Definitions
• Low birth weight (LBW) refers to infants with an absolute birth weight <2500 g regardless of gestational age.
• Small-for-gestational-age (SGA) fetuses are <10th percentile for gestational age. Fetuses >90th percentile are termed “large for gestational age” (LGA). Fetuses between the 10th and 90th percentiles are referred to as “appropriate for gestational age” (AGA). The correct assignment of the fetal weight category is dependent on accurate dating of the pregnancy because birthweight is a function of both gestational age and rate of fetal growth.
Intrauterine growth restriction
• Definition.
Intrauterine growth restriction (IUGR) refers to any fetus that fails to reach its full growth potential.
• Incidence.
Of fetuses 4–8% are diagnosed with IUGR.
• Classification.
IUGR can be classified as symmetric (in which the fetus is proportionally small, suggesting long-term compromise) or asymmetric (in which the fetal head is proportionally larger than the body, suggesting short-term compromise with “sparing” of the brain). This distinction is, however, of little clinical value.
• Causes.
IUGR represents the clinical end-point of many different fetal, uteroplacental, and maternal conditions. An attempt should be made to determine the cause before delivery in order to provide counseling, perform ultrasonographic evaluation for fetal growth and delineation of anatomy, and obtain neonatal consultation. Frequently, the cause is readily apparent.
CAUSES OF INTRAUTERINE GROWTH RESTRICTION (IUGR)
Genetic factors (5–15%)
• Fetal chromosomal anomalies (2–5%) including trisomies (18 >13 >21) and sex chromosome
abnormalities. Most chromosomally abnormal IUGR fetuses have associated structural abnormalities, but 2% do not.
• Single gene defects (3–10%) such as phenylketonuria, dwarfism
• Confined placental mosaicism (rare)
Fetal structural anomalies (1–2%)
• Cardiovascular anomalies
• Bilateral renal agenesis
Multiple pregnancy (2–3%)
• Risk of IUGR increases with fetal number
• Worse in poly/oligo sequence (twin–twin transfusion syndrome)
Uteroplacental causes
Uteroplacental insufficiency (25–30%)
• Chronic hypertension, preeclampsia
• Antiphospholipid antibody syndrome (25% of chromosomally and structurally normal IUGR fetuses have mothers who have circulating lupus anticoagulant [LAC] or anticardiolipin antibodies
[ACA])
• Unexplained chronic proteinuria (25% risk of IUGR)
• Chronic placental abruption
Velamentous insertion of umbilical cord
Maternal causes
Drug and/or toxin exposure
• Illicit drugs (cocaine)
• Heavy cigarette smoking (effect is most
pronounced in older mothers)
Malnutrition (especially gestational malnutrition
superimposed on poor prepregnancy nutritional
status)
Maternal medical conditions
• Poorly controlled hyperthyroidism
• Hemoglobinopathies
• Chronic pulmonary disease
• Cyanotic heart disease
• Anemia
Infections (5–10%)
• Malaria (the single greatest cause of IUGR
worldwide)
• Rubella
• Cytomegalovirus
• ? Varicella
• Risk factors.
Numerous pre-existing and acquired conditions predispose the fetus to IUGR
• Hypertension (both chronic and gestational hypertension)
• Multifetal pregnancies
• Prior IUGR infant
• Poor maternal weight gain
• Severe maternal anemia
• Antiphospholipid antibody syndrome
• Diabetes with vascular disease
• Maternal drug/tobacco abuse
• Discrepancy between fundal height measurement and gestational age >3–4 cm
• Diagnosis. The clinical diagnosis of IUGR is unreliable, but a fundal height measurement significantly less than expected (3–4 cm) for gestational age may suggest the diagnosis. IUGR is confirmed by sonographic measurements.
• Suspect the diagnosis in patients at high risk
• Clinical examination will fail to identify >50% of IUGR fetuses
• Confirm the diagnosis by ultrasound:
(i) estimated fetal weight <5th percentile (2 standard deviations from the mean) for gestational age
OR
(ii) estimated fetal weight <10th percentile for gestational age with evidence of fetal compromise (oligohydramnios, abnormal umbilical artery Doppler blood flow)
• Serial ultrasound examinations are more useful than a single scan to confirm the diagnosis of IUGR, to follow fetal growth, and to detect oligohydramnios or umbilical artery Doppler velocimetry abnormalities
• Pathophysiology.
- IUGR most commonly results from a compromise of uteroplacental blood flow
- Compromise in uteroplacental blood flow
- Decreased nutrients (glucose, oxygen, amino acids, growth factors) to fetus
- Fetal growth begins to diminish in a fixed sequence (subcutaneous tissue axial skeleton vital organs such as brain, heart, liver, kidney)
- Nutrient, oxygen and energy demands of the growing fetoplacental unit begin to exceed supply leading to hypoxia, acidosis, and death
Changes in antepartum fetal testing reflect the pathophysiological changes (in sequence):
- Umbilical systolic/diastolic ratio increases as placental vascular resistance increases
- Fetal growth on ultrasound slows or stops
- Oligohydramnios develops due to diminished perfusion of fetal kidneys
- Loss of fetal heart rate variability with subsequent decelerations
- Intrauterine fetal demise (IUFD)
Prevention.
