IUGR (Fetal Growth Restriction) and Antepartum Fetal Surveillance

Fetal growth restriction (FGR), traditionally called intrauterine growth restriction (IUGR), is the failure of a fetus to meet its growth potential because of a pathological process — most commonly placental dysfunction. It is a leading cause of stillbirth, neonatal death and short- and long-term morbidity worldwide.

Small for gestational age (SGA) is a size label: estimated fetal weight (EFW) or birth weight below the 10th centile for gestational age. Because true growth potential is hard to measure, SGA is the usual screening proxy, but it has limits. Most SGA fetuses are constitutionally small and healthy; some growth-restricted fetuses stay above the 10th centile; ultrasound weight estimation carries an error of up to plus or minus 15–20%; and the result depends on which growth chart is used.

To reduce false-positive and false-negative diagnoses, an international Delphi consensus (Gordijn et al.) defined placenta-mediated FGR by combining fetal size (EFW and abdominal circumference) with abnormal Doppler in the umbilical, uterine and middle cerebral arteries. FIGO's best-practice advice adopts these criteria and splits FGR at 32 weeks.

Early-onset FGR is strongly associated with early pre-eclampsia (maternal vascular malperfusion), is easier to detect, and tends to follow a predictable sequence of umbilical artery then ductus venosus deterioration. The management challenge is timing delivery between the risks of stillbirth and prematurity. Late-onset FGR is more common (prevalence about 5–10%); umbilical artery and ductus venosus Doppler are often normal, so diagnosis rests on cerebral redistribution, and sudden decompensation and stillbirth can occur.

Using head circumference, biparietal diameter, abdominal circumference and femur length, FGR is classically divided into symmetrical (all parameters proportionally reduced) and asymmetrical (abdominal circumference reduced below the 10th centile with relative preservation of the head and brain). The pattern hints at timing and cause.

• Fetal genetic anomalies are found in about 5% of FGR; half of fetuses with trisomy 13 or 18 develop FGR, and symmetric FGR before 20 weeks suggests aneuploidy.
• Fetal infection explains 5–10% of FGR, with malaria the most common cause globally; others include cytomegalovirus, toxoplasmosis, varicella-zoster, syphilis and herpes simplex.
• Maternal factors such as smoking, chronic hypertension, anaemia and pregestational diabetes reduce placental perfusion or nutrient supply.

Umbilical artery (UA) Doppler reflects placental vascular resistance. As resistance rises, the pulsatility index (PI) increases and diastolic flow falls; at the extreme, end-diastolic flow becomes absent (AEDV) and then reversed (REDV). These waveforms indicate increased perinatal mortality and morbidity and are linked to placental pathology and fetal hypoxaemia.

Middle cerebral artery (MCA) Doppler shows the fetal adaptive response. Hypoxaemia lowers cerebral vascular resistance (brain sparing or redistribution), so the MCA PI falls. The cerebroplacental ratio (CPR), calculated from MCA and UA PI, falls as well and is more closely related to fetal hypoxia than either component. About 20% of term SGA fetuses with a normal UA Doppler have a low MCA PI, associated with intrapartum distress and poorer outcomes.

Ductus venosus (DV) Doppler reflects cardiac function. With worsening placental or cardiac function, forward flow during atrial systole falls: the venous PI rises and the a-wave becomes absent or reversed. An abnormal DV is seen mainly in early-onset FGR and signals acidaemia and a high stillbirth risk.

The non-stress test (NST) records fetal heart rate (FHR) on a cardiotocograph with the patient in left lateral or semi-Fowler position for at least 20 minutes, extended to 40 minutes to allow for fetal sleep cycles. A reactive NST shows FHR accelerations of at least 15 bpm above baseline lasting at least 15 seconds, indicating intact fetal autonomic function. Vibroacoustic stimulation with an artificial larynx can provoke accelerations and reduce non-reactive results.

Gestational age matters. Up to 50% of NSTs are non-reactive at 24 weeks and about 15% between 28 and 32 weeks because of immaturity rather than distress, so between 24 and 32 weeks a lower acceleration threshold of at least 10 bpm is used.

The biophysical profile (BPP) combines an NST with four ultrasound observations made over 30 minutes. Each component scores 2 if present to the required degree or 0 if absent, for a maximum of 10. As hypoxia and acidosis develop, fetal breathing movements are lost first, followed by body movements and then tone.

• 8 or 10: fetal well-being.
• 6: equivocal — repeat or further testing depending on gestation.
• 4 or less: abnormal — delivery is often indicated unless the pregnancy is below 32 weeks, when extended monitoring may be chosen.
• Oligohydramnios with any score needs further evaluation, including for ruptured membranes — fluid volume is the chronic marker, and see amniotic fluid.
• Modified BPP: reactive NST plus deepest vertical pocket above 2 cm; if either is abnormal, proceed to a full BPP or CST.

Delivery timing balances stillbirth against prematurity and is guided by Doppler and fetal heart rate findings. Pregnancies with early-onset FGR do best in units with high-level fetal medicine and neonatal care and a uniform protocol. FIGO's summary of monitoring and timing is below.

• Antenatal corticosteroids are given when early delivery is anticipated; a transient improvement in end-diastolic flow after steroids should not change management, while no change predicts deterioration.
• Magnesium sulphate for fetal neuroprotection reduces perinatal death, cerebral palsy and gross motor dysfunction when preterm birth is expected.
• Prevention: aspirin started at or before 16 weeks in people at high risk of pre-eclampsia nearly halved FGR in a meta-analysis (RR 0.56), favouring 100–150 mg — see pre-eclampsia.