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    Fetal Growth Restriction



    Maternal conditions including hypertension and antiphospholipid antibody syndrome are considered strong risk factors for FGR. Importantly, PB 134 reminds us that the hereditary thrombophilias such as factor V Leiden, the prothrombin G20210A mutation, and methylenetetrahydrofolate reductase gene mutations have not consistently been associated with FGR.

    Pregnant women with small fetuses often ask about the adequacy of their nutrition. However, even famine-level caloric intake (600–900 kcal/day) has only a modest effect on birth weight.1 Conversely, increased caloric intake is very unlikely to alter the growth of an FGR fetus.

    Viral titers often are recommended for assessment of FGR, although viral infections cause a small fraction of reported cases. Depending on maternal history and other findings such as intracranial or peritoneal calcifications, viral testing may be useful. Most infectious-mediated FGR worldwide is caused by malaria.

    Chromosomal malformation can cause FGR, especially trisomies 13 and 18, so in the presence of FGR with malformations, and often associated polyhydramnios, it is prudent to offer invasive testing. Although not addressed in the PB, I discourage maternal cell-free fetal DNA testing in this circumstance because it does not offer microarray analysis. It is also becoming clear that copy number variants (eg, microdeletions and microduplications) are associated with FGR.

    Among placental anomalies, a single umbilical artery has recently been more convincingly shown to be associated with FGR. Consequently, although not addressed in the PB, I recommend a growth check at 32 weeks for affected pregnancies, with no further testing if it is normal. A similar recommendation can be made for velamentous and perhaps even marginal cord insertions.


    Should all patients have a screening “growth scan” in the third trimester? Should we adopt first- or second-trimester uterine artery Doppler velocimetry or use serum analytes for this purpose? The PB is quite clear that the basic screening modality is fundal height measurements and that there is no evidence of value for a routine growth scan in normal pregnancies.

    Maternal obesity or the presence of large uterine myomas, if they make fundal height measurement difficult, can be indications for serial sonograms for fetal size estimation.

    There is little benefit to uterine artery Doppler in the first trimester because it has a high false-positive rate and there is no evidence of improved outcomes with its use. Evidence of the association between FGR and low Pregnancy Associated Plasma Protein A (PAPP-A) in the first trimester or high serum alpha-fetoprotein in the second trimester is sufficient to check a third-trimester growth scan in affected pregnancies, but I would not order these tests to predict FGR alone.

    The major advance of the past 20 years in mangement of FGR has been the incorporation of umbilical artery Doppler velocimetry. Doppler does not work as a screening test because there are many etiologies of FGR that do not result in aberrant umbilical artery flow. However, there is a utility to Doppler flow studies in the setting of demonstrable FGR. Abnormal results, especially absent or reversed end-diastolic flow, can be used to modify frequency of fetal surveillance with other traditional tests (ie NST, BPP) with improved perinatal survival.

    Although PB 134 categorizes the value of Doppler investigation of other vessels such as the middle cerebral artery and ductus venosus as uncertain, many experts use these tests to supplement the information obtained from the umbilical artery.



    Joshua A. Copel, MD
    DR. COPEL is Professor, Division of Maternal-Fetal Medicine, Department of Obstetrics, Gynecology and Reproductive Sciences, Director of ...


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