Fetal growth restriction and macrosomia

• Fetal growth restriction (FGR) is a fetus that has not reached its own growth potential, usually because the placenta is not supplying it well; it is not the same as simply being small.
• Small-for-gestational-age (SGA) means an estimated fetal weight (EFW) or abdominal circumference (AC) measured on ultrasound is below the 10th centile for gestation; most, but not all, growth-restricted fetuses are SGA, and some SGA fetuses are constitutionally small and healthy. ^[1]
• Screening is done with symphysis fundal height (SFH), ultrasound EFW, and Doppler of the umbilical artery (UA): a raised UA pulsatility index with reduced or absent/reversed end-diastolic flow signals worsening placental function. ^[7]
• Once significant restriction is seen, the balance is between prematurity (deliver early) and intrauterine danger (wait and monitor); delivery thresholds range from around 30 weeks for reversed Doppler to 38 to 40 weeks when findings are milder.
• Macrosomia is excessive fetal size, usually EFW or birth weight above 4 kg (4.5 kg in many high-risk contexts), most often from maternal diabetes or obesity: it raises the risk of prolonged labour, shoulder dystocia, birth injury, and postpartum haemorrhage. ^[5]
• Management differs by guideline: RCOG green-top (No. 31, 2024), ACOG (Practice Bulletin 227, 2021), NICE (NG201, 2021), and WHO antenatal care (2016) give broadly similar surveillance but different thresholds and timing, as summarised below.

By the end of this page you should be able to:

1. Explain the difference between SGA and FGR, and between early- and late-onset FGR.
2. List the causes of FGR and of macrosomia, including the indirect effect of maternal diabetes.
3. Interpret symphysis fundal height, biometry, UA pulsatility index, cerebroplacental ratio and ductus venosus (DV) Doppler in surveillance.
4. Decide, from Doppler findings and gestational age, when delivery is appropriate, and how the main guidelines differ.
5. Describe the complications of macrosomia for mother and baby, including shoulder dystocia.
6. Adapt surveillance and delivery planning to low-resource settings.

RCOG green-top guideline No. 31 (2024) makes this distinction central: SGA is a size diagnosis, FGR is a pathological diagnosis, and the likelihood of FGR rises the smaller the fetus is and the more abnormal the Doppler or liquor findings are. ^[1]

Classification by gestational age is the most useful for management. ^[7]

• Early-onset FGR: diagnosed before 32 weeks of gestation. It is more often linked to placental insufficiency and pre-eclampsia and tends to be severe. ^[7]
• Late-onset FGR: manifests at or after 32 weeks of gestation. It is more common overall, usually milder, but still carries risk of stillbirth and neonatal morbidity near term. ^[7]

By severity. An EFW or AC below the 3rd centile increases the specificity (likelihood that a small fetus is truly growth-restricted rather than constitutionally small), though it misses milder restriction. ^[7] Conversely, EFW or AC under the 10th centile alone includes many constitutionally small fetuses. A "declining growth trajectory" (crossing centiles on serial scans) and abnormal Doppler or reduced liquor complete the diagnosis.

Macrosomia. There is no single cut-off, but there are conventional levels. ^[3]

• Fetal macrosomia: usually defined as an estimated fetal weight (or birth weight) above 4000 g, regardless of gestational age; 4500 g is used as a higher "severe" threshold in most guidelines. ^[3]
• Large for gestational age (LGA): EFW or birth weight above the 90th centile for gestation; some of these are constitutionally large.
• Fetal overgrowth or "gigantism": used informally for very large fetuses at the extreme of the distribution; it carries the highest complication rates.

• FGR affects about 5% to 10% of pregnancies worldwide. ^[7]
• SGA (below the 10th centile) by definition occurs in 10% of pregnancies in any given population, but only a proportion are growth-restricted.
• Early-onset FGR is less common than late-onset, yet accounts for a disproportionate share of neonatal deaths and hypoxic-ischaemic injury.
• Macrosomia occurs in roughly 5% to 10% of births in high-income countries and is more common with maternal obesity and diabetes; in parts of East Africa, prevalence is lower, but birth trauma rates rise sharply where Caesarean section is not easily available.

