Diagnose and manage fetal growth restriction, including Doppler, timing and route of delivery

In one line

Fetal growth restriction (FGR) is the failure of a fetus to reach its genetically determined growth potential, almost always from placental insufficiency — and the entire management problem is a single trade-off: balancing the rising risk of intrauterine demise against the iatrogenic harms of prematurity, arbitrated by a Doppler-driven surveillance ladder and a gestation-specific delivery threshold.

This chapter assumes the Intermediate groundwork on growth-restriction pathophysiology and SFH screening and the macrosomia counterpart; it does not re-teach what SGA is or how a basic umbilical-artery Doppler waveform is obtained. The Final-level work is to phenotype the small fetus, read the deterioration sequence, and time delivery against a moving target — so the words below are spent on the subtype distinctions, the staging systems, the appraisal of the timing trials, and the consultant judgement calls.

Assessment

FGR is not the same as small-for-gestational-age (SGA), and the most consequential cognitive error at consultant level is treating "small" as a single disease. There are at least four populations under the <10th-centile umbrella, each with a different driver and a different management consequence:

• Constitutionally small (true "SGA"). Normal placenta, normal Dopplers, appropriate interval growth, no perinatal-risk signal. The error is over-delivering this fetus — iatrogenic prematurity for a healthy baby.
• Early-onset placental FGR (<32 weeks). The "respiratory failure of the placenta" phenotype: severe placental disease, steeply escalating UA→DV Doppler abnormality, a strong association with pre-eclampsia, and high mortality and morbidity. Prevalence ~1%. This is the phenotype that follows the classic deterioration cascade and forces a viability-versus-prematurity decision.
• Late-onset placental FGR (≥32 weeks). Mild placental disease, a normal or near-normal umbilical artery (only an extensive lesion lifts the UA-PI), and the abnormality declared instead by the middle cerebral artery / cerebroplacental ratio — "brain-sparing" without UA derangement. Far commoner (~60% of FGR), lower mortality, but it accounts for a large share of unexplained term stillbirth precisely because the UA looks reassuring and the clinician is falsely reassured.
• Non-placental smallness. Aneuploidy, early CMV/malaria, structural anomaly, or simply wrong dates. The signature is a symmetrically small fetus with normal Doppler and often normal liquor — the placenta is innocent and the work-up is genetic/infective, not a delivery-timing problem.

The mechanism→consequence link that drives surveillance: in early FGR the UA is the index test because gross placental loss is what drives it, so the UA leads the deterioration sequence; in late FGR the placental reserve loss is too subtle to move the UA, so the CPR (more sensitive to hypoxia than either vessel alone) and the MCA become the discriminators, and a normal UA must never be read as "reassured."

The diagnostic definition — and why it is built the way it is

• Diagnosis (Delphi consensus, Gordijn 2016). Early FGR (<32 weeks): a solitary criterion — AC or EFW <3rd centile, or absent end-diastolic flow (AEDF) in the umbilical artery — or AC/EFW <10th centile combined with UA-PI or uterine-artery PI >95th centile. Late FGR (≥32 weeks): AC/EFW <3rd centile alone, or AC/EFW <10th centile with either CPR <5th centile or UA-PI >95th centile, or AC/EFW crossing >2 quartiles on serial charts. The architecture is deliberate: a <3rd-centile fetus is defined as restricted (the fixed low centile carries an adverse-outcome signal on its own — an isolated EFW <3rd centile predicts adverse perinatal outcome irrespective of Doppler), whereas a 4th–10th-centile fetus is "small enough to be suspicious but not enough to be certain" and so requires Doppler or interval-growth corroboration before it earns the FGR label.
• The customised-versus-population chart controversy. Population charts call constitutionally small-but-healthy fetuses "abnormal" and miss the large baby who has dropped below his own potential; customised/GROW charts (adjusting for maternal height, weight, parity, ethnicity) reclassify a meaningful fraction and improve the correlation with stillbirth, but the GAP/DESiGN cluster-randomised evidence did not show that mandating customised charts reduces stillbirth at a programme level, so this remains a tool that sharpens individual judgement rather than a proven population intervention. State the limitation; do not present customised charts as a settled win.
• Confirm dating first. A wrong LMP manufactures false FGR; first-trimester CRL trumps a late scan. An undated fetus presenting late and small is a diagnostic trap — you cannot distinguish "small" from "younger than you think" without a growth interval.

History and the SA risk landscape

• History/risk-stratify. Prior FGR/stillbirth/pre-eclampsia, chronic hypertension, renal/SLE/APS disease, smoking, multiple pregnancy, antepartum haemorrhage. In SA, add HIV (and the PVT cascade), TB and under-nutrition as population drivers — and remember the antiretroviral nuance, that older protease-inhibitor regimens were associated with growth restriction whereas the current dolutegravir-based first-line is not, so the modern SA HIV cohort's FGR is more often the placenta than the drug.

Investigations and what each one is actually telling you

• EFW + AC on customised or population charts; liquor volume (oligohydramnios = redistribution of cardiac output away from the kidneys, i.e. a decompensation marker, not a primary diagnostic criterion — its inclusion in management protocols is, on the meta-analytic evidence, of doubtful independent value); umbilical artery Doppler (the index test that changes outcomes); MCA-PI and CPR for the late/term phenotype; ductus venosus (DV) for early severe disease; uterine artery PI to confirm the placental aetiology. Screen for the cause: anomaly scan, and where indicated karyotype/microarray and CMV/malaria serology — a structurally abnormal or symmetrically tiny fetus with normal Doppler is more likely aneuploid or infective than placental.
• Read the venous Dopplers as a hierarchy, not a checklist. The deterioration sequence in early FGR is stereotyped: raised UA-PI → absent end-diastolic flow → reversed end-diastolic flow (arterial/placental side) running in parallel with CPR fall and MCA brain-sparing, then aortic isthmus reversal (the bridge between arterial and venous compromise — it precedes DV abnormality by roughly a week but does not predict mortality better than the DV, so it is physiologically informative but not the trigger), and finally the venous signs of cardiac decompensation: DV-PI >95th centile → absent then reversed a-wave, with UV pulsations and a falling cCTG short-term variation as the terminal events. The DV is the single strongest predictor of short-term risk of fetal death; it precedes the loss of cCTG short-term variability in ~50% of cases and precedes a biophysical-profile deterioration by 48–72 h in ~90%.