Cocaine

From: Exposure to Psychotropic Medications and Other Substances during Pregnancy and Lactation: A Handbook for Health Care Providers

On this page:

Summary and recommendations
Fetal effects
Neonatal effects
Long-term effects on the child
Breastfeeding
Withdrawal effects on the mother

Street names

Blow, C, coke, dust, flake, powder lines, snow

Crack cocaine: freebase, rock

Cocaine is a stimulant that readily crosses the placenta.¹ Cocaine hydrochloride, a white crystalline powder, can be snorted or injected. Powder cocaine can also be chemically changed to create crystals or “rocks”—known as “freebase” or “crack”—that can be smoked.

Most women who use cocaine use at least one other drug (e.g., alcohol, tobacco, cannabis)² and have other risk factors related to poor pregnancy outcome, including poor nutrition, high gravidity and lack of prenatal care.³

Summary and Recommendations

Abstinence from cocaine use throughout pregnancy is recommended. However, discontinuing cocaine at any time during pregnancy can improve the fetal outcome.
Careful monitoring of neonates is recommended; comfort measures, especially touch, reduced stimulation (e.g., a quiet room with dim lighting, no excessive testing, keeping interventions to a minimum) and breastfeeding, are generally sufficient.
Breastfeeding while using cocaine is not recommended. If a woman uses cocaine, she should not breastfeed within three days of using the drug (i.e., she should pump and discard the milk). The risks of breastfeeding while using cocaine must be weighed against the overall benefits of breastfeeding.

Fetal effects

Women who use cocaine during pregnancy are more likely than those who do not use the drug to have placental abruption (which may cause fetal hypoxia and ischemia) and preterm premature rupture of membranes.³ When cocaine crosses the placenta into the fetus’s circulation, fetal hypertension and increased cardiac output could also increase the risk of intracranial lesions and hemorrhage.¹

An infant prenatally exposed to cocaine is more likely than non-exposed infants to be born prematurely and to have intrauterine growth retardation (IUGR), lower birth weight and a smaller head circumference.^4–6

In addition, the combination of cocaine with other fetotoxins (e.g., cigarette smoke and/or alcohol) may result in a negative synergistic effect. For example, one study found that the percentage of babies weighing less than 2,500 grams at birth (i.e., low birth weight) was significantly higher among mothers who combined cocaine and cigarettes (50 per cent) than among those who used cocaine alone (eight per cent). Also, the infants exposed in utero to cocaine and tobacco were, on average, 500 grams smaller than those exposed to cocaine alone.⁷

Another study⁸ compared three groups of women: one group used cocaine throughout pregnancy, a second group used cocaine during the first trimester only and a third group did not use cocaine at all. Women who used cocaine in only the first trimester experienced placental abruption more frequently than women who did not use cocaine at all, but had similar rates of preterm delivery and low-birth-weight and IUGR infants to those of women who did not use cocaine. The effects of use were more significant in the women who used cocaine throughout their pregnancies—they were significantly more likely (25 per cent) than the drug-free controls (five per cent) to deliver low-birth-weight infants.⁸

Major malformations

While there is no established cause-and-effect relationship between prenatal cocaine exposure and increased major malformations, there is enough evidence to suggest that cocaine use during pregnancy is a significant concern for maternal and fetal effects.⁹ A meta-analysis¹⁰ of 20 papers compared (i) women who used only cocaine versus a control group of women who did not use substances, (ii) women with polysubstance use involving cocaine versus a control group of women who did not use substances and (iii) women with polysubstance use that included cocaine versus women with polysubstance use that did not include cocaine. The meta-analysis found a significantly greater likelihood of neonatal genitourinary malformations in cocaine-exposed infants,¹⁰ which appears to be dose related.¹¹ Other studies^9,12 did not observe any other congenital abnormalities in cocaine-exposed infants.

Spontaneous abortion

A meta-analysis reported an increase in spontaneous abortions in women who used cocaine, even when there was control for polysubstance use.¹⁰

Neonatal effects

Infants exposed in utero to cocaine may have significant neurobehavioural impairments during the neonatal period; they usually occur on days two and three.¹³ An increased degree of irritability, tremulousness and muscular rigidity have been observed; gastrointestinal symptoms (e.g., vomiting, diarrhea) and seizures have also been reported.¹² All of these effects seem to be more consistent with cocaine exposure rather than with cocaine withdrawal.^13,14

Long-term effects on the child

Long-term effects of maternal cocaine use on children are not known. Language delays (i.e., delays in expressive and verbal comprehension) and behavioural problems may be encountered at school.^15,16 Two primary risk factors that are also associated with cocaine use are poor maternal functioning and an inadequate caring environment.¹⁷

One study¹⁸ followed children of 28 women who reported light to moderate cocaine use (i.e., an average of 3.3 grams per month [approximately 3.7 lines per day]) during their first trimester. The children were examined at delivery and at eight months, 18 months, three years and six years of age. The comparison group consisted of 523 women who used no cocaine for the entire duration of the study as well as the year before pregnancy. The study only reported on the status of the children at the six-year mark, at which time no significant effects of prenatal cocaine exposure on growth, intellectual ability, academic achievement or teacher-rated classroom behaviour were reported. (Note: More of the women in this study who used cocaine were working or attending school; their monthly income was also higher than the income of those in the comparison group.)

