Before birth. Delay intrauterine development may be associated with an abnormality of the fetus or the inability of the placenta to supply it with necessary substances. Detection of developmental delay is based primarily on measuring the height of the uterus and on an ultrasound of the 3rd trimester, during which measurements are taken of the abdominal cavity and head of the unborn child. During the first two trimesters, fetal growth is usually normal and retardation is rare.
Additional tests (uterine Doppler and umbilical cord Doppler) can detect the causes of developmental delay and prescribe treatment depending on the results.
After birth. A low birth weight newborn is weaker than others. He needs to be monitored by doctors as he may have some metabolic abnormalities. The number of feedings increases (7 or 8 per day) due to the risk of glycemia; Sometimes a feeding tube is needed to ensure continuous food intake. To prevent possible hypocalcemia (calcium levels in the blood below normal), the baby is given vitamin D. Finally, if the newborn's temperature is too low, he is placed in an incubator.
This is a consequence of intrauterine growth retardation, or malnutrition.
First of all, the problem of placental insufficiency affects smokers. The symbolism is absolutely eloquent and a straightforward mother does not give her child proper life support. In this regard, smoking, and information about these relationships has long been known, almost always represents a half-conscious attack on the unborn child. The fetus reacts to each cigarette as a painful blow much more sensitively than the mother, or about the same as the mother did when smoking the first cigarette. Newborn children of smokers suffer from withdrawal symptoms and lack of adaptability, which can be expressed in the form of frequent crying, lack of appetite and sleep disturbances.
However, one should not “pounce” on smokers and accuse them of all mortal sins. It would be much better to understand that they suffer from a painful addiction consciously, and they are helpless in turn, and they do not need anything as urgently as help.
In our country, placental insufficiency occurs not only in smokers, but also in alcoholics and drug addicts, primarily heroin addicts. In third world countries, placental insufficiency is also often a consequence of poor nutrition of the expectant mother. And although these women did not have a good basis for pregnancy, they still conceived. Internal denial of pregnancy is not enough developed countries the third world as a whole is less common than among modern women. In our country, this picture of the disease most often affects unconscious, internally unstable women who do not have immune barriers - including against unwanted children.
Placental insufficiency- a symptom of many types of pregnancy complications; it is not an independent disease, but a manifestation of disturbances in the structure and function of the nutrition of the fetus and the correctness of its development.
Based on the time of occurrence, primary, secondary and mixed forms of placental insufficiency are distinguished. Primary placental insufficiency develops before 16 weeks of pregnancy, under the influence of implantation disorders, early embryogenesis under the influence of genetic defects of the embryo; immunological incompatibility of the blood of mother and fetus according to blood group or Rh blood type; endocrine deficiency of the ovaries, and again we return to the problem of STIs that disrupt communication ovum with the wall of the uterus. Placental insufficiency is manifested by changes in its structure, poor vascular blood supply, improper attachment (lower segment, placenta previa), and a violation of the time of formation of the chorion. This form is often combined with a stop in the development of pregnancy (frozen pregnancy), and fetal malformations.
Secondary placental insufficiency develops after 16 weeks, occurs under the influence of external influences and internal negative factors body of a pregnant woman. Secondary placental insufficiency is associated with complications of pregnancy and manifests itself in impaired blood flow in the vessels of the uterus and placenta, which impairs the supply of oxygen and nutrients to the fetus, and simultaneous oxygen starvation of the fetus occurs (chronic hypoxia) and its intrauterine development is delayed. Often, primary placental insufficiency becomes secondary.
According to the course, acute and chronic forms of placental insufficiency are distinguished. Acute insufficiency of uteroplacental blood flow occurs with placental abruption, normally located or presenting, with rupture of the marginal sinus of the placenta, uterine rupture and other acute conditions in obstetrics. If professional help is delayed, fetal death quickly occurs and the woman’s life is threatened. Chronic failure placenta occurs over several weeks and develops at the beginning of the second half of pregnancy. It is associated with the presence of diseases internal organs pregnant woman, exacerbation of chronic diseases during pregnancy, their development and decompensation, which causes dysfunction of the placenta (see below).
According to the state of possibility of compensation, absolute and relative placental insufficiency are distinguished. In the relative form of placental insufficiency, compensatory mechanisms in the placenta are still preserved; this form is treatable.
If the situation during childbirth is unfavorable - persistent weakness of labor, prolonged stimulation of labor or prolonged induction of labor - fetal hypoxia occurs - a violation of its oxygen supply.
With absolute insufficiency of the placenta, the ability to compensate is depleted, a chronic form of oxygen deficiency and hypoxia occurs, and this results in intrauterine growth retardation and a lag in fetal size from the standards of height and weight corresponding to the gestational age. Chronic hypoxia can lead to fetal death.
Modern diagnostics make it possible to distinguish decompensated, subcompensated and compensated forms of placental insufficiency. The presence of one or another form of compensation for placental insufficiency is determined by the degree of lag in size of the fetus from the standards of a given period of pregnancy, the severity of chronic intrauterine hypoxia, the depth of vascular insufficiency of the placental-uterine and fetal-placental blood flow, the hormone-forming function of the placenta and the effectiveness of the treatment.
Placental insufficiency most often develops with diseases of the internal organs of a pregnant woman - hypertension, kidney disease and urinary tract, chronic anemia (anemia), a combined form of diseases of internal organs, for example rheumatoid diseases, which affect the joints and valves of the heart, connective tissue throughout the body.
In second place are the causes of complications of pregnancy itself: long-term threat of miscarriage, anemia of pregnant women, gestosis.
Diagnosis of placental insufficiency is based on determining the hormonal function of the placenta. A decrease in the levels of hormones synthesized in the placenta by 30-50% indicates placental insufficiency. But ultrasound is the most informative. In this case, the location, thickness and degree of structure of the placenta are assessed. The third degree of maturity of the placenta in periods up to 36-37 weeks of pregnancy indicates its early aging- violation of functional mechanisms, placental insufficiency. In some cases, cysts are detected in the placenta - traces of catastrophic circulatory disorders - placental infarctions. Sometimes even many small cysts do not disturb the condition of the fetus. But large cysts lead to the death of part of the placental tissue and chronic fetal hypoxia. Excessive thinning of the placenta with the threat of miscarriage, with gestosis in pregnant women, or thickening of the placenta with diabetes mellitus and hemolytic conflict of the blood of the mother and fetus by more than 0.5 cm indicates placental insufficiency and requires complex treatment and repeated ultrasound. Doppler testing makes it possible to clarify the nature of blood flow disturbances in the uterine arteries and fetal vessels.
