-20 and 5-6%, respectively.

In 1/3 of cases, conjoined twins are stillborn or die on the 1st day of life. Survival of children depends on the type of fusion and associated anomalies.

In conjoined twins, anatomical developmental anomalies are always detected, which are most likely caused by a violation of embryonic division.

Thoracopagus have a common liver in 100%, a common gastrointestinal tract in 50%, congenital heart defects in 75%, of which 90% have varying degrees of pericardial fusion. Often there is a fusion of the heart with the formation of two ventricles and a different number of atria. Ventricular septal defect occurs in almost all twins of this group.

The prognosis is determined by the degree of fusion. With a common heart, twins die within 3 months.

Omphalopagus and Xyphopagus. With this type, the liver fuses in 80% of cases, the sternum cartilage in 26%, the diaphragm in 17%, and the genitourinary tract in 3%. In 1/3 of cases, omphalocele (embryonic hernia) and common distal ileum are found. Heart defects (ventricular septal defect and tetralogy of Fallot) are observed with a frequency of up to 25%.

Craniopagus. In the partial type of craniopagus, when the brain is divided by the bones of the skull or dura mater, each fetus has a separate pia mater.

With the complete type, the brain is connected. Cerebral connection occurs in 43% of cases and is more often formed with the temporo-parietal fusion variant.

Pygopagus, connected in the region of the buttocks and lower spine, have a common part of the canal of the sacral spine, a common rectum and anus, a common bladder and urethra, and fused external genitalia.

The prognosis is quite favorable, since vital organs are not involved in the pathological process.

Ishiopagus, connected in the area of ​​the lower part of the sacrum and coccyx, have a common pelvic girdle. Ishiopagus have 3 or 4 legs. They share a lower gastrointestinal tract. There may be a common bladder and urethra.

Feto-fetal blood transfusion syndrome (FTS) occurs in 5-25% of cases in monozygotic twins with a monochorionic biamniotic type of placentation. Perinatal mortality with this pathology ranges from 60 to 100%.

With monochorionic twins, anastomoses are often formed in the placenta between the vascular systems of both fetuses (arterio-arterial, arteriovenous or veno-venous).

If blood pressure is symmetrical in the placental vascular system, both twins develop under the same conditions. The arterio-arterial anastomoses available in the monochorionic type compensate for the hemodynamic imbalance that can be caused by arteriovenous shunts. However, this balance can be disrupted due to asymmetric placental circulation.

The prerequisites for the development of FPG are laid in monochorionic twins already in the process of development of the vascular network of the placenta, when conditions are formed for the twins to share certain vascular zones (cotyledons). Moreover, both twins are associated with the same group of cotyledons at the same time. The resulting arteriovenous anastomoses, which pass through the capillary bed of the cotyledon, promote the outflow of blood from one twin (donor) to the other (recipient).

The severity of FFH (mild, moderate, severe) depends on the degree of blood redistribution through these anastomoses, which vary in size, number and direction.

The impaired condition of the donor fetus is caused by hypovolemia due to insufficient blood supply and hypoxia due to placental insufficiency. He develops developmental delay, oligohydramnios, arterial hypotension and often anemia (hemoglobin concentration can be 80 g/l or less).

The recipient fetus has hypervolemia and hyperosmolarity, leading to heart failure, polyuria, polyhydramnios and hydrops (general edema, ascites, pericardial or pleural effusion). In addition, there is arterial hypertension, cardiac hypertrophy, hypervolemia, a high hematocrit number and a tendency to thrombosis.

Differences in size and weight between both fetuses (developmental dissociation) may appear at different stages of pregnancy. The degree of their dissociation can vary. Often the situation becomes dangerous between the 20th and 30th weeks of pregnancy, when premature termination is most likely.

Due to the resulting disturbances, the death of one of the fetuses may occur. If the fetus dies in the first 2 weeks of pregnancy (before the onset of ossification), then its complete resorption is possible. If the fetus dies later and has not undergone resorption, then it first macerates, then dehydrates, decreases in size, flattens and is pressed into the chorionic plate of its placenta or into the amnion outside the placenta. This mummified fruit is called a “paper fruit.” It is usually discovered after the birth of the surviving twin when examining the placenta. Following the death of one twin in a monochromatic twin, the survivor may be rapidly exsanguinated by massive shunting of blood into the vasculature of the dead twin, causing acute hypotension and ischemic brain damage. Occurring hemodynamic disturbances can lead to the death of the second twin.

One of the signs of FFH is an increase in the nuchal space in one or both fetuses during pregnancy 10-44 weeks, which may be due to heart failure due to hypervolemia.

