Fetal hypoxia is an intrauterine syndrome characterized by a complex of changes on the part of the fetus caused by insufficient oxygen supply to its tissues and organs. Fetal hypoxia is characterized by disorders of vital organs, primarily the central nervous system. Diagnosis of fetal hypoxia includes cardiotocography, dopplerometry of uteroplacental circulation, obstetric ultrasound, amnioscopy. Treatment of fetal hypoxia is aimed at normalizing uteroplacental blood flow, improving blood rheology; sometimes this condition requires early delivery of a woman.
Fetal hypoxia is registered in 10.5% of the total number of pregnancies and births. Fetal hypoxia can develop at different times of intrauterine development, characterized by varying degrees of oxygen deficiency and consequences for the child’s body. Fetal hypoxia, developed in the early stages of gestation, causes malformations and slowing of embryo development. In late pregnancy, hypoxia is accompanied by a delay in fetal growth, central nervous system damage, and a decrease in the adaptive capabilities of the newborn.
Fetal hypoxia can be a consequence of a wide range of adverse processes occurring in the body of the child, mother or placenta. The probability of developing hypoxia in the fetus increases with diseases of the maternal body – anemia, cardiovascular pathology (heart defects, hypertension), kidney diseases, respiratory system (chronic bronchitis, bronchial asthma, etc.), diabetes mellitus, pregnancy toxicosis, multiple pregnancies, STIs. Alcoholism, nicotine, narcotic and other types of dependence of the mother negatively affect the supply of oxygen to the fetus.
The risk of fetal hypoxia increases with disorders of the fetal-placental circulation caused by the threat of miscarriage, pregnancy overgrowth, umbilical cord pathology, fetoplacental insufficiency, abnormal labor and other complications of pregnancy and the birth process. Risk factors in the development of intranatal hypoxia include fetal hemolytic disease, congenital malformations, intrauterine infection (herpetic infection, toxoplasmosis, chlamydia, mycoplasmosis, etc.), multiple and tight entanglement of the umbilical cord around the baby’s neck, prolonged compression of the head during childbirth.
In response to hypoxia in the fetus, first of all, the nervous system suffers, since the nervous tissue is the most sensitive to oxygen deficiency. Starting from 6-11 weeks of embryo development, lack of oxygen causes a delay in brain maturation, disorders in the structure and functioning of blood vessels, slowing down the maturation of the blood-brain barrier. Also, hypoxia is experienced by the tissues of the kidneys, heart, and intestines of the fetus.
Minor fetal hypoxia may not cause clinically significant damage to the central nervous system. With severe fetal hypoxia, ischemia and necrosis develop in various organs. After birth, a child who has developed under hypoxia conditions may experience a wide range of disorders – from neurological disorders to mental retardation and severe somatic abnormalities.
According to the time of the course and the rate of occurrence, acute and chronically developing fetal hypoxia is distinguished.
The occurrence of acute fetal hypoxia is usually associated with anomalies and complications of labor – rapid or prolonged labor, pressing or umbilical cord prolapse, prolonged compression of the head in the birth canal. Sometimes acute fetal hypoxia can develop during pregnancy: for example, in the case of uterine rupture or premature placental abruption. In acute hypoxia, disorders of the functions of the vital organs of the fetus are rapidly increasing. Acute hypoxia is characterized by increased fetal heart rate (more than 160 beats. in min.) or its reduction (less than 120 units. in min.), arrhythmia, tone deafness; increased or decreased motor activity, etc. Often, against the background of acute hypoxia, fetal asphyxia develops.
Chronic hypoxia is caused by a prolonged moderate oxygen deficiency, in which the fetus develops. With chronic oxygen deficiency, intrauterine hypotrophy occurs; in case of exhaustion of the compensatory capabilities of the fetus, the same disorders develop as in the acute variant of the course. Fetal hypoxia can develop during pregnancy or childbirth; hypoxia that occurs in a child after birth due to hyaline membrane disease, intrauterine pneumonia, etc. is considered separately.
Taking into account the compensatory and adaptive capabilities of the fetus, hypoxia can acquire compensated, subcompensated and decompensated forms. Since, under unfavorable conditions, the fetus experiences not only hypoxia, but also a whole complex of complex metabolic disorders, in world practice this condition is defined as a “distress syndrome”, which is divided into prenatal, developed during childbirth and respiratory.
The severity of changes developing in the fetus under the influence of hypoxia is determined by the intensity and duration of the oxygen deficiency experienced. The initial manifestations of hypoxia cause the fetus to have a rapid heartbeat, then its slowing down and muffling of heart tones. Meconium may appear in the amniotic fluid. With mild hypoxia, the motor activity of the fetus increases, with severe hypoxia, movements are reduced and slowed down.
