Cocaine use during pregnancy

Could you please discuss the impact of cocaine use during pregnancy?


Peg Plumbo CNM

Peg Plumbo has been a certified nurse-midwife (CNM) since 1976. She has assisted at over 1,000 births and currently teaches in the... Read more

There are many dangers associated with cocaine use during pregnancy. Cocaine use in pregnant women can cause spontaneous abortion (38 percent); placental abruption (2 to 15 percent); placenta previa (2 percent); and an increased incidence of stillbirths, as the result of placental abruption (8 percent). The increased incidence of spontaneous abortions among pregnant women who use cocaine is due to an increase in maternal plasma norepinephrine, which increases uterine contractility, constricts placental vessels, and decreases blood flow to the fetus. Even when cocaine use is limited to the first trimester of pregnancy, the incidence of placental abruption is increased, in comparison with pregnant women who do not use cocaine.

Cocaine stimulates uterine contractions. The risk of premature rupture of membranes and preterm labor is significantly increased among pregnant women who use cocaine. Preterm delivery (giving birth at 37 weeks or earlier) has been found to occur in 17 to 29 percent of these pregnancies.

The most frequent consequences to the fetus of in utero cocaine exposure are intrauterine growth restriction (IUGR) and low birth weight. 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. Low birth weight (under 2500 gm or five pounds) has been found to occur in 22 to 34 percent of all infants exposed to cocaine in utero.

Cocaine also significantly suppresses the mother-to-be's appetite, which contributes to poor maternal and fetal nutrition. 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. Higher than expected concentrations of cocaine (and its metabolite norcocaine) occur in the fetus for any given intake of cocaine by the mother. This is because cocaine rapidly crosses the placenta (and fetal and maternal blood concentrations of cocaine rapidly becomes similar); the metabolism of cocaine and excretion of metabolites is prolonged in the mother and fetus; and pregnant women metabolize cocaine to the pharmacologically active norcocaine to a much greater extent than do women who are not pregnant.

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.

Following the birth, withdrawal symptoms are experienced in 31 percent of newborns exposed to cocaine in utero. These include seizures, depression, lethargy, feeding problems, hyperactive reflexes, vomiting, diarrhea, high-pitched cry, and restlessness. These symptoms may indicate damage to the central nervous system that may prevail throughout life.

On long-term follow-up, cocaine-exposed infants demonstrate significant cognitive and developmental delay.

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