- Email: [email protected]
Fetal and Neonatal Effects of Maternal Cocaine Use
HEATHER PETERS, RN, MSN C A T H E R I N E J U R S I C H THEORELL, R N C , M S N
Fetal and Neonatal Eflects of Maternal Cocaine Use
Marijuana was the drug of the 1960s and herotn the drug of the 1970s. Cocaine was the popular drug of the 1980s, and cocaine’s populartty appears to have contlnued tnto the 1990s. Cocaine use tncreased dramatically between 1974 and 1985. This article reviews the trends of cocaine use, fetal and maternal pharmacodynamics of cocatne, intrautertne effects of cocaine on the fetus, and the neonatal mangestatdons of cocaine exposure. Accepted: May 1990
March/April 1991
on the street and was often referred to as the “champagne of drugs.” Since the 1970s, however, cocaine has become less expensive, more available, and purer. The number of people using cocaine increased from 5.4 million in 1974 to 22.2 million in 1985.’ In recent years, the Colombian drug carteis have been successful in greatly expanding coca-leaf production and processing.* Currently, cocaine enters the United States mainly through Miami from Colombia, Peru, and Bolivia. From Miami, cocaine is distributed in a number of different forms to rural and metropolitan areas. Consequently, cocaine is now used by more people than ever. Beginning in the late 1970s, the dosages of cocaine increased. For example, between 1970 and 1978, recreational users inhaled intranasal doses of 1-4 grams per month, whereas from 1978 to 1982, they used 1-3 grams per week. In addition to taking cocaine intranasally, smoking the alkaloid form known as crack has become increasingly popular. The frequency of experimental practices with cocaine, such as taking cocaine free base intranasally and smoking coca paste, rose during the early 1 9 8 0 ~ ~ Demographic studies describe the typical cocaine user as a young man with a higher-than-average income and a high level of responsibilitywho is a professional in a position of authority. Cocaine use is most prevalent among young white men (aged 18-25 years) residing in the western and northeastern areas of the United state^.^ Similar to users of other types of drugs, cocaine users have a greater tendency to abuse more than one substance;*for instance, cocaine is often used in combination with marijuana. Many young adult users use cocaine occasionally and alcohol or marijuana more frequently. Cocaine use by women is also increasing, and many women receive cocaine as gifts from m e n 3 The extent of cocaine use during pregnancy is difficult to estimate. However, cocaine use by women has implications for nurses who take care of women in their childbearing years and their offspring.
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Women of childbearing age constitute 15-17% of all regular users of cocaine.
Cocaine often leads to a pattern of compulsive use that is dangerous to one’s health and psychologic well-being. The drug is absorbed effectively through mucus membranes and has a relatively short biologic half-life, which can lead to greater use to maintain the feeling of well-being. Because the perception of well-
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being increases the probability that the cocaine will be used again, cocaine has reinforcing properties3
cocaine can still produce effects for one and a half hours.
Pharmacology of Cocaine
Metabolism of Cocaine
Cocaine is prepared from the leaves of the Erythroxylon coca plant. Pure cocaine is an alkaloid, whereas cocaine hydrochloride is a salt made by dissolving the alkaloid form in hydrochloride. Cocaine hydrochloride is available in crystals, granules, or white powder; it is about 89% cocaine by weight and has a molecular weight of 339.81. The cocaine alkaloid, also known as free base or crack, is a colorless, odorless, and transparent crystalline substance that melts at 98°C and vaporizes at higher temperatures; thus, it is not destroyed by heating. These properties allow crack to be smoked or heated and inhaled. Cocaine causes central nervous system and peripheral effects. Centrally, cocaine acts by stimulating the dopaminergic neuronal systems, resulting in feelings of euphoria and psychologic addiction. Cocaine affects dopaminergic neurotransmission by blocking the reabsorption of dopamine. Long-term use of cocaine depletes dopamine at the nerve terminals, which may contribute to the dysphoria during withdrawal and subsequently lead to the craving for more ~ocaine.~ Peripherally, cocaine acts as an inhibitor of nerve conduction. Cocaine blocks the reabsorption of the neurotransmitters norepinephrine and dopamine at the presynaptic site, resulting in an excess of norepinephrine at the postsynaptic receptor site. Norepinephrine activates the sympathetic nervous system to produce vasoconstriction, which results in an acute rise in arterial pressure, tachycardia, and a predisposition to seizures and ventricular arrhythmia^.^ Because of its high water and lipid solubility, cocaine probably crosses the placental barrier by simple diffusion. Cocaine’s low molecular weight and low ionization at physiologic pH further facilitate placental diffusion.’
Cocaine is metabolized and excreted into two different compounds: ecgonine methyl ester and benzoyl ecgonine.6 Ecgonine methyl ester is a major metabolite of cocaine, making up 32-49% of the metabolites in urine. Plasma cholinesterase hydrolyzes cocaine to ecgonine methyl ester. The human liver also contains esterase activity with the ability to hydrolyze cocaine to ecgonine methyl ester. This liver esterase is a different enzyme than the plasma enzyme. At high substrate concentrations, cocaine is hydrolyzed slower in serum than in the liver. In vivo serum concentrations of cocaine, however, are hydrolyzed by plasma cholinesterase and liver esterase at comparable rates6 Benzoyl ecgonine is the other major metabolite of cocaine and was reported to be 29-45% of a dose of cocaine found in the urine. Benzoyl ecgonine is formed by nonenzymatic hydrolysis at physiologic pH. Esterases do not contribute to the formation of benzoyl ecgonine.6 Plasma cholinesterase activity is much lower in fetuses, neonates, elderly men, patients with liver disease, and pregnant women than in normal adults3 In average adults, this benzoyl ecgonine persists in the urine for up to 27 hours after intranasal use of co~ a i n eIn . ~one case study, for example, it was found to linger in a neonate’s urine for four days7An immature cholinesterase system was found to begin to develop in the neonate at the age of two weeks.* Because the pregnant woman and her fetus have a decreased ability to metabolize cocaine, the cocaine ingested by a pregnant woman will remain in the body longer than in a normal adult. This could lead to greater detrimental effects for the pregnant woman and her fetus.