In some cases, arteriovenous anastomoses can be detected using color Doppler mapping. Signs that may indicate the presence of FFH include differences in the weight of newborns by 20% or more, the formation of polyhydramnios from the 16th to 24th week of pregnancy. Pathognomonic echographic signs of severe FFH are the presence of a large bladder in the recipient fetus against the background of severe polyhydramnios and lack of bladder filling in the donor fetus due to anuria. The latter is also characterized by a decrease in motor activity against the background of severe oligohydramnios. An additional echographic criterion is the presence of a hypertrophic, dilated heart in the recipient fetus. In the donor fetus, the heart may also be dilated, which, along with hyperechoic intestines, is a manifestation of hypoxia.

When studying blood flow in the umbilical cord arteries in patients with FFH, changes in Doppler indices are noted in both fetuses. In the donor fetus, this is due to the indicated pathology of placental development; in the recipient fetus, impaired blood flow is associated with compression of the umbilical cord as a result of polyhydramnios.

When severe oligohydramnios is detected in one fetus and polyhydramnios in the other in monochorionic twins, the frequency of intrauterine death of both fetuses is 90%, which dictates the need for earlier diagnosis of this pathology.

To treat FFH, excess amniotic fluid is removed by ultrasound-guided amniocentesis. This treatment method primarily prevents the risk of spontaneous abortion or premature birth.

The effectiveness of this treatment method is 30-83%, which depends on the severity of FFH.

As an alternative treatment method for severe FFH, endoscopic laser coagulation of anastomosing placental vessels under constant echographic control can be used. The effectiveness of this method is 70%. During this treatment procedure, a fetoscope is inserted transabdominally into the amniotic cavity of the recipient fetus. Visually and with the help of echography, the condition of the chorionic plate along the entire interfetal septum is studied, the vessels crossing it are identified and coagulated. At the final stage, amniotic fluid is drained to normalize its quantity.

With the help of endoscopic laser coagulation, it is possible to prolong pregnancy by an average of 14 weeks, which contributes to a significant reduction in perinatal mortality

One of the manifestations of transfusion syndrome is reverse arterial perfusion in twins (acardia syndrome, acardiac monster, acephalic acardia, holocardia, pseudocardial anomaly). The incidence of this anomaly is 1:35,000 newborns.

Reverse arterial perfusion occurs only in monozygotic twins with placentas fused.

In all cases, PDA reveals umbilical cord anastomoses, which in the early stages of embryogenesis can lead to reverse blood circulation in the umbilical cord. This, in turn, causes a disruption in the development of organs and systems in one of the fetuses due to a lack of oxygen and nutrients. Thus, with PDA, a recipient twin and a donor twin are formed (Fig. 12.5).

This hemodynamic disturbance is due to the fact that in one of the twins, the umbilical cord vessels form earlier and cover most of the chorion. In the second fetus, this process is delayed, and it receives a smaller part of the chorion that does not meet its needs. The vessels of the umbilical cord of the second fetus tend to a greater extent to the vessels of the first fetus, and not to the placenta.

The donor twin, as a rule, is morphologically healthy, his chromosome set is within normal limits. However, this fetus has signs of cardiac overload characterized by hydrops, IUGR, right ventricular hypertrophy, and hepatosplenomegaly.

Rice. 12.5. The nature of fetoplacental blood flow in reverse arterial perfusion syndrome.

The recipient twin may lack any other organ besides the heart, and the appearance of the fetus takes on different forms.

The most common forms of lesions are the following (Fig. 12.6):

Acardia anceps: the affected fetus has the most preserved appearance, the head is fully or partially formed with the remains of the bones of the cranial vault and brain tissue, the facial skull is with clefts, the limbs and individual parts of the body are distinguished;

Acardia acephalus: missing head, upper body with chest organs, upper limbs; a rudimentary diaphragm, rudiments of the abdominal organs, pelvic bones and lower limbs are identified;

Acardia acormus: lacks a trunk, head or head-like structure, attached to the placenta directly or through a short umbilical cord;

Acardia amorphus: the most severe lesion of the fetus, which is an amorphous mass.

The mortality rate of recipient twins is almost 100%. The mortality rate of donor fetuses is 50%.

Ultrasound can most reliably identify the listed abnormalities in the condition of fetuses during multiple pregnancies.

Morbidity and mortality in polyhydramnios pregnancy. Compared to singleton pregnancies, the incidence of twins is 5 times higher. Even full-term twins, especially triplets, often show signs of morpho-functional immaturity. These children require further special care and feeding. Signs of morphofunctional immaturity are especially pronounced in premature twins. According to available data, 16% of all children born immature are twins.

