Fetal effects of crack

Although no single approach can accurately determine the presence or amount of drug used during pregnancy, it is more likely that fetal exposure will be identified if a biological specimen is collected along with a structured interview.

Self-reported history is an inexpensive and practical method for identifying prenatal drug exposure and is the only method available in which information can be obtained regarding the timing of the drug use during pregnancy and the amount used. Unfortunately, self-report suffers from problems with the veracity of the informant and recall accuracy. Several biological specimens can be used to screen for drug exposure. Each specimen has its own individual variations with regard to the window of detection, the specific drug metabolites used for identification, methods of adulteration of the sample, and analytical techniques, thus altering the sensitivity and specificity for each drug of interest.

The most common analytical method used for screening biological specimens is an immunoassay designed to screen out drug-free samples. Threshold values generally are set high to minimize false-positive test results but may be too high to detect low-dose or remote exposure. In addition, confirmation of the presence of a drug is not always associated with drug abuse. Alternative explanations include passive exposure to the drug, ingestion of other products contaminated with the drug, or use of prescription medications that either contain the drug or are metabolized to the drug.

Urine testing identifies only recent drug use, because threshold levels of drug metabolites generally can be detected in urine only for several days. A notable exception to this is marijuana, the metabolites of which can be excreted for as long as 10 days in the urine of regular users 15 or up to 30 days in chronic, heavy users. Urine is a good medium as well for the detection of nicotine, opiate, cocaine, and amphetamine exposure. Meconium is also easy to collect noninvasively.

It is hypothesized that drugs accumulate in meconium throughout pregnancy, and thus, meconium is thought to reflect exposure during the second and third trimester of pregnancy when meconium forms. However, use of meconium to determine the timing or extent of exposure during pregnancy is controversial 18 because of a lack of studies regarding the effects of the timing and quantity of the postpartum specimen collection as well as the effects of urine or transitional stool contamination of the meconium samples.

Hair is easy to collect, although some people decline this sampling method because of cosmetic concerns and societal taboos.

Drugs become trapped within the hair and, thus, can reflect drug use over a long period of time. Unfortunately, using hair to determine timing and quantity of exposure also is controversial. In addition, environmental contamination, natural hair colors and textures, cosmetic hair processing, and volume of the hair sample available all affect the rational interpretation of the results.

Other biological specimens have been studied for use in the detection of in utero drug exposure but are not commonly used in the clinical setting. These include such specimens as cord blood, human milk, amniotic fluid, and umbilical cord tissue.

In , the Keeping Children and Families Safe Act Public Law was passed by Congress, requiring physicians to notify their state child protective services agency of any infant identified as affected by illegal substances at birth or experiencing drug withdrawal. Currently, issues of whether to use biological specimens to screen for drug abuse; whether to screen the mother, her infant, or both; and which women and infants to screen are issues complicated by legal, ethical, social, and scientific concerns.

Each of these concerns must be taken into account as obstetricians, neonatologists, and pediatricians work to develop protocols for identifying prenatal drug exposure. Targeted screening of high-risk women is problematic, because it can be biased toward women of racial or ethnic minorities and those who are economically disadvantaged or socially disenfranchised. Universal screening of pregnant women is impractical and not cost-effective.

Drugs can affect the fetus in multiple ways. Early in gestation, during the embryonic stage, drugs can have significant teratogenic effects.

These are considered to be the direct effects of drugs. However, drugs also can exert a pharmacologic effect on the mother and, thus, indirectly affect the fetus.

Drugs of abuse mimic naturally occurring neurotransmitters, such that marijuana acts as anandamides, opiates act as endorphins, and cocaine and stimulants act within the mesolimbic dopaminergic pathways to increase dopamine and serotonin within the synapses.

Nicotine concentrations are higher in the fetal compartment placenta, amniotic fluid, fetal serum compared with maternal serum concentrations. Although the exact mechanisms by which nicotine produces adverse fetal effects are unknown, it is likely that hypoxia, undernourishment of the fetus, and direct vasoconstrictor effects on the placental and umbilical vessels all play a role.

