What are the causes and management strategies for small for gestational age (SGA) or low birthweight?

Causes of Small for Gestational Age (SGA) and Low Birthweight

SGA and low birthweight result from a complex interplay of maternal, placental, fetal, and environmental factors, with placental insufficiency being the most common pathological cause, though approximately 18-22% of SGA infants are constitutionally small but healthy.

Maternal Risk Factors

Pre-existing Maternal Characteristics

• Short maternal stature, low pre-pregnancy weight, and nulliparity are established risk factors for SGA 1
• Indian or Asian ethnicity increases risk of delivering an SGA infant 1
• Mother herself born SGA predisposes to having SGA offspring 1

Maternal Medical Conditions

• Chronic hypertension, renal disease, and anti-phospholipid syndrome are strongly associated with increased SGA risk 1
• Maternal schizophrenia increases odds of SGA (OR 1.64-1.54 depending on study quality) 2
• Malaria in endemic regions contributes to SGA 1

Pregnancy-Related Complications

• Pre-eclampsia and gestational hypertension are major contributors to pathological growth restriction 1
• Placental abruption significantly increases SGA risk 1
• Heavy bleeding in early pregnancy is associated with subsequent SGA 1

Behavioral and Substance Factors

• Cigarette smoking is a confirmed modifiable risk factor 1
• Cocaine use during pregnancy increases SGA risk 1

Placental Factors

Placental Insufficiency

• Uteroplacental dysfunction is considered the most common cause of pathological intrauterine growth restriction 3
• Abnormal umbilical artery Doppler (elevated resistance, absent or reversed end-diastolic flow) confirms placental insufficiency and indicates pathological growth restriction 4

Fetal Factors

Genetic and Chromosomal

• Fetal structural malformations are strongly associated with growth restriction 3
• Metabolic and genetic disorders contribute to a broad spectrum of SGA cases 5

Infectious Causes

• TORCH infections (toxoplasmosis, other, rubella, cytomegalovirus, herpes) are established fetal causes of growth restriction 3

Paternal Factors

• Changed paternity, short paternal stature, and father born SGA also contribute to risk 1

Obstetric History Factors

• Previous SGA infant or previous stillbirth increases recurrence risk 1
• Short inter-pregnancy interval (<6 months) or very long interval (>5 years) are associated with increased SGA 1

Protective Factors

• High maternal milk consumption is associated with reduced SGA risk 1
• High intakes of green leafy vegetables and fruit appear protective 1

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Management Strategies for SGA and Low Birthweight

Antenatal Screening and Prevention

Early Risk Assessment

• All guidelines recommend early pregnancy risk selection, with 5 of 6 (83%) recommending low-dose aspirin for women with major risk factors for placental insufficiency 2
• Smoking cessation interventions should be prioritized as a modifiable risk factor 2

Fundal Height Surveillance

• Universal recommendation exists for third-trimester fundal height measurement using a tape measure, with measurement in centimeters correlating to gestational age in weeks between 18-32 weeks 6
• Three of six guidelines (50%) recommend customized growth charts for fundal height plotting, which improve detection of SGA and reduce stillbirth 2, 6
• When fundal height lags >2-3 cm behind expected gestational age, ultrasound evaluation for fetal growth restriction should be performed 6
• In women with obesity and/or fibroids, ultrasound scans should replace fundal height measurements as they are unreliable in these populations 6

Diagnostic Approach

Ultrasound Criteria

• SGA is defined as estimated fetal weight (EFW) or abdominal circumference (AC) <10th percentile for gestational age 4
• Severe FGR is defined as EFW <3rd percentile, associated with stillbirth rates up to 2.5% 4
• Four of six international guidelines (67%) recommend using customized EFW rather than population references 2

Doppler Assessment

• Umbilical artery Doppler should be performed when SGA is suspected, as abnormal findings confirm placental insufficiency and guide management intensity 4, 6
• Middle cerebral artery or cerebroplacental ratio abnormalities indicate fetal brain-sparing redistribution and confirm pathological FGR 4