Rice. 12.6. Forms of lesions in the recipient fetus with reverse arterial perfusion syndrome.

With multiple pregnancy, there is usually a direct relationship between the weight of the placenta and the weight of the fetus. The weight of each individual placenta or the total weight of placentas divided by the number of fetuses (with a monochorionic type of placentation or fused placentas), as a rule, is lower than the weight of placentas in a singleton pregnancy of the same period.

It is natural that the Apgar score in multiple pregnancies is also often lower than in singleton pregnancies.

In monozygotic twins, there is more often a tendency to lag in the physical and neuropsychic development of newborns, and an increase in the number of cases of birth injuries.

The neonatal period in the recipient fetus as a result of transfusion syndrome can be complicated by dangerous cardiac overload and heart failure.

The increased incidence of complications in multiple pregnancies on both the maternal and fetal sides leads to a significant increase in perinatal mortality.

Perinatal mortality in multiple pregnancies is 6-10 times higher than in singleton pregnancies and is directly dependent on the body weight of the children.

In developed countries, perinatal mortality for twins is 47-120%, and for triplets - between 93 and 203%. Such a high mortality rate among twins persists during the 1st year of life, and only by the 2nd year does the mortality rate among dizygotic twins equal that after a singleton pregnancy.

The morbidity and mortality of monozygotic twins is 2-3 times higher than that of dizygotic twins. Considering that approximately 1% of monozygotic twins are monochorionic and monoamniotic, the mortality rate for these twins can be as high as 50%.

The high incidence among monozygotic twins is most often due to transfusion syndrome, twin fusion and umbilical cord pathology. At the same time, the perinatal mortality of the second fetuses with twins is higher than the first.

The leading causes of morbidity and mortality in twins are associated with preterm birth. At the same time, the leading place in the structure of complications of premature birth is occupied by:

Respiratory distress syndrome;

Asphyxia;

Intraventricular hemorrhages;

Necrotizing enterocolitis.

Another group of causes of morbidity in twins includes:

Fetal growth restriction (IUGR);

Intrapartum complications;

Transfusion syndrome;

Pathology of the umbilical cord;

Developmental anomalies.

Failed miscarriage is a disease in which the fertilized egg dies already in the relatively early stages of pregnancy, but it is still not expelled, despite bleeding, indicating an incipient miscarriage. Such a retained egg is called a hemorrhage; it is a dense, voluminous formation consisting of blood layers surrounding the dead and decaying embryo (fetus).

When bleeding is delayed in the uterine cavity for a longer time, blood clots become organized, thicken, become discolored, and take on the appearance of meat when cut. This form is called a fleshy mole.

A dead fertilized egg can remain in the uterus for several months, sometimes even years. If previous authors categorically denied the possibility of long-term retention of the fertilized egg in the uterine cavity, modern authors adhere to the opposite point of view.

Speaking about changes in the fertilized egg when it is retained in the uterine cavity, we cannot ignore the question of the embryo (fetus), which undergoes various transformations.

In early miscarriages (up to 2 months), the embryo may dissolve. What process occurs in this case has not yet been precisely established.

At a later date, the fetus undergoes, depending on the absence or presence of bacteria in the uterus, either a process of maceration or ichorous decay.

During maceration, the integument of the fruit is imbibed, and then autolysis occurs. Due to hemolysis, amniotic fluid becomes bloody, the umbilical cord turns brown, and the skin color turns red - foetus sanguinolentus.

Much less often, with a failed miscarriage, mummification of the fetus is observed. In this case, the amniotic fluid is absorbed, the fetus shrinks and dries out, its skin adheres closely to the bone, and the body becomes denser.

This process is most often observed on fetuses older than 3 months.

Even less common is skeletonization, i.e., the disintegration of soft parts with exposure of bones, which occurs without the access of bacteria.

In isolated cases, petrification of the fetus (litopaedion) is observed with the deposition of salts both in its tissues and in the egg shells (kelyhopaedion).

With identical twins, one of the dead fetuses may undergo flattening (foetus compressus) at the expense of the second, correctly developing fetus, and eventually becomes thin, transparent, turning into the so-called paper fruit - foetus papyraceus (Fig. 44).

Rice. 44. Paper fruit.

The reasons for the death of the fertilized egg are very diverse and are not always amenable to clarification.

The basis for the long-term retention of a dead fertilized egg in the uterus is a decrease in the reflex activity of the latter, caused both by disturbances on the part of the receptor apparatus of the uterus itself, and by disorders of the functional state of the central nervous system (cortex and subcortical centers), which is directly related to the state of hormonal balance ( qualitative and quantitative nature). As a result, there is a decrease in the level of pituitrin, acetylcholine and an increase in progesterone levels.

