Medical Complications of Cocaine Abuse

Cregler, Louis L.; Mark, Herbert

doi:10.1056/nejm198612043152327

Cited by 744 publications

(179 citation statements)

References 61 publications

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“…Poorer cognitive and motor outcomes are consistent with cocaine's known actions on neurotransmitter systems during fetal growth, which may interfere with neuronal development (Cregler and Mark, 1986;Volpe, 1992). Cocaine may also indirectly affect cognitive and motor functions through several other mechanisms, including vascular disruption leading to uterine hypoxia (Wood, Plessinger, & Clark, 1989), nutritional deficits associated with fetal growth retardation (Frank et al, 1990;Hadeed & Siegal, 1989;Lester et al, 1991;Singer, Arendt, Song, Warshawsky, & Kliegman, 1994;Zuckerman et al, 1989), and an increased incidence of subtle brain lesions (Chasnoff, Bussey, Savic, & Stack, 1986;Frank, McCarten, Cabral, Levinson, & Zuckerman, 1994;.…”

Section: Discussionmentioning

confidence: 85%

Relationship of prenatal cocaine exposure and maternal postpartum psychological distress to child developmental outcome

et al. 1997

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Maternal cocaine use during pregnancy can affect the infant directly through toxic effects or indirectly through cocaine's influence on maternal psychological status. We followed 160 cocaine exposed and 56 nonexposed infants and their mothers identified at birth through interview and/or urine screen. Although cocaine exposure defined the groups, infant exposure to alcohol, marijuana, and tobacco was allowed to vary. Infants were 99% African American and poor. All mothers completed the Brief Symptom Inventory (BSI) and infants were given the Bayley Scales of Mental (MDI) and Motor (PDI) Development at a mean corrected age of 17 ± 8 months. Both MDIs (94 ± 17 vs. 103 ± 16) and PDIs (101 ± 16 vs. 108 ± 12) were lower for cocaine exposed infants. Psychological distress was greater in cocaine using mothers. Hierarchical multiple regression was used to assess the relative effects of gestational age, maternal psychological distress, and cocaine and polydrug exposure on infant outcomes. Both psychological distress and cocaine and alcohol exposure predicted lower MDIs after controlling for prematurity. Neither psychological distress nor alcohol exposure predicted motor outcome, while cocaine had a significant effect. Tobacco and marijuana exposure were unrelated to outcome. These findings provide further support for direct effects of cocaine and alcohol on infant development, as well as highlight the need for studies to document maternal psychological factors, which may increase child risk for poorer outcomes.

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Section: Discussionmentioning

confidence: 85%

Relationship of prenatal cocaine exposure and maternal postpartum psychological distress to child developmental outcome

et al. 1997

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“…These characteristics include absent, late, or inadequate prenatal care; a previously documented or admitted history of drug abuse; a previous unexplained late fetal demise; precipitous labor; abruptio placentae; hypertensive episodes; severe mood swings; cerebrovascular accidents; myocardial infarction; and repeated spontaneous abortions. 80,[83][84][85][86][87][88] The legal implications of testing and the need for consent from the mother may vary among the states. 89 Each hospital should consider adopting a policy for maternal and newborn screening to avoid discriminatory practices and to comply with local laws.…”

Section: Differential Diagnosismentioning

confidence: 99%

Neonatal Drug Withdrawal

Hudak¹,

Tan²,

Frattarelli³

et al. 2012

Pediatrics

738

608

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Maternal use of certain drugs during pregnancy can result in transient neonatal signs consistent with withdrawal or acute toxicity or cause sustained signs consistent with a lasting drug effect. In addition, hospitalized infants who are treated with opioids or benzodiazepines to provide analgesia or sedation may be at risk for manifesting signs of withdrawal. This statement updates information about the clinical presentation of infants exposed to intrauterine drugs and the therapeutic options for treatment of withdrawal and is expanded to include evidence-based approaches to the management of the hospitalized infant who requires weaning from analgesics or sedatives.

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“…The phenomenon of "cocaine abuse" by pregnant women received widespread media attention due to observations of serious, life-endangering consequences for the mother and fetus (Burkett et al, 1990;Critchley et al, 1988;Henderson and Torbey, 1988;Mercado et al, 1989;Morild and Stajic, 1990). Known catastrophic cardiovascular and central nervous system effects of cocaine use in adults (Cregler and Mark, 1986;Farrar and Kearns, 1989;Gawin and Ellinwood, 1988;Tarr and Macklin, 1987) clearly raised concerns that maternal use of cocaine, especially crack cocaine, would cause long-term, irreparable damage to the developing infant and young child. However, numerous limitations in study design among the earliest published studies on the effects of in utero cocaine exposure have been noted and results have been inconsistent for most aspects of infant and child developmental outcomes (Bandstra and Burkett, 1991;Carmichael Olson and Toth, 1999;Frank et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

Severity of Prenatal Cocaine Exposure and Child Language Functioning Through Age Seven Years: A Longitudinal Latent Growth Curve Analysis

Bandstra

Vogel

Morrow

et al. 2004

Substance Use & Misuse

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The current study estimates the longitudinal effects of severity of prenatal cocaine exposure on language functioning in an urban sample of full-term African-American children (200 cocaineexposed, 176 noncocaine-exposed) through age 7 years. The Miami Prenatal Cocaine Study sample was enrolled prospectively at birth, with documentation of prenatal drug exposure status through maternal interview and toxicology assays of maternal and infant urine and infant meconium. Language functioning was measured at ages 3 and 5 years using the Clinical Evaluation of Language Fundamentals-Preschool (CELF-P) and at age 7 years using the Core Language Domain of the NEPSY: A Developmental Neuropsychological Assessment. Longitudinal latent growth curve analyses were used to examine two components of language functioning, a more stable aptitude for language performance and a time-varying trajectory of language development, across the three time points and their relationship to varying levels of prenatal cocaine exposure. Severity of prenatal cocaine exposure was characterized using a latent construct combining maternal self-report of cocaine use during pregnancy by trimesters and maternal and infant bioassays, allowing all available information to be taken into account. The association between severity of exposure and language functioning was examined within a model including factors for fetal growth, gestational age, and IQ as intercorrelated response variables and child's age, gender, and prenatal alcohol, tobacco, and marijuana exposure as covariates. Results indicated that greater severity of prenatal cocaine exposure was associated with greater deficits within the more stable aptitude for language performance (D = −0.071, 95% CI = −0.133, −0.009; p = 0.026). There was no relationship between severity of prenatal cocaine exposure and the time-varying trajectory of language development. The observed cocaineassociated deficit was independent of multiple alternative suspected sources of variation in language performance, including other potential responses to prenatal cocaine exposure, such as child's intellectual functioning, and other birth and postnatal influences, including language stimulation in the home environment.

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Medical Complications of Cocaine Abuse

Cited by 744 publications

References 61 publications

Relationship of prenatal cocaine exposure and maternal postpartum psychological distress to child developmental outcome

Relationship of prenatal cocaine exposure and maternal postpartum psychological distress to child developmental outcome

Neonatal Drug Withdrawal

Severity of Prenatal Cocaine Exposure and Child Language Functioning Through Age Seven Years: A Longitudinal Latent Growth Curve Analysis

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