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The major emphasis in fetal medicine involves (1) assessment of fetal growth and maturity, (2) evaluation of fetal well-being or distress, (3) assessment of the effects of maternal disease on the fetus, (4) evaluation of the effects of drugs administered to the mother on the fetus, and (5) identification and when possible treatment of fetal disease or anomalies.
One of the most important tools used to access fetal well-being is ultrasonography (ultrasound, US); it is both safe and reasonably accurate. Indications for antenatal US include estimation of gestational age (unknown dates, discrepancy between uterine size and dates, or suspected growth restriction), assessment of amniotic fluid volume, estimation of fetal weight and growth, determination of the location of the placenta and the number and position of fetuses, and identification of congenital anomalies. Fetal MRI is a more advanced imaging method that is thought to be safe to the fetus and neonate and is used for more advanced diagnostic and therapeutic planning ( Fig. 115.1 ).
Fetal growth can be assessed by US as early as 6-8 wk of gestation by measurement of the crown-rump length. Accurate determination of gestational age can be achieved through the 1st half of pregnancy; however, first-trimester assessment by crown-rump length measurement is the most effective method of pregnancy dating. In the second trimester and beyond, a combination of biometric measures (i.e., biparietal diameter, head and abdominal circumference, femoral diaphysis length) is used for gestational age and growth assessment ( Fig. 115.2 ). If a single US examination is performed, the most information can be obtained with a scan at 18-20 wk, when both gestational age and fetal anatomy can be evaluated. Serial scans assessing fetal growth are performed when risk factors for fetal growth restriction (FGR) are present. Two patterns of FGR have been identified: symmetric FGR, typically present early in pregnancy, and asymmetric FGR, typically occurring later in gestation. The most widely accepted definition of FGR in the United States is an estimated fetal weight (EFW) of less than the 10th percentile ( Fig. 115.3 ). Some aspects of human fetal growth and development are summarized in Chapter 20 .
Fetal maturity and dating are usually assessed by last menstrual period (LMP), assisted reproductive technology (ART)–derived gestational age, or US assessments. Dating by LMP assumes an accurate recall of the 1st day of LMP, a menstrual cycle that lasted 28 days, and ovulation occurring on the 14th day of the cycle, which would place the estimated delivery date (EDD) 280 days after LMP. Inaccuracies with any of these parameters can lead to an incorrectly assigned gestational age if the LMP is used for dating. Dating by ART is the most accurate method for assigning gestational age with EDD occurring 266 days after conception (when egg is fertilized by sperm). When US is used for dating, the most accurate assessment of gestational age is by first-trimester (≤ wk) US measurement of crown-rump length, which is accurate to within 5-7 days. In contrast, US dating in the second trimester is accurate to 10-14 days, and third trimester is only accurate to 21-30 days. Dating of a pregnancy is critical to determine when delivery should occur, if growth is appropriate during the pregnancy, and when testing and interventions should be offered. The earliest assessment of pregnancy dating should be used throughout the pregnancy unless methodologies used later in pregnancy are significantly different.
Fetal compromise may occur during the antepartum or intrapartum period. It may be asymptomatic in the antenatal period but is often suspected by maternal perception of decreased fetal movement. Antepartum fetal surveillance is warranted for women at increased risk for fetal death, including those with a history of stillbirth, intrauterine growth restriction (IUGR), oligohydramnios or polyhydramnios, multiple gestation, rhesus sensitization, hypertensive disorders, diabetes mellitus or other chronic maternal disease, decreased fetal movement, preterm labor, preterm rupture of membranes (PROM), and postterm pregnancy. The predominant cause of antepartum fetal distress is uteroplacental insufficiency, which may manifest clinically as IUGR, fetal hypoxia, increased vascular resistance in fetal blood vessels ( Figs. 115.4 and 115.5 ), and, when severe, mixed respiratory and metabolic (lactic) acidosis. The goal of antepartum fetal surveillance is to identify the fetus at risk of stillbirth such that appropriate interventions (i.e., delivery vs optimization of underlying maternal medical condition) can be implemented to allow for a healthy live-born infant. Table 115.1 lists methods for assessing fetal well-being.
