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FGR, also referred to as intrauterine growth restriction (IUGR), is defined as poor fetal growth due to an underlying pathological cause. Although small for gestational age (SGA) (birthweight <10th percentile) is sometimes used as a surrogate for FGR, the majority of SGA fetuses are healthy.^{42, 43} FGR represents 10–50 percent of SGA fetuses, with this proportion being dependent upon the population being studied and which growth curves are applied.^{42, 43} Distinguishing FGR from a constitutionally small baby prenatally is important, as it is specifically the FGR baby that is at risk of adverse perinatal outcomes, including intrauterine death, premature birth, neonatal sepsis, and neurological impairment.^44–46 Placental FGR is also a risk factor for adult‐onset diseases such as diabetes, hypertension, and cardiovascular disease.⁴⁷

To diagnose FGR prenatally, fetuses with abdominal circumference <10th percentile can be further assessed by uterine and umbilical artery Doppler to check for impeded blood flow to the placenta or fetus, amniotic fluid index, and other signs of fetal compromise (see Chapter 17). Altered protein levels in maternal serum have been associated with FGR caused by placental insufficiency, including lower levels of PlGF and increased levels of soluble fms‐like tyrosine kinase‐1 (sFLT‐1).^48–50 Placentas associated with FGR tend to be small and are associated with a range of pathologies that may be a cause or consequence of impaired maternal or fetal vascular supply.⁵¹ These findings can include increased syncytial knots, intervillous fibrin deposition, villous infarcts, villous agglutination, distal villous hypoplasia, villous hypermaturation, marginal abruption, thrombosis, and chorangioma, among others. Compromised placental vascularization can also be seen as microvascular regression (particularly at the placenta periphery).⁵² However, such findings can occur in the absence of FGR, and further research is needed to clarify these relationships.