The Fetus

Ultrasonography of the fetus, a common obstetric procedure, is both safe and accurate. Indications for antenatal ultrasonography 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, determination of the location of the placenta and the number and position of fetuses, and identification of congenital anomalies.

Fetal growth can be assessed by ultrasonography as early as 6-8 wk. The most accurate assessment of gestational age is by 1st-trimester ultrasound measurement of crown-rump length. The biparietal diameter is used to assess gestational age beginning in the 2nd trimester. Through 30 weeks the biparietal diameter accurately estimates gestation to within ± 10 days. Later in gestation, accuracy falls to ± 3 wk. Methods used to assess gestational age at term include measurement of abdominal circumference and femoral length. If a single ultrasound 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 may be useful in assessing fetal growth. Two patterns of fetal growth restriction have been identified: continuous fetal growth 2 standard deviations (SD) below the mean for gestational age or a normal fetal growth curve that abruptly slows or flattens later in gestation (Fig. 90-1).

Figure 90-1 A, Example of a “low-profile” growth retardation pattern in an uneventful pregnancy and labor. The baby cried at 1 min and hypoglycemia did not develop. Birthweight was below the 5th percentile for gestational age. B, Example of a “late-flattening” growth retardation pattern. The mother had a typical history of preeclampsia, and the infant had intrapartum fetal distress, a low Apgar score, and postnatal hypoglycemia. Birthweight was below the 5th percentile for gestational age.

(From Campbell S: Fetal growth, Clin Obstet Gynecol 1:41–65, 1974.)

Fetal maturity and dating are usually assessed by history (last menstrual period), physical examination, auscultation of fetal heart sounds at 16-18 wk, maternal perception of fetal movements at 18-20 wk, fundal height, and ultrasound (growth). Lung maturation may be estimated by determining the surfactant content of amniotic fluid (Chapter 95.3).

Fetal compromise may occur during the antepartum or intrapartum period; it may be asymptomatic in the antenatal period. 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, and post-term 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. 90-2 and 90-3), and, when severe, mixed respiratory and metabolic (lactic) acidosis. The goals of antepartum fetal surveillance are to prevent intrauterine fetal demise, to prevent hypoxic brain injury, and to either prolong gestation in women at risk for preterm delivery when such prolongation is safe or deliver a fetus when it is in jeopardy. Methods for assessing fetal well-being are listed in Table 90-1.

Figure 90-2 Normal Doppler velocity in sequential studies of fetal umbilical artery flow velocity waveforms from one normal pregnancy. Note the systolic peak flow with lower but constant heart flow during diastole. The systolic : diastolic ratio can be determined and, in normal pregnancies, is less than 3 after the 30th wk of gestation. The numbers indicate the weeks of gestation.

(From Trudinger B: Doppler ultrasound assessment of blood flow. In Creasy RK, Resnik R, editors: Maternal-fetal medicine: principles and practice, ed 5, Philadelphia, 2004, WB Saunders.)

Figure 90-3 Abnormal umbilical artery Doppler in which the diastolic component shows flow in a reverse direction. This finding occurs in severe intrauterine hypoxia and intrauterine growth restriction.

(From Trudinger C: Doppler ultrasound assessment of blood flow. In Creasy RK, Resnik R, editors: Maternal-fetal medicine: principles and practice, ed 5, Philadelphia, 2004, WB Saunders.)

Table 90-1 FETAL DIAGNOSIS AND ASSESSMENT

* DNA genetic analysis on chorionic villus samples, amniocytes from amniocentesis, or fetal cells recovered from the maternal circulation may obviate the need for direct fetal tissue biopsy if the gene or genetic marker is available (e.g., the gene for Duchenne muscular dystrophy).

The most commonly used noninvasive tests are the nonstress test (NST), the full and modified biophysical profile (BPP), and less commonly, the contraction stress test (CST). The NST monitors the presence of fetal heart rate accelerations that follow fetal movement. A reactive (normal) NST result demonstrates two fetal heart rate accelerations of at least 15 beats/min lasting 15 sec. A nonreactive NST result suggests fetal compromise and requires further assessment with a CST or the BPP. A CST observes the fetal heart rate response to spontaneous, nipple-stimulated, or oxytocin-stimulated uterine contractions. Fetal compromise is suggested when the majority of contractions in 10 min are followed by late decelerations. A CST is relatively contraindicated in women with preterm premature rupture of membranes, a previous uterine scar from a classic cesarean section, multiple gestations, incompetent cervix, and placenta previa. The goals of fetal monitoring are to prevent intrauterine fetal demise and hypoxic brain injury. Although the CST and NST have low false-negative rates, both have high false-positive rates. The full BPP assesses fetal breathing, body movement, tone, heart rate, and amniotic fluid volume, and it is used to improve the accurate and safe identification of fetal compromise (Table 90-2). A score of 2 is given for each observation present. 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 ultrasound 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 ultrasonography include reduced, absent, or reversed diastolic waveform velocity in the fetal aorta or umbilical artery (see Fig. 90-3 and Table 90-1). High-risk fetuses often have combinations of abnormalities, such as oligohydramnios, reversed diastolic Doppler umbilical artery blood flow velocity, and a low BPP.