METHOD | COMMENT(S) AND INDICATION(S) |
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IMAGING | |
Ultrasound (real-time) | Biometry (growth), anomaly detection, number of fetuses, sites of calcification |
Biophysical profile | |
Amniotic fluid volume, hydrops | |
Ultrasound (Doppler) | Velocimetry (blood flow velocity) |
Detection of increased vascular resistance in the umbilical artery secondary to placental insufficiency | |
Detection of fetal anemia (MCA Doppler) | |
MRI | Defining of lesions before fetal surgery |
Better delineation of fetal CNS anatomy | |
FLUID ANALYSIS | |
Amniocentesis | Karyotype or microarray (cytogenetics), biochemical enzyme analysis, molecular genetic DNA diagnosis, or α-fetoprotein determination |
Bacterial culture, pathogen antigen, or genome detection (PCR) | |
Cordocentesis (percutaneous umbilical blood sampling) | Detection of blood type, anemia, hemoglobinopathies, thrombocytopenia, polycythemia, acidosis, hypoxia, thrombocytopenia, IgM antibody response to infection |
Rapid karyotyping and molecular DNA genetic diagnosis | |
Fetal therapy (see Table 115.5 ) | |
FETAL TISSUE ANALYSIS | |
Chorionic villus biopsy | Cytogenetic and molecular DNA analysis, enzyme assays |
Circulating fetal DNA | Noninvasive molecular DNA genetic analysis including microarray analysis and chromosome number (screening method) |
MATERNAL SERUM α-FETOPROTEIN CONCENTRATION | |
Elevated | Twins, neural tube defects (anencephaly, spina bifida), intestinal atresia, hepatitis, nephrosis, fetal demise, incorrect gestational age |
Reduced | Trisomies, aneuploidy |
MATERNAL CERVIX | |
Fetal fibronectin | Indicates possible risk of preterm birth |
Transvaginal cervical length | Short length suggests possible risk of preterm birth |
Bacterial culture | Identifies risk of neonatal infection (group B streptococcus, Neisseria gonorrhoeae, Chlamydia trachomatis ) |
Amniotic fluid | Determination of premature rupture of membranes (PROM) |
ANTEPARTUM BIOPHYSICAL MONITORING | |
Nonstress test | Fetal distress; hypoxia |
Biophysical profile and modified biophysical profile | Fetal distress; hypoxia |
Intrapartum fetal heart rate monitoring | See Fig. 115.6 |
The most common noninvasive tests are the nonstress test ( NST ) and the biophysical profile ( BPP ). The NST monitors the presence of fetal heart rate ( FHR ) accelerations that follow fetal movement. A reactive (normal) NST result demonstrates 2 FHR accelerations of at least 15 beats/min above the baseline FHR lasting 15 sec during 20 min of monitoring. A nonreactive NST result suggests possible fetal compromise and requires further assessment with a BPP. Although the NST has a low false-negative rate, it does have a high false-positive rate, which is often remedied by the BPP. The full BPP assesses fetal breathing, body movement, tone, NST, and amniotic fluid volume. It effectively combines acute and chronic indicators of fetal well-being, which improves the predictive value of abnormal testing ( Table 115.2 ). A score of 2 or 0 is given for each observation. A total score of 8-10 is reassuring; a score of 6 is equivocal, and retesting should be done in 12-24 hr; and a score of 4 or less warrants immediate evaluation and possible delivery. The BPP has good negative predictive value. The modified BPP consists of the combination of an US estimate of amniotic fluid volume (the amniotic fluid index) and the NST. When results of both are normal, fetal compromise is very unlikely. Signs of progressive compromise seen on Doppler US include reduced, absent, or reversed diastolic waveform velocity in the fetal aorta or umbilical artery (see Fig. 115.5 and Table 115.1 ). The umbilical vein and ductus venosus waveforms are also used to assess the degree of fetal compromise. Fetuses at highest risk of stillbirth often have combinations of abnormalities, such as growth restriction, oligohydramnios, reversed diastolic Doppler umbilical artery blood flow velocity, and a low BPP.
BIOPHYSICAL VARIABLE | NORMAL SCORE (2) | ABNORMAL SCORE (0) |
---|---|---|
Fetal breathing movements (FBMs) | At least 1 episode of FBM of at least 30 sec duration in 30 min observation | Absence of FBM or no episode ≥30 sec in 30 min |
Gross body movement | At least 3 discrete body/limb movements in 30 min (episodes of active continuous movement considered a single movement) | 2 or fewer episodes of body/limb movements in 30 min |
Fetal tone | At least 1 episode of active extension with return to flexion of fetal limb(s) or trunk Opening and closing of hand considered evidence of normal tone |
Either slow extension with return to partial flexion or movement of limb in full extension or absence of fetal movement with the hand held in complete or partial deflection |
Reactive fetal heart rate (FHR) | At least 2 episodes of FHR acceleration of ≥15 beats/min and at least 15 sec in duration associated with fetal movement in 30 min | Less than 2 episodes of acceleration of FHR or acceleration of <15 beats/min in 30 min |
Quantitative amniotic fluid (AF) volume * | At least 1 pocket of AF that measures at least 2 cm in 2 perpendicular planes | Either no AF pockets or a pocket <2 cm in 2 perpendicular planes |
* Modification of the criteria for reduced amniotic fluid from <1 cm to <2 cm would seem reasonable. Ultrasound is used for biophysical assessment of the fetus.