Sometimes, or one might say most often, placental insufficiency is diagnosed only by signs of IUGR of the fetus - intrauterine growth retardation. This is called fetal malnutrition (malnutrition, lack of nutrition).
There are symmetrical and asymmetrical fetal growth retardation.
Symmetrical malnutrition is a proportional decrease in all sizes of the fetus according to ultrasound. This is observed in 10-35% of cases. This form of fetal growth restriction develops in the second trimester of pregnancy. If this is diagnosed at the border of the first and second trimesters, at 13-15 weeks of pregnancy, then there is a suspicion of missed genetic defects and chromosomal disorders (trisomy of the 18th pair of chromosomes, Down syndrome or Shereshevsky-Turner syndrome).
The diagnosis should be made after comparing a carefully determined gestational age, fetal size measurements over time (every 2 weeks) and data from previous pregnancies (if any) to identify a tendency towards low birth weight babies. For the development of this form of growth retardation, in addition to the above, smoking of the expectant mother and/or her alcoholism, and insufficient nutrition of the pregnant woman (hypovitaminosis) are important. Carriage forms are also characteristic viral infections- rubella, herpes, cytomegalovirus; venereal diseases - syphilis; toxoplasmosis.
Sometimes developmental defects such as microcephaly are detected (a sharp decrease in the size of the brain, its underdevelopment), birth defects heart, anomalies of the umbilical cord vessels (single artery), Potter's syndrome (hereditary anomalies of almost all internal organs, spine, facial skull, absence or underdevelopment of the kidneys, genitals), the fetus dies in the first hours of life. If such defects are detected, the woman is offered to terminate the pregnancy.
In connection with the above, it seems logical to perform amnio- or cordocentesis for genetic and chromosome analysis fetus
Asymmetrical fetal malnutrition is a condition when the dimensions of the fetal head and long bones of the limbs correspond to the calendar period of pregnancy, and the dimensions of the thoracic and abdominal cavities(circumferences, average diameters) are delayed by 2 weeks (I degree), by 3-4 weeks (II degree) and more than weeks (III degree). Placentometry is also carried out - examination of the placenta, determination of the degree of maturity, thickness, identification of cysts, sclerosis, and fossils. Amniotic fluid, its quantity, and suspension are also assessed.
Diagnosis is not difficult and is possible with the first ultrasound scan. Additional diagnostics - assessment of the state of the fetoplacental complex and the compensatory capabilities of the fetus should include Doppler measurements, a study of the degree of disturbance of the uteroplacental and fetal placental blood flow. And cardiotocography is necessary - a study of the fetal heartbeat, where a number of characteristics are performed conclusion about the condition of the fetus.
The choice of the date and method of delivery is determined by the duration of pregnancy, when diseases or defects of the fetus and placenta are established, the presence of hypoxia (poor oxygen supply), the degree of fetal malnutrition, retardation of its growth, the effectiveness of treatment of the form of placental insufficiency and the nature of the condition of the entire body of the pregnant woman, the presence of chronic diseases or abnormalities in the genital area.
Treatment of placental insufficiency is carried out under the control of ultrasound, Doppler, and cardiotocography. Ultrasound is repeated after 2 weeks, CTG - every 2 days, Doppler study - every 3-4 days.
In case of critical blood flow and gestational age lower than 32-34 weeks, studies are carried out daily. If blood flow is critical after 34 weeks, delivery must be carried out within the next 3-4 hours. If the treatment effect is present, pregnancy is prolonged to 36-37 weeks while treatment is ongoing. If there is no effect of treatment or the condition of the fetus worsens, early delivery is performed.
While carrying a long-awaited baby, unfortunately, not all expectant mothers can calmly enjoy their situation. In some conditions, a woman has to frequently visit her gynecologist, undergo various examinations, and constantly undergo tests. For example, if CPRF is diagnosed during pregnancy, then constant medical supervision is necessary, since such a pathology is fraught with oxygen starvation for the baby.
But this pathology does not occur in the same way in all pregnant women. Manifestations and consequences depend on the duration and severity of the condition. Fetoplacental insufficiency is a whole complex of disorders of the placenta and fetus as a result of complications during pregnancy or gynecological pathologies.
Signs and symptoms of pathology
Manifestations of CPRF depend on the form of the pathology; if there is compensated placental insufficiency, then the mother’s anemia is insignificant, as a rule, no pronounced symptoms are observed.
A pregnant woman feels fine, but if you do an ultrasound, the doctor will always be able to recognize the signs of fetoplacental insufficiency.
It is much more serious when an acute or chronic form develops. Anemia is more pronounced, so a woman may notice the following obvious signs:
- The baby's activity changes. The child begins to move actively, and then suddenly suddenly calms down. Every pregnant woman should know that after 28 weeks you should feel at least 10 movements of the baby per day; if this figure is lower, then you should visit a doctor, because most likely the woman develops anemia, the baby suffers from a lack of oxygen.
- One more characteristic symptom CPRF is a slow growth of the abdomen - the period becomes longer, but the volume of the abdomen changes slightly. This is already fraught with delays in the child’s development. The gynecologist will be able to determine this during a subsequent visit; each time the doctor measures the volume of the pregnant woman’s abdomen.
- If fetoplacental insufficiency develops with severe anemia in the mother, then there is a great threat of termination of pregnancy. This can be evidenced by the appearance of bloody issues. Such a symptom should immediately force a woman to see a doctor, maybe even call ambulance, because often the sign indicates the onset of placental abruption.
- If a woman has anemia and gradually develops FPN, this is reflected in weight gain. In the second trimester, weight should increase by at least 0.5 kg per week, as the fetus grows, the placenta enlarges, and fat deposits appear. If, at the next visit, the doctor discovers that the pregnant woman has not gained weight in a week, then he has every reason to suspect the development of pathology. The woman must be sent for tests, which will immediately show the presence of anemia and other abnormalities.
- Another symptom of the development of fetoplacental insufficiency is the growth of the child. You can determine how well it corresponds to the gestational age using an ultrasound.
- With the development of CPRF, a disorder of the intrasecretory function of the placenta is observed, so very often a woman gives birth prematurely or, conversely, there is a post-term pregnancy.
