Fetoplacental insufficiency is a complex of morphofunctional disorders on the part of the fetus and placenta, developing as a result of various extragenital and gynecological pathologies, as well as pregnancy complications. The presence of fetoplacental insufficiency may be accompanied by the threat of termination of pregnancy, hypoxia and fetal development delay, etc. Diagnosis of fetoplacental insufficiency is based on ultrasound, CTG, dopplerometry of uteroplacental blood flow. Treatment of fetoplacental insufficiency requires therapy of the underlying disease; conducting medical courses aimed at improving fetal and uterine blood flow, correction of hypoxic disorders of the fetus; if necessary, early delivery.
O43.8 Other placental disorders
Fetoplacental insufficiency is a factor of perinatal fetal death in more than 20% of cases, significantly complicates the course of pregnancy and childbirth. The manifestations and complications of fetoplacental insufficiency, as well as their consequences for the mother and fetus, are due to the degree of change in the functions of the placenta, the gestation period, the strength and duration of the disorder, the development of compensatory and adaptive mechanisms in the “mother-placenta-fetus” system.
In conditions of fetoplacental insufficiency, fetal hypoxia develops, a delay in its intrauterine growth and development; the probability of premature birth, various anomalies of labor activity, birth injuries of the fetus increases. In newborns, adaptation processes are subsequently more difficult, perinatal encephalopathy, congenital anomalies (hip dysplasia, torticollis) are more often detected; such children are more susceptible to respiratory and intestinal infections.
The nature of the development of this disease is multifactorial. Morphofunctional disorders of the placenta can develop due to somatic and gynecological diseases of the pregnant woman, fetal pathology:
1. Extragenital diseases of the pregnant woman:
- cardiovascular (heart defects, arterial hypertension or hypotension, circulatory insufficiency);
- renal (pyelonephritis, renal failure);
- pulmonary (bronchial asthma);
- neuroendocrine (diabetes mellitus, hypo- and hyperthyroidism, pathology of the adrenal glands and hypothalamus);
- hematological (anemia of pregnant women, blood clotting disorders). In anemia of pregnant women, fetoplacental insufficiency is caused by iron deficiency in the maternal-fetal bloodstream, which leads to a decrease in oxygen transport to the fetus and hypoxia. With antiphospholipid syndrome, microthrombs form in the vessels of the placenta, disrupting the fetal-placental blood flow;
- infections that occur acutely or worsen during pregnancy. In this case, the placenta is affected by viruses, protozoa, bacteria. Various infectious lesions (influenza, STIs, etc.) that occur in the first trimester often lead to spontaneous termination of pregnancy. In later periods of gestation, infection may be limited to local changes, the severity of which will depend on the pathogen and the ways of its spread.
2. Genital pathology of a pregnant woman:
- uterine abnormalities (bicornular, saddle-shaped uterus);
- uterine fibroma;
- chronic endocervicitis and endometritis;
- scar on the uterus.
3. Obstetric pathology:
- Rh incompatibility;
- placenta previa;
- pelvic presentation of the fetus;
- multiple pregnancy;
- early or late toxicosis of pregnancy (gestosis). In turn, gestosis can not only lead to fetoplacental insufficiency, but also aggravate its severity, creating a kind of vicious circle.
The risks of fetoplacental insufficiency increase in proportion to the age of the pregnant woman; with a history burdened with abortions, bad habits, environmental problems, social and household disorder. These conditions to one degree or another cause disorders of the uteroplacental, and then fetoplacental blood flow, which leads to irreversible morphological changes and disruption of the main functions of the placenta (gas exchange, trophic, excretory, protective and intersecretory, etc.). Usually, several etiofactors are involved in the pathogenesis of fetoplacental insufficiency, among which the leading one stands out.
According to the time of development, disease can be primary and secondary:
- Primary insufficiency occurs already in the early stages of gestation (16-18 weeks), at the stages of placenta formation and organogenesis under the influence of infectious, endocrine, iatrogenic factors.
- Secondary fetoplacental insufficiency develops with an initially normally formed placenta, as a rule, under the influence of maternal factors or pregnancy complications.
The clinical course of fetoplacental insufficiency can be acute or chronic:
- With acute insufficiency, which can develop both at any stage of pregnancy and in childbirth, first of all, the gas exchange function of the placenta is disrupted, which is accompanied by acute hypoxia and fetal death. The most common acute fetoplacental insufficiency is caused by premature placental abruption, hemorrhages in the marginal sinuses, placental infarction and thrombosis of its vessels.
- Obstetrics and gynecology face chronic fetoplacental insufficiency more often. The course and prognosis are determined by protective and adaptive reactions, and therefore compensated, subcompensated, decompensated and critical forms of fetoplacental insufficiency are distinguished.
The most favorable compensated form is determined by Dopplerometry; the fetus in this case does not suffer and continues to develop. With a compensated form of fetoplacental insufficiency, minor pathological changes are compensated due to protective and adaptive mechanisms that contribute to the progression of pregnancy. Adequate therapy and proper management of childbirth ensure the possibility of the birth of a healthy fetus.
In the case of a subcompensated form of fetoplacental insufficiency, protective and adaptive reactions are insufficient to ensure the normal course of pregnancy. With this form, there is a lag in the development of the fetus, the risks of various complications are high.
The decompensated form of fetoplacental insufficiency is characterized by overstrain and disruption of compensatory mechanisms, the impossibility of normal progression of pregnancy. Fetal suffering is manifested by severe cardiac disorders, developmental delay, severe hypoxia; intrauterine fetal death is excluded. With a critical form of insufficiency, irreversible morphofunctional changes in the fetoplacental complex inevitably lead to fetal death.