Uterine and Intrauterine Efects of Cocaine
Because cocaine is absorbed slowly through the mucous membranes, there is a delayed onset and a sustained duration. After smoking cocaine, a user’s feeling of euphoria usually last 20 minutes. The effects last for one and a half hours after intranasal administratiom3 Cocaine has a total half-life of about 30-40 minutes after administration.’ In other words, half of the cocaine administered is gone in 30-40 minutes, but
Cocaine causes a generalized vasoconstriction because of norepinephrine buildup. Vasoconstriction also occurs in the placenta and the uterine bed, resulting in decreased blood flow and diminished gas exchange. The higher norepinephrine levels increase uterine contractility. The increased maternal level of circulating norepinephrine crosses the placenta and causes vasoconstriction in the fetus, which results in fetal ta~hycardia.~ Research studies indicate that cocaine use in pregnancy results in more frequent contractions, fetal activity, and frequency of spontaneous abortions, premature labor, and abruptio pla~entae.~*~-’’ Many women
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Cocaine crosses the placenta by simple diffusion.
Effects
who used cocaine during pregnancy in these studies reported feeling contractions and more fetal activity within minutes of using cocaine. Abruptio placentae may occur because of the hypertensive and vasoconstrictive effect of cocaine, which causes disruption in the placental adherence to the uterine wall. These published reports and the frequent clinical experience of cocaine-induced abruptio placentae have led some medical centers to routinely screen the urine of women who have had an abruption and their fetuses for cocaine metabolites. Two published studies used a pregnant ewe and her fetus as a model for testing the effects of cocaine.l3.l4Woods et al. found that cocaine given parenterally produced a dose-dependent rise in maternal blood pressure with a dose-dependent fall in uterine blood Aow.13 They also found that maternal cocaine administration affected the fetus in one or both of the following ways. First, the vasoconstriction caused by norepinephrine reduced oxygen delivery to the fetus. The resultant hypoxia stimulated the release of catecholamines. Elevated catecholamine levels increased oxygen demands of the tissue and led to a cycle of decreasing fetal oxygenation. Second, the drug affected the fetus by direct diffusion of cocaine across the placenta. The cocaine in the fetus also caused a rise in circulating norepinephrine, which led to fetal vasoconstriction and an exaggerated fetal cardiovascular response to h y p ~ x e m i a . ' ~ A second study using the pregnant ewe and fetus showed similar response^.'^ Moore et al. demonstrated that the usual doses of cocaine exerted a negative effect on uterine blood flow, which lasted for about 20 minutes after parenteral administration. They also found that cocaine passed into the fetal circulation, reaching levels about one-eighth those seen in the mother.14 In the intrapartum period, fetal monitoring may show that the fetus exposed to cocaine has multiple variable decelerations and a baseline heart rate of 180-200 beats per m i n ~ t eFetal . ~ intolerance to labor and meconium staining of the amniotic fluid has been reported in the l i t e r a t ~ r e . ' ~ "Chasnoff ~"~ et al. also reported a greater frequency of precipitous 1ab0r.l~ In addition to these uterine effects, cocaine use in early pregnancy may have teratogenic effects. Bingo1 et al. found that cocaine used early in gestation resulted in a greater incidence of fetal skull abnormalities (e.g., encephalocele, exencephalia, and parietal bone defect^).^ They also reported that fetuses exposed to cocaine had lower birth weights, shorter lengths, and smaller head circumferences than expected for their gestational ages5 Chasnoff et al. reported the occurrence of prune-belly syndrome in an
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infant whose mother consumed a large dose of cocaine at five weeks' gestation.' In another study, Chasnoff et al. reported a slightly increased incidence of genitourinary tract malformations in infants whose mothers consumed ~ 0 c a i n e .This l ~ is consistent with the fact that the urogenital system forms in humans at five weeks' gestation, and a large dose of a teratogenic substance could interfere with development. An excessive incidence of cryptorchidism, exencephaly, eye malformations, hydronephrosis, and skeletal defects occurred in the fetuses of gravid mice that were administered cocaine on any of days 7-11 of gestation.17Many centers now advocate the routine screening of neonates exposed to cocaine during pregnancy for genitourinary anomalies.
Neonatal Manifestations of Maternal Cocaine Use It is very difficult to study the specific effects of maternal cocaine use on the neonate because other determinants, such as socioeconomic factors and the concomitant use of other drugs, may play a role. A report in 1986 by Madden et al. revealed that, from their study of maternal cocaine use and neonatal withdrawal symptoms, one of eight neonates exposed to cocaine in utero manifested symptoms of classic neonatal drug withdrawal." They also reported that one neonate was noted to be floppy, one neonate required gavage feedings, one neonate was premature, and two neonates were considered small for their gestational ages." Although the study sample was small, the results showed that six of the eight neonates demonstrated problems after intrauterine cocaine exposure. These and subsequent researchers found that infants exposed to cocaine in utero did not display the withdrawal symptoms more commonly seen in infants exposed to narcotics or other street d r ~ g s . ~ , ' ~ * ' ~ ~ ' ~ - * ~ MacGregor et al. and Chasnoff et al. reported that the infants exposed to cocaine in utero demonstrated depressed interactive abilities and significant impairment in organizational abilities.*~'~ These infants also had difficulty maintaining adequate state control in the neonatal p e r i ~ d . ~ Cocaine is metabolized slower by pregnant women, fetuses, and neonates than by normal adults.