Since folliculin is considered a stimulator of acetylcholine production, it is used to stimulate contractile activity of the uterus. For successful action, it is necessary to use relatively large doses (from 6,000 to 30,000 IU), and the shorter the pregnancy, the larger the dose should be, and vice versa. Instead of folliculin, you can also use sinestrol. Confirmation of the correctness of this view is that such an application of this method is quite successful in a number of cases.

Microscopic examination of the placenta in cases of failed miscarriage always reveals changes, in particular hyaline degeneration of the villi and obliteration of their blood vessels. According to some authors (N.N. Chukalov), these changes occur intravitally and gradually, and the fertilized egg dies due to the cessation of the influx of nutritional material. Other authors, such as K.P. Ulezko-Stroganova, consider these changes as posthumous.

Along with necrotic ones, sometimes there are small areas of unchanged villi, which, when the fetus has long died, penetrate deeply into the wall of the uterus. Removing such areas of the placenta is difficult.

Missed miscarriage is observed in 80% of multiparous women (V, A. Bulatov). In the origin of this kind of disease in multipregnant women, morphological changes in the tissues of the uterine wall are important, in particular the increased proliferation of connective tissue, due to inflammatory and traumatic disorders, intoxications, etc. In primigravidas, a failed miscarriage is observed with congenital hypoplasia of the uterus.

A missed miscarriage occurs completely unexpectedly. A woman who had a clear progression of pregnancy and experienced the sensations characteristic of the latter notes that they suddenly disappeared.

An objective examination reveals the absence of pre-existing signs of pregnancy. In such cases, the woman is placed under surveillance.

In the case of a missed miscarriage, as opposed to a hydatidiform mole, the discrepancy between the period of the delay in menstruation and the size of the uterus is expressed in the lag in the size of the uterus from the expected period of pregnancy (according to the duration of the delay in menstruation). This is the main symptom of the disease. Subsequently, the size of the uterus becomes increasingly reduced.

Due to the absorption of amniotic fluid and the cessation of hyperemia and serous saturation of the uterine tissue, common during progressive pregnancy, the consistency of the uterus changes, it becomes much denser.

Bleeding and pain in the abdomen and lower back usually appear when the ovum is detached; “dirty” discharge (sometimes with a putrid odor) alternating with slight bleeding is more often noted. An increase in body temperature is usually not observed. With the death of the egg, the pregnant woman notices the cessation of engorgement of the mammary glands and the disappearance of the usual signs of pregnancy. The woman’s condition is depressed, she is worried about a headache, she feels malaise and loss of strength, an aversion to meat food due to the body being overloaded with absorbed proteins (R. R. Makarov). Sooner or later, the dead fertilized egg is expelled from the uterine cavity, and its independent expulsion usually occurs closer to the end of a normal pregnancy.

Failed birth(missed labor) are observed extremely rarely. In recent years, only isolated cases of prolonged retention of a full-term dead fetus in the uterine cavity have been published in the world literature in recent years. There is no doubt that the number of cases of missed labor is much greater than what is published in the press.

The delay in the onset of birth with a dead fetus at term depends, apparently, on a sharp decrease in the excitability of the uterus, caused by a disorder in the work of the central (cortex and subcortex) and peripheral (lying in the uterus) nervous and neuro-hormonal mechanisms, as well as on the functional state conducting nerve pathways, as was proven by the research of G. M. Lisovskaya using electrohystero- and encephalography methods.

Fetal death depends on degenerative changes in the placenta, as a result of which this organ gradually loses its ability to deliver oxygen and nutrients to the fetus. The death of the fetus also depends on the intoxication of its body with carbon dioxide and decay products due to impaired blood circulation in the overripe and degenerated placenta.

A dead fetus can linger in the uterus for a long time - from several weeks to several years. In the case described by E. Z. Rabinovich, the fetus was in the uterus for 15 years, in the case of Kamerarius - 46 years (discovered during an autopsy of an old woman 96 years old).

Treatment. If a miscarriage does not occur, a wait-and-see approach is recommended. Active intervention should be used only for special indications (severe bleeding, pain, fever, etc.); deterioration in the general condition of the pregnant woman also serves as an indication for urgent emptying of the uterus. The patient must be explained the nature of the disease and be systematically monitored. Manipulation of instruments in the uterine cavity should be done with great care, since with this disease the uterus can be easily perforated (similar cases are described in the literature) or profuse bleeding occurs, which is often the cause of death of the patient.