Causes work through three mechanisms: reduced uteroplacental perfusion, maternal medical disease, and fetal factors.

Maternal vascular/placental. Pre-eclampsia and gestational hypertension, chronic hypertension, chronic renal disease, systemic lupus, severe anaemia, antiphospholipid syndrome, and smoking/alcohol/drug use. ^[1][7]

Placental. Small placenta, abnormal uterine artery Doppler, infarction, chorioamnionitis, and marginal/circumvallate placenta.

Maternal nutritional and metabolic. Low pre-pregnancy body mass index, poor weight gain, malabsorption.

Fetal. Chromosomal abnormalities (e.g. trisomies 13, 18, 21), congenital malformations, intrauterine infection (TORCH, parvovirus, malaria, syphilis), multiple pregnancy, and genetic syndromes. ^[1]

Obstetric. Prior pregnancy complicated by FGR or stillbirth, assisted conception with multiple gestation, and antepartum haemorrhage.

Social/regional. Short inter-pregnancy interval, poverty, adolescent or advanced maternal age, and in some regions, malaria, HIV, severe malnutrition and hypertensive disease in pregnancy.

Risk assessment should be performed at booking and again in the second trimester. ^[4]

Macrosomia arises from hyperinsulinaemia in utero, which accelerates fetal growth and fat deposition, especially in the shoulders and trunk.

Maternal.

• Pre-existing and gestational diabetes mellitus (the strongest driver). ^[5]
• Maternal obesity and excessive gestational weight gain.
• Multiparity and prior macrosomic baby. ^[5]
• Post-term pregnancy.
• Male fetal sex.
• Increasing maternal age.

Genetic/familial. Parental size and constitutional large stature (familial large baby).

Other. Non-diabetic hyperinsulinaemic states and post-dates pregnancy.

The common pathway is uteroplacental insufficiency. Reduced maternal perfusion of the placental bed (from failed physiological conversion of spiral arteries, as in pre-eclampsia) lowers delivery of oxygen and nutrients. The fetus responds in stages, each of which is a clinical sign: ^[1][7]

1. Compensated restriction. Growth of the abdominal circumference and length slow first, because glucose-dependent liver glycogen deposition (which drives AC) falls. Head circumference is relatively spared ("asymmetric" or "brain-sparing" FGR). The UA pulsatility index rises.
2. Brain sparing. Middle cerebral artery (MCA) resistance falls (vasodilation), so the cerebroplacental ratio (CPR = MCA pulsatility index ÷ UA pulsatility index) drops. This is evidence of redistribution of cardiac output.
3. Advanced compromise. DV Doppler becomes abnormal (raised pulsatility index, then absent or reversed "a" wave), reflecting altered right-sided diastolic flow; oligohydramnios develops as renal perfusion falls. These changes precede serious acidosis.
4. Decompensation. Abnormal computerised CTG, reduced short-term variation, and heart rate decelerations, with rising risk of stillbirth.

Early-onset FGR more often follows from a severe, intrinsic placental defect and is accompanied by pre-eclampsia; late-onset FGR more often reflects a milder maturation problem in the third trimester with normal or near-normal UA flow initially (though MCA changes may reveal it).

In non-diabetic pregnancies the fetus is usually mildly larger because of parental factors. In diabetes, macrosomia comes from fetal hyperinsulinaemia, which preferentially expands shoulders, trunk and fat mass, producing a baby with disproportionate shoulder girdle and a high risk of shoulder dystocia even at similar birth weights.

Maternal history. Reduced fetal movements may be the first complaint, or the baby may feel small. Risk factors from the aetiology list should be sought: blood pressure, renal disease, diabetes, prior SGA/stillbirth, smoking, bleeding, and multiple pregnancy.