Or0 and Dixon reported that infants exposed to cocaine in utero exhibited significant neurologic and physiologic alterations associated with abnormal sleep patterns, tremors, poor feeding, hypertonia, poor visual processing of faces and objects, long pe-
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riods of dull alert periods, and decreased spontaneous a ~ t i v i t y . ’Other ~ researchers report that, despite discontinuation of cocaine in the first trimester of pregnancy, the newborn may exhibit impaired organizational ability, orientation, and state contr01.**’~,~’ The neurobehavioral symptoms exhibited by cocaine-exposed neonates were confirmed by electroencephalographic (EEG) testing.20The EEGs of 17 of 38 neonates tested were abnormal during the first week of life. The EEGs normalized by three to 1 2 months of age. The EEG abnormalities could not be predicted based on the clinical neurologic dysfunctions or the perinatal variables. The neurobehavioral symptoms of increased tremulousness, more startle responses, and deficient interactive behavior and state control were found to be due to a direct neurotoxic effect rather than to withdrawal from cocaine. Currently, it is unknown whether these effects are permanent or transient. These results of the study are based on the fact that the clinical signs disappeared as the cocaine metabolites disappeared from the neonates’ urine.20 Cocaine exposure can also occur in neonates after delivery. A report of a two-week-old neonate who ingested cocaine via her mother’s breast milk was reported in 1987.8The neonate was brought to the hospital because of increasing irritability. On physical examination, the neonate demonstrated tachycardia, tachypnea, and neurobehavioral symptoms, such as a high-pitched cry, dilated pupils, an increased sucking reflex, a hyperactive Moro reaction, tremulous extremities, and a marked lability of mood. Twenty-four hours after discontinuation of the contaminated breast milk, the neonate began to show improvement. The irritability and tremulousness persisted for about 48 hours, and the cocaine metabolites persisted in the urine for at least 60 hours after ingestion. It is reasonable to assume that cocaine could pass into human milk because it is highly lipid soluble. In this case, benzoyl ecgonine remained in the breast milk for as long as 36 hours after maternal cocaine use.* Neonates affected bj! cocaine may demonstrate abnormal neurobehavioral symptoms, have lower gestational ages and birth weights, and deliver preterm.
Maternal cocaine use has been associated with a lower gestational age a t delivery, an increase in preterm labor and delivery, lower neonatal Apgar scores, lower birth weights, and delivery of small-for-gestational-age n e ~ n a t e s . ~ ”One ~ ” ~study ’ ~ ~ showed that a higher incidence of meconium staining occurred in
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cocaine-exposed infants.15 In the same study, 10 of 66 infants (15%) exposed to cocaine died of sudden infant death syndrome (SIDS), and five infants had episodes of prolonged apnea requiring resuscitation and ho~pita1ization.l~ Chasnoff et al. also found that intrauterine exposure to cocaine was associated with a 15% incidence of SIDS, as opposed to a 4% incidence of SIDS after prenatal exposure to opiates and a 0.27% incidence of SIDS in term infants. Newer studies link other neonatal effects with maternal cocaine use. For instance, one case study reported the presence of hyperplastic primary vitreous in o n e eye and retinopathy of prematurity-like changes in the other eye in a term neonate exposed to cocaine in utero. The vasoconstriction related to cocaine may have resulted in vasoconstriction of the developing retinal vessels.23
Nursing Implications Nurses must be aware of the effects of cocaine on mothers and their neonates during the antepartum, intrapartum, and postpartum periods. Prenatally and during the intrapartum period, clues such as a history of repeated first-trimester losses, stillbirths, preterm labor, previous preterm deliveries, chronic rhinitis, and ulcerations of mucous membranes should alert the nurse to obtain and review an updated patient history for possible cocaine use or abuse. Changes in the life-style of a woman using cocaine may lead the woman to disregard her nutritional intake and prenatal care. Prenatal care is vital for these women to assess and monitor adequate nutrition and growth of the fetus. Screening and assessment for substance abuse in pregnancy require a nonjudgmental assertiveness on the part of the nurse. If a nurse suspects that a patient is abusing drugs, the nurse can adapt assessment questions from the following sample questions: (1) What do you do to relax? (2) What is your idea of a good party? (3) Do you ever “overdo it” with drugs or alcohol? ( 4 ) Would you find it difficult to give up drugs or alcohol? Although some women will admit to cocaine use under direct questioning, many users will give evasive responses. Once a woman is found to use cocaine, counseling by specialized practitioners is the next step. Counseling can be implemented pre- and postnatally. Many educational, legal, and ethical issues may need to be addressed when dealing with the pregnant cocaine user. These issues can place the nurse in a legal or ethical dilemma and may involve nutrition; the detrimental effects of cocaine use; and social issues, such as housing, transportation, and employ-
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Efects qf Maternal Cocuine Use
ment. There is also a growing trend to report intrauterine cocaine exposure to the state child-abuse authorities, and a few women in the United States have been arrested and jailed for exposing their fetuses to cocaine. Labor and delivery nurses may care for cocaineusing women who present with abruptio placentae, acute hypertension and tachycardia, premature rupture of membranes, and preterm labor. Fetal monitoring may show a fetus with an increased baseline heart rate or d e e p variable decelerations. Meconium staining of the amniotic fluid can also occur. The effects of cocaine may also be seen in the postpartum period. Women may have headaches, seizures, or cardiopulmonary distress associated with cocaine use. Behavioral problems, such as marked mood shifts and disinterest in the neonate, also may occur. The nurse also should be aware that cocaine readily passes into breast milk, and any mother who continues to use cocaine after delivery should be discouraged from breastfeeding. The unpredictable environment of the neonatal intensive-care unit (NICU) places extraordinary demands on the neonate exposed to cocaine. The constant light, the loud, monotonous machinery and alarms, and the large number of people present often prohibit behavioral recovery of these neonates. The NICU nurse can facilitate the neonate’s recovery of normal behavior by promoting patterned sensory input. One way this can be accomplished is to enhance diurnal rhythms in the NICU by providing cycles of relative light and dark. Adverse auditory and light exposure should be decreased, and if possible, the neonates should be grouped together to minimize background stimulation. Intervention or procedures could be limited to 15 minutes and performed according to a time schedule. All perinatal nurses may have patients aflected by cocaine use.