Only in case of delayed pregnancy of a later date (missed labour), in order to stimulate the activity of the uterus, in some cases it is appropriate to prescribe folliculin, pituitrin, quinine, hot vaginal showers (45-46 ° C), as well as other means and methods that excite and enhance contractility ability of the uterus.

In exceptional cases, where rapid emptying of the uterus is required (heavy bleeding with a slight opening of the pharynx), vaginal or abdominal caesarean section is resorted to.

It is often necessary to resort to manual removal of the placenta, especially during a long-term pregnancy.

A pregnancy that ends in the birth of a child with signs of overmaturity is called post-term. Childbirth during a post-term pregnancy is called late.

Signs of postmaturity most often occur during pregnancy 42 weeks or more, but can also occur earlier - 40-41 weeks.

In addition to post-term pregnancy, there is a prolonged, physiologically longer pregnancy (up to 41-42 weeks or more), in which the child is born without signs of post-term pregnancy.

Postmaturity has an adverse effect on the condition of the fetus and newborn due to the following unfavorable factors:

Development of placental insufficiency due to dystrophic changes in the placenta and, as a consequence, chronic fetal hypoxia;

More mature central nervous system of the fetus, increasing the sensitivity of the brain to oxygen deficiency;

The appearance of intrauterine pathological respiratory movements of the fetus during pregnancy and childbirth, promoting aspiration of amniotic fluid containing meconium;

Increased density of the bones of the skull, narrowing of the sutures and fontanels complicating the configuration of the head during the passage of the birth canal.

Etiology and pathogenesis post-maturity has not been definitively established.

Etiological factors contributing to post-maturity include:

The pregnant woman is over 30 years old;

Neuroendocrine diseases combined with lipid metabolism disorders;

Predominance of the tone of the parasympathetic nervous system, lack of receptor between the cortex and subcortical structures of the brain;

Hormonal dysfunction, expressed in a decrease in the concentration of active fractions of estrogens, catecholamines, progesterone;

Absence of changes in the uterus necessary for the onset of labor: low level of metabolic reactions, synthesis of actin and myosin, receptors for uterotonic compounds (prostaglandins E, F 2 a, oxytocin);

Delayed or dissociated maturation of the placenta with the preservation of immune tolerance, preventing immunological rejection of the fetus at birth;

Malformations of the fetus, primarily the central nervous system and the pituitary-adrenal system, responsible for the synthesis of corticosteroids that activate the synthesis of estrogens and prostaglandins in the placenta.

In case of post-maturity, as a result of these features, the formation of the generic dominant is disrupted. Regressive changes in the placenta are observed. As a result of a decrease in blood flow, its thickness changes, signs of involutive processes appear: heart attacks, calcifications, areas of fatty degeneration.

The transparency and composition of amniotic fluid changes. With a slight overmaturity, the waters become opalescent and whitish due to the dissolution of the cheese-like lubricant and the surface layers of the fetal skin in them. With fetal hypoxia and meconium in the amniotic fluid, they become green or even yellow (meconium from the upper intestines of the fetus).

The phospholipid composition of amniotic fluid is changed. The ratio of lecithin and sphingomyelin, which determines the formation of a sufractant in the fetal lungs, is disrupted. In a post-term fetus, the surfactant system of the lungs is destroyed, which causes respiratory distress syndrome and the formation of hyaline membranes in the lungs of the newborn.

With a decrease in the amount and change in the physicochemical properties of amniotic fluid, its bactericidal capacity decreases, and the number of bacteria increases, increasing the risk of developing intrauterine pneumonia in the fetus.

Changes in the placenta, the quantity and quality of amniotic fluid, and a decrease in the amount of Wharton's jelly in the umbilical cord ("lean umbilical cord") affect the condition of the fetus and newborn.

The skin begins to lose its original lubricant. With the loss of this protective layer, the skin comes into direct contact with amniotic fluid and wrinkles. Hair and nail plates continue to grow; As pregnancy progresses, subcutaneous fat loss occurs. When meconium enters the amniotic fluid, the skin of the fetus becomes greenish or yellowish in color.

When pregnancy is carried beyond term, the fetus is often large, the size of the head approaches or exceeds the upper limit of normal. However, the weight of a post-term newborn may be small due to developing growth retardation. The length of the fetus during postmaturity often exceeds normal values ​​and is 54-56 cm or more. As the gestational age increases, the bones of the skull become dense, and the sutures and fontanelles become narrow.

Clinical picture and diagnosis. The diagnosis of postmaturity is established based on a combination of medical history and additional research methods.

