Diagnosing and Monitoring Growth Restriction
Studies show that hypertensive disorders, for one, are present in 30%–40% of pregnancies that involve fetal growth restriction, and that even without proteinuria, elevated diastolic blood pressure in pregnancy is associated with small-for-gestational-age infants. Preeclampsia is associated with a fourfold increase in the risk of having a small-for-gestational-age infant.
Maternal autoimmune disorders (lupus and antiphospholipid syndrome, for instance), various medications (including certain anticonvulsants, particular β-blockers, cancer chemotherapy, and steroids), cigarette smoking, and even moderate alcohol use, have also been implicated in causing fetal growth restriction. Treatment of some of these conditions, such as the hypertensive conditions, is necessary for the health of the mother but, unfortunately, will not necessarily improve fetal growth.
Treatment of other conditions, such as those involving maternal lifestyle, will definitely lower the severity of the complication. If the mother is a smoker, for instance, a smoking cessation program is absolutely critical. Her fetus's drop in birth weight will be significantly less if smoking is stopped after the first trimester than if it continues throughout the pregnancy.
Fetal chromosomal abnormalities and congenital malformations are also significantly associated with fetal growth restriction, as is perinatal infection. Malaria may be one of the most significant causes of growth restriction in many countries where this disease is endemic. Even in the United States about 5%–10% of all cases of fetal growth restriction can be attributed to viral or protozoan infections in utero.
Bacterial infections have not traditionally been implicated as causes, but there is emerging evidence that subclinical infection and inflammation, as well as extragenital infection, may be associated with growth restriction.
Experts have long recognized a strong association between fetal growth restriction and prematurity, though it's unclear whether there is a true casual relationship.
Monitoring the Growth-Restricted Baby
When a diagnosis of fetal growth restriction is made, our role then focuses on fetal surveillance and the recognition of fetal stress and compromise.
Ultrasonography, first of all, should be done every 2–4 weeks after the diagnosis is made. Of all the additional modalities that we can use for fetal surveillance, umbilical arterial Doppler, which measures blood-flow impedance in the placenta, is one of the most effective tests we have for detecting a fetus who is getting into trouble. It should be used as our primary test. We now have compelling evidence from more than 20 randomized trials that fetal Doppler surveillance significantly improves outcomes (deaths in utero and other medical outcomes) in well-defined, high-risk pregnancies—most notably those involving fetal growth restriction and preeclampsia.
We can supplement Doppler with traditional tests of fetal heart rate monitoring, namely the nonstress test (NST), and evaluation of amniotic fluid volume. Both nonreactive NST and oligohydramnios have been associated with adverse perinatal outcome.
We also can use the biophysical profile (BPP), which incorporates parameters relating to the heart rate pattern, the fluid levels, umbilical artery Doppler, and examination of growth via ultrasound.
Just as the nonstress test does, the BPP has a low false-negative rate but a high false-positive rate. None of these additional tests is backed by the “level 1” evidence (randomized controlled trials) that Doppler carries, but they have essentially become standards of care. When used once a week, the tests are a valuable part of management, and I have incorporated them into my own evidence-based management guidelines. (See chart below.)
Usually, ominous changes in the fetal heart rate pattern or the BPP will follow nonreassuing Doppler indices—a fact that is indicative not only of the value of umbilical arterial Doppler but the value of these other tests in helping us to assess fetal distress and compromise, and the need for delivery, as completely as possible.
If our umbilical arterial Doppler shows an absence of flow at the end of the cardiac cycle and the other tests are normal, we can—if the pregnancy hasn't reached 34 weeks—step up the frequency of our other tests and attempt to carry the gestation through a bit further. If the end-diastolic flow is reversed, however, we need to intervene promptly. Reversed end-diastolic flow is an ominous sign.
Other ominous signs are a BPP score of 4 or less; an amniotic fluid index of 5 cm or less or a single deepest pocket less than 2 cm; and nonreassuring fetal heart rate patterns such as persistent nonreactive NSTs, continuous deceleration, and poor heart rate variability from one cardiac cycle to another.
The use of venous Doppler sonography is getting more attention today as another back-up test for evaluating fetal well-being when the umbilical arterial Doppler shows absent end-diastolic flow.