The most dramatic symptoms of maternal cocaine use in the neonate are neurobehavioral ones, including irritability, restlessness, and tremulousness. These symptoms, which are characteristic of cocaine-exposed neonates, interfere with the neonate’s ability to interact with and respond to the caretaker, either the mother or the nursing staff, and could put the mother and neonate’s relationship at risk for further development problems. To optimize parent-neonate interaction, the parents must be readily involved in the neonate’s care and progress. For the parents to derive any satisfaction
March/April 1991
from their caretaking activities, they must recognize their individual neonate’s temperament and behavior to determine the nature and timing of intervention. The nurse should facilitate parental recognition and interpretation of these cues. For example, the immature, behaviorally disorganized neonate may not be able to tolerate visual activity for more than 30-60 seconds and will avert his or her eyes. Unless informed to the contrary, the parents may interpret this action as a rejection, as opposed to a time-out period. The parents should be taught to proceed slowly with any intervention and to speak in a calm, soothing voice. Parents can avoid startling cocaine-exposed neonates by gently touching them before changing their positions and allowing the neonates time to reorganize after each interaction to avoid losing control over their behavior. Neonates exposed to cocaine may require swaddling or the provision of physical boundaries around them when they sleep. Foam contour chairs have been used with good results in nurseries, and some parents have used beanbag chairs at home for their neonates. The environment these neonates will do well in is one that is consistent and predictable. The nurse should help the parents plan to regularize the routine care for their neonate after discharge. Parents should be informed of their need to participate in their neonate’s care from the time of admission. During the hospitalization, the nurse should establish a parent-neonate visiting record in the care plan to document visiting patterns, educational sessions, and parent-neonate interaction. Parents are expected to visit or call daily and to bring in clothing or toys for their neonate. Parents should be instructed during their visits about exercises and activities that they can conduct with their neonate. The nurse should facilitate the interpretation of the neonate’s response for the parents to help them realize the progress their neonate is making and to encourage appropriate interaction. The nurse can thereby reduce the frustration of caring for these neonates and promote healthy parentneonate relationships. This situation requires close follow-up of the family. Other educational concerns involve teaching the mother about the increased incidence of SIDS. The mother should learn the risk of SIDS, as well as how to perform cardiopulmonary resuscitation. Some perinatal centers provide all cocaine-exposed neonates with monitors upon discharge.
Summary Cocaine use during pregnancy has serious consequences for the mother and her neonate. Nurses can be instrumental in screening for cocaine use in preg-
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nant women and in educating mothers about t h e effects of cocaine use during pregnancy. Mothers with cocaine-exposed neonates need t o learn h o w t o interact with their neonates, as well as t o learn t h e risks and dangers of SIDS. T h e community pediatrician should be made aware of t h e neonate’s intrauterine cocaine exposure to promote consistency in care. Further stud-
ies are needed to assess the long-term effects of cocaine exposure on infants and children.
References 1. Kozel, N., and E. Adams. 1986. Epidemiology of drug abuse: An overview. Science. 234:970-74. 2. Morganthau, T., and M. Miller. 1988. Getting tough on cocaine. Newsweek, November 28,76-79. 3. Cregler, L., and H. Mark. 1986. Medical complications of cocaine abuse. N Engl JMed. 315:1495-1500. 4. MacGregor, S., L. Keith, I . Chasnoff, etal. 1987. Cocaine use during pregnancy: Adverse perinatal outcome. Am J Obstet Gjwecol. 157:686-90. 5. Bingol, N., M. Fuchs, V. Diaz, R. Stone, and D. Gromisch. 1987. Teratogenicity of cocaine in humans.JPediatr. 110:93-96. 6. Stewart, D., T. Inaba, M. Lucassen, and W. Kalow. 1979. Cocaine metabolism: Cocaine and norcocaine hydrolysis by liver and serum esterases. Clin Pbarmacol Tber. 25:464-68. 7. Chasnoff, I., M. Bussey, R. Savich, and C. Stack. 1986. Perinatal cerebral infarction and maternal cocaine use.J Pediutr. 108:456-59. 8. Chasnoff, I., D. Lewis, and L. Squires. 1987. Cocaine intoxication in a breast-fed infant. Pediatrics. 80:83638. 9. Chasnoff, I., W. Burns, S. Schnoll, and K. Burns. 1985. Cocaine use in pregnancy. N Engl J Med. 313:666-69. 10. Amaro, H., B. Zuckerman, and H. Cabral. 1989. Drug use among adolescent mothers: Profile of risk. Pediatrics. 84:144-51. 11. Townsend, R., F. Laing, and R. Jeffrey. 1988. Placental abruption associated with cocaine abuse. AJR. 150:1339-40. 12. Little, B., L. Snell, V. Klein, and L. Gilstrap. 1989. Cocaine abuse during pregnancy: Maternal and fetal implications. Obstet Gynecol. 75157-60. 13. Woods, J., M. Plessinger, and K. Clark. 1987. Effect of cocaine on uterine blood flow and fetal oxygenation. JAMA. 257:957-61.
14. Moore, T., J. Sort, L. Miller, T. Key, and R. Resnik. 1986. Hemodynamic effects of intravenous cocaine on the pregnant ewe and fetus. Am.] Obstet Gynecol. 155:88388. 15. Chasnoff, I., K. Burns, and W. Burns. 1987. Cocaine use in pregnancy: Perinatal morbidity and mortality. Neurotoxicol Teratol. 9:291-93. 16. Hadeed, A,, and S. Siefel. 1989. Maternal cocaine use during pregnancy: Effect on the newborn infant. Pediatrics. 84:205-10. 17. Mahahk, M., R. Gautieri, and D. Mann. 1980. Teratogenic potential of cocaine hydrochloride in CF-1 mice. J %arm Sci. 69:703-6. 18. Madden, J., T. Payne, and S. Miller. 1986. Maternal cocaine abuse and effect on the newborn. Pediatrics. 77~209-11, 19. Oro, A,, and S . Dixon. 1987. Perinatal cocaine and methamphetamine exposure: Maternal and neonatal correlates. J Pediatr. 111:571-78. 20. Doberczak, T., S. Shanzer, R. Senie, and S. Kandall. 1988. Neonatal neurologic and electroencephalographic effects of intrauterine cocaine exposure. J Pediatr. 115354-58. 21. Chasnoff, I., D. Griffith, S . MacGregor, K. Dirkes, and K. Burns. 1988. Temporal patterns of cocaine use in pregnancy. JAMA. 261:1741-44. 22. Chouteau, M., P. Namerow, and P. Leppart. 1988. The effect of cocaine abuse on birth weight and gestational age. Obstet Gynecol. 72351-54. 23. Teske, M., and M. Trese. 1987. Retinopathyofprematurity-like fundus and persistent hyperplastic primaryvitreous associated with maternal cocaine use. Am JOpbtbalmol. 105719-20. Address for correspondence: Heather Peters, RN, MSN, 10322 S. Austin, Chicago Ridge, IL 60415.
