Asymmetric Fetal Growth Restriction at 38 Weeks: Genetic vs. Placental Etiology
The asymmetric pattern of growth restriction (abdominal circumference at the 2nd percentile with estimated weight at the 20th percentile) strongly suggests placental insufficiency rather than genetic or constitutional smallness, and this distinction is critical because it determines surveillance intensity and delivery timing. 1, 2
Why This Is Likely Placental Insufficiency, Not Genetic
Asymmetric Growth Pattern Is the Key Diagnostic Feature
Asymmetric growth restriction—where the abdominal circumference is disproportionately smaller than the head measurements—is the hallmark of placental insufficiency and late-onset fetal growth restriction (FGR). 3, 4
Placental dysfunction causes the fetus to preferentially preserve brain growth at the expense of liver glycogen stores and abdominal fat, resulting in a small abdominal circumference while head size remains relatively preserved. 3, 4
Constitutionally small fetuses (genetic smallness) typically demonstrate symmetric growth—all biometric parameters track proportionally along lower percentiles—rather than the asymmetric pattern you describe. 5
Genetic Smallness Would Present Differently
If this were purely genetic or constitutional smallness, you would expect all fetal measurements to track consistently along the same lower percentile throughout pregnancy, not an isolated abdominal circumference at the 2nd percentile. 5
The family history of a petite relative and a 7-lb infant at 42 weeks does not explain the asymmetric pattern; genetic smallness produces proportionate reduction across all measurements. 6, 5
Genetic factors account for approximately 30-70% of variability in birth size, but this influence manifests as symmetric smallness rather than the disproportionate abdominal growth lag seen in placental insufficiency. 6
Immediate Diagnostic Steps Required
Umbilical Artery Doppler Is Mandatory
You must obtain umbilical artery Doppler velocimetry immediately if not already performed—this single test differentiates pathological placental insufficiency from constitutional smallness and determines the urgency of delivery. 1, 2
Normal Doppler with this degree of asymmetry would be unusual and might suggest a mixed picture, but abnormal Doppler (elevated pulsatility index >95th percentile, absent or reversed end-diastolic flow) confirms placental dysfunction. 1, 2, 7
At 38 weeks with an abdominal circumference at the 2nd percentile, if umbilical artery Doppler shows decreased end-diastolic flow, delivery should occur immediately rather than awaiting 39 weeks. 2, 8, 7
Middle Cerebral Artery Doppler and Cerebroplacental Ratio
Obtain middle cerebral artery (MCA) Doppler to assess for brain-sparing physiology (increased MCA diastolic flow), which is a marker of chronic hypoxia and confirms pathological FGR. 2, 7
An abnormal cerebroplacental ratio (MCA-PSV/UA-PI) indicates fetal redistribution of blood flow to protect the brain and is a severity marker for placental insufficiency. 2
Amniotic Fluid Assessment
Measure the amniotic fluid index (AFI) or maximum vertical pocket (MVP)—oligohydramnios (AFI <5 cm or MVP <2 cm) suggests chronic placental dysfunction and significantly increases perinatal risk. 8, 7
The combination of asymmetric FGR with oligohydramnios at 38 weeks is an independent indication for delivery and argues strongly against expectant management. 8
Management Algorithm Based on Findings
If Umbilical Artery Doppler Is Normal
Proceed with delivery at 38-39 weeks as planned; induction of labor is reasonable with continuous electronic fetal monitoring throughout labor. 2, 8, 7
Weekly non-stress testing (cardiotocography) should continue until delivery. 7
If Umbilical Artery Doppler Shows Decreased End-Diastolic Flow
Deliver immediately at 38 weeks; do not delay to 39 weeks. 2, 7
Twice-weekly cardiotocography is required if delivery is not immediate. 7
If Absent or Reversed End-Diastolic Velocity Is Present
Cesarean delivery should be strongly considered, as these Doppler findings indicate severe placental insufficiency and high risk of intrapartum fetal compromise. 2, 8, 7
Continuous fetal monitoring during labor is mandatory if vaginal delivery is attempted, with a low threshold for cesarean section if non-reassuring patterns develop. 7
Why the Family History Does Not Override the Clinical Picture
Maternal Genetic Restraint vs. Placental Pathology
Maternal genetic factors that restrain fetal growth are inherited through the maternal line and are most evident in first pregnancies, but they produce symmetric smallness, not asymmetric abdominal growth restriction. 6
A relative delivering a <7-lb infant at 42 weeks (approximately 3,175 g at term) is within the normal range and does not establish a pattern of pathological growth restriction. 2
The mitochondrial DNA 16189 variant and maternally expressed genes like H19 have been associated with birth size, but these genetic influences do not cause the asymmetric pattern or the severe abdominal circumference lag you describe. 6
Placental Insufficiency Is the Most Common Cause of Late-Onset FGR
Uteroplacental dysfunction due to inadequate nutrient and oxygen supply is the most frequent etiology for late-onset FGR (diagnosed after 32 weeks), accounting for the majority of cases presenting at 38 weeks. 3, 9, 4
Deficient remodeling of uterine spiral arteries during early pregnancy leads to placental malperfusion, villous damage, and reduced surface area for maternal-fetal exchange—all of which manifest as asymmetric growth restriction. 4
Maternal vascular malperfusion is the most common placental disease contributing to FGR and is identifiable through Doppler studies and, if delivered, placental pathology. 9, 4
Critical Pitfalls to Avoid
Do not assume this is "just genetic" based on family history when the growth pattern is asymmetric—this error can lead to inadequate surveillance and delayed recognition of fetal compromise. 1, 2, 5
Do not delay umbilical artery Doppler assessment; it is the single most important test to distinguish pathological restriction from constitutional smallness. 1, 2, 7
Approximately 18-22% of fetuses with estimated weight <10th percentile are constitutionally small with normal outcomes, but an abdominal circumference at the 2nd percentile with asymmetry is not consistent with this benign category. 7
Avoid relying solely on estimated fetal weight percentiles—the abdominal circumference percentile and the pattern of asymmetry are equally important diagnostic criteria. 2, 7
Neonatal and Long-Term Considerations
All infants with FGR require evaluation in a neonatal intensive care unit due to increased risks of hypoglycemia, hypothermia, polycythemia, and respiratory distress. 7
Children born after FGR have increased long-term risks of neurodevelopmental delay, childhood obesity, metabolic syndrome, type 2 diabetes, hypertension, and cardiovascular disease, warranting metabolic screening in childhood and adolescence. 1, 2, 7