From the anamnesis data, the following is taken into account:

The nature of menstrual function;

Date of last menstruation;

First fetal movement;

Pregnancy period at the first visit to the antenatal clinic;

Pregnancy dates according to ultrasound performed at 12-13 and 22-23 weeks.

Additional objective methods to clarify the diagnosis of post-term pregnancy include:

Lack of biological activity of the cervix during full-term pregnancy (38-40 weeks);

A decrease in abdominal circumference after the 40th week of pregnancy (indirect evidence of a decrease in the amount of amniotic fluid);

An increase in the height of the uterine fundus due to the larger size of the fetus, hypertonicity of the lower segment, high location of the presenting part of the fetus;

Reduced blood levels of estradiol, placental lactogen, corticosteroids, trophoblastic b-globulin;

Signs of chronic hypoxia according to CTG, biophysical profile, Doppler blood flow in the mother-placenta-fetus system;

Reduction in the thickness of the placenta according to ultrasound data and structural changes in it (petrificates, cysts), no increase in biometric parameters of the fetus during dynamic fetometry, thickening of the skull bones, decreased motor activity, a pronounced decrease in the amount of amniotic fluid (oligohydramnios!), the largest vertical size of the pocket free from the echostructure of the fetus in the area of ​​amniotic fluid is less than 2 cm;

Amnioscopy data: decreased transparency and change in color of amniotic fluid;

green color due to the presence of meconium in the amniotic fluid, disturbances in the biochemical composition (increased concentrations of total protein and glucose, creatinine levels, alkaline phosphatase, changes in the lecithin/sphingomyelin ratio).

It is important to differentiate between post-term and prolonged pregnancy. Clinical data and the results of special studies should be taken into account: electrocardiography, ultrasound, amnioscopy, amniocentesis, etc.

In prolonged pregnancy, the fetus is often large, and there are no changes in fetal cardiac activity on CTG; Ultrasound does not reveal pronounced signs of “aging” of the placenta and oligohydramnios, the contours of the head are normal; amnioscopy reveals a sufficient amount of normal-colored water.

A child born from a prolonged pregnancy has no signs of postmaturity.

Management of pregnancy and delayed childbirth.

Scheme 19.1. If signs of post-maturity are detected (oligohydramnios, dystrophic changes in the placenta), which are combined with symptoms of chronic fetal hypoxia (impaired blood flow in the mother-placenta-fetus system according to Doppler measurements, changes in CTG, green amniotic fluid) or with other obstetric complications (age of the primigravida 30 years or more, large fetus, fetal growth restriction, breech presentation, etc.) is carried out planned.

C-section

If the condition of the fetus is satisfactory and there are no aggravating factors, the immature cervix must be prepared for delivery. To prepare the cervix when its maturity is 3 points or less on the Bishop scale, it is advisable to first use kelp. These are algae, the volume of which increases in the moist environment of the cervical canal and expands it. When the cervix ripens to 4 points or more on the Bishop scale (or in the initial state corresponding to the indicated values), prostaglandins E 2 (prepidyl gel containing 0.6 mg of dinoprostone) are used. As a rule, after 6-24 hours, complete ripening of the cervix is ​​achieved, which allows for amniotomy and subsequent induction of labor; injecting the mother intravenously with enzaprost first, and then oxytocin).

If you are postterm, childbirth may be complicated by:

Untimely discharge of amniotic fluid;

Pathological preliminary period;

Bleeding in the afterbirth or early postpartum period.

During labor management, labor activity (tocography) and the condition of the fetus (CTG, color of amniotic fluid, their changes during labor) are monitored.

These conditions determine the labor management plan.

Delayed labor is best managed using epidural anesthesia.

Due to the poor configuration of the head of a large post-term fetus, it is necessary to exclude a clinically narrow pelvis during childbirth.

To prevent deterioration of the fetus' condition, a perineal or episiotomy is performed at the end of the expulsion period.

The diagnosis of postterm pregnancy is clarified after the birth of the child according to the Bellenstein-Runge signs:

Lack of vellus hair;

Lack of caseous lubrication;

Increased density of the skull bones (difficulty in the configuration of the head during childbirth);

Narrowness of sutures and fontanelles;

Nail lengthening;

Greenish skin tone;

Dry “parchment” macerated skin;

“bath” palms and feet;

Decreased skin turgor;

Weak expression of subcutaneous fat.

When examining the placenta, fatty degeneration, calcifications in the placenta, and yellow-green staining of the membranes are visible.

Classification of deformities

organism defect deformity hereditary

Single deformities

Persistent congenital anatomical abnormalities of one developing fetus are called single. They are distinguished by localization in the skeleton (skull, spine, limbs), in the brain and spinal cord, in the cardiovascular, respiratory, digestive, reproductive apparatus and classified according to the nature of the changes: persistence, atavism, agenesis, hypogenesis, hypergenesis, excessive formation of organs , organ fusion, dysraphism, atresia, dystopathy.

