Gestational age at delivery is an important factor affecting neonatal outcome. Accurate knowledge of gestational age is essential for risk assessment and providing appropriate care and counseling. In women with regular 28-day menstrual cycles, the mean duration of a singleton pregnancy is 280 days (40 weeks) from the first day of the last normal menstrual period. Term pregnancy is defined as the period from 37 weeks’ (259 days’) to 42 weeks’ (294 days’) gestation, with neonatal outcomes varying widely across this period. For this reason, the designations of early term (37 0/7 to 38 6/7 weeks’ gestation), full term (39 0/7 to 40 6/7 weeks’ gestation), and late term (41 0/7 to 41 6/7 weeks’ gestation) were adopted. Delivery prior to 37 weeks is considered preterm, with anticipated complications varying based on the gestational age at delivery. Evaluation of fetal growth, efficient use of screening and diagnostic tests, appropriate initiation of fetal surveillance, and optimal timing of delivery all depend on accurate dating of the pregnancy.

Recommendations for determining the gestational age and estimated due date (EDD) have been established by the American College of Obstetricians and Gynecologists (ACOG), the Society for Maternal-Fetal Medicine (SMFM), and the American Institute of Ultrasound in Medicine. Assigning the EDD by the first day of the last menstrual period (LMP) is limited by inaccurate recall, irregular cycle lengths, and variations in ovulation timing. Ultrasonographic measurement of the embryo or fetus can improve the accuracy of the EDD, particularly when performed earlier in pregnancy. Gestational age determination is most accurate when ultrasonographic measurement of the fetus or embryo is performed in the first trimester (up to and including 13 6/7 weeks’ gestation). For pregnancies achieved by assisted reproductive technology, the EDD should be assigned based on the age of the embryo and the date of transfer. When the LMP is recorded and the first accurate ultrasonographic examination is performed, the EDD should be determined, communicated to the patient, and documented in the medical record. Once established, the EDD should rarely be revised, as discrepancies between gestational age and fetal measurements may indicate an abnormality in fetal growth, such as macrosomia or fetal growth restriction (FGR).

In the first trimester, before 14 0/7 weeks’ gestation, the crown-rump length (CRL) measurement should be used to establish or confirm the gestational age; in the second and third trimesters, biometric measurements (i.e., biparietal diameter, head circumference, femur length, abdominal circumference) should be used. Assessment of gestational age in the third trimester (after 28 0/7 weeks’ gestation) is the least accurate.

Guidelines for revising the EDD are based on the initial ultrasonographic examination. Before 9 0/7 weeks’ gestation, if the CRL and LMP dating differ by more than 5 days, the EDD should be revised using the CRL measurement. Ultrasonographic and LMP dating difference greater than 7 days (between 9 0/7 and 15 6/7 weeks’ gestation), greater than 10 days (between 16 0/7 and 21 6/7 weeks’ gestation), greater than 14 days (between 22 0/7 and 27 6/7 weeks’ gestation), and greater than 21 days (at greater than 28 0/7 weeks’ gestation) should be revised based on the ultrasonographic examination. Pregnancies without ultrasonographic examination confirmation or revision of the EDD before 22 0/7 weeks’ gestation should be considered suboptimally dated. These pregnancies may benefit from a follow-up ultrasonographic examination 3 to 4 weeks later to confirm gestational age and assess interval growth.

Definitive prenatal fetal genetic information can be obtained by diagnostic testing via chorionic villus sampling (CVS) or amniocentesis . A needle is inserted into the uterus under ultrasonographic guidance to obtain fetal cells from a placental sample (for CVS, performed at 10 to 13 weeks’ gestation) or amniotic fluid (for amniocentesis, performed at 15 weeks’ gestation and beyond). Risks common to all invasive procedures include bleeding, infection, isoimmunization, and pregnancy loss. Women who are Rh negative should receive Rh ₀ (D) immune globulin before or after the procedure. Although risk for vertical transmission of viral infections (e.g., hepatitis B, hepatitis C, human immunodeficiency virus) with invasive procedures is low, the patient should be made aware of these risks as part of a shared decision-making process. The risk of pregnancy loss associated with CVS is approximately 1 in 500, while the risk of pregnancy loss associated with amniocentesis is between 1 in 500 and 1 in 900.