Heather Peters is a graduate student in the Maternal Child Program at Rush University, College of Nursing, Chicago, Illtnots. She currently works at the Unlversity of Illinols in labor and deltvery and for Women’s Health Ltd., a home birth service in Chicago. Ms. Peters is a member of the Illinois Nurses Association, the Midwives’ Alltance of North Amertca, and Sigma Theta Tau. Catherine Jursich Theorell is a practtttoner-teacher at Rush University, College of Nursing, Chicago, Illinots, and 1s a neonatal nurse practitioner in the Special Care Nursery. Ms. Theorell b a member of Alpha Sigma Nu, the National Associatton of Neonatal Nurses, and Sigma Theta Tau.
Notice to Copiers Authorization to photocopy items for internal or personal use, or the internalor personal use of specific clients, is granted by NAACOG. a division of the American College of Obstetricians and Gynecologists. for libraries and other users registered with the Copyright Clearance Center (CCC) Transactional Reporting Service, provided that the base fee of $00.80 per copy, plus $00.05 per page is paid directly to CCC, 21 Congress St.. Salem, MA 01970. 0884-2175191 $00.80 $00.05.
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Fetal and Neonatal Eflects of Maternal Cocaine Use
Marijuana was the drug of the 1960s and herotn the drug of the 1970s. Cocaine was the popular drug of the 1980s, and cocaine’s populartty appears to have contlnued tnto the 1990s. Cocaine use tncreased dramatically between 1974 and 1985. This article reviews the trends of cocaine use, fetal and maternal pharmacodynamics of cocatne, intrautertne effects of cocaine on the fetus, and the neonatal mangestatdons of cocaine exposure. Accepted: May 1990
March/April 1991
on the street and was often referred to as the “champagne of drugs.” Since the 1970s, however, cocaine has become less expensive, more available, and purer. The number of people using cocaine increased from 5.4 million in 1974 to 22.2 million in 1985.’ In recent years, the Colombian drug carteis have been successful in greatly expanding coca-leaf production and processing.* Currently, cocaine enters the United States mainly through Miami from Colombia, Peru, and Bolivia. From Miami, cocaine is distributed in a number of different forms to rural and metropolitan areas. Consequently, cocaine is now used by more people than ever. Beginning in the late 1970s, the dosages of cocaine increased. For example, between 1970 and 1978, recreational users inhaled intranasal doses of 1-4 grams per month, whereas from 1978 to 1982, they used 1-3 grams per week. In addition to taking cocaine intranasally, smoking the alkaloid form known as crack has become increasingly popular. The frequency of experimental practices with cocaine, such as taking cocaine free base intranasally and smoking coca paste, rose during the early 1 9 8 0 ~ ~ Demographic studies describe the typical cocaine user as a young man with a higher-than-average income and a high level of responsibilitywho is a professional in a position of authority. Cocaine use is most prevalent among young white men (aged 18-25 years) residing in the western and northeastern areas of the United state^.^ Similar to users of other types of drugs, cocaine users have a greater tendency to abuse more than one substance;*for instance, cocaine is often used in combination with marijuana. Many young adult users use cocaine occasionally and alcohol or marijuana more frequently. Cocaine use by women is also increasing, and many women receive cocaine as gifts from m e n 3 The extent of cocaine use during pregnancy is difficult to estimate. However, cocaine use by women has implications for nurses who take care of women in their childbearing years and their offspring.
-
Women of childbearing age constitute 15-17% of all regular users of cocaine.
Cocaine often leads to a pattern of compulsive use that is dangerous to one’s health and psychologic well-being. The drug is absorbed effectively through mucus membranes and has a relatively short biologic half-life, which can lead to greater use to maintain the feeling of well-being. Because the perception of well-
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being increases the probability that the cocaine will be used again, cocaine has reinforcing properties3
cocaine can still produce effects for one and a half hours.
Pharmacology of Cocaine
Metabolism of Cocaine
Cocaine is prepared from the leaves of the Erythroxylon coca plant. Pure cocaine is an alkaloid, whereas cocaine hydrochloride is a salt made by dissolving the alkaloid form in hydrochloride. Cocaine hydrochloride is available in crystals, granules, or white powder; it is about 89% cocaine by weight and has a molecular weight of 339.81. The cocaine alkaloid, also known as free base or crack, is a colorless, odorless, and transparent crystalline substance that melts at 98°C and vaporizes at higher temperatures; thus, it is not destroyed by heating. These properties allow crack to be smoked or heated and inhaled. Cocaine causes central nervous system and peripheral effects. Centrally, cocaine acts by stimulating the dopaminergic neuronal systems, resulting in feelings of euphoria and psychologic addiction. Cocaine affects dopaminergic neurotransmission by blocking the reabsorption of dopamine. Long-term use of cocaine depletes dopamine at the nerve terminals, which may contribute to the dysphoria during withdrawal and subsequently lead to the craving for more ~ocaine.~ Peripherally, cocaine acts as an inhibitor of nerve conduction. Cocaine blocks the reabsorption of the neurotransmitters norepinephrine and dopamine at the presynaptic site, resulting in an excess of norepinephrine at the postsynaptic receptor site. Norepinephrine activates the sympathetic nervous system to produce vasoconstriction, which results in an acute rise in arterial pressure, tachycardia, and a predisposition to seizures and ventricular arrhythmia^.^ Because of its high water and lipid solubility, cocaine probably crosses the placental barrier by simple diffusion. Cocaine’s low molecular weight and low ionization at physiologic pH further facilitate placental diffusion.’
