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Pregnancy & Baby 

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Cocaine use during pregnancy

There are many dangers associated with cocaine use during pregnancy. Cocaine use in pregnant women can cause spontaneous abortion (38%); placental abruption (two to 15%); placenta previa (two per cent); and an increased incidence of stillbirth as the result of placental abruption (eight per cent). The increased incidence of spontaneous abortions among pregnant women who use cocaine is caused by an increase in maternal plasma norepinephrine, which heightens uterine contractility, constricts placental vessels and lessens blood flow to the foetus. 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 the membranes and premature labour is significantly increased among pregnant women who use cocaine. Premature delivery (giving birth at 37 weeks or earlier) has been found to occur in 17 to 29% of these pregnancies.

The most frequent consequences to the foetus 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 the constriction of the uterine blood vessels. This reduces blood flow and impairs oxygen and nutrient transfer to the foetus. Low birth weight (under 2500 grams or five pounds) occurs in 22 to 34% of all infants exposed to cocaine in utero.

Cocaine also significantly suppresses the appetite, which contributes to poor maternal and foetal nutrition. In addition, in utero cocaine exposure depresses neo-natal fat stores and diminishes body mass.

Maternal cocaine use may have direct as well as indirect effects on the foetus. Cocaine crosses the placenta by simple diffusion. Higher than expected concentrations of cocaine (and its metabolite norcocaine) occur in the foetus for any given intake of cocaine by the mother. This is because cocaine rapidly crosses the placenta (and foetal and maternal blood concentrations of cocaine rapidly become similar); the metabolism of cocaine and excretion of metabolites is prolonged in the mother and foetus; and pregnant women metabolise cocaine to the pharmacologically active norcocaine to a much greater extent than do women who are not pregnant.

Congenital anomalies occur in seven to 26% of babies exposed to cocaine in utero. Cocaine can adversely affect embryonic and foetal development through interruption of uterine, placental and foetal blood flow. Evidence of brain malformation or haemorrhage is discovered in approximately 35% of babies exposed to cocaine in utero. Foetal cardiovascular abnormalities caused by maternal use of cocaine have been reported to occur in four to 40% of babies exposed to cocaine in utero. Defects or disruption of urinary and genital development have been found in 14% of babies exposed to cocaine in utero.

Following the birth, withdrawal symptoms are experienced by 31% of newborn infants exposed to cocaine in utero. These include seizures, depression, lethargy, feeding problems, hyperactive reflexes, vomiting, diarrhoea, high﷓pitched crying and restlessness. These symptoms may indicate damage to the central nervous system that may prevail throughout life.

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

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