Persistence (from the Latin persistens - remaining, persistent) is expressed by the preservation of parts of the fetus that disappear at the time of birth, for example, gill slits, the ductus botallus (the vessel connecting the pulmonary artery and the aorta), the umbilical duct (between the intestines and the gallbladder).

Atavism (from Latin atavus - ancestor) is the presence of anatomical features in the fetus that are absent in the parents, but inherent in distant ancestors.

Agenesis (aplasia) - congenital absence of an organ or part of the body, for example acrania (from the Greek cranion - skull) - absence of a head, acardia (from the Greek cardia - heart) - absence of a heart, amelia (from the Greek melos - limb) - absence limbs.

Peromelia is an inherited agnesia of the peripheral parts of the limbs in the presence of only rudimentary proximal parts. Often observed in cattle and pigs. In many breeds of cattle, peromelia is part of a syndrome that has become known and described as Acroteriasis congenita (congenital amputation of the limbs). Genetic studies suggest that the hereditary tendency behaves as recessive (Fig. 1).

Amputated limbs acroteriasis congenita (congenital acroteriasis) - the genetically determined absence of all four limbs occurs in pigs, cattle and humans. In calves with this defect, the limbs end near the elbow and hock joints and the rounded stumps are neatly covered with skin. This anomaly is accompanied by other defects: shortening of the jaws, bifurcation of the palate and the absence of most teeth (Fig. 4).

Hypogenesis (hypoplasia) - underdevelopment of an organ or part of the body, for example microcephaly - underdevelopment of the head, microphthalmia - an abnormal decrease in the size of one or both eyes and other organs.

Hypergenesis is a congenital enlargement of an organ, for example, macrosplenia is an enlargement of the spleen, macromegia is an enlargement of the limbs, macrophthalmia is an abnormal enlargement of the eyeball.

Excessive formation of organs, for example, polydactyly (from the Greek poly - many, daktylos - finger) - polycardia (from the Greek cardia - heart) - the presence of several hearts (K G. Bol described the presence of 10 hearts in one chicken), polythelia (from Greek thele - breast nipple) - excessive formation of nipples. Hyper- or polydactyly is known in almost all farm animals (Fig. 2). This term refers to an increase in the number of fingers on the limbs compared to the normal number for a given species. This enlargement begins at the carpus or tarsus, or distal to it in the region of the metapodium or acropodium, additional digits are formed. The most common type of polydactyly is in horses. In most cases, a doubling of the number of fingers is observed, less often - a tripling. Along with polydactyly, duplication of limbs above the carpus and tarsus (polymelia) is also found in various animal species. Such duplications are referred to as polymelia. Nothing is known yet regarding their inheritance (Fig. 3).

Fusion of parenchymal organs, for example cyclopia (from the Greek myth of the one-eyed Cyclops people) - one-eyed; fusion of limbs, horseshoe kidney.

Dystrophy (from the Greek raphe - suture) - non-closure of natural cavities, for example, “cleft lip” - cleft upper lip, “cleft palate” - absence of the sternum, rachischisis - non-closure of the spinal canal.

Atresia (from the Greek thresis - hole) - the absence of natural openings, for example oral, anal, genital.

Anal sphincter agenesis is the congenital absence of the anal sphincter. Also known as anal sphincter aplasia.

Anal artesia is a congenital absence of the anus, causing the accumulation of feces and subsequent distension of the abdomen.

Atresia, obstruction - congenital absence of the ileum (the distal part of the small intestine, passing from the small intestine to the cecum).

Cloaca - the absence of the anus causes the passage of feces and urine through the vulva.

Deformities of the reproductive apparatus are of particular importance in veterinary and zootechnical practice.

Dystopia (from the Greek topos - under) - displacement of organs due to underdevelopment of the septum, for example the diaphragm, and the abdominal organs are displaced into the chest cavity, and the lungs and heart into the abdominal cavity; When the scalp is underdeveloped, the brain is displaced under the scalp (“cerebral hernia”). In case of small defects of the calvarium, either one meninges or the parts of the brain covered by it come out through the hole, and the outer skin protrudes and covers the whole. The abnormal opening, most often located at the site of the suture between the bones, is a hernial orifice, reaching a size from several millimeters to several centimeters. The dura mater or parts of the brain together with the arachnoid membrane, also stretched by cerebrospinal fluid, form the contents of the hernial sac, and the outer skin with subcutaneous tissue forms the hernial sac, often with a narrowed base. The formation of small clefts in the calvarium, which serve as hernial orifices, can be caused by either amniogenic or genetic reasons. It has been established that in cattle and pigs, cerebral hernia is most likely caused by a simple recessive sublethal gene with variable penetrance and expressivity, which is of great importance. Among small laboratory animals, brain herniation has been described in guinea pigs, rabbits and mice. The mirror movement of organs is described: the heart is localized on the right half of the body, the liver on the left.