Cocaine is metabolized and excreted into two different compounds: ecgonine methyl ester and benzoyl ecgonine.6 Ecgonine methyl ester is a major metabolite of cocaine, making up 32-49% of the metabolites in urine. Plasma cholinesterase hydrolyzes cocaine to ecgonine methyl ester. The human liver also contains esterase activity with the ability to hydrolyze cocaine to ecgonine methyl ester. This liver esterase is a different enzyme than the plasma enzyme. At high substrate concentrations, cocaine is hydrolyzed slower in serum than in the liver. In vivo serum concentrations of cocaine, however, are hydrolyzed by plasma cholinesterase and liver esterase at comparable rates6 Benzoyl ecgonine is the other major metabolite of cocaine and was reported to be 29-45% of a dose of cocaine found in the urine. Benzoyl ecgonine is formed by nonenzymatic hydrolysis at physiologic pH. Esterases do not contribute to the formation of benzoyl ecgonine.6 Plasma cholinesterase activity is much lower in fetuses, neonates, elderly men, patients with liver disease, and pregnant women than in normal adults3 In average adults, this benzoyl ecgonine persists in the urine for up to 27 hours after intranasal use of co~ a i n eIn . ~one case study, for example, it was found to linger in a neonate’s urine for four days7An immature cholinesterase system was found to begin to develop in the neonate at the age of two weeks.* Because the pregnant woman and her fetus have a decreased ability to metabolize cocaine, the cocaine ingested by a pregnant woman will remain in the body longer than in a normal adult. This could lead to greater detrimental effects for the pregnant woman and her fetus.
Uterine and Intrauterine Efects of Cocaine
Because cocaine is absorbed slowly through the mucous membranes, there is a delayed onset and a sustained duration. After smoking cocaine, a user’s feeling of euphoria usually last 20 minutes. The effects last for one and a half hours after intranasal administratiom3 Cocaine has a total half-life of about 30-40 minutes after administration.’ In other words, half of the cocaine administered is gone in 30-40 minutes, but
Cocaine causes a generalized vasoconstriction because of norepinephrine buildup. Vasoconstriction also occurs in the placenta and the uterine bed, resulting in decreased blood flow and diminished gas exchange. The higher norepinephrine levels increase uterine contractility. The increased maternal level of circulating norepinephrine crosses the placenta and causes vasoconstriction in the fetus, which results in fetal ta~hycardia.~ Research studies indicate that cocaine use in pregnancy results in more frequent contractions, fetal activity, and frequency of spontaneous abortions, premature labor, and abruptio pla~entae.~*~-’’ Many women
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Cocaine crosses the placenta by simple diffusion.
Effects
who used cocaine during pregnancy in these studies reported feeling contractions and more fetal activity within minutes of using cocaine. Abruptio placentae may occur because of the hypertensive and vasoconstrictive effect of cocaine, which causes disruption in the placental adherence to the uterine wall. These published reports and the frequent clinical experience of cocaine-induced abruptio placentae have led some medical centers to routinely screen the urine of women who have had an abruption and their fetuses for cocaine metabolites. Two published studies used a pregnant ewe and her fetus as a model for testing the effects of cocaine.l3.l4Woods et al. found that cocaine given parenterally produced a dose-dependent rise in maternal blood pressure with a dose-dependent fall in uterine blood Aow.13 They also found that maternal cocaine administration affected the fetus in one or both of the following ways. First, the vasoconstriction caused by norepinephrine reduced oxygen delivery to the fetus. The resultant hypoxia stimulated the release of catecholamines. Elevated catecholamine levels increased oxygen demands of the tissue and led to a cycle of decreasing fetal oxygenation. Second, the drug affected the fetus by direct diffusion of cocaine across the placenta. The cocaine in the fetus also caused a rise in circulating norepinephrine, which led to fetal vasoconstriction and an exaggerated fetal cardiovascular response to h y p ~ x e m i a . ' ~ A second study using the pregnant ewe and fetus showed similar response^.'^ Moore et al. demonstrated that the usual doses of cocaine exerted a negative effect on uterine blood flow, which lasted for about 20 minutes after parenteral administration. They also found that cocaine passed into the fetal circulation, reaching levels about one-eighth those seen in the mother.14 In the intrapartum period, fetal monitoring may show that the fetus exposed to cocaine has multiple variable decelerations and a baseline heart rate of 180-200 beats per m i n ~ t eFetal . ~ intolerance to labor and meconium staining of the amniotic fluid has been reported in the l i t e r a t ~ r e . ' ~ "Chasnoff ~"~ et al. also reported a greater frequency of precipitous 1ab0r.l~ In addition to these uterine effects, cocaine use in early pregnancy may have teratogenic effects. Bingo1 et al. found that cocaine used early in gestation resulted in a greater incidence of fetal skull abnormalities (e.g., encephalocele, exencephalia, and parietal bone defect^).^ They also reported that fetuses exposed to cocaine had lower birth weights, shorter lengths, and smaller head circumferences than expected for their gestational ages5 Chasnoff et al. reported the occurrence of prune-belly syndrome in an
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infant whose mother consumed a large dose of cocaine at five weeks' gestation.' In another study, Chasnoff et al. reported a slightly increased incidence of genitourinary tract malformations in infants whose mothers consumed ~ 0 c a i n e .This l ~ is consistent with the fact that the urogenital system forms in humans at five weeks' gestation, and a large dose of a teratogenic substance could interfere with development. An excessive incidence of cryptorchidism, exencephaly, eye malformations, hydronephrosis, and skeletal defects occurred in the fetuses of gravid mice that were administered cocaine on any of days 7-11 of gestation.17Many centers now advocate the routine screening of neonates exposed to cocaine during pregnancy for genitourinary anomalies.