Bed rest and low-dose aspirin have been used to prevent IUGR in women at high risk, but with little or no benefit.
• Management
1 Attempt to determine etiology (ultrasound for fetal anomalies, check karyotype, exclude infectious etiology)
2 Regular (usually twice weekly) fetal testing
3 Consider delivery once a favorable gestational age is reached (>34 weeks), once fetal lung maturity is documented, or for worsening fetal testing (deterioration in biophysical profile,
the development of absent or reversed end-diastolic flow on umbilical artery Doppler velocimetry)
4 50–80% of IUGR fetuses will develop ‘fetal distress’ in labor requiring cesarean delivery
5 Send placenta/fetal membranes to pathology after delivery to look for evidence of vasculopathy
Principles of management include:
1 the identification of women at high risk for IUGR
2 early antepartum diagnosis
3 determination of etiology
4 regular (usually weekly) fetal testing with non-stress test (NST) or cardiotocography
5 appropriate timing of delivery.
• Complications.
IUGR infants have higher rates of perinatal morbidity and mortality at any given gestational age but have a better prognosis than infants with the same birthweight delivered at earlier gestational ages. Unfortunately, neonatal morbidity (meconium aspiration syndrome, hypoglycemia, polycythemia, pulmonary hemorrhage) will be present in 50% of IUGR neonates. Long-term studies show a 38-fold increase in the incidence of cerebral dysfunction (ranging from minor learning disabilities to cerebral palsy) in term IUGR infants and even more so if the infant was born preterm.
Fetal macrosomia
• Definition.
Fetal macrosomia is defined as an estimated weight (not birthweight) of ≥4500 g.
• Incidence.
In developing countries, 5% of infants weigh >4000 g at delivery and 0.5% weigh >4500 g.
• Risk factors.
Although a number of factors have been associated with macrosomia, most women with risk factors have normal weight babies:
1 Maternal diabetes (35–40% of all macrosomic infants) is the most common risk factor.
2 Post-term pregnancy (10–20%) is another common risk factor. Of all infants born at or beyond 42 weeks, 2.5% weigh >4500 g.
3 Maternal obesity (10–20%), defined as a pre-pregnancy body mass index (BMI) >30 kg/m2, predisposes to fetal macrosomia. Moreover, clinical and ultrasound estimates of fetal weight in obese women are technically more difficult and may be less accurate.
4 Other risk factors include multiparity, a prior macrosomic infant, a male infant, increased maternal height, advanced maternal age, and Beckwith–Wiedemann syndrome.
• Diagnosis.
Clinical estimates of fetal weight based on the Leopold maneuvers or fundal height measurements are often unreliable. Ultrasound is generally used to estimate fetal weight. However, currently available ultrasonographic techniques are accurate only to within 15–20% of actual fetal weight.
• Prevention.
Meticulous control of maternal diabetes throughout pregnancy reduces the incidence of fetal macrosomia.
• Management:
1 Antepartum. Women at high risk for having a macrosomic infant or who have a known LGA fetus should be followed with serial ultrasound examinations at 3–4 weeks to chart fetal growth.
2 Induction of labor. Despite the association between fetal macrosomia, and both birth trauma and cesarean section delivery, early induction of labor is not often recommended in patients with suspected fetal macrosomia at term. Induction of labor in this setting doubles the risk of cesarean section delivery without reducing shoulder dystocia or neonatal morbidity. However, the induction of labor for “impending macrosomia” does not decrease the cesarean section rate. As such, this approach should not be encouraged.
3 To prevent birth trauma, elective (prophylactic) cesarean section delivery should be offered to diabetic women with an estimated fetal weight >4500 g and non-diabetic women with estimated fetal weight >5000 g.
4 Vaginal delivery of a macrosomic infant should take place in a controlled fashion, with immediate access to anesthesia staff and a neonatal resuscitation team. It is prudent to avoid assisted vaginal delivery in this setting.
• Fetal morbidity and mortality. Macrosomic fetuses have an increased risk of intrauterine and neonatal death and birth trauma, especially shoulder dystocia and brachial plexus palsy. Other neonatal complications include hypoglycemia, polycythemia, hypocalcemia, and jaundice.
• Maternal morbidity. The increased maternal morbidity associated with the birth of a macrosomic infant is due primarily to a higher incidence of cesarean section delivery. Other maternal complications include postpartum hemorrhage, perineal trauma, and puerperal infection.