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(Лат.: natalis - относящийся к рождению, связанный с моментом рождения; 1826).
Учебное пособие. . Доступ к данному источнику = Access to the reference. URL: http://www.tryphonov.ru/tryphonov/serv_r.htm#0 quotation с. 18- PRENATAL DIAGNOSIS I. First-trimester screening. Maternal serum can be analyzed for certain biochemical markers that, in combination with ultrasound measurement of the fetal nuchal translucency, can be used to calculate a risk assessment for trisomies 18 and 21. In the first trimester, these serum markers are the free b-human chorionic gonadotropin (hCG) and pregnancy-associated plasma protein A (PAPP-A). It is an effective screening tool, with a detection rate of 87-92% for trisomy 21 and fewer falsepositive results than the traditional triple-screen test (alpha-fetoprotein [AFP], unconjugated estriol, and hCG). First-trimester screening is performed between 10 and 13 weeks' gestation and requires confirmation of a chromosomal abnormality by an invasive genetic test (usually chorionic villus sampling [CVS]). II. Second-trimester screening. Two common second-trimester tests are the maternal serum AFP (MSAFP) and the triple-screen test. The MSAFP is a sensitive marker for open neural tube defects, whereas the triple-screen test yields a risk assessment for open neural tube defects as well as trisomies 18 and 21. These tests are usually performed between 15 and 20 weeks' gestation and require an invasive test to confirm the diagnosis of a chromosomal abnormality (usually amniocentesis). The usefulness of the triple-screen test is limited by its high number of false-positive test results. III. Ultrasound testing. Ultrasound examination is used in the following circumstances. A. Calculation of gestational age. Measurement of the crown-rump length between 8 and 12 weeks' gestation allows for the most accurate assessment of gestational age, to within 5-7 days. After the first trimester, a combination of biparietal diameter, head circumference, abdominal circumference, and femur length is used to estimate gestational age and fetal weight. Measurements in the second trimester are accurate to within approximately 2 weeks and in the third trimester to within 3 weeks. B. Anatomic survey. A large number of congenital anomalies can be diagnosed reliably by ultrasonography, including anencephaly, hydrocephalus, congenital heart disease, gastroschisis, omphalocele, spina bifida, renal anomalies, diaphragmatic hernia, cleft lip and palate, and skeletal dysplasia. Identification of these anomalies before birth can help determine the safest type of delivery and the support personnel needed. Ultrasonography can also aid in determining fetal gender. C. Assessment of growth and fetal weight. Ultrasonography is useful to detect and monitor both intrauterine growth restriction (IUGR) and fetal macrosomia. Estimation of fetal weight is also important in counseling patients regarding expectations after delivering a premature infant. D. Assessment of amniotic fluid volume 1. Oligohydramnios (decreased amniotic fluid). This is associated with a major anomaly in 15% of cases. Rupture of membranes is the most common cause of oligohydramnios. Other causes include placental insufficiency, renal anomalies, bladder outlet obstruction, karyotypic abnormalities, and severe cardiac disease. The kidneys and the bladder can be seen with ultrasonography at ~14 weeks' gestation. 2. Polyhydramnios (hydramnios) (excess of amniotic fluid). Polyhydramnios is associated with major anomalies in 15% of cases. It is associated with gestational diabetes, anencephaly, neural tube defects, bowel obstruction such as duodenal atresia, multiple gestation, nonimmune hydrops fetalis, and exstrophy of the bladder. E. Assessment of placental location and presence of retroplacental hemorrhage. This is useful in suspected cases of placenta previa or abruptio placentae. F. Diagnosis of multiple pregnancy and determination of chorionicity. The determination of chorionicity is made by examination of the fetal membranes and is best done by 14 weeks' gestation. G. Determination of pregnancy viability. This is important in the first trimester, when fetal heart motion can be detected at 6-7 weeks' gestation. It is also important in the case of a suspected fetal demise later in pregnancy. H. Assessment of fetal well-being: 1. Biophysical profile. Ultrasonography is used to assess fetal movements and breathing activity. 