Fetal Growth and Development
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).
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.
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. ∗
4. Is there a difference between growth retardation and growth restriction? Define fetal growth restriction.
Symmetric IUGR is characterized by equal reduction in head, abdominal, and skeletal dimensions. It is indicative of an insult during the period of most active cell division, as seen in chromosomal or congenital abnormalities.
Asymmetric IUGR is distinguished by a reduction in abdominal circumference but sparing of head and skeletal growth. It most likely represents an insult during cell growth caused by extrinsic factors such as uteroplacental insufficiency or maternal vascular disease. ∗
5. How do you differentiate a growth-restricted infant from a small-for-gestational-age (SGA) infant and a low-birth-weight (LBW) infant?
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:
TABLE 2-1
RISK FACTORS FOR INTRAUTERINE GROWTH RESTRICTION
MATERNAL | PLACENTAL | FETAL |
Poor or inadequate nutritional intake | Mosaicism | Chromosomal abnormalities |
Medical disease | Abnormal implantation | Trisomy 13, 18, and 21 |
Preeclampsia | Previa | Turner syndrome |
Chronic hypertension | Accreta | Genetic syndromes |
Collagen vascular disease | Abnormal morphology | Russell–Silver |
Diabetes mellitus with vascular disease | Small size | Cornelia de Lange |
Thrombophilia (congenital or acquired) | Bilobed, battledore, or circumvallate | Congenital malformations |
Asthma | Velamentous cord insertion | Anencephaly |
Cyanotic heart disease | Lesions | Congenital heart defect |
Genetic disorder | Chorioangiomata | Congenital diaphragmatic hernia |
Environment | Abruptio placentae | Gastroschisis |
High altitude | Infarction | Omphalocele |
Emotional or physical stress | Secondary to maternal chronic disease | Renal abnormalities |
Medications and drugs | Chronic abruption | Multiple malformations |
Warfarin | Infection | Multiple gestation |
Anticonvulsants | Chorionitis | Twin-twin transfusion syndrome |
Retin-A | Chorioamnionitis | Infection |
Cigarette smoking | Funisitis | TORCH infections: Toxoplasmosis, other (syphilis and other viruses), rubella, cytomegalovirus, and herpes simplex virus |
Alcohol | ||
Cocaine | ||
Heroin | ||
Prior obstetric complications | ||
Spontaneous abortion | ||
Stillbirth | ||
Intrauterine growth restriction, low birth weight, or premature offspring |
Prior maternal history of fetal growth restriction
Maternal history of immunologic or collagen vascular disease
Maternal TORCH infection: Toxoplasmosis, Other (syphilis and other viruses), Rubella, Cytomegalovirus, and Herpes simplex virus
Maternal hypertension or preeclampsia
Genetic abnormalities in the fetus, including some aneuploidies and genetic syndromes
Teratogens: cigarette smoke, Retin-A, warfarin, alcohol
7. What is the initial work-up when fetal growth restriction is suspected?
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. ∗†‡§
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. ∗†‡
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. ∗
16. When in gestation do the five senses develop in the fetus?
Touch: Between 8 and 15 weeks of gestation, the fetal somatosensory system develops in a cephalocaudal pattern. By 32 weeks of gestation, the fetus consistently responds to temperature, pressure, and pain.
Taste: Taste buds are morphologically mature by 13 weeks of gestation. By 24 weeks of gestation, gustatory responses may be present.