Neonatal Manifestations of Maternal Cocaine Use It is very difficult to study the specific effects of maternal cocaine use on the neonate because other determinants, such as socioeconomic factors and the concomitant use of other drugs, may play a role. A report in 1986 by Madden et al. revealed that, from their study of maternal cocaine use and neonatal withdrawal symptoms, one of eight neonates exposed to cocaine in utero manifested symptoms of classic neonatal drug withdrawal." They also reported that one neonate was noted to be floppy, one neonate required gavage feedings, one neonate was premature, and two neonates were considered small for their gestational ages." Although the study sample was small, the results showed that six of the eight neonates demonstrated problems after intrauterine cocaine exposure. These and subsequent researchers found that infants exposed to cocaine in utero did not display the withdrawal symptoms more commonly seen in infants exposed to narcotics or other street d r ~ g s . ~ , ' ~ * ' ~ ~ ' ~ - * ~ MacGregor et al. and Chasnoff et al. reported that the infants exposed to cocaine in utero demonstrated depressed interactive abilities and significant impairment in organizational abilities.*~'~ These infants also had difficulty maintaining adequate state control in the neonatal p e r i ~ d . ~ Cocaine is metabolized slower by pregnant women, fetuses, and neonates than by normal adults.
Or0 and Dixon reported that infants exposed to cocaine in utero exhibited significant neurologic and physiologic alterations associated with abnormal sleep patterns, tremors, poor feeding, hypertonia, poor visual processing of faces and objects, long pe-
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riods of dull alert periods, and decreased spontaneous a ~ t i v i t y . ’Other ~ researchers report that, despite discontinuation of cocaine in the first trimester of pregnancy, the newborn may exhibit impaired organizational ability, orientation, and state contr01.**’~,~’ The neurobehavioral symptoms exhibited by cocaine-exposed neonates were confirmed by electroencephalographic (EEG) testing.20The EEGs of 17 of 38 neonates tested were abnormal during the first week of life. The EEGs normalized by three to 1 2 months of age. The EEG abnormalities could not be predicted based on the clinical neurologic dysfunctions or the perinatal variables. The neurobehavioral symptoms of increased tremulousness, more startle responses, and deficient interactive behavior and state control were found to be due to a direct neurotoxic effect rather than to withdrawal from cocaine. Currently, it is unknown whether these effects are permanent or transient. These results of the study are based on the fact that the clinical signs disappeared as the cocaine metabolites disappeared from the neonates’ urine.20 Cocaine exposure can also occur in neonates after delivery. A report of a two-week-old neonate who ingested cocaine via her mother’s breast milk was reported in 1987.8The neonate was brought to the hospital because of increasing irritability. On physical examination, the neonate demonstrated tachycardia, tachypnea, and neurobehavioral symptoms, such as a high-pitched cry, dilated pupils, an increased sucking reflex, a hyperactive Moro reaction, tremulous extremities, and a marked lability of mood. Twenty-four hours after discontinuation of the contaminated breast milk, the neonate began to show improvement. The irritability and tremulousness persisted for about 48 hours, and the cocaine metabolites persisted in the urine for at least 60 hours after ingestion. It is reasonable to assume that cocaine could pass into human milk because it is highly lipid soluble. In this case, benzoyl ecgonine remained in the breast milk for as long as 36 hours after maternal cocaine use.* Neonates affected bj! cocaine may demonstrate abnormal neurobehavioral symptoms, have lower gestational ages and birth weights, and deliver preterm.
Maternal cocaine use has been associated with a lower gestational age a t delivery, an increase in preterm labor and delivery, lower neonatal Apgar scores, lower birth weights, and delivery of small-for-gestational-age n e ~ n a t e s . ~ ”One ~ ” ~study ’ ~ ~ showed that a higher incidence of meconium staining occurred in
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cocaine-exposed infants.15 In the same study, 10 of 66 infants (15%) exposed to cocaine died of sudden infant death syndrome (SIDS), and five infants had episodes of prolonged apnea requiring resuscitation and ho~pita1ization.l~ Chasnoff et al. also found that intrauterine exposure to cocaine was associated with a 15% incidence of SIDS, as opposed to a 4% incidence of SIDS after prenatal exposure to opiates and a 0.27% incidence of SIDS in term infants. Newer studies link other neonatal effects with maternal cocaine use. For instance, one case study reported the presence of hyperplastic primary vitreous in o n e eye and retinopathy of prematurity-like changes in the other eye in a term neonate exposed to cocaine in utero. The vasoconstriction related to cocaine may have resulted in vasoconstriction of the developing retinal vessels.23
Nursing Implications Nurses must be aware of the effects of cocaine on mothers and their neonates during the antepartum, intrapartum, and postpartum periods. Prenatally and during the intrapartum period, clues such as a history of repeated first-trimester losses, stillbirths, preterm labor, previous preterm deliveries, chronic rhinitis, and ulcerations of mucous membranes should alert the nurse to obtain and review an updated patient history for possible cocaine use or abuse. Changes in the life-style of a woman using cocaine may lead the woman to disregard her nutritional intake and prenatal care. Prenatal care is vital for these women to assess and monitor adequate nutrition and growth of the fetus. Screening and assessment for substance abuse in pregnancy require a nonjudgmental assertiveness on the part of the nurse. If a nurse suspects that a patient is abusing drugs, the nurse can adapt assessment questions from the following sample questions: (1) What do you do to relax? (2) What is your idea of a good party? (3) Do you ever “overdo it” with drugs or alcohol? ( 4 ) Would you find it difficult to give up drugs or alcohol? Although some women will admit to cocaine use under direct questioning, many users will give evasive responses. Once a woman is found to use cocaine, counseling by specialized practitioners is the next step. Counseling can be implemented pre- and postnatally. Many educational, legal, and ethical issues may need to be addressed when dealing with the pregnant cocaine user. These issues can place the nurse in a legal or ethical dilemma and may involve nutrition; the detrimental effects of cocaine use; and social issues, such as housing, transportation, and employ-
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ment. There is also a growing trend to report intrauterine cocaine exposure to the state child-abuse authorities, and a few women in the United States have been arrested and jailed for exposing their fetuses to cocaine. Labor and delivery nurses may care for cocaineusing women who present with abruptio placentae, acute hypertension and tachycardia, premature rupture of membranes, and preterm labor. Fetal monitoring may show a fetus with an increased baseline heart rate or d e e p variable decelerations. Meconium staining of the amniotic fluid can also occur. The effects of cocaine may also be seen in the postpartum period. Women may have headaches, seizures, or cardiopulmonary distress associated with cocaine use. Behavioral problems, such as marked mood shifts and disinterest in the neonate, also may occur. The nurse also should be aware that cocaine readily passes into breast milk, and any mother who continues to use cocaine after delivery should be discouraged from breastfeeding. The unpredictable environment of the neonatal intensive-care unit (NICU) places extraordinary demands on the neonate exposed to cocaine. The constant light, the loud, monotonous machinery and alarms, and the large number of people present often prohibit behavioral recovery of these neonates. The NICU nurse can facilitate the neonate’s recovery of normal behavior by promoting patterned sensory input. One way this can be accomplished is to enhance diurnal rhythms in the NICU by providing cycles of relative light and dark. Adverse auditory and light exposure should be decreased, and if possible, the neonates should be grouped together to minimize background stimulation. Intervention or procedures could be limited to 15 minutes and performed according to a time schedule. All perinatal nurses may have patients aflected by cocaine use.
