Several placental abnormalities may cause poor fetal growth. These are discussed further throughout Chapter 6 and include chronic placental abruption, extensive chorioangioma, velamentous cord insertion, placenta previa, and umbilical artery thrombosis. Growth failure in these cases is presumed secondary to uteroplacental insuiciency. Abnormal placental implantation leading to endothelial dysfunction may also limit fetal growth (Brosens, 2015). This pathology is implicated in pregnancies complicated by preeclampsia (Chap. 40, p. 714). If the placenta is implanted outside the uterus, the fetus is usually growth restricted (Chap. 19, p. 383). Finally, some uterine malformations have been linked to impaired fetal growth (Chap. 3, p. 44).
Pregnancy with two or more fetuses is more likely to be complicated by diminished growth of one or more fetuses compared with that ofnormal singletons. This is illustrated in Figure 44-5 and discussed in Chapter 45 (p. 872).
Drugs with Teratogenic and Fetal Effects
Several drugs and chemicals are capable oflimiting fetal growth. Some are teratogenic and afect the fetus before organogenesis is ::,1500
FIGURE 44-5 Birthweight and gestational age relationships in multifetal gestations without malformations delivered at Parkland Hospital.
complete. Some exert-or continue to exert-fetal efects after embryogenesis ends at 8 weeks. Many ofthese are considered in detail in Chapter 12, and examples include anticonvulsants and antineoplastic agents. Cigarette smoking, opiates and related drugs, alcohol, and cocaine may also cause growth restriction, either primarily or by decreasing maternal food intake. he link with cafeine use and fetal-growth restriction remains speculative (American College of Obstetricians and Gynecologists, 2016b). In contrast, Cyganek and colleagues (2014) studied growth restriction in pregnancies complicated by renal and liver transplants and concluded that common immunosuppressive drugs-prednisone, azathioprine, cyclosporine A, and tacrolimus-did not significantly afect fetal-growth rates.
Viral, bacterial, protozoan, and spirochetal infections have been implicated in up to 5 percent of fetal-growth restriction cases and are discussed throughout Chapters 64 and 65. The best known of these are rubela and cytomegalovirus inection. Both promote calcifications in the fetus that are associated with cell death, and infection earlier in pregnancy correlates with worse outcomes. Toda and colleagues (2015) described a Vietnamese epidemic in which 39 percent of 292 term newborns with congenital rubella syndrome were low birthweight. In one study of 238 primary cytomegalovirus infections, no severe cases were observed when infection occurred after 14 weeks' gestation (Picone, 2013). hese investigators later identified sonographic findings in 30 of 69 cases of congenital infection, and growth restriction was noted in 30 percent of these 30 cases (Picone, 2014).