- Quantity changes amniotic fluid, usually the amount decreases, and ultrasound diagnoses oligohydramnios, but with diabetes mellitus and intrauterine infections, polyhydramnios is noted.
In serious cases, deficiency can cause a missed abortion.
If a pregnant woman takes her situation responsibly and cares about the health of her baby, then she will definitely register with the authorities on time. antenatal clinic. In this case, the doctor will always be able to recognize the pathology at the very beginning of its development.
What can trigger the development of CPRF?
We can name some factors that can lead to the development of placental insufficiency:
- The presence of chronic diseases in a pregnant woman, especially with regard to heart and vascular diseases, thyroid pathologies, diabetes mellitus and heart disease.
- Infectious diseases of the respiratory system.
- Viral diseases.
- Venereal diseases.
- Complications during pregnancy in the form of gestosis, Rh conflict or threat of miscarriage can also cause the development of fetoplacental insufficiency.
- The presence of pathologies of the uterus and reproductive system.
- Disturbances in the attachment of the placenta.
- A history of abortions or miscarriages.
- Love of cigarettes during pregnancy greatly increases the risk of developing anemia, and therefore CFRD.
- Unsatisfactory living conditions.
- Late or early pregnancy.
Treatment of CPRF
Therapy when fetoplacental insufficiency is detected is reduced to solving the following problems:
- Improving blood circulation in the uterus and placenta.
- Correct the blood clotting process.
- Improve gas exchange.
- Eliminate anemia in the mother.
- Normalize the tone of the uterus.
- Improve metabolism.
A pregnant woman should understand that there is no special treatment that would 100% eliminate the pathology. You can only stabilize the condition and reduce the risk of abnormalities in fetal development to a minimum.
The first step is to prescribe drug therapy:
- Curantil is prescribed, it eliminates anemia, improves blood circulation, and prevents irreversible changes in the placenta. The advantages of the drug include the almost complete absence of side effects. The course of treatment lasts at least a month.
- Actovegin is also often prescribed to activate metabolic processes and improve blood circulation. The pregnant woman's condition improves significantly. But among negative consequences such treatment can be called birth large child, therefore, if the ultrasound determines the high weight of the fetus, then the medicine is not prescribed.
- In the hospital, treatment is carried out with the appointment of droppers with Eufillin, as well as a mixture of glucose and Novocaine.
- To relax the uterus, a dropper with Magnesia or Ginipral is recommended.
- If coagulability is increased, then the woman is prescribed Clexane, Heparin.
- To normalize antioxidant protection, the expectant mother is prescribed vitamins E and C.
- If there is a risk of miscarriage, then tocolytics are prescribed, for example, Fenoterol, Hexoprenaline.
There are quite a few medications for the treatment of fetoplacental insufficiency, but in each specific case the doctor prescribes the drugs individually.
Prevention of the development of fetoplacental insufficiency
To avoid the need for long-term treatment of the pathology, it is better to take all measures to prevent it.
The following can be considered as preventive measures::
- Pregnancy needs to be planned, but, unfortunately, most couples take this advice lightly.
- Before pregnancy begins, a woman must undergo a complete examination to identify the presence of risk factors and existing chronic pathologies.
- Eliminate exposure to factors such as smoking and alcohol abuse.
- Do not take any medications without the advice of a specialist.
- Prevent infectious diseases whenever possible.
- Adjust your diet, it should include a large number of vegetables and fruits.
- Avoid overwork and frequent stress.
- Provide the body with proper rest.
- If pregnancy occurs with complications, then constant monitoring by a doctor is necessary to prevent CPRF.
Placental insufficiency is a serious problem, but if you follow all the doctor’s recommendations and take a responsible approach to the birth of your baby, you can minimize the risk and give birth to a healthy baby.
Placental insufficiency during pregnancy has Negative influence on fetal development. If the disturbances are severe, then the functional ability of the shell to provide nutrients and oxygen is reduced. Hypoxia develops, which threatens the baby's life.
Symptoms of placental insufficiency during pregnancy
Placental insufficiency during pregnancy manifests itself depending on the form of pathology:- In the chronic compensated form, there are no pronounced symptoms. It is possible to determine that uterine placental insufficiency is developing only with the help of ultrasound and other examinations.
- Decompensated - characterized by erratic movements of the fetus inside the womb. The doctor may notice signs of tachycardia (increased heart rate) and later bradycardia (slow heart rate) in the child.
One of the most dangerous symptoms is the presence of bloody discharge from the vagina, which indicates pathological processes - detachment or premature aging placenta.
Causes of placental insufficiency during pregnancy
The reasons for which the disease develops can be divided into two categories. Primary - imply an initially incorrectly formed placenta and secondary, which were formed under the influence of various factors already during the gestation period.Among the main reasons are:
- hereditary diseases or genetic disorders;
- infectious reactions in the mother's body;
- limited production of progesterone;
- woman's age over 35 years;
- smoking and alcohol abuse;
- lack of normal nutrition;
- contact with harmful chemicals during professional activity;
- previous interruption, including abortions;
- conflict of Rh factors;
- abnormal structure of the uterus.
Inflammatory reactions threaten the penetration of harmful bacteria into the baby. The consequences of such a pathological process, in the later stages, most often depend on the type of infection or virus.
Placental insufficiency during pregnancy
Fetoplacental insufficiency (FPI) during pregnancy is a pathological process that significantly reduces blood flow between woman and baby. The situation is also dangerous because the placenta reduces the supply of oxygen and nutrients to the fetus. The synthesis of hormones becomes slower, while the normal formation of the baby suffers, and there is a danger of birth defects.There are several forms of FPN:
- impaired hemodynamic function;
- pathology associated with the transfer of substances.
The chronic form is accompanied by gestosis, and treatment is carried out under the constant threat of interruption, which often ends in the third trimester, labor ahead of schedule.
The causes of the disease mainly depend on the production of hormones. This affects long-term post-term pregnancy and the risk of hypoxia.
Infectious diseases that develop in the vagina penetrate through the ascending path to the placenta. Thus, harmful microorganisms reduce the protective barrier, infect the fetal membrane, and contribute to infection of the baby inside the womb.
Failure of the excretory function leads to oligohydramnios or, conversely, to polyhydramnios in diabetes mellitus.
But the main danger is delayed fetal development, accompanied by progressive hypoxia.
