Chapter 2

Fetal growth assessments can be made clinically by assessing the fundal height; clinical assessment of fetal weight can be made by performing Leopold maneuvers ( Fig. 2-1).

Fundal height is measured from the upper edge of the symphysis pubis to the top of the uterine fundus. Between 20 and 34 weeks of gestation, fundal height measurements (in centimeters) approximate the gestational age (in weeks). A discrepancy between measured and expected fundal height measurements of 3 centimeters or more is suggestive of fetal growth restriction.

Leopold maneuvers involve the palpation of the fetus through the maternal abdomen. Advantages of Leopold maneuvers include the fact that the procedure is relatively easy to perform and does not incur the expense of ultrasound; disadvantages include a low sensitivity for macrosomia. In general, clinical estimates of fetal weight are more likely to underestimate the weight of macrosomic infants than to overestimate the weight.

Ultrasound is generally used to evaluate possible fetal growth abnormalities. Biometric measurements used to assess fetal growth are as follows:

When a single sonographic measurement is used, the BPD or FL is generally the most reliable indicator of fetal age, whereas the AC is the most sensitive indicator of fetal growth.

When fetal growth is estimated, several individual biometric parameters are commonly entered into a standard formula to calculate a composite weight. Because two-dimensional estimates of fetal weight do not account for variation in fetal body composition and because of the margin of error inherent in sonographic measurement of fetal biometries, sonographic assessments of fetal weight are associated with a significant (~10% to 20%) margin of error. ^∗†

Macrosomia is a term used to describe excessive fetal growth. No threshold weight has been universally accepted, but common definitions include a birth weight above 4000 or 4500 grams. In contrast to macrosomia, which is determined solely by birth weight, the term large for gestational age is used to describe any fetus with an estimated weight above the 90th percentile for a given gestational age. ^∗

Because of the pejorative nature of the term retardation, the term restriction has been substituted. Intrauterine growth restriction (IUGR) is a deviation in the rate of growth of a fetus that is less than its genetically predetermined growth potential. Prenatally, intrauterine growth restriction is often defined as an estimated fetal weight that is less than the 10th percentile for a given gestational age.

Both IUGR and SGA refer to fetal growth potential. In contrast to IUGR, which is diagnosed using estimated fetal weights, SGA refers to an infant whose birthweight is below a preset weight cutoff, typically the 10th percentile for gestational age, when compared with reference population norms.

The LBW classification refers to any infant who weighs less than 2500 grams at birth, independent of gestational age. This category includes term (≥37 weeks’ gestation) SGA infants as well as premature infants who may be SGA or of appropriate size relative to their gestational age.

Factors that affect fetal growth are typically categorized as fetal, placental, or maternal in origin and are summarized in Table 2-1. Common examples include the following:

In pregnancies at risk for IUGR, Doppler analysis is used to evaluate placental resistance and fetal status and may improve fetal and neonatal outcomes. Normal umbilical arterial Doppler flow is reassuring and rarely associated with significant morbidity. Absence of end-diastolic flow in the umbilical artery is indicative of significant placental resistance; reversal of flow is suggestive of worsening fetal status and impending demise. Abnormalities in venous circulation (e.g., ductus venosus a-wave reversal) represent worsening circulatory compromise and may reflect a greater risk of fetal death than abnormalities in the arterial circulation. ^∗†‡§

The brain-sparing effect observed in asymmetric IUGR refers to the fetal adaptive response to chronic hypoxia, in which the fetus preferentially redistributes its blood flow to the brain, myocardium, and adrenal glands. A decreased middle cerebral artery pulsatility index may provide direct evidence of brain sparing.

Once IUGR is suspected, fetal well-being should be closely monitored with serial antenatal testing (biophysical profile ± non-stress test; Doppler studies); the frequency of testing will be influenced by the gestational age as well as the maternal and the fetal condition. The timing of delivery is based on fetal maturity, signs of fetal distress, or worsening maternal disease. ^∗†‡§

The timing of delivery is determined by the gestational age and clinical status of the fetus. For an IUGR fetus at term or near term, delivery is indicated if fetal lung maturity has been documented, there has been minimal fetal growth observed over serial ultrasounds, significant fetal compromise is evident on testing or Doppler study, or maternal status is worsening (e.g., hypertension). The IUGR fetus is at increased risk of metabolic acidosis and hypoxia, which may be apparent in the fetal heart tracing; continuous monitoring is indicated in labor. ^∗†‡

The PI is a widely used measurement of the infant’s relative thinness or fatness independent of race, gender, and gestational age. It is calculated from the following formula: (weight × 100)/ length³ with weight in grams and length in centimeters. Normal PI values range between 2.32 and 2.85. The PI is normal in symmetric IUGR, low in asymmetric IUGR, and high in the macrosomic fetus.

