MD Notes

creation date: 2026-01-13 09:57
tags: Pathologies

Fetal Growth Restriction

Background

Definitions

Fetal growth restriction (FGR), previously referred to as intrauterine growth restriction, refers to the pathological failure of a fetus to reach its full genetically determined growth potential.

This is often defined as an estimated fetal weight or abdominal circumference <10th percentile but must be distinguished from a naturally small fetus.

Small for gestational age (SGA) typically use the same cutoffs to describe neonatal size but may or may not be associated with pathological etiology.

Etiology and Risk Factors

Approximately 60% of small for gestational age fetuses are associated with pathological etiology. These etiologies can overlap.

Fetal causes
In 5% of cases, fetal genetic anomalies are responsible:

  • Aneuploidy
  • Uniparental disomy
  • Single-gene mutations
  • Partial deletions or duplications
  • Ring chromosomes
  • Aberrant genomic imprinting

Other fetal causes include:

  • Fetal infection (eg. malaria, CMV)
  • Nonchromosomal congenital anomalies

Maternal causes
Maternal conditions may interfere with uteroplacental-fetal blood flow resulting in SGA and FGR:

Increased risk is associated with:

  • Substance misuse
  • Multiple gestations
  • Low prepregnancy weight
  • Poor gestational weight gain
  • Teratogenic medications/procedures
  • Uterine malformations

Placental and umbilical cord causes
Placental causes include:

  • Bilobate or circumvallate placenta
  • Placental abruption
  • Infarction
  • Placenta accreta spectrum
  • Placental mesenchymal dysplasia

Umbilical cord anomalies include:

  • Single artery
  • Velamentous
  • Marginal cord insertion

Pathogenesis

FGR most commonly occurs due to inadequate remodelling of the uterine spiral arteries. Cord obstruction (eg. compression or hypercoiling) may precipitate growth restriction as well.

In 20-30% of cases, poor placental function that begin in early first trimester may cause symmetric fetal growth restriction, of which the fetus’ growth is uniformly restricted.

In 70-80% of FGR cases, intrauterine insult occurs in the late second or third trimester of pregnancy results in disproportionate restriction. This is sometimes referred to as “head-sparing” growth restriction, whereby the head circumference is preserved while the abdominal circumference is reduced due to the preferential blood supply for the brain.

Clinical Presentation

Signs & Symptoms

Palpation of the fundal height (pubic symphysis to top of uterus) ≥4 cm discordant with expected size suggests possible FGR.

  • Week 12: level of pubic symphysis (0 cm)
  • Week 20: level of umbilicus
  • Week 24+: ±3 cm of gestational age

Findings may be incidental during anatomy ultrasound (18-22 weeks)

History & Physical Exam

An assessment of maternal medical conditions and risks for FGR should have been obtained in the first prenatal visit.

Diagnosis

Criteria

Diagnosis of FGR is based on sonographic estimation of fetal weight <10th percentile or fetal abdominal circumference <10th percentile.

Abnormal doppler parameters and decreasing growth trajectory support the diagnosis of pathologic FGR. Other supporting findings include:

  • EFW or AC <3rd percentile
  • Oligohydramnios (reduced urination due to reduced fetal renal perfusion)

Work-up

Ultrasound
In all fetus suspected of FGR, ultrasound is used to determine:

  • Sizing
  • Congenital anomalies (10% of etiologies)

Selected cases
In some cases, further testing may be indicated:

  • Fetal ECG (if uncertainty about normal cardiac development)
  • Genetic testing
  • Infection testing via amniocentesis (if sonographic markers or history suggests infectious etiology)

Differential

  • Misdated pregnancy
  • Oligohydramnios
  • Genetically/naturally small fetus

Red Flags / Complications

Complications generally manifests following delivery. However, there is an increased risk of prematurity.

Management

Prenatal Care

Fetal surveillance

The following parameters are assessed:

  • Estimated fetal weight every 3 weeks
  • Doppler ultrasonography
  • Nonstress test and biophysical profile

Interventions

A course of antenatal betamethasone is given to pregnancies <34+0 weeks gestation in the 7 days prior to anticipated preterm birth.

For patients with reversible risk factors, targeted intervention may be beneficial such as:

  • Nutrition
  • Smoking cessation
  • Antihypertensive therapy

Delivery

The exact timing of delivery depends on the weighing of the benefit of longer gestation versus the risk associated with fetal instability.

The timing is thus based on:

  • NST and BPP score
  • Amniotic fluid volume
  • Umbilical artery Doppler flow

It is not recommended to postpone delivery beyond 39 week gestation. Delivery timing range from prompt delivery (very unstable) to delivering between 38-39 weeks of gestation if all parameters are normal with no comorbidities.

Intrapartum management includes:

  • Magnesium sulfate for neuroprotection
  • Continuous fetal heart rate monitoring

Postpartum Management

Neonatal

The most common neonatal morbidities are:

  • Respiratory distress syndrome
  • Sepsis
  • Retinopathy of prematurity

Early-onset FGR and concerning parameters of prenatal testing are associated with worse mortality.

Long-term morbidities include:

  • Increased risk of hypertension, diabetes, coronary heart disease, and CKD
  • Neurodevelopmental abnormalities and impaired cognitive performance

Maternal

Maternal risk for the following is elevated:

  • Cardiovascular disease
  • Subsequent SGA births

Management consist of addressing risk factors (eg. smoking cessation). Additionally, accurate dating by early ultrasonography is important for subsequent pregnancies.

References

Tools / Guidelines

Additional Reading