The risk of premature rupture of membranes and preterm labor is significantly increased among pregnant women who use cocaine. Decreased intrauterine growth is due to the intermittent slowing in placental blood flow, caused by constriction of the uterine blood vessels. This decreases blood flow and impairs oxygen and nutrient transfer to the fetus. In addition, in utero cocaine exposure depresses neonatal fat stores and diminishes body mass. Maternal cocaine use may have direct, as well as indirect, effects on the fetus.
Cocaine crosses the placenta by simple diffusion.
Congenital anomalies occur in 7 to 26 percent of infants exposed to cocaine in utero. Cocaine can adversely affect embryonic and fetal development through interruption of uterine, placental, and fetal blood flow. Evidence of brain malformation or hemorrhage occurs in approximately 35 percent of infants exposed to cocaine in utero. Fetal cardiovascular abnormalities caused by maternal use of cocaine have been reported to occur in 4 to 40 percent of babies exposed to cocaine in utero. Defects or disruption of urinary and genital development have been found in 14 percent of infants exposed to cocaine in utero.