A unique CVS consideration involves the interpretation of the genetic test results. Because the fetus and placenta arise from the same cell, it is assumed that the genetic complements are identical, but this is not always the case. Confined placental mosaicism refers to the situation in which the karyotype of the chorionic villus is a mosaic (i.e., it contains two or more populations of cells with different karyotypes, usually one normal and one trisomic) but the karyotype of the fetus is normal. If mosaicism is detected on a CVS sample, it may be necessary to repeat the fetal karyotype with amniocentesis to provide additional information and to test for uniparental disomy, if indicated. Confined placental mosaicism can be associated with increased risk of growth restriction and warrants additional monitoring.

An ultrasonographic examination is recommended for all pregnant women, given its ability to accurately determine gestational age, viability, fetal number, and placental location, and screen for fetal structural abnormalities in the second trimester. Significant variability exists in the sensitivity of routine ultrasonographic examinations for the detection of fetal anomalies; in a large review of 36 studies with over 900,000 fetuses, the detection rate for fetal anomalies ranged from 15% to 80%. The detection rates for fetal malformations are improved when the examination is performed by an experienced operator at a tertiary center. Central nervous system and urinary tract abnormalities are easier to detect than cardiac anomalies, and imaging of all abnormalities is more difficult in patients with high body mass index.

The indications for first-trimester ultrasonography, which is performed before 14 0/7 weeks’ gestation, are different from those for second- and third-trimester ultrasonography. The first trimester is the ideal time to establish gestational age, fetal number (i.e., singleton versus multiple gestation), and chorionicity. First-trimester ultrasonography between 11.5and 14 weeks’ gestation can include assessment of the nuchal translucency, which, when thickened, is associated with an increased risk for aneuploidy and certain anomalies, such as cardiac, abdominal wall, and diaphragmatic defects.

Some aspects of fetal anatomy can be assessed in the first trimester, but ideally, a detailed fetal anatomic survey is performed at 18 to 22 weeks’ gestation in all pregnant women to assess for fetal growth and anatomy. Placental location in relation to the cervix should also be documented at this time. If placenta previa is identified at 18 to 22 weeks’ gestation, serial ultrasonographic examinations should follow placental location because only about 10% of placenta previas identified in the second trimester persist to term. Other ultrasonographic elements that should be examined include the umbilical cord (i.e., number of vessels, placental and fetal insertion) and amniotic fluid volume. In pregnancies at high risk for fetal cardiac anomalies or preterm birth, fetal echocardiography and cervical length measurements, respectively, may be indicated. Certain fetal anomalies (e.g., achondroplasia, duodenal atresia) may only become evident later in pregnancy as the fetus develops.

During routine or indicated visits throughout pregnancy, fetal well-being is assessed by confirming the FHR and fetal movements (quickening). Typically reported by 18 to 20 weeks’ gestation by nulliparous women and by 16 to 18 weeks’ gestation by parous women, the presence of fetal movements is correlated with fetal health. Decreased fetal movement, which is often observed with increasing gestational age, smoking, low amniotic fluid volume, anterior placentation, and antenatal corticosteroid therapy, is associated with adverse pregnancy events (e.g., umbilical cord compromise, placental abruption, stillbirth). For these reasons, a subjective decrease in perceived fetal movements in the third trimester should prompt an immediate investigation.