2. Doppler studies. Doppler ultrasonography of fetal vessels, particularly the umbilical artery, is a useful adjunct in the management of high-risk pregnancies, especially those complicated by IUGR. Changes in the vascular Doppler pattern (ie, absent or reversed end-diastolic flow in the umbilical artery) signal a deterioration in placental function and possibly a worsening fetal condition. The use of Doppler ultrasonography has been associated with a 38-50% decrease in perinatal mortality in high-risk pregnancies; however, no benefit in using this technique to screen a low-risk population has been proven. I. Visual guidance for procedures such as amniocentesis, CVS, percutaneous umbilical blood sampling (PUBS), and some fetal surgeries (eg, placement of bladder or chest shunts). IV. Amniocentesis. Amniotic fluid can be analyzed for prenatal diagnosis of karyotypic abnormalities, in fetuses diagnosed with congenital defects, to determine fetal lung maturity, to monitor the degree of isoimmunization by measurement of the content of bilirubin in the fluid, and for the diagnosis of chorioamnionitis. Testing for karyotypic and congenital abnormalities is usually done at 16-20 weeks' gestation. A sample of amniotic fluid is removed under ultrasound guidance. Fetal cells in the fluid can be grown in tissue culture for genetic study. With visual guidance from the ultrasonogram, the pregnancy loss rate related to amniocentesis is usually quoted at between 0.3% and 0.5%. Early amniocentesis (before 13 weeks) is associated with a higher rate of fetal loss. This is indicated · In women older than 35 years, because of the increased incidence of aneuploidy (ie, trisomies 13, 18, and 21). · In those who have already had a child with a chromosomal abnormality. · In those in whom X-linked disorders are suspected. · To rule out inborn errors of metabolism. V. Chorionic villus sampling. CVS is a technique for first-trimester genetic studies. Chorionic villi are withdrawn either through a needle inserted through the abdomen and into the placenta or through a catheter inserted through the vagina and cervix into the placenta. The cells obtained are identical to those of the fetus and are grown and analyzed. CVS can be performed in the first trimester (usually between 10 and 12 weeks' gestation). Results can be obtained more quickly than with other methods via fluorescence in situ hybridization (FISH) rapid chromosome analysis, thus enabling the patient to have a diagnosis before the end of the first trimester. Indications are the same as for amniocentesis. Reported complications after CVS can include pregnancy loss and limb abnormalities; however, if CVS is performed after 70 days' gestation, there is no increased incidence of limb reduction defects. Pregnancy loss rates after CVS are usually quoted as ranging from 0.6-0.8% but are highly operator dependent. VI. Percutaneous umbilical blood sampling. Under ultrasound guidance, a needle is placed transabdominally into the umbilical vein. Samples of fetal blood can be obtained for karyotype, viral studies, fetal blood type, and hematocrit. This also provides a route for in utero transfusion. This technique is most often used in cases of fetal hydrops. ANTEPARTUM TESTS OF FETAL WELL-BEING I. Nonstress test. The nonstress test (NST) is used to detect intact fetal brainstem function. Fetal wellbeing is confirmed if the baseline heart rate is normal and there are periodic increases in the fetal heart rate. These accelerations are often associated with fetal movement. The following guidelines can be used, although there may be variations between institutions. A. Reactive NST. In a 20-min monitoring period, there are at least two accelerations of the fetal heart rate 15 beats/min above the baseline fetal heart rate; each acceleration lasts at least 15 s. B. Nonreactive NST. Fetal heart rate does not meet the criteria just mentioned during a prolonged period of monitoring (usually at least 1 h). Note: There are many causes of a nonreactive NST besides fetal compromise, including a fetal sleep cycle, chronic maternal smoking, and exposure to medications such as central nervous system depressants and propranolol. Because of this low specificity, a nonreactive NST should be followed by more definitive testing such as a biophysical profile or a contraction stress test. II. Biophysical profile. The biophysical profile (Table 1-1) is another test used to assess fetal wellbeing, often when the NST has been nonreactive. An NST is performed along with an ultrasound examination to evaluate fetal breathing movements, gross body movements, tone, and amniotic fluid volume. A score of 8-10 is considered normal, 4-6 indicates possible fetal compromise, and 0-2 predicts high perinatal mortality. This test has not been adequately assessed at early gestational ages. III. Contraction stress test. The contraction stress test (CST) is used to assess a fetus at risk for uteroplacental insufficiency. A monitor is placed on the mother's abdomen to continuously record the fetal heart rate and uterine contractions. An adequate test consists of at least three contractions, each lasting at least 40- 60 s, within a period of 10 min. If sufficient contractions do not occur spontaneously, the mother is instructed to perform nipple stimulation or oxytocin is administered by intravenous pump. If oxytocin is needed to produce contractions for the CST, it is called an oxytocin challenge test (OCT). Normally, the fetal heart rate increases in response to a contraction, and no decelerations occur during or after the contraction. If late decelerations occur during or after contractions, uteroplacental insufficiency may be present. The CST is contraindicated in patients with placenta previa, those who have had a previous cesarean section with a vertical