Examination. SFH measured from the pubic symphysis to the fundus (after 24 weeks) plotted on a customised growth chart. ^[4]

• A single measurement below the 10th centile, or two consecutive measurements crossing centiles downward, suggests SGA/FGR and warrants an ultrasound for fetal growth and wellbeing. ^[4]
• A measurement large for dates warrants an ultrasound too (large baby or polyhydramnios). ^[4]

Fetal movements and liquor. Decreased fetal movements, reduced liquor on scan, and a persistently empty bladder on scan point to restriction.

Fetal well-being signs. Normal movements and reassuring fetal heart rate pattern are reassuring; an abnormal cardiotocograph indicates a need for urgent delivery planning.

Suspicion comes from maternal size, maternal diabetes or obesity, previous large baby, prolonged pregnancy, and a clinical impression of a large uterus. Excessive weight gain, difficulty palpating small parts, and polyhydramnios may be present. Firm diagnosis relies on ultrasound EFW (not on clinical palpation, which is inaccurate).

The diagnosis is built up in three steps: estimate gestation, measure the fetus, and assess placental function.

The Delphi consensus criteria (Gordijn 2016, as summarised by Caetano 2026) define FGR as: early onset before 32 weeks with AC or EFW below the 3rd centile, or UA-PI/RI above the 95th centile, or absent/reversed end-diastolic flow, or cerebroplacental ratio below the 5th centile; and late onset at 32 weeks or more with growth below the 3rd centile, or at least two of AC/EFW below the 10th centile, growth velocity fall, CPR below the 5th centile, or UA-PI above the 95th centile. ^[7]

• Confirm estimated fetal weight with ultrasound (Hadlock or similar). Clinical palpation alone is inaccurate.
• Shoulder and abdominal diameter proportions (e.g. the difference between abdominal and biparietal circumference) and MRI in selected cases can help predict shoulder dystocia, though no single test is reliable. ^[3]
• In women with diabetes, serial growth scans every 4 weeks from 28 to 36 weeks are recommended to detect overgrowth. ^[5]

• Gestational diabetes / maternal diabetes: overgrowth with excess shoulder fat; screen with OGTT. ^[5]
• Constitutionally large baby: normal Doppler, normal liquor, family history; often above 90th centile without risk.
• Fetal macrosomia without diabetes: obesity alone can produce large abdomens.
• Polyhydramnios with large baby: consider diabetes, fetal anomaly or isoimmunisation.
• Hydrops (immune/non-immune): widespread oedema, ascites and skin thickening, not simple macrosomia.

1. Decide whether the fetus is restricted, not just small.
2. Assess severity and speed of deterioration with Doppler and CTG.
3. Time delivery so that premature birth complications do not outweigh intrauterine risk.
4. Manage maternal conditions (especially pre-eclampsia and diabetes).

• Treat modifiable factors: smoking cessation, good nutrition, treatment of anaemia and infection, and aspirin for women at high risk of pre-eclampsia (in line with hypertension guidance). ^[4]

  United Kingdom (NICE)

  NICE NG201 supports risk assessment for FGR at booking and again in the second trimester, plus serial SFH and targeted ultrasound. ^[4]
• Treat maternal disease (hypertension, renal, thyroid) and manage antiphospholipid syndrome or diabetes as its own guideline requires.
• Antenatal corticosteroids for fetal lung maturation whenever preterm delivery is planned before 34 to 35 weeks. ^[7] (Betamethasone or dexamethasone per standard regimen; magnesium sulphate for neuroprotection before 30 to 32 weeks, per the preterm-birth guideline.) Avoid doses not specified in an source: follow the RCOG/NICE preterm-birth guideline in your unit.
• No drug has been proven to improve growth in FGR in routine practice; aspirin is used for prevention (see below), not treatment.

A typical schedule, combining RCOG/SFM recommendations and the open literature (Caetano 2026): ^[1][7]

• Early-onset FGR (under 32 weeks). Biometry every 2 weeks; UA Doppler weekly or more often; MCA and DV Doppler regularly; cardiotocography or computerised CTG for high-risk cases; liquor assessment each scan. Delivery is triggered by the most severe abnormality (see table). ^[4]
• Late-onset FGR (from 32 weeks). Biometry every 2 to 3 weeks; UA, MCA/CPR Doppler and liquor assessment weekly; daily fetal movements count; cardiotocography weekly or as indicated.