A diaphragmatic hernia is a congenital hole in the thoracic diaphragm that allows the abdominal organs to be displaced into the chest.

The prolapse of organs onto the surface of the body or into an adjacent cavity is called ectopia.

Hermaphroditism (from the Greek myth about the son of Hermes and Aphrodite, fused with the nymph Salmacis) - bisexuality. In humans and various species of domestic animals, there are intermediate sexual forms, which are characterized by a mixture of sexual characteristics of both sexes in one individual. In this case, it is often difficult or even impossible to establish the true sex of an individual. Determination of sex in animals is carried out on the basis of genetic (chromosomal), gonadal or somatic sex. True - the presence of testes and ovaries in one creature, false - when the gonads do not correspond to the external genitalia. The latest research has repeatedly confirmed that the cause of various forms of intersexuality is hormonal disorders at a certain stage of development. It was found that primary differentiation of sex, regardless of genetic sex, proceeds towards the female sex. Due to the suppression of male sex hormones and another still unknown factor, this development is inhibited and the formation of either male individuals or intersex individuals occurs. Despite the fact that individual cases of intersexuality have been known since the middle of the last century, evidence of its genetic cause was obtained only in 1912. Although it has not yet been possible to accurately determine the type of inheritance (Fig. 5).

Males have monorchidism (from the Greek monos - one, orchis - testis) - congenital absence, underdevelopment or delay in the abdominal cavity of one testis, and cryptorchidism (from the Greek kripto - hidden) - retention in the abdominal cavity of both testes or their underdevelopment (enorchidism ). In females, frumartinis is detected - underdevelopment of the vagina. Such anomalies include: choristia, hamartia, dysplasia.

Choristia (from the Greek horso - I separate) are small additional organs or their rudiments, split off from one or another organ, for example the spleen, pancreas. Adnexal aplasia is a complete or partial disruption of the development of the epididymis of the ovary. Ovarian aplasia is defective development, or complete absence of the ovaries.

Hamartia (from the Greek amartia - error) - formations consisting of an incorrect relationship of tissues, for example birthmarks, liver angiomas, inclusion of adrenal tissue in the kidney, liver tissue in the spleen.

Dysplasia (heteroplasia) is an unusual localization of tissue in an organ, for example the presence of sections of the intestinal mucosa in the esophagus.

These anomalies can disappear over time, persist for life without developing, and sometimes reach significant sizes, taking on the form of tumors called choristomas, hamartomas or teratomas (from the Greek teratos - miracle). For example, dermoid cysts are found in the skin - closed cavities lined with epithelium with rudiments or formed horn formations and teeth; in the mammary gland - tumor-like nodes consisting of bone, cartilage, fatty, glandular tissue. Such tumors sometimes become malignant and metastasize.

The discovery of tumors originating from embryonic rudiments gave Conheim the basis for creating an embryonic theory of the origin of tumors. It can explain the origin of only some neoplasms, since in most cases they appear in adulthood under the influence of physical, chemical factors and viruses, regardless of the disruption of tissue development in the embryonic period.

Multiple deformities

Multiple deformities are the simultaneous development of several twin fetuses (lat. gemini - twins). Multiple births of some animals are not considered deformities. There are identical and polyzygotic twins. They can be free and non-free, symmetrical and asymmetrical.

Identical twins develop due to the complete or partial separation of a fertilized egg at the stage of the first blastomeres. Free symmetrical twins are always of the same sex and are very similar to each other, develop normally and are viable. But sometimes one of the fruits dies, dries out and looks like a plate similar to parchment (“parchment” fruit, lat. fetus papyrocens), the second fruit may be normal. Or both fetuses have some anatomical deviations - underdeveloped, with rudimentary or absent organs - free asymmetrical twins.

Fraternal twins occur as a result of the simultaneous release of several eggs into the female’s reproductive tract and their subsequent fertilization. Some animals have this feature: pigs, sheep, dogs, cats. This is a normal species property of them. The fetuses in these cases are of different sexes, do not look similar to each other, are anatomically normal, viable, and, as a rule, free. Sometimes some of them die before birth, are underdeveloped, and have deformities.