First described by Leopold and Sporlin in 1894, a systematic physical examination of the gravid abdomen can determine the size, presentation, and lie of the fetus. Although the value of an abdominal examination is limited in the setting of a small fetus, maternal obesity, multiple pregnancy, uterine fibroids, or polyhydramnios, it is safe, well tolerated, and likely to add information to assist in antepartum management. The uterus can be palpated above the pelvic brim at approximately 12 weeks’ gestation. Thereafter, fundal height should increase by approximately 1 cm per week, reaching the level of the umbilicus at 20 to 22 weeks’ gestation ( Fig. 6.1 ). Between 20 and 32 weeks’ gestation, the fundal height (incentimeters) is approximately equal to the gestational age (in weeks) in healthy women of average weight with an appropriately growing fetus. However, a wide range of values exists for normal fundal height measurements, and maximal fundal height occurs at approximately 36 weeks’ gestation, after which the lower uterine segment elongates and the fetus drops into the pelvis. For these reasons, fundal height measurements alone fail to identify growth restriction in more than 50% of fetuses.

Fundal height measurements in a singleton pregnancy with normal fetal growth.

If clinical findings suggest a fetal growth discrepancy between size and gestational age, ultrasonography is the modality of choice to evaluate alternative explanations, such as growth restriction, macrosomia, multifetal pregnancy, polyhydramnios, and uterine fibroids. FGR is associated with an increased risk of stillbirth as well as neonatal morbidity and mortality; once this diagnosis is made, management includes increasing antenatal surveillance and consideration for an earlier planned delivery.

Obstetric ultrasonography utilizes fetal measurements to estimate fetal weight; however, this approach has inherent limitations. First, regression equations used to create weight estimation formulas are derived primarily from cross-sectional data for infants delivered within an arbitrary period after the ultrasonographic examination. Second, growth curves for “normal” infants between 24 and 37 weeks’ gestation rely on data collected from pregnancies delivered preterm, which may be complicated by some element of uteroplacental insufficiency, regardless of whether the delivery was spontaneous or indicated/iatrogenic. Third, ultrasonographic estimates of fetal weight are derived from mathematical formulas that use a combination of fetal measurements, most commonly the biparietal diameter, abdominal circumference, and femur length. The abdominal circumference is the single most important measurement and is weighted more heavily in these formulas. Unfortunately, abdominal circumference is also the most difficult measurement to acquire, and small differences in the measured value result in large changes in the estimated fetal weight (EFW). A systematic review of ultrasonographic estimations of fetal weight found a significant margin of error, approximately 15%, across all studies. Although the use of an intrauterine standard of EFW across gestation generally performed better than the use of a birthweight standard in predicting neonatal morbidity or mortality, neither significantly improved the accuracy of this detection. Despite these limitations, ultrasonographic estimation of fetal weight with the use of an intrauterine growth standard remains the preferred approach for pregnancies at risk for growth restriction.

Serial ultrasonographic evaluations of fetal weight are more useful than a single measurement in diagnosing abnormal fetal growth. The ideal interval for fetal growth evaluations is every 3 to 4 weeks; more frequent determinations may be misleading due to variations in the ultrasonographic measurements. However, in pregnancies complicated by growth restriction or fetal anomalies, evaluations can be performed as frequently as every 2 weeks. The use of customized fetal growth curves has not yet been shown to improve outcomes.

Antepartum fetal assessment is based on the theory that a change in fetal behavior can indicate a change in fetal status. With the goal of identifying the fetus at risk for preventable neurologic injury or death, antepartum fetal surveillance attempts to screen for neonatal hypoxemia and acidosis associated with infection, anemia, trauma, hypotension, or metabolic derangements. Testing cannot reliably predict or detect all causes of hypoxemia and acidosis, but those associated with progressive uteroplacental insufficiency are most likely to be identified. Antenatal fetal testing relies on the following assumptions: (1) progressive fetal asphyxia can lead to fetal death or permanent neurologic injury, (2) antenatal tests can discriminate between asphyxiated and nonasphyxiated fetuses, and (3) early detection of asphyxia with subsequent intervention can reduce the likelihood of an adverse perinatal outcome. Unfortunately, it is not clear whether these assumptions are reliable, and many adverse outcomes may not be anticipatable or preventable.

Despite these limitations, antepartum fetal testing, including the nonstress test (NST), biophysical profile (BPP), umbilical artery (UA) Doppler assessment, and contraction stress test (CST), are routinely used for high-risk pregnancies. While these tests can be used individually, given the wide variability in findings in normal and at-risk fetuses, a combination of testing modalities offers a more reliable assessment.