incision, and those with high-risk factors for preterm delivery (ie, premature rupture of membranes or incompetent cervix). Test results are interpreted as follows: A. Negative (normal) test. No late decelerations occur during adequate uterine contractions. The baseline fetal heart rate is normal. This result is associated with a very low perinatal mortality rate in the week after the test. B. Positive (abnormal) test. Late decelerations occur with at least two of three contractions over a 10-min interval. This result can signify poor fetal outcome, and depending on gestational age, delivery is usually recommended. C. Equivocal (suspicious) test. A late deceleration occurs with one of three contractions over a 10- min interval. Prolonged fetal monitoring is usually recommended. INTRAPARTUM TESTS OF FETAL WELL-BEING I. Fetal heart rate monitoring. Continuous fetal heart rate monitoring has been the standard clinical practice since the 1970s. However, it has not been shown to improve perinatal mortality compared with intermittent auscultation of the fetal heart rate. The only clear benefit to continuous fetal monitoring in labor is a decrease in neonatal seizures. An abnormal fetal heart rate pattern is 50% predictive of low Apgar scores. Fetal heart rate monitoring may be internal, with an electrode attached to the fetal scalp, or external, with a monitor attached to the maternal abdomen. The baseline heart rate, beat-to-beat variability, and long-term variability are measured. A. Baseline fetal heart rate. The baseline fetal heart rate is the rate that is maintained apart from periodic variations. The normal fetal heart rate is 110-160 beats/min. Fetal tachycardia is present at 160 beats/min or more. Causes of fetal tachycardia include maternal or fetal infection, fetal hypoxia, thyrotoxicosis, and maternal use of drugs such as parasympathetic blockers or beta-mimetic agents. Moderate fetal bradycardia is defined as a heart rate of 90-110 beats/min with normal variability. Severe fetal bradycardia is a heart rate of <90 beats/min. Common causes of bradycardia include hypoxia, complete heart block, and maternal use of drugs such as b-blockers. B. Variability. Fetal heart rate variability has traditionally been broken down into categories of short-term (beat-to-beat) and long-term variability, although for most practical purposes they are assessed together. In the normal mature fetus, there are slight rapid fluctuations in the interval between beats (beat-to-beat variability). This indicates a functioning sympathetic-parasympathetic nervous system interaction. An amplitude range (baseline variability) >6 beats/min indicates normal beat-to-beat variability and suggests the absence of fetal hypoxia. Absence of variability may be caused by severe hypoxia, anencephaly, complete heart block, and maternal use of drugs such as narcotics or magnesium sulfate. Long-term variability refers to fluctuations in the fetal heart rate over longer periods of time (minutes rather than seconds). C. Accelerations. Accelerations are often associated with fetal movement and are an indication of fetal well-being. D. Decelerations. There are three types of decelerations (Figure 1-1). 1. Early decelerations. Early decelerations (decelerations resulting from physiologic head compression) occur secondary to vagal reflex tone, which follows minor, transient fetal hypoxic episodes. These are benign and are not associated with fetal compromise. 2. Late decelerations. Two types of late decelerations exist. a. Late decelerations with maintained beat-to-beat variability. These are seen in the setting of normal fetal heart rate variability. They are associated with a sudden insult (eg, maternal hypotension) that affects a normally oxygenated fetus and signifies uteroplacental insufficiency. The normal variability of the fetal heart rate signifies that the fetus is physiologically compensated. b. Late decelerations with decreased beat-to-beat variability. These are associated with decreased or absent fetal heart rate variability. They may represent fetal hypoxia resulting from uteroplacental insufficiency. Maneuvers such as maternal oxygen supplementation and maternal positioning in the left lateral decubitus position may improve fetal oxygenation and placental circulation and should be attempted. 3. Variable decelerations. These are most frequently associated with umbilical cord compression. They are classified as severe when the fetal heart rate decreases to <60 beats/min, the deceleration is longer than 60 s in duration, or the fetal heart rate is 60 beats/min below baseline. If beat-to-beat variability is maintained, the fetus is compensated physiologically and oxygenated normally. II. Fetal scalp blood sampling. Fetal scalp blood sampling is used during labor to determine the fetal acid-base status when the fetal heart rate tracing is non-reassuring or equivocal. This procedure can be performed only after rupture of membranes. It is contraindicated in cases of possible blood dyscrasias in the fetus and with maternal infections caused by herpesvirus or HIV. A blood sample is obtained from the fetal presenting part (usually