Fetoplacental insufficiency can manifest itself in various clinical forms. Most often, this condition is accompanied by the threat of termination of pregnancy, fetal hypoxia and a delay in its intrauterine development. The risk of spontaneous termination of pregnancy usually occurs in the early stages of gestation and can be expressed in the development of a threatening, incipient abortion or an abortion in progress. In some cases, with fetoplacental insufficiency, a frozen pregnancy is observed.
In the II-III trimesters, fetoplacental insufficiency, as a rule, is manifested by a delay in fetal development. At the same time, there is a decrease in the circumference of the pregnant woman’s abdomen, a discrepancy in the height of the uterine fundus to the gestation period. Ultrasound reveals a lag in fetal development. Fetal hypoxia in fetoplacental insufficiency is associated with impaired transport and gas exchange function of the placenta. The severity of the fetal lesion is determined by the size of the affected area of the placenta: for example, when a section of more than 1/3 of the placenta is turned off from the circulation, disorders critical for the fetus develop. Signs of hypoxia experienced by the fetus are initially increased disorderly motor activity, and then a decrease in the number of fetal movements until their complete absence.
Disorder of intersecretory function in fetoplacental insufficiency of the placenta may contribute to pregnancy or premature birth. Due to a violation of the excretory function of the placenta, there is a change in the amount of amniotic fluid – usually lack of water, but with some concomitant pathology (diabetes mellitus, intrauterine infection, hemolytic disease of the fetus) – polyhydramnios. Placental changes in fetoplacental insufficiency may be accompanied by calcinate deposition, expansion of the interstitial space, placental cysts. Against the background of a violation of the hormonal function of the placenta and insufficient activity of the vaginal epithelium, colpitis often develops in a pregnant woman.
Taking into account the multifactorial nature of etiopathogenetic mechanisms, the diagnosis of fetoplacental insufficiency should include a comprehensive dynamic examination of the pregnant woman. When collecting anamnesis, the leading factor contributing to the development of fetoplacental insufficiency (age, gynecological and extragenital diseases, operations, habits, professional and living conditions, etc.) is revealed. Complaints of a pregnant woman with fetoplacental insufficiency may be abdominal pain, increased uterine tone, white from the genital tract, activation or suppression of fetal movements, spotting.
- Physical examination. An obstetrician-gynecologist measures the circumference of the abdomen, assesses the standing of the bottom of the uterus, weighs the pregnant woman, which suggests a delay in fetal development, high or low water. Conducting a gynecological examination allows you to assess the nature of secretions, identify signs of inflammation, and take material for bacteriological and microscopic examination.
- Ultrasound of the fetus. The importance of ultrasound in the diagnosis of fetoplacental insufficiency consists in the possibility of determining fetometric parameters (the size of the head, trunk, limbs of the fetus) and comparing them with the norm indicators for a given gestation period. In addition, the thickness of the placenta is measured and the degree of its maturity is determined. Dopplerography of the uterine-fetal blood flow evaluates blood circulation in the vessels of the umbilical cord, uterus and the fetal part of the placenta.
- Functional research. With the help of fetal phonocardiography and cardiotocography, the nature of fetal cardiac activity is determined – the frequency and rhythm of the heartbeat. Signs of hypoxia can serve as tachycardia, bradycardia, arrhythmia.
Treatment of a compensated form of fetoplacental insufficiency, provided that the dynamics of therapy is positive and there is no threat to the development of pregnancy, can be carried out on an outpatient basis. In other cases, immediate hospitalization with intensive therapeutic measures is indicated. Given the multifactorial development of pathology, there can be no standard treatment regimen for fetoplacental insufficiency. The main place in the treatment of fetoplacental insufficiency is given to the elimination of the leading etiological factor and the maintenance of compensatory mechanisms for the continuation of gestation.
In microcirculatory disorders and vascular tone disorders in the placenta, the first-line drugs are antiplatelet agents and anticoagulants (pentoxifylline, dextran, dipyridamole, heparin, etc.). In order to correct hypotrophy and fetal growth retardation, transfusion of plasma-substituting and protein solutions is used. In hemodynamic disorders accompanying fetoplacental insufficiency, calcium antagonists (nifedipine, verapamil) are prescribed, improving organ perfusion, normalizing myocardial contractile function, having a hypotensive effect. Detection of hypertonicity of the myometrium requires the appointment of antispasmodic drugs (drotaverine, glucosonocaine mixture, etc.).
As part of the normalization of antioxidant protection and transport function of the placenta, vitamins E, C, hepatoprotectors are prescribed. Vitamin B6, thiamine pyrophosphate, folic acid, glucose, multivitamins, and calf blood hemoderivate are used for metabolic therapy in fetoplacental insufficiency. In case of a threat of early termination of pregnancy, it is advisable to prescribe tocolytics (phenoterol, hexoprenaline).
The decision on the time and method of delivery is made taking into account the effectiveness of fetoplacental insufficiency therapy. With a compensated form, natural childbirth is possible in the prognosis; with a subcompensated one, the choice is made in favor of cesarean section; with the development of decompensation, emergency surgical delivery is indicated.
Preventive measures are based on careful preparation of a woman for pregnancy. It is necessary to identify and correct existing risk factors, to determine early in pregnant women the likelihood of developing fetoplacental insufficiency, to manage pregnancy in this group of patients with increased control.
Prevention of the development of fetoplacental insufficiency may be facilitated by preventive medication courses at 14-16 weeks and 28-34 weeks of gestation. Pregnant women with a compensated form of fetoplacental insufficiency require constant monitoring of the condition and development of the fetus using laboratory and ultrasound screening.