Symmetric vs. Asymmetric IUGR: Key Distinctions
Symmetric IUGR occurs predominantly in early gestation (typically <28-32 weeks) due to chromosomal anomalies, congenital syndromes, and viral infections, while asymmetric IUGR with head-sparing develops later (≥32 weeks) from placental insufficiency related to maternal hypertensive disease. 1
Timing and Gestational Age Thresholds
- Symmetric IUGR is more common earlier in gestation, with proposed thresholds at 28,32, or 34 weeks representing different pathologies and etiologies 1
- Asymmetric IUGR with "head-sparing" characteristically appears later in gestation when placental insufficiency predominates 1, 2
- The distinction matters because early-onset disease (<32 weeks) warrants genetic testing including chromosomal microarray analysis, which provides 4-10% incremental diagnostic yield over standard karyotyping 2
Etiology and Pathophysiology
Symmetric IUGR (Proportionate Growth Restriction)
- Chromosomal anomalies, genetic syndromes, and viral infections are the primary causes in early gestation 1
- Chromosomal disorders and congenital malformations together account for approximately 20% of all FGR cases 2
- All fetal parameters (head circumference, abdominal circumference, femur length) are proportionately reduced 3
- The insult typically occurs early in pregnancy, affecting the fundamental growth potential of all fetal structures 3
Asymmetric IUGR (Head-Sparing Growth Restriction)
- Placental insufficiency is the dominant cause, accounting for 25-30% of all FGR cases 2
- Maternal hypertensive disorders and vascular disease are key associations with late-onset asymmetric FGR 2
- The fetus redistributes blood flow preferentially to protect the brain at the expense of abdominal/somatic growth 2
- Abdominal circumference is disproportionately reduced while head circumference and length are relatively preserved 3
Important caveat: Recent evidence challenges the traditional teaching that asymmetric IUGR is confined to the third trimester. A 2011 study found that 58% of severe, early-onset IUGR cases (<33 weeks) due to placental insufficiency demonstrated an asymmetric phenotype with elevated head circumference/abdominal circumference ratio ≥95th percentile—more than 10-fold greater than expected 4. This suggests asymmetric patterns can occur earlier than previously believed when placental disease is severe.
Ultrasound and Doppler Findings
Biometric Assessment
- Symmetric IUGR: All biometric parameters (biparietal diameter, head circumference, abdominal circumference, femur length) fall proportionately below the 10th percentile 1
- Asymmetric IUGR: Head circumference/abdominal circumference ratio ≥95th percentile indicates preferential head-sparing 4
- Estimated fetal weight (EFW) below the 10th percentile defines FGR; below the 3rd percentile defines severe FGR with stillbirth rates up to 2.5% 5, 6
Doppler Velocimetry Patterns
- Umbilical artery Doppler is essential for differentiating pathological growth restriction from constitutional smallness 6, 7
- Elevated pulsatility index, resistance index, or absent/reversed end-diastolic velocity confirms placental insufficiency 5, 6
- Middle cerebral artery Doppler and cerebroplacental ratio demonstrate brain-sparing redistribution in asymmetric IUGR 1, 5
- Ductus venosus Doppler with reversed A-wave flow is abnormal throughout gestation and indicates severe fetal compromise 1
- Uterine artery Doppler combined with umbilical artery Doppler offers better prediction of adverse perinatal outcomes than either measure alone 1
Additional Sonographic Markers
- Oligohydramnios suggests chronic placental dysfunction 5
- Reduced growth velocity (AC change <5mm over 14 days or >30% reduction in growth velocity) indicates progressive pathology 5, 6
- Approximately 10% of fetuses with FGR have congenital anomalies, and 20-60% of fetuses with congenital anomalies are SGA, necessitating detailed structural surveys 1, 2
Clinical Management Approach
Initial Diagnostic Workup
For Early-Onset IUGR (<32 weeks):
- Perform detailed fetal structural survey to identify the 10% with congenital anomalies 1, 2
- Offer chromosomal microarray analysis (CMA) for unexplained isolated IUGR (GRADE 1C recommendation) 2
- When amniocentesis is performed, offer PCR testing for cytomegalovirus 2
- Do not routinely screen for toxoplasmosis, rubella, or herpes without specific risk factors—this wastes resources and delays appropriate management 2
For Late-Onset IUGR (≥32 weeks):
- Focus on placental insufficiency as the predominant etiology 1
- Evaluate for maternal hypertensive disorders and vascular disease 2
- Genetic testing is less commonly indicated unless structural anomalies are present 2
Surveillance Protocol
For EFW 3rd-9th percentile with normal umbilical artery Doppler:
- Umbilical artery Doppler every 1-2 weeks initially 6
- If stable, extend interval to every 2-4 weeks 6
- Biophysical profile (BPP) remains the mainstay of fetal well-being evaluation, assessing fetal breathing, movements, tone, and amniotic fluid volume 1
For severe IUGR (EFW <3rd percentile):
- Weekly umbilical artery Doppler evaluation 6
- Weekly cardiotocography (CTG) 6
- More intensive monitoring is required regardless of Doppler findings due to 2.5% stillbirth risk 5
For abnormal umbilical artery Doppler (absent/reversed end-diastolic velocity):
- Doppler assessment 2-3 times per week for absent end-diastolic velocity 6
- Add middle cerebral artery and venous Doppler (especially ductus venosus) to assess fetal well-being and assist with delivery timing 1
- Consider hospital admission if fetal surveillance more than 3 times per week is necessary 6
Delivery Timing Considerations
- The predominant theme for all FGR pregnancies is individualized timing of surveillance and delivery based on gestational age, Doppler abnormalities, fetal well-being, and presence of structural defects or chromosomal abnormalities 1
- Preterm FGR carries 2- to 5-fold increased perinatal death rates compared to term FGR 5
- Knowledge of specific gestational age thresholds (28,32, or 34 weeks) helps guide management as these represent varying etiologies and pathologies 1
Long-Term Implications
- IUGR is linked with lifelong health consequences including impaired intellectual performance in childhood and adult diseases such as hypertension, obesity, and cardiovascular disease 5
- Acute neonatal consequences include perinatal asphyxia, respiratory distress from meconium aspiration, persistent pulmonary hypertension, abnormalities of glucose regulation, temperature instability, and polycythemia 3
- IUGR preterm infants face increased incidence of chronic lung disease, necrotizing enterocolitis, retinopathy of prematurity, and postnatal growth failure 3