Antepartum fetal tests should be interpreted in relation to the gestational age, presence or absence of congenital anomalies, and underlying clinical risk factors. For example, a nonreassuring NST in a fetus with severe growth restriction at 32 weeks’ gestation in the setting of heavy maternal vaginal bleeding has a much higher predictive value in identifying an adverse fetal outcome than an identical FHR tracing in a well-grown fetus at 40 weeks’ gestation. The efficacy of antenatal fetal testing in preventing long-term neurologic injury has not been, nor will likely ever be, validated by prospective randomized clinical trials. Current recommendations rely predominantly on expert opinion and observational data.

Nonstress Test

The fetal NST, also known as fetal cardiotocography (CTG) , investigates changes in the FHR pattern with time, reflecting the maturity of the autonomic nervous system; for this reason, it is less useful in the very preterm fetus (<28 weeks’ gestation). The NST is noninvasive, simple to perform, inexpensive, and readily available in all obstetric units. Most obstetric care providers use the FHR interpretation criteria established in 1997, and updated in 2008, by the National Institute of Child Health and Human Development Research Planning Workshop ( Table 6.1 ) (see Chapter 8 ).

TABLE 6.1

Interpretation of Antepartum Nonstress Test Results

Data from the National Institute of Child Health and Human Development Research Planning Workshop. Electronic fetal heart rate monitoring: research guidelines for interpretation. Am J Obstet Gynecol . 1997;177:1385–1390.

Criterion	Definition
Baseline FHR	Defined as the approximate mean FHR during a 10-min segment and lasting at least 2 min. The normal FHR is defined as 110–160 bpm.
Baseline FHR variability	Described as fluctuations in baseline FHR ≥ 2 cycles/min. It is quantified visually as the amplitude of the peak to the trough in bpm. Variability is classified as follows: • Absent: amplitude range undetectable • Minimal: amplitude range detectable but less than or equal to 5 bpm • Moderate: amplitude range 6–25 bpm • Marked: amplitude range > 25 bpm The normal baseline FHR variability is defined as moderate variability.
Accelerations	Defined as an abrupt increase in FHR above baseline. • At and after 32 weeks’ gestation, an acceleration is defined as 15 bpm or more above baseline for 15 s or more but less than 2 min. • Before 32 weeks’ gestation, an acceleration is defined as 10 bpm or more above baseline for 10 s or more but less than 2 min. A prolonged acceleration is defined as an acceleration lasting 2 min or more but less than 10 min. If the duration is longer than 10 min, it is referred to as a “change in baseline” and not a prolonged acceleration.
Decelerations	Decelerations are not normal. However, some decelerations are a more serious sign of fetal compromise than others. The following three types of decelerations are recognized: • Early decelerations are characterized by a gradual decrease and return to baseline FHR associated with a uterine contraction. The onset, nadir, and recovery of the deceleration are coincident with the beginning, peak, and ending of the uterine contraction. • Variable decelerations are characterized by an abrupt decrease in the FHR to 15 bpm or more below the baseline and lasting for 15 s or more but less than 2 min. Abrupt is defined as less than 30 s from baseline to the nadir of the deceleration. When variable decelerations are associated with uterine activity, their onset, depth, and duration commonly vary with successive contractions. • Late decelerations are characterized by a gradual decrease and return to baseline FHR associated with a uterine contraction. Importantly, the deceleration is delayed in timing, with the nadir of the deceleration occurring after the peak of the contraction. Onset, nadir, and recovery of the deceleration occur after the beginning, peak, and ending of the uterine contraction. A prolonged deceleration is defined as a deceleration lasting 2 min or more but less than 10 min. If the duration is longer than 10 min, it is referred to as a “change in baseline” and not a prolonged deceleration. Recurrent decelerations describe the presence of decelerations with more than 50% of uterine contractions in any 20-min period

FHR , Fetal heart rate.