Fetal compromise during labor may be detected by monitoring the FHR, uterine pressure, and fetal scalp blood pH ( Fig. 115.6 ). Continuous fetal heart rate monitoring detects abnormal cardiac patterns by instruments that compute the beat-to-beat FHR from a fetal electrocardiographic signal. Signals are derived either from an electrode attached to the fetal presenting part, from an ultrasonic transducer placed on the maternal abdominal wall to detect continuous ultrasonic waves reflected from the contractions of the fetal heart, or from a phonotransducer placed on the mother's abdomen. Uterine contractions are recorded from an intrauterine pressure catheter or from an external tocotransducer applied to the maternal abdominal wall overlying the uterus. FHR patterns show various characteristics, some of which suggest fetal compromise. The baseline FHR is determined over 10 min devoid of accelerations or decelerations. Over the course of pregnancy, the normal baseline FHR gradually decreases from approximately 155 beats/min in early pregnancy to 135 beats/min at term. The normal range throughout pregnancy is 110-160 beats/min. Tachycardia (>160 beats/min) is associated with early fetal hypoxia, maternal fever, maternal hyperthyroidism, maternal β-sympathomimetic drug or atropine therapy, fetal anemia, infection, and some fetal arrhythmias. Arrhythmias do not generally occur with congenital heart disease and may resolve spontaneously at birth. Fetal bradycardia (<110 beats/min) may be normal (e.g., 105-110 beats/min) but may occur with fetal hypoxia, placental transfer of local anesthetic agents and β-adrenergic blocking agents, and occasionally, heart block with or without congenital heart disease.
Normally, the baseline FHR is variable as a result of opposing forces from the fetal sympathetic and parasympathetic nervous systems. Variability is classified as follows: absence of variability, if an amplitude change is undetectable; minimal variability, if amplitude range is ≤5 beats/min; moderate variability, if amplitude range is 6-25 beats/min; and marked variability, if amplitude range is >25 beats/min. Variability may be decreased or lost with fetal hypoxemia or the placental transfer of drugs such as atropine, diazepam, promethazine, magnesium sulfate, and most sedative and narcotic agents. Prematurity, the sleep state, and fetal tachycardia may also diminish beat-to-beat variability.
Accelerations or decelerations of the FHR in response to or independent of uterine contractions may also be monitored (see Fig. 115.6 ). An acceleration is an abrupt increase in FHR of ≥15 beats/min in ≥15 sec. The presence of accelerations or moderate variability reliably predicts the absence of fetal metabolic acidemia. However, their absence does not reliably predict fetal acidemia or hypoxemia. Early decelerations are a physiologic vagal response to uterine contractions, with resultant fetal head compression, and represent a repetitive pattern of gradual decrease and return of the FHR that is coincidental with the uterine contraction ( Table 115.3 ). Variable decelerations are associated with umbilical cord compression and are characterized by a V or U shaped pattern, are abrupt in onset and resolution, and may occur with or without uterine contractions.
LATE DECELERATION |
|
EARLY DECELERATION |
|
VARIABLE DECELERATION |
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Late decelerations are associated with fetal hypoxemia and are characterized by onset after a uterine contraction is well established and persists into the interval following resolution of the contraction. The late deceleration pattern is usually associated with maternal hypotension or excessive uterine activity, but it may be a response to any maternal, placental, umbilical cord, or fetal factor that limits effective oxygenation of the fetus. The significance of late decelerations varies according to the underlying clinical context. They are most likely to be associated with true fetal hypoxemia/acidemia when they are recurrent and occur in conjunction with decreased or absent variability. Late decelerations represent a compensatory, chemoreceptor-mediated response to fetal hypoxemia. The transient decrease in FHR serves to increase ventricular preload during the peak of hypoxemia (i.e., at the crest of a uterine contraction). If fetal acidemia progresses, late decelerations may become less pronounced or absent, indicating severe hypoxic depression of myocardial function. Prompt delivery is indicated if late decelerations are unresponsive to oxygen supplementation, hydration, discontinuation of labor stimulation, and position changes. Approximately 10–15% of term fetuses have terminal (just before delivery) FHR decelerations that are usually benign if they last <10 min before delivery.
A 3-tier system has been developed by a panel of experts for interpretation of FHR tracings ( Table 115.4 ). Category I tracings are normal and are strongly predictive of normal fetal acid-base status at the time of the observation. Category II tracings are not predictive of abnormal fetal status, but there is insufficient evidence to categorize them as category I or III; therefore further evaluation, surveillance, and reevaluation are indicated. Category III tracings are abnormal and predictive of abnormal fetal acid-base status at the time of observation. Category III tracings require prompt evaluation and efforts to resolve expeditiously the abnormal FHR as previously discussed for late decelerations.
CATEGORY I |
|
CATEGORY II |
|
Baseline Rate |
|
Baseline FHR Variability |
|
Accelerations |
|
Periodic or Episodic Decelerations |
|
CATEGORY III |
|
Umbilical cord blood samples obtained at delivery are useful to document fetal acid-base status. Although the exact cord blood pH value that defines significant fetal acidemia is unknown, an umbilical artery pH <7.0 has been associated with greater need for resuscitation and a higher incidence of respiratory, gastrointestinal, cardiovascular, and neurologic complications. Nonetheless, in many cases, even when a low pH is detected, newborn infants are neurologically normal.
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