A more recent study showed that potential long-term risks for the child are more closely related to low birth weight and the environmental risks associated with cocaine exposure in the caregiving environment, than to cocaine exposure itself.⁹

Breastfeeding

Cocaine passes into breast milk, and both powder cocaine and crack have been known to cause the baby to experience irritability, trembling, vomiting, diarrhea and seizures.¹² However, there are no known data to confirm this and the percentage dose in breast milk is unknown.

Withdrawal effects on the mother

About 10 per cent of people who use cocaine meet the diagnostic criteria for cocaine dependence.¹⁹ Symptoms of withdrawal may include fatigue, nightmares, insomnia, increased appetite, anxiety, psychomotor agitation or retardation, and dysphoric mood. Withdrawal from cocaine is primarily a psychological process, and can be safely undertaken. Women should be provided supportive care and monitored for suicidal ideation.

People who have been bingeing on cocaine will sometimes sleep heavily for one or two days after the binge. They may then experience several weeks or months of depression and insomnia, with vivid dreams and strong cravings for cocaine. Medical treatments have not yet been shown to be effective for cocaine withdrawal or cravings.

References

Plessinger, M.A. & Woods, J.R. (1998). Cocaine in pregnancy: Recent data on maternal and fetal risks. Obstetrics and Gynecology Clinics of North America, 25 (1), 99–118.
Gingras, J.L. & O’Donnell, K. (1998). State control in the substance-exposed fetus. I. The fetal neurobehavioral profile: An assessment of fetal state, arousal, and regulation competency. Annals of the New York Academy of Sciences, 846, 262–276.
Sprauve, M.E., Lindsay, M.K., Herbert, S. & Graves, W. (1997). Adverse perinatal outcome in parturients who use crack cocaine. Obstetrics & Gynecology, 89 (5 Pt. 1), 674–678.
Kliegman, R.M., Madura, D. & Kiwi, R. (1994). Relation of maternal cocaine use to the risks of prematurity and low birth weight. Journal of Pediatrics, 124 (5 Pt. 1), 751–756.
Bateman, D.A., Ng, S.K., Hansen, C.A. & Heagarty, M.C. (1993). The effects of intrauterine cocaine exposure in newborns. American Journal of Public Health, 83 (2), 190–193.
Eyler, F.D., Behnke, M., Conlon, M., Woods, N.S. & Frentzen, B. (1994). Prenatal cocaine use: A comparison of neonates matched on maternal risk factors. Neurotoxicology and Teratology, 16 (1), 81–87.
Forman, R., Klein, J., Meta, D., Barks, J., Greenwald, M. & Koren, G. (1993). Maternal and neonatal characteristics following exposure to cocaine in Toronto. Reproductive Toxicology, 7 (6), 619–622.
Chasnoff, I.J., Griffith, D.R., MacGregor, S., Dirkes, K. & Burns, K.A. (1989). Temporal patterns of cocaine use in pregnancy: Perinatal outcome. Journal of the American Medical Association, 261 (12), 1741–1744.
Messinger, D.S., Bauer, C.R., Das, A., Seifer, R., Lester, B.M., Lagasse, L.L. et al. (2004). The maternal lifestyle study: Cognitive motor and behavioral outcomes of cocaine-exposed and opiate-exposed infants through three years of age. Pediatrics, 113 (6) 1677–1685.
Lutiger, B., Graham, K., Einarson, T.R. & Koren, G. (1991). Relationship between gestational cocaine use and pregnancy outcome: A meta-analysis. Teratology, 44 (4), 405–414.
Chiriboga, C.A., Brust, J.C., Bateman, D. & Hauser, W.A. (1999). Dose-response effect of fetal cocaine exposure on newborn neurologic function. Pediatrics, 103 (1), 79–85.
Briggs, G.G., Freeman, R.K. & Yaffe, S.J. (2002). Drugs in Pregnancy and Lactation: A Reference Guide to Fetal and Neonatal Risk (6th ed.). Philadelphia, PA: Lippincott Williams & Wilkins.
American Academy of Pediatrics Committee on Drugs. (1998). Neonatal drug withdrawal. Pediatrics, 101 (6), 1079–1088.
Bauer, C.R., Langer, J.L., Shankaran, S., Bada, H.S., Lester, B., Wright, L. et al. (2005). Acute neonatal effects of cocaine exposure during pregnancy. Archives of Pediatrics and Adolescent Medicine, 159 (9), 824–834.
Delaney-Black, V., Covington, C., Templin, T., Kershaw, T., Nordstrom-Klee, B., Ager, J. et al. (2000). Expressive language development of children exposed to cocaine prenatally: Literature review and report of a prospective cohort study. Journal of Communication Disorders, 33 (6), 463–480; Quiz 480–481.
Nulman, I., Rovet, J., Greenbaum, R., Loebstein, M., Wolpin, J., Pace-Asciak, P. et al. (2001). Neurodevelopment of adopted children exposed in utero to cocaine: The Toronto Adoption Study. Clinical and Investigative Medicine, 24 (3), 129–137.
Lester, B.M. (2000). Prenatal cocaine exposure and child outcome: A model for the study of the infant at risk. The Israel Journal of Psychiatry and Related Sciences, 37 (3), 223–235.
Richardson, G.A., Conroy, M.L. & Day, N.L. (1996). Prenatal cocaine exposure: Effects on the development of school-age children. Neurotoxicology and Teratology, 18 (6), 627–634.
O’Grady, C.P. & Skinner, W.J.W. (2007). A Family Guide to Concurrent Disorders. Toronto: Centre for Addiction and Mental Health.