An NST is performed before the onset of labor via an externally placed Doppler ultrasound probe positioned on the maternal abdomen over the fetal heart. Sound waves emitted from the transducer are deflected by heart and heart valve movements. The shift in wave frequency is detected by a sensor and converted into a heart rate. The FHR is recorded for a period of 20 to 40 minutes during which the tracing is evaluated for the presence of periodic changes. Simultaneously, an external tocometer records myometrial tone, providing information about the timing and duration of contractions. The tocometer does not assess intrauterine pressure or the intensity of the contractions. A FHR tracing is designated reactive if there are two or more accelerations that peak (but do not necessarily remain) at least 15 bpm above the baseline for 15 seconds in a 20-minute period ( Fig. 6.2 ). In fetuses less than 32 weeks’ gestation, FHR tracing is designated as reactive if there are two or more accelerations of at least 10 bpm above the baseline for 10 seconds. A reactive NST is regarded as evidence of fetal health.

A Normal (Reactive) Fetal Heart Rate (FHR) Tracing. The baseline FHR is normal (110–160 bpm), there is moderate variability (defined as 6 to 25 bpm from peak to trough), there are no decelerations, and there are two or more accelerations (defined as an increase in FHR of 15 bpm or more above baseline lasting at least 15 s) in a 20-min period.

A nonreactive NST does not achieve sufficient accelerations within a 40-minute period; this finding does not necessarily indicate a compromised fetus, as most often it is secondary to a fetal sleep cycle. The interpretation of a nonreactive NST must consider gestational age, the underlying clinical circumstance, and the results of previous NSTs. Only 65% of fetuses have a reactive NST by 28 weeks’ gestation, whereas 95% do so by 32 weeks. However, once a reactive NST has been documented, it should generally remain reactive throughout the remainder of the pregnancy. A nonreactive NST at term is associated with a poor perinatal outcome in only a minority of cases. It has a sensitivity of 57%, a positive predictive value of 13%, and a negative predictive value of 98% (assuming a prevalence of 4%) for a 5-minute Apgar score < 7. For permanent neurologic injury, a nonreactive NST at term has a 99.8% false-positive rate.

Visual interpretation of the FHR tracing involves assessment of the following components: (1) baseline FHR, (2)baseline FHR variability, (3) presence of accelerations, (4) presence of periodic or episodic decelerations, and (5) changes of FHR pattern over time (see Table 6.1 ; see Fig.8.4 ). The patterns are categorized as baseline , periodic (i.e., associated with uterine contractions), or episodic (i.e., not associated with uterine contractions). Periodic changes are described as abrupt or gradual (defined as onset-to-nadir interval < 30 seconds or > 30 seconds, respectively).

A normal FHR tracing (Category 1) is defined as having a normal baseline rate (110 to 160 bpm), normal baseline variability (i.e., moderate variability, defined as 6 to 25 bpm from peak to trough), presence of accelerations, and absence of decelerations. FHR accelerations typically occur in response to fetal movement and usually indicate fetal health and adequate oxygenation (see Box 8.3 ). Abnormal FHR patterns (Category 3) demonstrate absence of baseline variability combined with recurrent late or variable decelerations or substantial bradycardia. Indeterminant FHR patterns (Category 2) have characteristics between the two extremes of normal and abnormal tracings.

Persistent fetal tachycardia (defined as an FHR > 160 bpm) may be associated with fetal hypoxia, maternal fever, chorioamnionitis (intrauterine infection), maternal administration of an anticholinergic or beta-adrenergic receptor agonist, fetal anemia, or tachyarrhythmia ( Table 6.2 ). Persistent fetal bradycardia (FHR < 110 bpm) may be a result of congenital heart block, administration of a beta-adrenergic receptor antagonist, hypoglycemia, or hypothermia; it may also indicate fetal hypoxia. Both tachyarrhythmias and bradyarrhythmias require immediate evaluation.

