Lucan · Conditions

Fetal growth restriction

Australian guidance: RANZCOG FGR Statement

1. Definition and epidemiology

Fetal growth restriction (FGR) is defined as a failure of the foetus to reach its genetically determined growth potential, most commonly operationalised as an estimated foetal weight (EFW) or abdominal circumference (AC) below the 10th centile for gestational age, with evidence of placental insufficiency or abnormal Doppler findings. In Australia, FGR affects approximately 5 to 10% of all pregnancies, though rates vary depending on the centile threshold and population reference charts used. Aboriginal and Torres Strait Islander women carry a disproportionate burden due to higher rates of underlying placental disease, preeclampsia, and hypertensive disorders of pregnancy, all of which are independent drivers of uteroplacental insufficiency.

2. Pathophysiology

The predominant mechanism in placental FGR is defective trophoblastic invasion of the maternal spiral arteries. During normal early placentation, cytotrophoblasts remodel the spiral arteries from high-resistance muscular vessels into wide-bore, low-resistance conduits. When this remodelling fails, the intervillous space remains underperfused, generating chronic uteroplacental ischaemia. The hypoxic placenta releases antiangiogenic factors including soluble fms-like tyrosine kinase 1 (sFlt-1) and endoglin, which impair maternal endothelial function and reduce foetal nutrient delivery. The foetus responds with a redistribution of cardiac output toward the brain, adrenal glands, and heart at the expense of somatic growth, producing the characteristic brain-sparing pattern seen on Doppler studies. In severe or early-onset FGR, absent or reversed end-diastolic flow in the umbilical artery signals critically elevated placental vascular resistance, predicting imminent foetal compromise. Non-placental causes include foetal chromosomal or structural anomalies, congenital infection (cytomegalovirus, toxoplasmosis, rubella), and maternal factors such as smoking, malnutrition, and substance use. Robbins Ch 10 characterises placental insufficiency FGR under the broader category of placental disease linked to abnormal villous vascularisation, with accelerated villous maturation and infarction as hallmark pathological findings.

3. Clinical presentation and diagnostic criteria

FGR is often clinically silent and detected through surveillance rather than symptoms. The primary screening tool in Australia is symphysis-fundal height (SFH) measurement at each antenatal visit from 24 weeks gestation; a measurement that plots below the 10th centile or shows growth faltering over two or more visits prompts ultrasound referral. On ultrasound, the key biometric parameters are AC, EFW, and head circumference to abdominal circumference ratio (HC:AC). FGR is classified as early-onset (before 32 weeks) or late-onset (at or after 32 weeks), a distinction that carries prognostic and management implications. Early-onset FGR is more often associated with severe placental disease, abnormal umbilical artery Doppler findings, and a higher risk of perinatal mortality. Late-onset FGR is more common, more likely to have a normal umbilical artery Doppler, and is identified primarily through AC or EFW below the 3rd centile or through evidence of growth faltering with abnormal cerebroplacental ratio. Risk factors for FGR include antepartum haemorrhage, gestational hypertension, preeclampsia, previous stillbirth, prolonged pregnancy, multiple pregnancy, and single umbilical artery.

4. Investigations and AU-specific cutoffs

Investigations are tiered from surveillance to confirmation to monitoring.

First-line surveillance: - Serial SFH measurement from 24 weeks; plot on an Australian customised growth chart - Referral for ultrasound if SFH below the 10th centile or growth faltering over 2 to 3 consecutive measurements

Confirmatory ultrasound: - AC or EFW below the 3rd centile: high-probability FGR regardless of Doppler - AC or EFW between the 3rd and 10th centile with abnormal uterine artery pulsatility index (UtPI) or umbilical artery Doppler: probable placental FGR - Cerebroplacental ratio (CPR) below the 5th centile is an additional marker for late-onset FGR where umbilical artery Doppler is normal

Doppler indices and AU thresholds: - Umbilical artery pulsatility index (UA PI) above the 95th centile for gestational age indicates increased placental resistance - Absent end-diastolic flow (AEDF) or reversed end-diastolic flow (REDF) in the umbilical artery indicates critical placental compromise and triggers hospitalisation and consideration of delivery - Middle cerebral artery pulsatility index (MCA PI) below the 5th centile indicates cerebrovascular redistribution (brain-sparing) - Ductus venosus (DV) PI above the 95th centile or absent/reversed a-wave is a late pre-terminal sign

Ancillary investigations: - Detailed foetal anatomical survey to exclude structural anomalies - Amniocentesis for foetal karyotype and chromosomal microarray if early-onset FGR, especially if structural anomalies are present - Serology for TORCH infections (cytomegalovirus IgG/IgM, toxoplasma, rubella) when structural anomalies coexist - Maternal full blood count, urea and electrolytes, liver function tests, and uric acid to screen for underlying preeclampsia - PAPP-A and PlGF measured in first trimester: low PAPP-A (below the 5th centile) and reduced PlGF are associated with placental FGR

5. Management

Management is guided by gestational age at diagnosis, severity of Doppler abnormality, and the presence of coexisting conditions. The overarching goal is to balance the risk of continued intrauterine compromise against the risks of iatrogenic prematurity.