the scalp but sometimes the buttocks), and the fetal blood pH is determined. A pH of і7.25 has been shown to correlate (with 92% accuracy) with a 2- min Apgar score of і7. The protocol for interpreting fetal scalp blood pH varies among institutions. Complications of this test are scalp infections (in <1% of infants) and soft tissue damage to the scalp. An example of one such protocol is as follows. A. pH і7.20. Fetus is not acidotic; no intervention required. B. pH 7.10-7.19. Fetus is preacidotic. Repeat sampling in 15-20 min. C. pH <7.10. Fetus may be acidotic. Delivery is indicated. III. Scalp stimulation/vibroacoustic stimulation. An acceleration in fetal heart rate in response to either manual stimulation of the fetal presenting part or vibroacoustic stimulation through the maternal abdomen has been associated with a fetal pH of >7.20. These tests are often used in labor to determine fetal well-being in lieu of a scalp blood sampling; however, a lack of fetal response to stimulation is not predictive of acidemia. IV. Fetal pulse oximetry. This promising new technique is designed as an adjunct to nonreassuring fetal heart rate tracings in order to reduce the number of unnecessary interventions. A normal fetal oxygen saturation as measured by pulse oximetry (SpO2) is 30-70%. A pulse oximetry reading of at least 30% has good correlation with a fetal pH of at least 7.20. Long-term studies are still needed to evaluate this technique. FIGURE 1-1. Examples of fetal heart rate monitoring. FHR, Fetal heart rate (beats per minute); UC, uterine contraction (mm Hg); HC, head compression; UPI, uteroplacental insufficiency; CC, cord compression. (Modified and reproduced, from McCrann JR, Schifrin BS: Fetal monitoring in high-risk pregnancy. Clin Perinatol 1974;1:149 with permission from Elsevier Science.) TESTS OF FETAL LUNG MATURITY I. Lecithin-sphingomyelin (L-S) ratio. Lecithin, a saturated phosphatidylcholine (the condensation product of a phosphatidic acid and choline), can be measured specifically in amniotic fluid and is a principal active component of surfactant. It is manufactured by type II alveolar cells. Sphingomyelin is a phospholipid found predominantly in body tissues other than the lungs. The L-S ratio compares levels of lecithin, which increase in late gestation, with levels of sphingomyelin, which remain constant. The L-S ratio is usually 1:1 by 31-32 weeks' gestation and 2:1 by 35 weeks' gestation. The following are guidelines to L-S ratios. · L-S і 2:1: Lungs are mature (98% accuracy). Only 2% of these infants will experience respiratory distress syndrome (RDS). · L-S = 1.5-1.9:1: 50% of infants will experience RDS. · L-S <1.5:1: 73% of infants will experience RDS. Some disorders are associated with delayed lung maturation, and higher than normal L-S ratios may be needed before fetal lung maturity is ensured. The two most common disorders are diabetes mellitus (an L-S ratio of 3:1 is usually accepted as indicating maturity) and Rh isoimmunization associated with hydrops fetalis. Acceleration of fetal lung maturity is seen in sickle cell disease, maternal narcotic addiction, prolonged rupture of membranes, chronic maternal hypertension, intrauterine growth restriction, and placental infarction. Differences may also occur in various racial groups. II. Phosphatidylglycerol. Phosphatidylglycerol appears in amniotic fluid at ~35 weeks, and levels increase at 37-40 weeks. This substance is a useful marker for lung maturation late in pregnancy. It is reported as either present or absent. TABLE 1-1. BIOPHYSICAL PROFILE SCORING SYSTEM USED TO ASSESS FETAL WELL-BEING Variable Normal (2) Abnormal (0) Fetal breathing One episode >30 s in 30 min None or episode <30 s in 30 min Body movement Three or more movements in 30 min Fetal tone One episode or active limb or trunk extension with flexion Two or less movements in 30 min No movement Nonstress test Reactive Nonreactive Amniotic fluid One pocket of amniotic fluid 1 cm or more No fluid pockets or pocket <1 cm Based on guidelines from Manning FA et al: Fetal biophysical profile scoring: a prospective study in 1184 high-risk patients. Am J Obstet Gynecol 1981;140:289. Reprinted with permission from Elsevier Science III. TDx fetal lung maturity (TDx FLM). This test (Abbott Laboratories, North Chicago, IL) measures the relative concentrations of surfactant and albumin (milligrams of surfactant per gram of albumin) in amniotic fluid and gives a result that helps assess fetal lung maturity. TDx FLM has several advantages over L-S ratio: (1) Less technical expertise is required; (2) this test can be performed more easily; and (3) results are obtained more quickly. Results are interpreted in the following ways. 30-70 mg/g: The infant is at risk for immature lungs. Other conditions may weigh more heavily on the decision to deliver early. 70 mg/g: The likelihood of RDS is small. СИСТЕМА РЕПРОДУКЦИИ: ОГЛАВЛЕНИЕ СИСТЕМА РЕПРОДУКЦИИ: ТАБЛИЦЫ СИСТЕМА РЕПРОДУКЦИИ: ИЛЛЮСТРАЦИИ СИСТЕМА РЕПРОДУКЦИИ: ЛИТЕРАТУРА
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Санкт-Петербург, Россия, 1996-2015
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