Delivery timing is the area where guidelines differ most in detail but agree in principle: use gestational age plus the most severe monitoring abnormality, balancing preterm risk against stillbirth risk. ^[1][2][7]

Guideline differences.

• RCOG GTG 31 (2024): stratifies care by severe features; delivery timing based on the most severe abnormality present. ^[1]
• ACOG PB 227 (2021): antenatal surveillance with UA Doppler from 24 to 28 weeks for suspected FGR; delivery by 38 weeks for uncomplicated late-onset FGR, and by 34 to 37 weeks if there are additional risk factors or abnormal Doppler; continuous intrapartum surveillance preferred. ^[2]
• NICE NG201 (2021): risk assessment at booking and in the second trimester; SFH after 24 weeks; one scan if third-trimester concern; delivery timing deferred largely to obstetrician decision using RCOG-style guidance. ^[4]
• WHO (2016/2022): recommends at least one ultrasound before 24 weeks for gestational age, plus monitoring according to context; delivery timing is not protocolised and follows national guidance. ^[6]

Macrosomic babies and their mothers face specific mechanical and metabolic problems. ^[3][5]

Maternal.

• Prolonged labour and failure to progress, leading to emergency Caesarean section.
• Severe perineal tears (third/Fourth degree) and pelvic floor injury.
• Postpartum haemorrhage from uterine atony.
• Shoulder dystocia (descent of the head but arrested shoulders), which risks both mother and baby.

Fetal-neonatal.

• Shoulder dystocia itself: a delay of only minutes can cause fetal hypoxia.
• Brachial plexus injury (Erb's or Klumpke's palsy), especially with shoulder dystocia; many resolve, but some do not.
• Clavicle or humerus fracture.
• Birth asphyxia and neonatal encephalopathy.
• Erb's palsy (C5-C6 root injury) is the characteristic brachial plexus injury of shoulder dystocia.
• Neonatal hypoglycaemia, hyperbilirubinaemia and polycythaemia, especially with maternal diabetes.
• Long-term: childhood overweight, type 2 diabetes risk and metabolic syndrome. ^[5]

Management.

• Discuss the risks and benefits of vaginal birth, induction of labour and Caesarean section with the woman. ^[5]
• In women with diabetes, offer elective birth between 37 and 38 weeks plus 6 days for type 1 or 2 diabetes, and no later than 40 weeks plus 6 days for gestational diabetes; consider earlier delivery with complications such as macrosomia or hydramnios. ^[5]
• Suspected macrosomia is not on its own an indication for Caesarean section in most guidelines, but the discussion must include shoulder dystocia explicitly, and induction for suspected macrosomia is a recognised option.
• If shoulder dystocia occurs: McRoberts manoeuvre, suprapubic pressure, all-fours position, internal manoeuvres, and delivery of the posterior arm in sequence; call senior help early.
• Neonatal side: check blood glucose at 2 to 4 hours of age in babies of diabetic mothers; monitor for respiratory distress. ^[5]

• Antepartum and intrapartum stillbirth.
• Preterm birth and its complications (respiratory distress syndrome, intraventricular haemorrhage, necrotising enterocolitis) when delivery is early.
• Hypoxic-ischaemic encephalopathy from chronic placental failure.
• Neonatal hypoglycaemia, hypothermia, polycythaemia and thrombocytopenia.
• Growth restriction in adulthood: neurodevelopmental impairment, hypertension, ischaemic heart disease and type 2 diabetes (the Barker hypothesis), especially after preterm birth.