Table 90-2 BIOPHYSICAL PROFILE SCORING: TECHNIQUE AND INTERPRETATION

* Modification of the criteria for reduced amniotic fluid from less than 1 cm to less than 2 cm would seem reasonable. Ultrasound is used for biophysical assessment of the fetus.

From Creasy RK, Resnik R, Iams JD, editors: Maternal-fetal medicine: principles and practice, ed 5, Philadelphia, 2004, Saunders.

Fetal compromise during labor may be detected by monitoring the fetal heart rate, uterine pressure, and fetal scalp blood pH (Fig. 90-4). Continuous fetal heart rate monitoring detects abnormal cardiac patterns by instruments that compute the beat-to-beat fetal heart rate from a fetal electrocardiographic signal. Signals are derived 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 simultaneously recorded from an amniotic fluid catheter and pressure transducer or from a tocotransducer applied to the maternal abdominal wall overlying the uterus. Fetal heart rate patterns show various characteristics, some of which suggest fetal compromise. The baseline fetal heart rate is the average rate between uterine contractions, which gradually decreases from about 155 beats/min in early pregnancy to about 135 beats/min at term; the normal range at term 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. The last 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.

Figure 90-4 Patterns of periodic fetal heart rate (FHR) deceleration. The tracing in A shows early deceleration occurring during the peak of uterine contractions as a result of pressure on the fetal head. B, Late deceleration caused by uteroplacental insufficiency. C, Variable deceleration as a result of umbilical cold compression. Arrows denote the time relationship between the onset of FHR changes and uterine contractions.

(From Hon EH: An atlas of fetal heart rate patterns, New Haven, CT, 1968, Harty Press.)

Normally, the baseline fetal heart rate is variable. Variability is classified as follows: absence of variability, if an amplitude change is undetectable; minimal variability if amplitude range is ≤ 5 beats/min (beats/min); moderate variability if amplitude range is 6-25 beats/min; 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.

Periodic accelerations or decelerations of the fetal heart rate in response to uterine contractions may also be monitored (see Fig. 90-4). An acceleration is an abrupt increase in fetal heart rate 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 deceleration associated with head compression is a repetitive pattern of gradual decrease and return of the fetal heart rate that is coincidental with the uterine contraction (Table 90-3). Variable deceleration (associated with cord compression) is characterized by variable shape, abrupt onset and occurrence with consecutive contractions, and return to baseline at or after the conclusion of the contraction. Late deceleration, associated with fetal hypoxemia, occurs repetitively after a uterine contraction is well established and persists into the interval following contractions. 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. Reflex late decelerations with normal beat-to-beat variability are associated with chronic compensated fetal hypoxia, and they occur during uterine contractions that temporarily impede oxygen transport to the heart. Nonreflex late decelerations are more ominous and indicate severe hypoxic depression of myocardial function.

If late decelerations are unresponsive to oxygen supplementation, hydration, discontinuation of labor stimulation, and position changes, prompt delivery is indicated. A three-tier system has been developed by a panel of experts for interpretation of fetal heart rate tracings (Table 90-4). 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; 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 expeditiously resolve the abnormal fetal heart rate as previously discussed for late decelerations.

Fetal scalp blood sampling during labor through a slightly dilated cervix may aid in confirming fetal distress suspected on the basis of variations in fetal heart rate or the presence of meconium in amniotic fluid. The proper use of this technique may result in earlier delivery of depressed infants, who thus have a better chance of successful resuscitation, increased survival, and less morbidity. Alternatively, when continuous fetal heart rate monitoring or general clinical evaluation suggests that a fetus is at risk, a normal fetal scalp blood sample may help avert obstetric intervention.

Fetal scalp blood pH in normal labor decreases from about 7.33 early in labor to approximately 7.25 at the time of vaginal delivery; the base deficit is about 4-6 mEq/L. Changes in the buffer base may be particularly helpful in assessing fetal status, because they correspond to the accumulation of fetal lactic acid. A pH <7.25 suggests fetal distress, and a pH <7.20 is an indication for further assessment and intervention. Determination of the lactate concentration in fetal scalp blood is another tool for monitoring the condition of the fetus.

Umbilical cord blood samples obtained at the time of 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.