The signs and sensations of the disease are individual for each woman. During examination, doctors may suspect it by measuring the size of the abdomen and the ratio of the height of the uterine fundus. Minor symptoms and specialist suspicions indicate the need to undergo an ultrasound examination to determine the pathology for more early and start her treatment.
Treatment of placental insufficiency
Ultrasound determines and compares with normal indicators weight and length of the child. In case of significant deviations, especially if disproportionate indicators are observed (length is normal, weight is lagging), additional studies are prescribed.After all diagnostic procedures and confirmation of the diagnosis, treatment is carried out in a hospital setting, which involves the prescription of drugs depending on the main indicators of the occurrence of pathology.
The main goals for improving the functionality of the placenta are identified:
- improving the quality of blood flow;
- preventive measures to eliminate developmental delays;
- determining the acceptable date premature birth and choice of delivery.
"Placental insufficiency"
Placental dysfunction is one of the main causes of perinatal morbidity and mortality. In recent years, it has become common to talk about placental insufficiency; this concept does not yet have clinical content, but at the same time it is included in the international statistical classification of diseases.
Placental insufficiency should be understood as a decrease in its ability to maintain adequate exchange between the organisms of the mother and fetus.
According to the classification of Fedorova and Kalashnikova /1936/, primary placental insufficiency that occurs before 16 weeks is distinguished. pregnancy, and secondary, arising in more late dates. According to these data, primary placental insufficiency occurs during the period of implantation, early embryogenesis and placentation under the influence of various factors: genetic, endocrine, infectious; acting on the gametes of the parents, the zygote, the blastocyst, the developing placenta and the female reproductive apparatus as a whole. Of great importance in the development of primary placental insufficiency is the enzymatic failure of the decidual tissue (for example, with ovarian hypofunction), which carries out trophism of the fetal egg. Primary placental insufficiency is manifested by anatomical disorders of the structure, location and attachment of the placenta, as well as defects in vascularization and disorders of chorion maturation.
Secondary placental insufficiency develops against the background of an already formed placenta under the influence of exogenous Factors. As a rule, this pathology is observed in the second half of pregnancy.
Placental insufficiency can have an acute and chronic course. Most often, acute placental insufficiency occurs as a consequence of extensive disturbances in the circulatory system, in urgent situations in obstetrics (uterine rupture, placental abruption, intraplacental thrombosis, sudden death of the mother, etc.). Chronic placental insufficiency is a more common pathology, observed in approximately every 3rd pregnant woman at high risk of perinatal pathology.
Perinatal mortality with placental insufficiency reaches 60 ppm. Chronic placental insufficiency can develop relatively early (at the beginning of the second half of pregnancy) and last for a long time from several weeks to several months.
Depending on the compensatory-adaptive reserve of the placentas, this pathology is usually divided into decompensated, subcompensated and compensated forms, based on the condition of the fetus and the degree of its underdevelopment.
Etiology and pathogenesis of placental insufficiency
1. The causes of acute dysfunction of the placenta are complications of pregnancy and extragenital diseases that arise during gestation and childbirth. These primarily include late gestosis/nephropathy. preeclampsia, eclampsia/, chronic glomerulo- and pyelonephritis, diabetes, influenza, acute respiratory viral infections, etc. Often the cause of acute dysfunction of the placenta is anomalies in its location (presentation, low attachment), as well as developmental defects (umbilical cord nodes, short umbilical cord, etc.).
The pathogenesis of acute placental insufficiency depends on its form. With acute hemorrhagic infarction of the placenta, changes occur in both the maternal and fetal parts of the placenta. It is believed that maternal circulation in the intervillous space is initially damaged as a result of changes in the spiral arteries.
Acute placental insufficiency is caused by the formation of intraplacental blood clots. Local cessation of fetal circulation in one of the catheledons is known as “nodular ischemia”.
The most dangerous thing for mother and fetus is premature abruption of a normal and low-lying placenta. In this case, in the genesis of placental apoplexy, the leading role is played by stagnation in the intervillous space.
With mechanical damage to the fetal blood flow in the umbilical cord, secondary damage occurs in the intervillous space of the placenta.
2. Chronic placental insufficiency syndrome is of a multifactorial nature. Diseases of the mother, fetus and placenta can lead to its development.
Primary placental insufficiency is formed on early stages development of the placenta as a consequence of the influence of various factors /genetic, endocrine, infectious, etc./..
Changes in the production and maturation of gametes may be caused by exposure to certain physical factors /ionizing radiation/ or chemical substances, including drugs /chronic intoxication/.
The structure and degree of development of the vascular network of the uterus, the presence of anomalies in its development and myomatous nodes, etc. are important in the formation of the placenta. Disturbances in the mother's body's adaptation to pregnancy also play a certain role.
Secondary chronic placental insufficiency develops, as a rule, against the background of an already formed placenta due to a complicated course of pregnancy, caused either by its pathology (gestosis, threat of miscarriage, etc.), or by infectious and extragenital diseases.
Despite the variety of forms of placental insufficiency, they are all, to one degree or another, accompanied by pathology of blood circulation in the uterus and placenta.
As is known, dysfunction of the peripheral arteries, which can conditionally include the uterine ones during pregnancy, can be caused by disturbances in their vasomotility / functional expansion or narrowing /, with structural changes in the walls / arteriolosclerosis / or complete or partial blockage of the vascular lumen due to arteriolosclerosis, thrombosis or embolism. The degree of circulatory disturbance /placental insufficiency/ depends on where these changes occur, in most vessels or in individual parts of the system.
A decrease in blood flow in individual parts of the system does not necessarily lead to a significant decrease in blood circulation throughout the entire organ. As a rule, collateral inflow and outflow of blood occurs. Therefore, blood supply is almost always gradually restored. If the collateral blood flow is insufficient, then a sharp weakening of microcirculation occurs, and ischemia and degenerative processes form in the corresponding areas of the tissue.
Pathological blood circulation in the uterus and placenta can be caused by a very large number of different reasons. For example. disorder of innervation mechanisms. Neurogenic factors have a great influence on the normal functioning of the heart and the condition of the blood vessels of a pregnant woman.
Biologically active substances circulating in the blood as exogenous. and endogenous ones can change vascular tone, tissue destruction, etc. Under their influence, an increase or decrease in vascular tone may occur. Humoral transport system /in foreign. literature - mass transfer /, includes general blood circulation and fluid movement in the chain: blood-tissue-lymph-blood is functionally unified. Similar processes occur in the lymphatic system.