Ethanol easily crosses the placenta into the fetus, with a significant concentration of the drug identified in the amniotic fluid as well as in maternal and fetal blood. These include direct teratogenic effects during the embryonic and fetal stage of development as well as toxic effects of alcohol on the placenta, altered prostaglandin and protein synthesis, hormonal alterations, nutritional effects, altered neurotransmitter levels in the brain, altered brain morphology and neuronal development, and hypoxia thought to be attributable to decreased placental blood flow and alterations in vascular tone in the umbilical vessels.

In addition, smoking marijuana produces as much as 5 times the amount of carbon monoxide as does cigarette smoking, perhaps altering fetal oxygenation. In humans, opiates rapidly cross the placenta, with drug equilibration between the mother and the fetus. Pharmacologic studies of cocaine in animal models using a variety of species have demonstrated that cocaine easily crosses both the placenta and the blood-brain barrier and can have significant teratogenic effects on the developing fetus, directly and indirectly.

Thus, functions such as arousal, attention, and memory may be adversely affected by prenatal cocaine exposure. Thus, cocaine exposure occurring during development of the nervous system might be expected to result in permanent changes in brain structure and function, which can produce altered responsiveness to environmental or pharmacologic challenges later in life.

Methamphetamine is a member of a group of sympathomimetic drugs that stimulate the central nervous system. It readily passes through the placenta and the blood-brain barrier and can have significant effects on the fetus.

It is possible that the mechanism of action of methamphetamine is an interaction with and alteration of these neurotransmitter systems in the developing fetal brain as well as alterations in brain morphogenesis.

Fetal tobacco exposure has been a known risk factor for low birth weight and intrauterine growth restriction for more than 50 years, with decreasing birth weight shown to be related to the number of cigarettes smoked. An independent effect of prenatal cocaine exposure on intrauterine growth has been the most consistent finding across studies of prenatally exposed infants. However, the literature available is limited at this time. Several reviews on the effects of prenatal drug exposure on growth contain additional details.

Nicotine has been associated with oral facial clefts in exposed newborn infants, , — although the data are relatively weak. There is a vast literature on the teratogenic effects of prenatal alcohol exposure after the first description of fetal alcohol syndrome in However, Little et al reported no increase in the frequency of major anomalies in a small sample of exposed infants when compared with nonexposed infants.

No convincing studies are available that document a neonatal withdrawal syndrome for prenatal nicotine exposure. Although several authors describe abnormal newborn behavior of exposed infants immediately after delivery, the findings are more consistent with drug toxicity, which steadily improves over time, , as opposed to an abstinence syndrome, in which clinical signs would escalate over time as the drug is metabolized and eliminated from the body.

There is 1 report of withdrawal from prenatal alcohol exposure in infants with fetal alcohol syndrome born to mothers who drank heavily during pregnancy, but withdrawal symptoms have not been reported in longitudinal studies available in the extant literature. Neonatal abstinence symptoms have not been observed in marijuana-exposed infants, although abnormal newborn behavior has been reported with some similarities to that associated with narcotic exposure.

Neonatal abstinence syndrome includes a combination of physiologic and neurobehavioral signs that include such things as sweating, irritability, increased muscle tone and activity, feeding problems, diarrhea, and seizures. Infants with neonatal abstinence syndrome often require prolonged hospitalization and treatment with medication. Methadone exposure has been associated with more severe withdrawal than has exposure to heroin.

The AAP clinical report on neonatal drug withdrawal contains in-depth information on neonatal drug withdrawal, including treatment options. Abnormalities of newborn neurobehavior, including impaired orientation and autonomic regulation and abnormalities of muscle tone, , , have been identified in a number of prenatal nicotine exposure studies.

Poor habituation and low levels of arousal along with motor abnormalities have been identified in women who drank alcohol heavily during their pregnancy. Using the Brazelton Newborn Behavioral Assessment Scale, reported effects of prenatal cocaine exposure on infants have included irritability and lability of state, decreased behavioral and autonomic regulation, and poor alertness and orientation.