Antenatal surveillance schedule (RANZCOG FGR Statement framework): - Fortnightly to weekly growth ultrasound depending on severity - Umbilical artery Doppler at each surveillance visit; more frequent assessment if abnormal - Biophysical profile (BPP) scoring or amniotic fluid index (AFI) as adjuncts when Doppler abnormalities are present - Cardiotocography (CTG) is indicated for intrapartum monitoring of all FGR pregnancies given their elevated risk of fetal compromise in labour

Delivery timing (RANZCOG FGR Statement guidance): - EFW or AC below the 3rd centile with normal Doppler: deliver at 37 weeks - Abnormal umbilical artery Doppler (raised PI, no AEDF/REDF): deliver at 34 to 37 weeks depending on trajectory - AEDF: delivery at or after 34 weeks; consider steroids before 34 weeks - REDF or DV abnormality: delivery at 30 weeks or sooner if foetal distress is imminent; administer antenatal corticosteroids and consider magnesium sulphate for neuroprotection below 30 weeks - Foetuses below 34 weeks should receive a course of antenatal corticosteroids (betamethasone 11.4 mg IM two doses 24 hours apart) to promote foetal lung maturation before delivery

Mode of delivery: - Vaginal birth is appropriate in many cases; continuous intrapartum CTG is mandatory - Caesarean birth is indicated for REDF, non-reassuring CTG, or clinical deterioration

6. Pharmacology and AU PBS notes

There is no pharmacological treatment that reverses established FGR, but the following agents are relevant to prevention and management of associated complications.

Aspirin (preventive in high-risk pregnancies): - Low-dose aspirin 100 to 150 mg orally at night, commenced before 16 weeks in women at high risk of preeclampsia-related FGR (including those with prior FGR, hypertension, renal disease, or an abnormal first-trimester screening result) - Strong RANZCOG recommendation (GRADE: Moderate) - Available as generic aspirin 100 mg (AU brand: Astrix, Cartia); not PBS-listed specifically for FGR prevention but is PBS General Schedule for cardiovascular indications

Betamethasone (antenatal corticosteroids for foetal lung maturation): - Betamethasone sodium phosphate and betamethasone acetate (Celestone Chronodose) 11.4 mg IM two doses 24 hours apart - Indicated for anticipated delivery before 34 to 35 weeks - PBS-listed under Section 85 for foetal lung maturation (no streamlined authority required at standard dose)

Magnesium sulphate (neuroprotection): - Magnesium sulphate IV for foetal neuroprotection when delivery is anticipated before 30 weeks - Loading dose 4 g IV over 20 to 30 minutes, followed by infusion 1 g/hour until delivery or 24 hours - Not PBS-listed as outpatient therapy; administered in hospital

Tocolysis: - Not indicated to delay delivery once foetal compromise is established; short-term tocolysis (nifedipine or atosiban) may be used for 24 to 48 hours solely to allow completion of corticosteroid course

7. Complications and monitoring

Foetal and neonatal complications: - Intrauterine foetal death (IUFD): the most serious outcome; risk is highest with REDF and DV abnormality - Preterm birth with associated complications of prematurity: intraventricular haemorrhage, necrotising enterocolitis, respiratory distress syndrome, retinopathy of prematurity - Perinatal asphyxia and hypoxic-ischaemic encephalopathy (HIE) - Neonatal polycythaemia, hypoglycaemia, and hypothermia from chronic hypoxia and poor nutritional reserves - Meconium aspiration syndrome, particularly in late-onset FGR with subacute compromise

Long-term sequelae: - Neurodevelopmental impairment from chronic hypoxia and preterm birth - Metabolic programming: increased lifetime risk of type 2 diabetes mellitus, hypertension, and cardiovascular disease (Barker/foetal origins of adult disease hypothesis, Robbins Ch 10)

Surveillance schedule summary: - Well-compensated FGR (normal Doppler): fortnightly ultrasound, weekly CTG from 32 weeks - Raised UA PI: weekly ultrasound with Doppler, twice-weekly CTG - AEDF: hospitalise; daily Doppler and CTG or BPP; plan delivery at or after 34 weeks - REDF or DV abnormality: immediate senior obstetric review; delivery planning within 24 to 48 hours; continuous CTG in labour

Written for Australian practice and grounded in the guidance named above. Study material only — not medical advice. Always check against current guidelines.