Therefore, the biologically active substances present in these systems, a change in their concentration or the introduction of new ones can affect the functioning conditions of the lymph and blood circulation and the formation of functional or organic damage.
Insufficiency of the uteroplacental circulation is largely determined by the nature of pregnancy complications. With different pathologies, the pathogenesis of MPC may be different.
In case of OPG-preeclampsia, the pathogenesis of circulatory damage" was presented to you in previous lectures.
In case of miscarriage, the main role is played by the central mechanisms of blood circulation regulation. In cases of habitual miscarriages, frequent instability of the cervical vascular reaction and impaired vascular reactivity of the uterus and placenta were found. Serov et al. It is believed that the leading pathogenetic mechanism of miscarriage is myometrial hypoxia as a result of hemodynamic disturbances in the uterus. If there is a threat of miscarriage, increased BMD leads to a decrease in excitability and contractile activity of the uterus.
When placental insufficiency occurs, regardless of the etiology, the same changes occur in the body of the fetus, indicating damage to humoral regulation, leading to damage to the biophysical properties of its blood. Increased viscosity is recorded in the fetal blood. In response to hypoxia in the fetus, increased amounts of norepinephrine and other amines are released from the chromoile tissues.
With Rh sensitization, primary disorders occur in the fetal body, subsequently damaging the placental and then the uteroplacental circulation. The same mechanism of damage to the BMD occurs in other fetal diseases, for example infectious, some genetically determined.
With placental insufficiency, according to Kalashnikova, widespread circulatory disorders from the maternal and fetal parts of the placenta lead to nonspecific morphological disorders: premature maturation of the strema, involutively destructive changes in the structural elements of the villous chorion and depidual tissue.
The effect of placental insufficiency on the fetus and newborn Acute placental insufficiency leads to acute fetal hypoxia and asphyxia of the newborn, the severity of which is determined by the size / size / of the affected area of the placenta and the time interval from the onset of disturbance of placental blood flow to delivery. Chronic placental insufficiency can cause a terratogenic effect (cerebral palsy, heart defects), as well as fetopathy in the form of prenatal dystrophy, chronic hypoxia, their combination, and disruption of the period of adaptation to extrauterine life.
According to the WHO classification of the IX revision, 2 categories of impaired growth and development of the fetus are distinguished. "Slow growth and malnutrition of the fetus", "Disorders associated with prolonged gestation and high birth weight." In addition, in accordance with generally accepted criteria, all newborns, depending on intrauterine growth /gestograms/, are divided into 9 groups. The first 3 groups are full-term, premature and post-term children corresponding to the gestational age. 4,5,6 include full-term, premature and post-term infants who are too large for their gestational age. Groups 7,8,9 included full-term, premature and post-term children. small for this stage of pregnancy.
In order to differentiate the assessment of the correspondence of the weight and length of the child’s body to the gestational age, percentile tables and Dementieva curves are used. The average norm is located between the 25.50 and 75 percentiles. Values below the 25th percentile or above the 75th percentile are considered deviations from the norm.
Of the various forms of impaired physical development of newborns with placental insufficiency, growth retardation (low weight in relation to gestational age, or small children for term) and fetal malnutrition (intrauterine or congenital malnutrition) are most often observed. The distinction between these forms, with the exception of congenital metabolic disorders, is extremely difficult.
Depending on the lag in anthropometric data, 3 degrees of delayed fetal development are distinguished. At grade 1, the data are located between the 25th and 2nd percentiles. and the delay from gestational age is about 2 weeks. Developmental delay of 2 and 3 degrees is characterized by a simultaneous decrease in the weight and length of the newborn’s body. At grade 2, body weight is between the 10th and 4th percentiles, at grade 3 - at the 3rd percentile and below.
In addition, the weight-height coefficient is used: with normal anthropometric data, this parameter varies above 60, with 1st degree malnutrition - from 60 to 55, with 2nd degree malnutrition - 55 - 50, and 3rd degree - below 50.
We analyzed the course of pregnancy in 255 patients /from the general population/, whose children were born with signs of intrauterine malnutrition of 1st degree /75.5%/, 2nd degree /17.6%/, and 3rd degree /6.7%/. Of these, young primiparas /under 19 years old/ accounted for 8.6%, women in labor over 35 years old - 6.7%, 13.7% of women were short in stature /below 155 cm/. Thus, it was proven that symmetrical malnutrition is genetically caused and not a pathology.
Chronic fetal hypoxia, resulting from a violation of transplacental gas exchange, does not develop in every pregnant woman with placental insufficiency and depends on the stage of development and the nature of changes in the placenta. Chronic hypoxia often leads to the birth of children with asphyxia and ante- or intranatal fetal death, but in some cases it does not significantly affect the general condition of the child at birth.
As studies carried out at our department have shown, oxygen deficiency leads to characteristic changes in metabolism, hemodynamics and microcirculation, well known to you, at birth in every second child and disrupts adaptation processes in the first days of life in 50-75% of children.
Studies of metabolism in the mother-water-fetus system and newborns indicate a nonspecific response of the fetus to acute and chronic hypoxia.
Clinic of placental insufficiency.
Placental insufficiency has some general and local manifestations, despite extremely mild clinical symptoms. As a rule, pregnant women do not complain. However, some pregnant women do not experience physiological weight gain. Metabolic and hormonal imbalances are possible. Local manifestations of placental insufficiency include changes in the body of the fetus and placenta. There are disturbances in the growth and development of the fetus, its condition suffers, which is expressed in changes in its motor activity and cardiac activity. Changes in the placenta /structural and functional/ can only be determined using objective research methods.
A comprehensive examination carried out for the purpose of diagnosing placental insufficiency should include: 1/.assessment of the growth and development of the fetus by carefully measuring the height of the uterine fundus, taking into account the abdominal circumference and body weight of the pregnant woman, ultrasound biometry of the blanket, 2/.assessment of the condition of the fetus by studying its motor function activity and cardiac activity, 3/.ultrasound assessment of the condition of the placenta, 4/.study of placental circulation, blood flow in the vessels of the umbilical cord and large vessels of the fetus, 5/.determination of the level of hormones in the blood and specific proteins of pregnancy, 6/.assessment of the state of metabolism and hemostasis in the body of a pregnant woman.