An IUGR infant is initially at risk for perinatal asphyxia, intraventricular hemorrhage, meconium aspiration, respiratory distress syndrome, impaired thermoregulation, fasting and alimented hypoglycemia, hypocalcemia, hyperviscosity–polycythemia syndrome, immunodeficiency, and necrotizing enterocolitis. The potential long-term complications are cerebral palsy, behavioral and learning problems, and altered postnatal growth. ^∗

David Barker and colleagues postulated that impaired fetal growth may be a key determinant of later development of adult diseases such as obesity, insulin resistance, type 2 diabetes mellitus, and cardiovascular disease. Poor fetal nutrition results in developmental adaptations that permanently alter subsequent postnatal physiology and thereby “program” an infant’s future predisposition to disease.

Postmaturity refers to an infant born of a post-term pregnancy, defined as a pregnancy beyond 42 weeks of gestation. Dysmaturity may occur in term or preterm infants and describes an infant who exhibits characteristics of placental insufficiency, such as loss of subcutaneous fat and muscle mass or meconium staining of the amniotic fluid, skin, and nails.

The BPP is an antenatal test that is used to assess fetal well-being before birth. Five parameters are assessed:

The presence of a normal assessment is scored as 2 points, and the absence of the finding is scored as 0. The maximum score is 10, and the minimum score is 0. If all of the ultrasound measurements are normal (i.e., BPP = 8), fetal heart monitoring may be omitted because it will not improve the test’s predictive accuracy. If oligohydramnios is detected, further fetal evaluation is necessary, regardless of the BPP. ^∗

A regular pattern of fetal breathing movements is observed by 20 to 21 weeks of gestation. Fetal breathing movement is controlled by centers on the ventral surface of the fourth ventricle. As a result, the presence of fetal breathing indicates an intact central nervous system. Fetal breathing movements appear to assist the movement of fetal lung fluid into the amniotic cavity and also tone the respiratory muscles for the initiation of breathing at the time of birth. ^∗

Fetal sleep cycles are generally approximately 20 minutes in length. Accordingly, to account for the possibility of fetal sleep during an observation period, a BPP must be performed over a minimum of 30 minutes before absence of fetal breathing can be diagnosed. ^∗

The BPP is applicable in cases of acute or chronic intrauterine hypoxia. In response to hypoxia, the individual components of the BPP theoretically disappear in the inverse of their appearance. Nonreactive fetal heart rate activity should be the first sign of fetal compromise, followed by absence of fetal breathing movements, gross body movement, and, lastly, tone.

Whereas the other BPP parameters reflect more acute changes, amniotic fluid volume assessment is a measure of chronic fetal status. Oligohydramnios may be seen in response to impaired uteroplacental perfusion. ^∗

Figure 2-2 reveals the relationship between the fetal BPP and mean umbilical venous pH. ^∗

Figure 2-3 depicts the relationship between the fetal BPP and risk of any perinatal morbidity, meconium aspiration, and major congenital anomaly. A normal BPP is never associated with fetal acidemia. The perinatal mortality rate is 0.8 per 1000 live births after a normal BPP. However, a BPP of 0 is almost always associated with fetal compromise.

Fetal anomalies can be classified as either major or minor. Minor anomalies are those that may have cosmetic significance but rarely require medical or significant surgical treatment. In contrast, major anomalies are those that have a serious impact on the health, development, or functional ability of the affected individual. Although some women—such as those with diabetes, those born with a congenital anomaly, or those who have had a prior affected child—are at higher risk of having a baby with a birth defect, the majority of infants with congenital anomalies are born to women with no risk factors.

The goal of prenatal screening is the early detection of major birth defects before delivery. Prenatal detection of anomalies allows time for referral to a tertiary care facility for consultation with appropriate pediatric subspecialists, delivery planning, and coordination of neonatal care.