Growth Velocity Monitoring

• Crossing centiles downward or inadequate interval growth (AC change <5mm over 14 days, or >30% reduction in growth velocity) indicates progressive pathology 4

Antenatal Surveillance Based on Severity

Normal Doppler (EFW 3rd-10th percentile)

• Serial umbilical artery Doppler every 2 weeks is recommended 7
• Delivery at 38-39 weeks gestation for isolated SGA with normal Doppler 7

Decreased End-Diastolic Flow

• Weekly umbilical artery Doppler surveillance 7
• Delivery at 37 weeks gestation 7

Absent End-Diastolic Velocity (AEDV)

• Doppler assessment 2-3 times per week 7
• Delivery at 33-34 weeks gestation, with national guidelines showing consensus ranging from 32-34 weeks 7
• Antenatal corticosteroids if delivery anticipated before 33 6/7 weeks, with universal agreement across all national guidelines 7

Reversed End-Diastolic Velocity (REDV)

• Hospitalization with cardiotocography 1-2 times per day 7
• Delivery at 30-32 weeks gestation 7
• Magnesium sulfate for fetal neuroprotection for pregnancies <32 weeks, with general consensus across guidelines 7

Mode of Delivery Considerations

• FGR alone is not an indication for cesarean delivery when umbilical artery end-diastolic flow is present 7
• Continuous fetal monitoring in labor is recommended for all SGA pregnancies 7
• Cesarean delivery is recommended for very preterm FGR or severe umbilical artery Doppler abnormalities (AEDV/REDV) 7

Neonatal Management

Immediate Postnatal Period

• SGA newborns are at greater risk of life-threatening conditions including hypoglycemia, hypercoagulability, necrotizing enterocolitis, direct hyperbilirubinemia, and hypotension 5
• Accurate anthropometry at birth including weight, length, and head circumference should be documented 8

Distinguishing Pathological from Constitutional SGA

• Constitutionally small but healthy infants (18-22% of SGA) require only standard newborn care 4
• IUGR infants face acute complications including perinatal asphyxia, hypothermia, hypoglycemia, and polycythemia, plus long-term risks requiring interdisciplinary follow-up 4

Long-Term Follow-Up

Growth Monitoring

• Early surveillance in a growth clinic is recommended for those without catch-up growth 8
• Approximately 10% of SGA children do not achieve catch-up growth and remain short (≥-2 SDS) into adulthood 5
• Most SGA children experience spontaneous catch-up growth usually completed by age 2 years 9

Growth Hormone Treatment

• SGA children aged >4 years with no spontaneous catch-up and height ≥-2.5 SD should be considered for growth hormone treatment 5
• Early intervention with GH for severe growth retardation (height SD score <-2.5; age 2-4 years) should be considered at a dose of 35-70 mcg/kg/day 8

Metabolic and Endocrine Surveillance

• SGA infants with rapid catch-up growth and marked weight gain are at increased risk of premature adrenarche, early puberty, polycystic ovary syndrome (girls), insulin resistance, and obesity 9
• SGA individuals have increased incidence of metabolic syndrome, coronary artery disease, stroke, low bone density, and osteoporosis in adulthood 5

Neurodevelopmental Assessment

• Early neurodevelopment evaluation and interventions are warranted in at-risk children 8
• SGA status can affect different areas of neurodevelopment manifesting at different life stages, with better outcomes in those with spontaneous catch-up growth 9

Key Pitfalls to Avoid

• Accurate pregnancy dating using first-trimester crown-rump length is essential before diagnosing FGR 4
• Do not rely on fundal height alone in obese patients—proceed directly to ultrasound 6
• Abandon the term "intrauterine growth restriction (IUGR)" for prenatal diagnosis—use "fetal growth restriction (FGR)" instead, reserving "SGA" for newborns with birthweight <10th percentile 4