Growth and development of the fetus. The growth and development of the fetus during pregnancy is determined using external obstetric examination (measurement and palpation) and ultrasound scanning. Each of these methods has its own advantages and disadvantages. A screening test is to measure the height of the uterine fundus above the womb and compare it with the abdominal circumference, body weight and height of the pregnant woman. UMR before 30 weeks is 0.7-1.9 cm/week, between 30-36 - 0.6-1.2 cm/week and after 36 weeks -0.1-0.4 cm/week. When verifying data on this indicator with the weight of newborns, it was found that the difference can only be detected between healthy fetuses, fetuses with severe malnutrition (below the 10th percentile) and large fetuses (above the 90th percentile).
Establishing fetal growth using clinical methods presents certain difficulties; in these situations, ultrasound provides invaluable assistance.
In the early stages of pregnancy, the size of the ovum is measured, and the outer and inner diameter of the ovum is measured. The error in this case is up to 1 week of development.
When establishing the gestational age and fetal weight after the 1st trimester, measuring the biparietal size of the head, or fetal cephalometry, remains the most common method. In addition to the BPR, the heads use such parameters as the area and circumference of the head and the fronto-occipital diameter. Up to 30 weeks pregnancy, BPD increases by 3 mm/week, at 30-34 weeks - by 1.3 mm/week, and after 34 weeks - by 1 mm/week_
In recent years, in addition to BPD, determination of fetal femur length has been used to determine the gestational age of the fetus. The growth rate of the femur up to 24 weeks is 3 mm/week, from 25 to 35 weeks. is 2.2 mm/week, after 35 weeks - 1.8 mm/week.
In our country, measuring two fetal sizes has become widespread: average diameters chest the fetus at the level of the leaflet valves of the heart and abdomen at the origin of the umbilical cord.
In addition, it was proposed to measure the volumes of the fetus and uterus and other anatomical formations of the fetus and uterus. There are many different nomograms, and this is not our topic. The ultrasound will be read separately.
Condition of the fetus. The condition of the fetus with placental insufficiency depends on the degree of preservation of the compensatory mechanisms of the placenta. Information about disorders in the fetal body during pregnancy can be obtained by assessing its cardiac activity, hemodynamics and motor activity, including respiratory movements, studying the composition of amniotic fluid and some parameters of maternal homeostasis. Cardiovascular monitoring allows us to identify initial signs of intrauterine hypoxia or metabolic disorders.
The state of fetal cardiac activity during placental insufficiency mainly reflects the nature of changes in the placenta and is less dependent on pregnancy complications. Chronic fetal hypoxia is detected during a non-stress test; most often, monotony of the rhythm, lack of acceleration in response to fetal movements, or the occurrence of decelerations, often turning into bradycardia, are observed.
With intrauterine growth retardation, in addition to the signs listed above, peak-shaped decelerations of type deep 0 are often recorded. Particular attention should be paid to the reaction of the fetal cardiac activity in response to its movements. Krause identifies five types of responses, three of which reflect the good state of the fetus with the appearance of accelerations, a volley of high oscillations, and a saltatory rhythm. the reaction is considered doubtful when peak-shaped decelerations of the dip 0 type occur. The absence of any reaction to fetal movement is a bad sign. Spontaneous abnormalities in fetal cardiac activity (score 6 or lower on the Fisher scale) detected during cardiac monitoring are an unfavorable sign for the fetus. If placental insufficiency is suspected, it is advisable to take into account motor activity fetus The counting of movements is carried out by the pregnant woman herself within 30 minutes. Normally, the average frequency of fetal movements is about 3 in 10 minutes. Their increase in frequency and intensification, as well as a sharp decrease in the frequency of motor activity, indicates the occurrence of fetal pathology.
Valuable information about the condition of the fetus during ultrasound examination can be obtained by assessing the respiratory movements of the fetus. Assessment of this biophysical parameter can provide, albeit indirect, fairly accurate information about the state of the central nervous system of the fetus. Normally, the fetal respiratory rate reaches 50 per minute at the age of 35-40 weeks. They are not constant and are combined with periods of apnea. for which time intervals of 6 seconds or more should be taken. The absence or change in fetal respiratory movements at the end of pregnancy is a poor prognostic sign, especially the type of shortness of breath. A decrease in respiratory activity has been established when the fetus is delayed in development.
The use of ultrasound in widespread practice makes it possible to determine biophysical profile fetus Most authors include five parameters in this concept: the results of a non-stress test conducted during cardiac monitoring, and four indicators determined by echography (respiratory rate, physical activity, muscle tone fetal volume of amniotic fluid. Vinceleus also takes into account the degree of maturity of the placenta. The maximum score is 12 points, with 6-7. scores, a repeat study is necessary. With a score of 6-4 points, there is significant fetal suffering, and pregnancy management tactics depend on the degree of fetal maturity and the preparedness of the birth canal for childbirth.
The cordocentesis currently used is worthy of attention - puncture of the umbilical cord vessels and determination of acid-base balance of fetal blood and other studies of microdoses of fetal blood.
In addition to the listed methods, the biochemical composition of amniotic fluid is examined during amniocentesis. They contain an increased content of acidic metabolic products, a decrease in pH, a change in the ratio of biologically active substances, and the activity of a number of enzymes.
Assessment of the condition of the placenta and placental circulation.
Ultrasonography for placental insufficiency can detect some pathological changes in the placenta /cysts, calcification, fibrinoid necrosis, areas of detachment, etc./. There are 4 degrees of placental maturity. The combination of disturbances in the placenta with its premature aging may indicate placental insufficiency and the need for delivery. Placentometry provides valuable information about the condition of the placenta. those. determination of its thickness, area and volume. A decrease in the area and volume of the placenta indicates the presence of placental insufficiency.
In order to assess blood circulation in the placenta, methods are used that allow one to get an idea of the uterine, utero-placental. fetal-placental and fetal blood flow. Rheography and radioisotope placentoscintigraphy have been used for a relatively long time, while Doppler ultrasound began to be used only in recent years.
Based on the results of reogray of the abdominal organs, you can get a rough idea of the blood supply to the uterus. The method has not yet been fully developed and can be used as a screening method.
More accurate data on blood circulation in the intervillous space of the placenta can be obtained using radioisotope placentoscintigraphy. This method is based on visualization of the organ, obtaining from its shielded areas the dynamic characteristics of the intake and distribution of radiopharmaceuticals administered to the mother.