2D ultrasound is the primary tool used to screen for fetal structural abnormalities. Although the majority of anomalies are detected in the second or third trimester, some major birth defects can be diagnosed already in the first trimester. Measurement of the nuchal translucency between 11 and 14 weeks of gestation can be used as an early screening tool for aneuploidy, fetal congenital heart disease, and other structural anomalies. ^∗

Although many birth defects can be diagnosed prenatally, some major and many minor anomalies are not detected until birth (or later). Several factors can affect the ability to detect a fetal malformation prenatally. In general, major anomalies are generally more likely to be detected before birth than minor abnormalities, but some major anomalies—such as congenital heart disease and orofacial clefts—have relatively low detection rates despite routine prenatal screening. In addition to the nature of the ultrasound facility and the experience of the sonographer or sonologist, ultrasound detection rates can also be affected by maternal factors, such as obesity and abdominal wall scarring, which can make it difficult to see fetal structures prenatally. Furthermore, some anomalies cannot be detected early in gestation either because the structure is not developed at the time the ultrasound is performed or because the abnormality may develop after the scan was done. ^∗

In some cases, three-dimensional ultrasound or fetal magnetic resonance imaging (MRI) may be used to further characterize a structural abnormality or to screen for other malformations. In particular, fetal MRI may be used to evaluate abnormalities of the fetal brain because it can sometimes detect abnormalities that cannot be seen with ultrasound alone.

Fetal echocardiogram is recommended in all cases of suspected fetal congenital heart disease as well as in women at increased risk of fetal cardiac anomalies (e.g., personal or family history of congenital heart disease, pregestational diabetes, conception by way of in vitro fertilization, presence of other fetal structural anomalies). ^∗†

TTTS is defined as the presence of oligohydramnios in one amniotic sac and polyhydramnios in the other sac in a monochorionic diamniotic twin gestation. TTTS results from an unbalanced interfetal transfusion from a net unidirectional flow through arteriovenous anastomoses deep within the shared placenta. The severity of clinical presentation is modulated by the degree of bidirectional flow from superficial anastomoses. ^∗

Complications specific to the recipient twin are polycythemia, systemic hypertension, biventricular cardiac hypertrophy, and congestive heart failure. The donor twin is at risk for growth failure, anemia, high-output cardiac failure, and hydrops. Both twins are at increased risk of congenital anomalies, in utero demise, and cerebral palsy. ^∗

The Quintero staging system grades the severity of TTTS and may aid in determining the prognosis and selection of treatment modalities.

The major concern in fetuses with tachyarrhythmia (e.g., supraventricular tachycardia and atrial flutter) is compromised cardiac output leading to the development of fetal hydrops. When cardiac output is compromised, maternal antiarrhythmic therapy may be initiated. If the fetal arrhythmia remains refractory, direct fetal therapy with antiarrhythmic medications may be considered.

CVR is an ultrasonographic measurement used as a prognostic tool for fetuses with a prenatal diagnosis of congenital cystic adenomatoid malformation (CCAM). CVR is calculated using the formula: [(mass length × height × width) × 0.52] / fetal head circumference; all variables should be in centimeters. ^∗

Neonatal survival approaches 100% in the absence of hydrops. The CVR identifies fetuses at high risk for developing hydrops, and a CVR greater than 1.6 is associated with an 80% risk of developing hydrops; these fetuses may benefit from closer surveillance and possible fetal intervention. ^∗

LHR is an ultrasonographic measurement used in fetuses between 24 and 26 weeks of gestation with congenital diaphragmatic hernia. LHR is calculated according to the following formula: right lung length × right lung length/fetal head circumference; all variables should be in millimeters. ^∗

In general, LHR greater than or equal to 1.4 is considered a good prognostic indicator, whereas LHR below 0.6 is associated with poor outcomes. Nevertheless, there is a degree of unpredictability in the clinical course despite an accurate LHR measurement. ^∗

The major neonatal diseases that may benefit from fetal intervention are listed in Table 2-2. In utero therapy has been successfully performed for diseases such as primary fetal pleural effusion, lower urinary tract obstruction, neural tube defect, some obstructive heart defects, CCAM, and sacrococcygeal teratoma. Fetal intervention for congenital diaphragmatic hernia is currently investigational. ^∗†‡

Left-sided lesions

Right-sided lesions

As shown in Figure 2-5, the ex utero intrapartum treatment (EXIT) is a technique by which a mother undergoes partial cesarean delivery so that placental support to the fetus can be maintained while airway identification, stabilization, and, if necessary, mass resection are performed. The procedure is currently used for the delivery and management of fetal airway compromise resulting from extrinsic mass compression or intrinsic airway defect.

Maternal mirror syndrome is a preeclampsia-like state that occurs in the setting of fetal hydrops; other terms that are used interchangeably are Ballantyne syndrome and pseudotoxemia. When the syndrome is identified, immediate delivery is generally indicated. Although the symptoms are similar to those of true preeclampsia, mothers with this syndrome typically exhibit anemia caused by hemodilution rather than hemoconcentration and do not commonly develop thrombocytopenia.