With severe hypoxia, the fetus develops circulatory disorders: there is a short-term tachycardia and an increase in blood pressure, followed by bradycardia and a decrease in blood pressure. Rheological disorders are manifested by blood thickening and plasma discharge from the vascular bed, which is accompanied by intracellular and tissue edema. As a result of increased fragility and permeability of vascular walls, hemorrhages occur. A decrease in vascular tone and slowing of blood circulation leads to ischemia of organs. With hypoxia, acidosis develops in the fetal body, the balance of electrolytes changes, tissue respiration is disrupted. Changes in the vital organs of the fetus can cause its stillbirth, asphyxia, intracranial birth trauma.
Suspicion that the fetus is experiencing hypoxia may occur when its motor activity changes – restless behavior, increased and increased frequency of movements. Prolonged or progressive hypoxia leads to a weakening of fetal movements. If a woman notices such changes, she should immediately contact a gynecologist who performs pregnancy management. When listening to the fetal heartbeat with an obstetric stethoscope, the doctor evaluates the frequency, sonority and rhythm of heart tones, the presence of noise. To detect fetal hypoxia, modern gynecology uses cardiotocography, fetal phonocardiography, dopplerometry, ultrasound, amnioscopy and amniocentesis, laboratory tests.
During cardiotocography, it is possible to track the fetal heart rate and its motor activity. By changing the heartbeat, depending on the rest and activity of the fetus, its condition is judged. Cardiotocography, along with phonocardiography, is widely used in childbirth. Dopplerography of the uteroplacental blood flow studies the speed and nature of blood flow in the vessels of the umbilical cord and placenta, the violation of which leads to fetal hypoxia. Cordocentesis under ultrasound control is performed to collect umbilical cord blood and study acid-base balance. An echoscopic sign of fetal hypoxia can serve as a detectable delay in its growth. In addition, during obstetric ultrasound, the composition, volume and color of amniotic fluid are evaluated. Pronounced polyhydramnios or lack of water can signal trouble.
Conducting amnioscopy and amniocentesis through the cervical canal allows you to visually assess the transparency, color, amount of amniotic fluid, the presence of inclusions in it (flakes, meconium), conduct biochemical tests (pH measurement, study of hormones, enzymes, CO2 concentration). Amnioscopy is contraindicated in placenta previa, colpitis, cervicitis, and the threat of termination of pregnancy. A direct assessment of the amniotic fluid is carried out after its outpouring in the first period of labor. In favor of fetal hypoxia, an admixture in the amniotic fluid of meconium and their greenish color indicates.
If fetal hypoxia is detected, the pregnant woman is hospitalized in an obstetric and gynecological hospital. The presence of fetal hypoxia requires correction of the existing obstetric and extragenital pathology of the mother and normalization of fetoplacental circulation. The pregnant woman is shown strict rest, oxygen therapy. Therapy is carried out aimed at reducing uterine tone (papaverine, drotaverine, eufillin, hexoprenaline, terbutaline), reducing intravascular coagulability (dipyridamole, dextran, calf blood hemoderivate, pentoxifylline).
Chronic fetal hypoxia requires the administration of drugs that improve cellular permeability to oxygen and metabolism (essential phospholipids, vitamins E, C, B6, glutamic acid, glucose), antihypoxants, neuroprotectors. If the condition of the pregnant woman improves and the phenomena of fetal hypoxia decrease, breathing exercises, aquagymnastics, UFO, inductothermy may be recommended to the pregnant woman. If complex measures are ineffective and signs of fetal hypoxia persist for more than 28 weeks, an emergency delivery (emergency caesarean section) is indicated.
Childbirth is carried out using cardiomonitoring, which allows for timely application of additional measures. With acute hypoxia developed during childbirth, the child needs intensive care. Timely correction of fetal hypoxia, rational management of pregnancy and childbirth help to avoid the development of gross violations in the child. In the future, all children who have developed in hypoxia are observed by a neurologist; they often need the help of a psychologist and a speech therapist.
Severe fetal hypoxia is accompanied by severe multiple organ dysfunctions in the newborn. With hypoxic damage to the central nervous system, perinatal encephalopathy, cerebral edema, areflexia, convulsions may develop. On the part of the respiratory system, posthypoxic pneumopathy, pulmonary hypertension are noted; cardiovascular disorders include heart and vascular defects, ischemic necrosis of the endocardium, etc.
The effect of fetal hypoxia on the kidneys may be manifested by renal insufficiency, oliguria; on the gastrointestinal tract – regurgitation, vomiting, enterocolitis. Often, due to severe perinatal hypoxia, a newborn develops DIC syndrome, secondary immunodeficiency. Birth asphyxia in 75-80% of cases develops against the background of previous fetal hypoxia.
Preventing the development requires a woman to prepare responsibly for pregnancy: treatment of extragenital pathology and diseases of the reproductive system, rejection of unhealthy habits, rational nutrition. Pregnancy management should be carried out taking into account risk factors and timely monitoring of the condition of the fetus and the woman. Prevention of the development of acute fetal hypoxia consists in the correct choice of the method of delivery, prevention of birth injuries.