Few sources are available documenting the prevalence of drug use during breastfeeding. Women who used various amounts of alcohol or marijuana and moderate amounts of cocaine during their pregnancy were not deterred from breastfeeding their infants. Thus, the pediatrician is faced with weighing the risks of exposing an infant to drugs during breastfeeding against the many known benefits of breastfeeding.

For most street drugs, including marijuana, opiates, cocaine, and methamphetamine, the risks to the infant of ongoing, active use by the mother outweigh the benefits of breastfeeding, because most street drugs have been shown to have some effect on the breastfeeding infant. Nicotine is secreted into human milk , and has been associated with decreased milk production, decreased weight gain of the infant, and exposure of the infant to environmental tobacco smoke.

Heavy alcohol use has been shown to be associated with decreased milk supply and neurobehavioral effects on the infant. Marijuana has an affinity for lipids and accumulates in human milk, as can cocaine 26 and amphetamines. Several available reviews provide more detailed information with regard to breastfeeding and substance abuse.

The effects of prenatal tobacco exposure on long-term growth are not clear-cut. Reports in the literature of effects on height and weight , — have not been substantiated by research teams able to control for other drug use in the sample.

Although poor growth is 1 of the hallmarks of fetal alcohol syndrome, it is the least sensitive of the diagnostic criteria. Although several studies document the negative effects of prenatal cocaine exposure on postnatal growth, , — others do not. However, 1 study of unspecified amphetamine use suggests that in utero exposure may be associated with poor growth throughout early childhood.

After controlling for a variety of potentially confounding socioeconomic, psychosocial, family, and health variables, a number of studies have identified independent effects of prenatal tobacco exposure on long-term behavioral outcomes extending from early childhood into adulthood.

For example, impulsivity and attention problems have been identified in children prenatally exposed to nicotine. Kelly et al published an in-depth review of the effects of prenatal alcohol exposure on social behavior. Inattention and impulsivity at 10 years of age have been associated with prenatal marijuana exposure.

However, 1 study of unspecified amphetamine use during pregnancy suggests a possible association with externalizing behaviors and peer problems. The link between prenatal nicotine exposure and impaired cognition is not nearly as strong as the link with behavioral problems. However, studies of both young and older children prenatally exposed to nicotine have revealed abnormalities in learning and memory , and slightly lower IQ scores.

Although IQ scores are lower in alcohol-exposed offspring, , they can be variable. Additionally, prenatal alcohol exposure has been associated with poorer memory and executive functioning skills.

Although developmental scores tend to be lower in exposed infants, these differences no longer exist when appropriate medical and environmental controls are included in the analyses. Poor language development in early childhood after prenatal nicotine exposure has been reported, , , as have poor language and reading abilities in 9- to year-olds.

The literature available evaluating academic achievement is limited. In nicotine-exposed children, Batstra et al identified poorer performance on arithmetic and spelling tasks that were part of standardized Dutch achievement tests. Howell et al reported poorer performance in mathematics on achievement tests in adolescents who had been exposed prenatally to alcohol.

Streissguth et al describe a variety of significant academic and school problems related to prenatal alcohol exposure, primarily associated with deficits in reading and math skills throughout the school years. Reported effects of cocaine exposure on school achievement are variable. However, other studies do not support significant cocaine effects on school achievement.

Cernerud et al reported on 65 children prenatally exposed to amphetamines. At 14 to 15 years of age, the children in their cohort scored significantly lower on mathematics tests than did their classmates who were not exposed to amphetamines prenatally and had a higher rate of grade retention than the Swedish norm. A limited number of studies are available that have investigated the association between prenatal substance exposure and subsequent drug abuse in exposed offspring.