Prognosis tracks gestational age at delivery and the depth of growth failure. ^[1][7]

• Early-onset FGR delivered before 32 weeks without an urgent trigger carries a high perinatal death rate and neurodevelopmental risk.
• Late-onset FGR at term has a much better outcome, but stillbirth risk is raised unless monitored and delivered by the late 38th to 39th week.
• Neonates below the 3rd centile have worse outcomes than those between the 3rd and 10th centiles.
• Macrosomia without birth injury usually has an excellent neonatal outcome; the long-term metabolic risks are managed through childhood.

• Identify risk at booking and again in the second trimester. ^[4]
• Low-dose aspirin from the first trimester to the end of the second trimester reduces early-onset pre-eclampsia and its downstream FGR in high-risk women. ^[1]
• Stop smoking; manage hypertension, renal disease and diabetes; correct severe anaemia; screen for and treat syphilis/HIV/malaria in endemic regions.
• WHO's antenatal guidance supports at least one ultrasound before 24 weeks for accurate dating and morphology, which is the backbone of later growth assessment. ^[6]
• NICE encourages SFH measurement after 24 weeks and targeted ultrasound when concern arises. ^[4]

• Optimise maternal blood glucose before conception and throughout pregnancy. ^[5]
• Manage maternal weight gain and obesity.
• Accurate dating to avoid post-term overgrowth.

Pregnancy. Diabetes, obesity, hypertension and multiple pregnancy magnify both restrictions and overgrowth; teams should use the respective guidelines in parallel. ^[5]

Children. This page describes the fetus; paediatric follow-up is needed after FGR (neurodevelopment, growth) and after macrosomia (hypoglycaemia surveillance). Toddlers born FGR need monitoring for catch-up growth and adult metabolic risk.

Older adults. Not directly relevant (the patient is the mother), but maternal age 35 years and above increases placental dysfunction and macrosomia risk; earlier and closer surveillance is warranted. ^[1]

• Clinical suspicion and symphysis fundal height plotted on a chart are the main screening tools when ultrasound is scarce.
• Universal third-trimester ultrasound is not feasible everywhere; target high-risk women (hypertension, previous stillbirth, smoking).
• Umbilical artery Doppler may not be available; deliver on clinical judgment (reduced movements, severe thinness/oligohydramnios, abnormal CTG) and maternal indication.
• If delivery before 37 weeks is likely, give antenatal steroids and arrange transfer to a facility with neonatal care.
• For macrosomia, timely access to a skilled birth attendant and Caesarean section reduces shoulder dystocia injury; McRoberts is deliverable everywhere.

• SGA is a size category (EFW/AC/birth weight below the 10th centile); FGR is a failure to reach growth potential and needs restriction-specific findings.
• Early-onset FGR is diagnosed before 32 weeks and late-onset from 32 weeks; the earlier and lower the growth, the worse the outlook.
• Risk factors are assessed at booking and in the second trimester; surveillance combines SFH, biometry, liquor and UA/MCA/DV Doppler, with reduced short-term variation on CTG.
• UA-PI above the 95th centile with increased resistance, absent or reversed end-diastolic flow, low CPR or abnormal DV all signal worsening placental function. ^[7]
• Delivery timing trades prematurity against stillbirth: severe Doppler may justify delivery around 30 to 32 weeks, while mild late-onset FGR is usually induced at 37 to 39 weeks.
• Macrosomia (usually over 4000 g, or 4500 g in diabetic women) raises the risk of prolonged labour, shoulder dystocia, brachial plexus and clavicular injury, and postpartum haemorrhage.
• Major guidelines agree on the principles but differ in timing cut-offs; maternal deterioration always overrides Doppler numbers.
• WHO supports at least one ultrasound before 24 weeks, NICE supports SFH after 24 weeks, RCOG gives detailed Doppler-based timing and ACOG publishes PB 227 for FGR and PB 216 for macrosomia.

• Pregnancy diagnosis and physiology; preeclampsia, HELLP and eclampsia; gestational and chronic hypertension in pregnancy; diabetes in pregnancy; neonatal hypoglycaemia; prematurity and its complications; antepartum fetal surveillance; invasive prenatal testing and prenatal care. All topic names are given here as plain text planning entries (MedGrasp topic pages to be linked individually once verified).