The results of placentoscintigraphy in a patient are shown. Slide. Studies conducted by us and other authors have shown that normally OC in the intervillous space of the placenta fluctuates within 100 ml/min per 100 g of placental tissue. In pathology, there is a significant decrease of 30% or more from the norm, and various parameters of the activity-time curves also change.
With the introduction of Doppler ultrasound into obstetric practice, it became possible to study blood flow in the arcuate arteries, which at the end of pregnancy represent cords with a diameter of about 3 mm. The state of diastolic and systolic blood flow in the arcuate arteries of the uterus in the last trimester of a physiological pregnancy ranges between 62 and 70%. A decrease in this ratio to 52% and below indicates a significant decrease in blood flow in the uterine arteries, and consequently in the intervillous space of the placenta.
The study of fetal blood flow in the umbilical cord has great diagnostic significance. Blood flow in the umbilical cord vein normally fluctuates within 100 ml/min. It is customary to study blood flow in the umbilical cord arteries using pulsogram analysis. as in the arcuate arteries. During the physiological course of pregnancy, the ratio of diastolic and systolic blood flows is about 60-70%, the resistance of the umbilical vessels does not exceed 2. Pi, according to our data, ranges from 0.9 to 1.5. With a pathological course of pregnancy, Pi reaches 3.
Hormonal imbalances. An important diagnostic criterion for placental insufficiency is the level of hormones in the blood of a pregnant woman. In the early stages of pregnancy, the most informative indicator is the concentration of hCG-chorian gonadotropin, a decrease in which, as a rule, is accompanied by a delay or arrest of embryo development. At a later stage, in the second half of pregnancy, the concentration of placental lactogen is of great importance. With placental insufficiency, the concentration of PL in the blood decreases by 50%, and with fetal hypoxia by almost 2 times. The role of progesterone determination is controversial. To a large extent, the function of the fetoplacental system is characterized by the concentration of estriol. since when the fetus suffers due to placental insufficiency, the production of this hormone by the liver decreases. A decrease in the level of estriol in the blood of pregnant women by more than 50% is an indicator of a threatening condition of the fetus. Oncofetoproteins, such as alpha-fetoprotein, alpha-2-fertility microglobulin, PAPP, etc., are of great diagnostic significance in determining placental insufficiency. In cases of fetal development disorders, prenatal damage and placental insufficiency, the level of these substances varies significantly from control data.
Indicators of hemostasis and metabolism. Placental insufficiency of any etiology is based on disturbances in placental circulation, including microcirculation and metabolic processes, which are closely related. They are accompanied by changes in blood flow not only in the placenta, but also in the body of the mother and fetus.
It should be noted that micropiriculation disorders are detected early, even before the appearance of clinical symptoms of gestosis and placental insufficiency. The criteria for placental insufficiency are an increase in erythrocyte aggregation against the background of hyperfibrinogenemia, a decrease in the number of platelets and an increase in their aggregation. In the diagnosis of placental insufficiency, an increase in platelet aggregation on collagen is of great importance. With satisfactory placental function, the activity of thermostable alkaline sosphotase accounts for more than 50% of the total phosphatase activity. If TAS activity is less than 25%, this indicates severe placental insufficiency and a poor prognosis for the fetus.
In amniotic fluid with placental insufficiency, the concentration of non-essential amino acids increases and the concentration of essential amino acids decreases. The concentration of urea and potassium increases, acidic metabolic products accumulate, the activity of histidine catabolism enzymes increases, etc.
TREATMENT OF PLACENTAL INSUFFICIENCY
Abroad, when identifying placental insufficiency and BMD deficiency. as a rule, after 28 weeks of gestation they resort to early delivery, since thanks to intensive therapy, newborns often even with a low weight (up to 1000 g) survive in 95% of cases. When delivering a child, the overwhelming number of obstetricians take into account the gestational age, fetal weight and the severity of the condition of the mother or placental insufficiency. This is due to the fact that until now, the second leading cause of PS in the vast majority of countries in the world is the mortality of premature infants. In 1948 At the 1st World Health Assembly of the League of Nations, it was proposed that all children born with a body weight of less than 2500 g be considered premature. In fact, many newborns weighing less than 2500 g show signs of sufficient maturity and should not be considered preterm. On the other hand, some newborns (a typical example are children of mothers with diabetes), despite their large body weight, may not be mature enough in their development.
Fetoplacental insufficiency during pregnancy (FPI) occurs in 7 out of 10 expectant mothers. This frightening statistic has many reasons, such as pathological condition has a multifactorial etiology. As gynecologists emphasize, such a problem can appear in any trimester. The term FNP refers to a number of disorders in the “mother-placenta-fetus” system.
General information
A woman's body changes in many ways while bearing a child. Normally, by 15–16 weeks, “ children's place" - placenta. This organ exists only during pregnancy and serves as a link between mother and fetus. The importance of the placenta is difficult to exaggerate:
- Provides an influx of oxygen and removes carbon dioxide;
- Supplies nutrients and removes “waste”;
- Protects against infections;
- Produces active substances necessary for the growth and development of the fetus.
Thus, any pathological changes in the placenta harm the unborn baby.
The essence of FNP is the disruption of blood circulation in the part of the body where fetal maturation occurs.
The nature and course of the pathology depend on the age and health status of the woman. Medical practice shows that most often FNP develops in young girls (under 17 years old) and mature women (after 35 years old). In 20% of cases, placental insufficiency leads to spontaneous abortion and fetal death due to hypoxia (oxygen starvation), in 10% - to the fact that the child is born with physical and mental disabilities.
Nature of origin of FNP
Experts say that the cause of placental insufficiency can be almost any disease of the expectant mother. Infectious diseases are a source of danger, since microbes and viruses can have a detrimental effect on the “children’s place.” If a pregnant woman has anemia, iron deficiency leads to poor blood flow. Problems from outside of cardio-vascular system provoke damage to the placenta due to the formation of microthrombi.
Negative factors influencing the development of FNP include:
- Anatomical abnormalities of the uterus;
- Multiple pregnancy;
- Asthma;
- Diabetes and other endocrine diseases;
- Kidney failure;
- Toxicoses;
- Uterine fibroids;
- Mismatch between the Rh factor of the woman and the fetus.
The danger increases many times if the expectant mother has had abortions and STDs, has bad habits, antisocial image life.
