Clinical Review

Fetal growth restriction

OBG Manag. 2004 June;16(6):48-64

3 keys to successful management

A rational strategy for antepartum identification, close fetal surveillance, and individualized intervention is based on meta-analyses, Cochrane reviews, and current standards of care.

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References

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10. Lindhard A, Nielsen PV, Mouritsen LA, Zachariassen A, Sorensen HU, Roseno H. The implications of introducing the symphyseal-fundal height measurement. A prospective randomized controlled trial. Br J Obstet Gynaecol. 1990;97:675-680.

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KEYS TO SUCCESS

Antepartum recognition of fetal growth restriction is essential for proper surveillance and management.
Because growth-restricted fetuses are at risk for adverse outcomes in utero, fetal surveillance is vital for timely recognition and intervention.
Once growth restriction is identified, management should be individualized to ensure optimal gestational development and safe delivery.

Not only is fetal growth restriction (FGR) associated with perinatal mortality and morbidity, but it may be linked to adverse consequences in adulthood.¹ Its many causes involve diverse pathological processes; thus, it should not be considered a single disease. Many aspects remain unclear, a substantial number of affected infants are not identified before birth, and effective antepartum prevention and treatment remain elusive.

Fortunately, managing FGR has hopeful aspects. Meaningful recent advances elucidate its etiologic and pathophysiologic mechanisms and help clarify diagnosis and management.

This article offers an up-to-date, evidence-based approach and includes guidelines on 3 keys to success: antepartum recognition, fetal surveillance, and antepartum and intrapartum management. These guidelines are not intended as a strict protocol, since the clinical course of FGR is highly variable, but as the starting point for individualized care.

An amorphous entity: FGR terminology

Fetal growth restriction implies failure to realize genetically determined growth potential. Terms include fetal growth restriction, intrauterine growth restriction, and small for gestational age (SGA). The pejorative term growth retardation is obsolete.

Traditionally, FGR refers to prenatally identified fetal growth deficiency, whereas SGA refers to suboptimal birth weight for the gestational age. However, some small fetuses are merely constitutionally small, not growth-restricted. Conversely, not all growth-restricted fetuses are small in size or weight for gestational age. Yet defining these groups is difficult, as the tools are imprecise and controversial.

This article uses these definitions:

Fetal growth restriction identified in the antepartum period refers to a fetus with sonographically measured fetal dimensions, particularly abdominal circumference or estimated weight, below an age-specific threshold, typically the 10th percentile.

Fetal growth restriction identified at birth is birth weight below the 10th percentile for gestational age, or SGA. Unfortunately, this definition may fail to identify some fetuses that are truly growth-restricted. Alternative, more sensitive definitions, such as the Ponderal index or birth weight ratio, are used primarily in research.

Consequences of FGR

Perinatal outcomes. Perinatal morbidities include prematurity, oligohydramnios, nonreassuring fetal heart rate patterns with a higher incidence of cesarean delivery, birth asphyxia, low Apgar score, neonatal hypoglycemia, hypocalcemia, polycythemia, hyperbilirubinemia, hypothermia, apnea, seizure disorders, and infection.

Fetal and neonatal mortality is significantly increased. Perinatal mortality is influenced by many factors, including severity of growth restriction, timing of onset, gestational age, and cause of growth restriction. The lower the birth-weight percentile for gestational age, the higher the mortality rate.

Effects in infancy. Although many SGA infants “catch up” growth in infancy, the pattern varies. Height and weight catch-up growth of preterm FGR infants lags behind that of preterm infants that are appropriate for gestational age (AGA) at birth.² Those with early-onset or severe growth deficit continue to lag behind in postnatal growth. Although recent studies indicate that rapid postnatal growth in SGA infants may lead to increased risk of chronic diseases, including type 2 diabetes, others have found tangible short-term benefits of less frequent morbidity and mortality in infancy.³

FGR has been linked to a spectrum of neurodevelopmental risks, including subtle behavioral abnormalities, immature sleep patterns, decreased visual fixation, decreased general activity, altered early mother-infant interaction, altered motor skills, and hyperactivity.^4,5 Infants born SGA at 32 to 42 weeks were 4 to 6 times more likely to have cerebral palsy, yet those whose birth weight was above the 97th percentile also had increased risk. It remains uncertain whether deviant growth is the cause or a consequence of this disability.⁶

Long-term effects. Lifetime sequelae of early nutritional deprivation have been demonstrated in animals.⁷ Moreover, epidemiological evidence suggesting an association between SGA at birth or infancy and increased risk of abnormal blood lipid values, diabetes, hypertension, and ischemic heart disease in adult life led Barker and associates to propose the fetal origins hypothesis.¹

1. Antepartum recognitionDetermine gestational age

A reliable estimate of gestational age is central to identification of fetal growth compromise in utero or at birth. In pregnancies at risk for fetal growth restriction, gestational age should be established early, preferably in the first trimester.

The method of determining gestational age influences the observed frequency of FGR and SGA births. Estimates are more accurate when based on early ultrasound biometry than on menstrual history. The latter, if well documented, regular, and ovulatory, may be reliable if it differs by no more than 1 week from the sonographic gestational age. Otherwise, early-pregnancy, ultrasoundbased age is more accurate.