TABLE 6.2

Drugs That Can Affect the Fetal Heart Rate Tracing

Effect on the Fetus	Drug
Fetal tachycardia	Atropine
	Epinephrine (adrenaline)
	Beta-adrenergic agonists (ritodrine, terbutaline)
Fetal bradycardia	Antithyroid medications (including propylthiouracil)
	Beta-adrenergic antagonists (e.g., propranolol)
	Intrathecal or epidural analgesia
	Methylergonovine (contraindicated before delivery)
	Oxytocin (if associated with excessive uterine activity)
Sinusoidal fetal heart rate pattern	Systemic opioid analgesia
Diminished variability	Atropine
	Anticonvulsants (but not phenytoin)
	Beta-adrenergic antagonists
	Antenatal corticosteroids (betamethasone, dexamethasone)
	Ethanol
	General anesthesia
	Hypnotics (including diazepam)
	Insulin (if associated with hypoglycemia)
	Magnesium sulfate
	Systemic opioid analgesia
	Promethazine

Baseline FHR variability, perhaps the most important component of the NST, is determined on a beat-to-beat basis by the competing influences of the sympathetic and parasympathetic nervous systems on the fetal sinoatrial node. The presence of FHR variability, characterized by fluctuations that are irregular in both amplitude and frequency, indicates that the autonomic nervous system is functioning and that the fetus has normal acid-base status.

Variability is defined as absent, minimal, moderate, or marked. The older terms short-term variability and long-term variability are no longer used. Normal (moderate) variability indicates the absence of cerebral hypoxia. In the setting of acute hypoxia, variability may be minimal or marked. Persistent or chronic hypoxia is typically associated with loss of variability. Reduced variability may be the result of maternal drug administration (see Table 6.2 ), fetal arrhythmia, or neurologic abnormality (e.g., anencephaly, structural abnormality, prior injury).

Contraction Stress Test

Also known as the oxytocin challenge test, the CST assesses the response of the FHR to uterine contractions induced by either intravenous oxytocin administration or nipple stimulation (which causes release of endogenous oxytocin from the maternal neurohypophysis). A minimum of three contractions for at least 40 seconds in a 10-minute period is required to interpret the test. A negative CST (no late or severe late decelerations with contractions) is reassuring and suggestive of a healthy, well-oxygenated fetus.

A positive CST (late or severe variable decelerations with at least 50% of the contractions) is suggestive of a fetus suffering from impaired maternal-to-fetal oxygen exchange during uterine contractions and is associated with adverse perinatal outcome in 35% to 40% of cases. A CST is defined as equivocal if FHR decelerations occur in the presence of contractions that occur more frequently than every 2 minutes or last longer than 90 seconds, equivocal-suspicious if there are intermittent late decelerations or significant variable decelerations, and unsatisfactory if there are fewer than three contractions in 10 minutes or the FHR tracing is uninterpretable. The combination of a positive CST and absence of FHR variability is especially ominous. It should be noted, however, that the false-positive rate of this test exceeds 50%. If the CST is uninterpretable or equivocal, the test should be repeated in 24 to 72 hours. Studies suggest that more than 80% of repeated tests are negative. The rate of antepartum intrauterine fetal demise within 1 week of a negative CST is 0.04%.

Because this test is time-consuming, requires skilled nursing care, and necessitates an inpatient setting owing to the possibility of precipitating fetal compromise requiring emergency cesarean delivery, the CST is reserved for specific clinical indications. Moreover, there are contraindications to its use, including placenta previa, placental abruption, prior classical (high-vertical) cesarean delivery, and risk for preterm labor. Despite these limitations, the CST allows for indirect evaluation of fetal oxygenation during periods of uterine contractions and diminished uteroplacental perfusion and may therefore provide a better assessment of fetal well-being and fetal reserve than either the NST or the BPP ( Table 6.5 ).

TABLE 6.5

False-Positive and False-Negative Rates for the Nonstress Test, Biophysical Profile, and Contraction Stress Test

Data from References.

Test	False-Negative Rate (per 1000 Live Births) a
Nonstress test	1.9
Biophysical profile	0.8
Contraction stress test	0.3

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