Signs of FNP
Symptoms of fetoplacental insufficiency at the stage of the onset of disorders and during the transition to the chronic form do not clearly appear. Doctors strongly recommend that pregnant women listen to their bodies and immediately seek professional help in the following situations:
- Ankles and feet swell;
- Worried about pain in the lower abdomen;
- The uterus is regularly tense;
- Colic torments;
- Bloody discharge from the vagina appeared.
IMPORTANT! From the 28th week of fetal ripening, a woman should normally feel its movements at least 10 times a day. IN otherwise ordered to urgently report to a gynecologist for an unscheduled examination.
Classification
There are acute and chronic forms of FNP depending on the course of the pathological process. The first option is rarely observed. It is characterized by the fact that a rapid deterioration in blood circulation causes placental abruption and leads to spontaneous abortion.
Chronic placental insufficiency is of two types: compensated and decompensated. In the first case, damage to the placenta does not affect the maturation and development of the fetus, since it adapts to these changes due to the protective and compensatory abilities of the maternal body. Competent and timely treatment of fetoplacental insufficiency of this form ends successfully in 99% of patients, without complications.
Decompensated FNP is characterized by a persistent deterioration in blood flow. In this condition, the placenta is unable to perform its functions. As a result future baby does not receive enough oxygen, which results in intrauterine growth retardation or death.
Severe consequences of FNP most often occur if violations appear on early stage pregnancy. As gynecologists note, fetoplacental insufficiency, the development of which began in the last trimester, does not cause such complications. Thus, primary FNP (up to 4 months) and secondary (in the later months of pregnancy) are classified according to timing. The primary form of pathology, developing during the period of structure and attachment of the placenta, in many cases provokes the death of the embryo, since the incorrectly formed “baby place” is not able to perform its functions and the embryo does not develop. Most often, this type of placental system disorder is caused by hormonal imbalances, anomalies and diseases of the uterus.
The secondary form of FNP in most patients is associated with external factors. Under the influence of inflammatory processes, physical activity, stress, and exacerbation of chronic diseases, the normally maturing placenta becomes damaged and ceases to function fully.
Diagnostic methods
Considering that pathology appears for a number of reasons, complex dynamic examinations are necessarily carried out to establish the form and stage of FPN. This is especially true for patients at risk:
- Primipara after 35 years;
- Women under 18 years of age;
- Expectant mothers with a history of gynecological and cardiovascular diseases, problems with endocrine system, STD;
- Pregnant women leading an unhealthy lifestyle.
The doctor’s main task is to determine the degree of fetal development and rule out (or confirm) low or polyhydramnios. To do this, the weight of the expectant mother is determined, the abdominal circumference is measured, and the level of the uterine fundus is assessed.
If fetoplacental insufficiency is suspected, diagnosis includes the following manipulations:
- Examination on a gynecological chair;
- Collection of material for laboratory research(blood, smear);
- Ultrasound - allows you to determine the degree of maturity and thickness of the placenta, whether the size of the fetus is normal, its motor activity, the volume of amniotic fluid;
- Dopplerography of utero-fetal blood flow - helps to establish how blood circulates in the vessels of the umbilical cord, uterus and placenta;
- Phonocardiography and cardiotocography (CTG) of the fetus - the frequency and rhythm of the heartbeat of the unborn child are determined.
IMPORTANT! CTG is performed daily if a diagnosis of FNP is made.
Treatment
Treatment of fetoplacental insufficiency depends on the severity, form and stage of the disorder. With compensated FNP, when it is precisely determined that there is no risk of miscarriage and threat of fetal growth retardation, there is no need for hospitalization. Treatment is aimed at eliminating the specific factor that caused the deterioration of blood flow in the placental system. The main task is to correct the development of the fetus and restore the condition and functionality of the “baby place”.
To avoid complications, the following medications are prescribed:
- Medicines and vitamins that improve microcirculation and blood circulation;
- Means for activating metabolism;
- Drugs to reduce uterine tone;
- Sedatives to normalize sleep and stabilize the nervous system.
IMPORTANT! Take medications strictly according to the doctor's instructions. Self-medication, use traditional methods is strictly contraindicated.
Drug therapy should be combined with proper nutrition and good rest.
If no positive dynamics are observed, the patient is hospitalized and treatment continues in a maternity hospital. If there are no further results, the possibility of a cesarean section is considered.
The decompensated form of FNP requires immediate hospitalization of the pregnant woman. The complex of therapeutic measures includes taking “Curantil” (improves microcirculation, eliminates fetal hypoxia), oxygen cocktails. Among the procedures, droppers with magnesium, aminophylline, and a glucose-novocaine mixture are prescribed. There is no standard treatment regimen, it all depends on individual characteristics patients (age, medical history), root causes of FNP, condition of the placenta and fetus.
In many cases it is possible natural childbirth with a diagnosis of “fetoplacental insufficiency”. Subject to constant monitoring of the condition of the pregnant woman and the development of the baby, and in the case of a positive prognosis, doctors allow such an outcome of events. As a rule, obstetrics proceeds without complications, and a full-fledged child is born.
Preventive measures
Pregnancy is an exceptional time in the life of every woman. It is advisable to prepare for it in advance. This will be the most effective prevention any complications, including FNP.
If the expectant mother is suffering chronic diseases, you need to make every effort to cure them or bring them to the stage of compensation.
- Try to undergo a full examination before becoming pregnant (ophthalmologist, endocrinologist, cardiologist, etc.);
- Get rid of bad habits(smoking, alcohol abuse);
- Lead a healthy lifestyle, play sports, get your immune and nervous system in order;
- While carrying a child, avoid hypothermia, stress, and excessive physical activity;
- Observe personal hygiene extremely strictly;
- Stick to a daily routine, get enough rest, go to fresh air, get a good night's sleep ( night sleep should be 9–10 hours);
- Eat right, providing your body with proteins, vitamins, and microelements;
- During pregnancy, regularly visit your obstetrician-gynecologist, carefully monitor your health, undergo examinations and tests on time;
- During pregnancy, take a mineral-vitamin complex (as recommended by your doctor);
- Visit together with the child’s father special courses for future parents.
These rules and restrictions will help you bear and give birth to a healthy baby.
Let's sum it up
Placental insufficiency is a common complication during pregnancy. Causes of placental dysfunction may include various factors, as a result of which the intrauterine development of the baby may be defective. Only by doing everything possible for her own health can the expectant mother reduce the danger to zero. Even with the development of strong FNP resources, healthy body will be enough to compensate for the pathology.
We wish easy pregnancy and successful birth!