These studies did not document cause and effect, and it remains to be determined how much of the association can be linked to prenatal exposure versus socioeconomic, environmental, and genetic influences. Studies available for prenatal nicotine exposure suggest an increased risk of early experimentation and abuse of nicotine in exposed offspring. Mounting clinical data support an increased risk of ethanol abuse later in life after prenatal exposure. Although methodologic differences between studies and limited data in the extant literature make generalization of the results for several of the drugs difficult, some summary statements can be made by using the current knowledge base Table 2.

The negative effect of prenatal nicotine exposure on fetal growth has been known for decades; however, longitudinal studies do not reveal a consistent effect on long-term growth. Clinical studies have failed to reach a consensus regarding congenital anomalies, and there is no evidence of a withdrawal syndrome in the newborn infant.

Recent studies document a negative effect of prenatal exposure on infant neurobehavior as well as on long-term behavior, cognition, language, and achievement. Alcohol remains the most widely studied prenatal drug of abuse, and the evidence is strong for fetal growth problems, congenital anomalies, and abnormal infant neurobehavior.

There has been no convincing evidence of a neonatal withdrawal syndrome. Ongoing longitudinal studies continue to document long-term effects on growth, behavior, cognition, language, and achievement, and alcohol is the most common identifiable teratogen associated with intellectual disability. Although there have been studies revealing subtle abnormalities in infant neurobehavior related to prenatal marijuana exposure, there have been no significant effects documented for fetal growth, congenital anomalies, or withdrawal.

Long-term studies reveal effects of prenatal exposure on behavior, cognition, and achievement but not on language or growth. The most significant effect of prenatal opiate exposure is neonatal abstinence syndrome. There have been documented effects on fetal growth but not on long-term growth and infant neurobehavior as well as long-term effects on behavior. There is not a consensus as to the effects of prenatal opiate exposure on cognition, and few data are available regarding language and achievement.

Prenatal cocaine exposure has a negative effect on fetal growth and subtle effects on infant neurobehavior. However, there is little evidence to support an association with congenital anomalies or withdrawal. There is not a consensus regarding the effects of prenatal cocaine exposure on either long-term growth or achievement; however, there are documented long-term effects on behavior and subtle effects on language.

Although there is little evidence to support an effect on overall cognition, a number of studies have documented effects on specific areas of executive function. Studies on prenatal methamphetamine exposure are still in their infancy. Early studies have documented an effect of prenatal exposure on fetal growth and infant neurobehavior but no association with congenital anomalies and no data regarding infant withdrawal or any long-term effects.

This document is copyrighted and is property of the American Academy of Pediatrics and its Board of Directors. All authors have filed conflict of interest statements with the American Academy of Pediatrics. Any conflicts have been resolved through a process approved by the Board of Directors. The American Academy of Pediatrics has neither solicited nor accepted any commercial involvement in the development of the content of this publication.

The guidance in this report does not indicate an exclusive course of treatment or serve as a standard of medical care. Variations, taking into account individual circumstances, may be appropriate.

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Close mobile search navigation Article navigation. Volume , Issue 3. Previous Article Next Article. Identification of Prenatal Exposure. Mechanisms of Action of Drugs on the Fetus. Medical Issues in the Newborn Period. Fetal Growth. Congenital Anomalies. Predisposed to Own Drug Use. Lead Authors. Committee on Substance Abuse, — Placental oxidative stress and classical parameters of maternal and fetal evaluation were studied, in addition to the morphometric analysis of the fetal metamers.

Even in the absence of changes in body weight gain and feed intake, crack altered the reproductive performance of dams. Exposure to the drug promoted late closure of the fetal fontanel. Privacy Copyright. Examining the effects of fetal "crack" cocaine exposure on the development of infants during the neonatal period Israel Feliciano , Pace University Abstract This study was conducted in an effort to assess the possible teratogenic effects of fetal exposure to "crack" cocaine on the development of infants during the neonatal period.

Subject Area Cellular biology Obstetrics Gynecology Toxicology Recommended Citation Feliciano, Israel, "Examining the effects of fetal "crack" cocaine exposure on the development of infants during the neonatal period" View More. Search Enter search terms:.