Small for Gestational Age

Definitions

• Small for gestational age (SGA) – a fetus with an estimated fetal weight (EFW) or abdominal circumference (AC) <10^th centile. A liveborn infant with a birth weight <10^th centile is also described as SGA.
  • Severe SGA – an EFW, AC or birth weight <3^rd centile.
• Fetal growth restriction (FGR) – a fetus that has failed to achieve its genetically determined growth potential. The current consensus (and RCOG GTG 31) defines FGR as an EFW or AC <3^rd centile, or an EFW or AC <10^th centile combined with abnormal Doppler studies (uterine or umbilical artery) or reduced growth velocity.
  • FGR may be classified as early (<32 weeks) or late (≥32 weeks), which differ in their clinical course and surveillance.
  • Not all SGA fetuses are growth restricted, and a fetus can be growth restricted without being SGA.
• Low birth weight – a birth weight <2500g, irrespective of gestation.

The complementary condition – where the fetus grows above the expected centile – is large for gestational age (LGA), which is covered in a dedicated article.

Aetiology and Pathophysiology

Constitutionally (Normally) Small

The majority of SGA fetuses are constitutionally small. They are small at all stages of pregnancy but grow consistently along their centile, with no underlying pathology. Contributing factors include maternal ethnicity, fetal sex, and parental height and build.

Placenta-Mediated Growth Restriction

Growth is often normal initially but slows in utero as a result of placental insufficiency. This is the commonest cause of FGR. Contributing maternal factors include low pre-pregnancy weight, smoking and substance misuse, autoimmune disease (e.g. antiphospholipid syndrome), renal disease, pre-existing diabetes with vascular disease, and chronic or pregnancy-related hypertension.

Non-Placenta-Mediated Growth Restriction

Growth is restricted by fetal factors such as chromosomal or structural anomalies, inborn errors of metabolism, or congenital infection.

Risk Factors

All women should be assessed for risk factors for small for gestational age and fetal growth restriction at booking and again at the 20-week scan. This assessment determines whether a woman enters a surveillance pathway.

* Chronic hypertension, renal impairment, diabetes with vascular disease, and antiphospholipid syndrome.

^ PAPP-A = pregnancy-associated plasma protein A, produced by the placenta; a low level is associated with placental dysfunction.

Women with ≥3 minor risk factors are referred for uterine artery Doppler at 20-24 weeks. Women with a major risk factor are referred for serial ultrasound assessment of fetal growth and umbilical artery Doppler, usually from 26-28 weeks.

Diagnosis and Clinical Features

Clinicians use ultrasound to diagnose and monitor the SGA fetus. Biometry, including EFW and AC, should be plotted on customised centile charts that adjust for maternal characteristics (height, weight, ethnicity and parity), gestational age and fetal sex. Customised charts improve the detection of pathological smallness compared with population-based charts.

Symphysis-fundal height (SFH) measurement screens for SGA in women not already on a serial scan pathway. A single measurement <10^th centile, or slow or static growth across measurements, prompts referral for ultrasound. However, SFH measurement is unreliable where maternal BMI >35, with large fibroids, or in polyhydramnios — these women should have serial ultrasound instead.

The pattern of smallness may give a clue to the cause. A symmetrically small fetus (head and abdomen proportionately small) is more likely to be constitutionally small or to reflect an early insult such as a chromosomal anomaly or infection. In contrast, an asymmetrically small fetus (relative sparing of the head, with a smaller abdomen) is more suggestive of placental insufficiency.

As a result of placental insufficiency, blood flow may be redistributed to the fetal brain — the ‘brain-sparing’ effect — which can be detected as abnormal middle cerebral artery (MCA) Doppler. Placental insufficiency may also reduce fetal renal perfusion, causing reduced amniotic fluid volume (oligohydramnios).

Investigations

Where a fetal anomaly or non-placental cause is suspected, further investigations may include:

• Detailed fetal anatomical survey
• Uterine artery Doppler (to assess for placental dysfunction, particularly when EFW is <10^th centile at the 20-week scan)
• Karyotyping / microarray (especially if structural anomalies are present or growth restriction is early and severe)
• Screening for congenital infection (e.g. cytomegalovirus, toxoplasmosis; syphilis and malaria where relevant)

Management

Prevention

Modifiable risk factors should be addressed, including smoking cessation support and optimising maternal medical conditions.

Women at high risk of pre-eclampsia or placental dysfunction should be offered aspirin (75-150 mg daily) from 12 weeks of gestation until birth (NICE NG133). This reduces the risk of preterm pre-eclampsia and preterm placenta-mediated SGA. (Note: this is the dose and timing for pre-eclampsia/placental dysfunction prophylaxis; it differs from older guidance that quoted 75 mg from 16 weeks.)

Surveillance

Once a fetus is identified as SGA, repeat ultrasound biometry approximately every 2 weeks to assess growth velocity (measuring more frequently risks false detection of apparent growth changes).

Umbilical artery Doppler is the primary surveillance tool in the SGA fetus and should be performed at diagnosis and during follow-up:

• If normal, repeat as a minimum every 14 days.
• If abnormal but end-diastolic flow is present (raised pulsatility/resistance index), increase surveillance to twice weekly.
• If absent or reversed end-diastolic flow, admit for intensive monitoring (e.g. daily assessment) and plan delivery.

Additionally, the following tools complement umbilical artery Doppler in surveillance:

• Middle cerebral artery (MCA) Doppler – most useful in the late/term SGA fetus (after 32 weeks), where the umbilical artery Doppler is often normal. A low MCA pulsatility index, or a low cerebroplacental ratio, can help time delivery.
• Ductus venosus (DV) Doppler – used in the preterm SGA fetus with an abnormal umbilical artery Doppler, and to help time delivery.
• Computerised cardiotocography (CTG) and amniotic fluid volume (single deepest vertical pocket) – used as adjuncts, but not as the sole form of surveillance.

Delivery

If preterm birth is anticipated, give a single course of antenatal corticosteroids if birth is expected before 34⁺⁶ weeks, and offer magnesium sulfate for fetal neuroprotection if birth is anticipated before 30 weeks (and consider it between 30 and 34 weeks).

The principles for timing and mode of birth are summarised below.

Induction of labour in a SGA fetus carries a higher rate of emergency caesarean section. Consequently, continuous fetal heart rate monitoring remains essential from the onset of contractions.

Complications of Small for Gestational Age

Increased morbidity and mortality are most strongly associated with FGR rather than constitutional smallness. The use of customised growth charts and structured surveillance reduces perinatal morbidity and mortality. Consequently, early identification of FGR and close surveillance are essential — antenatally, the principal risk is stillbirth.

Many of the long-term associations reflect the developmental origins of health and disease hypothesis, linking impaired fetal growth to adult metabolic and cardiovascular risk.

References and Further Reading

• Royal College of Obstetricians and Gynaecologists. Investigation and Care of a Small-for-Gestational-Age Fetus and a Growth Restricted Fetus. Green-top Guideline No. 31 (3^rd edition). London: RCOG; 2024.
• National Institute for Health and Care Excellence. Hypertension in pregnancy: diagnosis and management. NICE guideline NG133. London: NICE; 2019.
• National Institute for Health and Care Excellence. Antenatal care. NICE guideline NG201. London: NICE; 2021.
• NHS England. Saving Babies’ Lives Care Bundle (Version 3). NHS England; 2023.