The most dramatic symptoms of maternal cocaine use in the neonate are neurobehavioral ones, including irritability, restlessness, and tremulousness. These symptoms, which are characteristic of cocaine-exposed neonates, interfere with the neonate’s ability to interact with and respond to the caretaker, either the mother or the nursing staff, and could put the mother and neonate’s relationship at risk for further development problems. To optimize parent-neonate interaction, the parents must be readily involved in the neonate’s care and progress. For the parents to derive any satisfaction
March/April 1991
from their caretaking activities, they must recognize their individual neonate’s temperament and behavior to determine the nature and timing of intervention. The nurse should facilitate parental recognition and interpretation of these cues. For example, the immature, behaviorally disorganized neonate may not be able to tolerate visual activity for more than 30-60 seconds and will avert his or her eyes. Unless informed to the contrary, the parents may interpret this action as a rejection, as opposed to a time-out period. The parents should be taught to proceed slowly with any intervention and to speak in a calm, soothing voice. Parents can avoid startling cocaine-exposed neonates by gently touching them before changing their positions and allowing the neonates time to reorganize after each interaction to avoid losing control over their behavior. Neonates exposed to cocaine may require swaddling or the provision of physical boundaries around them when they sleep. Foam contour chairs have been used with good results in nurseries, and some parents have used beanbag chairs at home for their neonates. The environment these neonates will do well in is one that is consistent and predictable. The nurse should help the parents plan to regularize the routine care for their neonate after discharge. Parents should be informed of their need to participate in their neonate’s care from the time of admission. During the hospitalization, the nurse should establish a parent-neonate visiting record in the care plan to document visiting patterns, educational sessions, and parent-neonate interaction. Parents are expected to visit or call daily and to bring in clothing or toys for their neonate. Parents should be instructed during their visits about exercises and activities that they can conduct with their neonate. The nurse should facilitate the interpretation of the neonate’s response for the parents to help them realize the progress their neonate is making and to encourage appropriate interaction. The nurse can thereby reduce the frustration of caring for these neonates and promote healthy parentneonate relationships. This situation requires close follow-up of the family. Other educational concerns involve teaching the mother about the increased incidence of SIDS. The mother should learn the risk of SIDS, as well as how to perform cardiopulmonary resuscitation. Some perinatal centers provide all cocaine-exposed neonates with monitors upon discharge.
Summary Cocaine use during pregnancy has serious consequences for the mother and her neonate. Nurses can be instrumental in screening for cocaine use in preg-
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nant women and in educating mothers about t h e effects of cocaine use during pregnancy. Mothers with cocaine-exposed neonates need t o learn h o w t o interact with their neonates, as well as t o learn t h e risks and dangers of SIDS. T h e community pediatrician should be made aware of t h e neonate’s intrauterine cocaine exposure to promote consistency in care. Further stud-
ies are needed to assess the long-term effects of cocaine exposure on infants and children.
References 1. Kozel, N., and E. Adams. 1986. Epidemiology of drug abuse: An overview. Science. 234:970-74. 2. Morganthau, T., and M. Miller. 1988. Getting tough on cocaine. Newsweek, November 28,76-79. 3. Cregler, L., and H. Mark. 1986. Medical complications of cocaine abuse. N Engl JMed. 315:1495-1500. 4. MacGregor, S., L. Keith, I . Chasnoff, etal. 1987. Cocaine use during pregnancy: Adverse perinatal outcome. Am J Obstet Gjwecol. 157:686-90. 5. Bingol, N., M. Fuchs, V. Diaz, R. Stone, and D. Gromisch. 1987. Teratogenicity of cocaine in humans.JPediatr. 110:93-96. 6. Stewart, D., T. Inaba, M. Lucassen, and W. Kalow. 1979. Cocaine metabolism: Cocaine and norcocaine hydrolysis by liver and serum esterases. Clin Pbarmacol Tber. 25:464-68. 7. Chasnoff, I., M. Bussey, R. Savich, and C. Stack. 1986. Perinatal cerebral infarction and maternal cocaine use.J Pediutr. 108:456-59. 8. Chasnoff, I., D. Lewis, and L. Squires. 1987. Cocaine intoxication in a breast-fed infant. Pediatrics. 80:83638. 9. Chasnoff, I., W. Burns, S. Schnoll, and K. Burns. 1985. Cocaine use in pregnancy. N Engl J Med. 313:666-69. 10. Amaro, H., B. Zuckerman, and H. Cabral. 1989. Drug use among adolescent mothers: Profile of risk. Pediatrics. 84:144-51. 11. Townsend, R., F. Laing, and R. Jeffrey. 1988. Placental abruption associated with cocaine abuse. AJR. 150:1339-40. 12. Little, B., L. Snell, V. Klein, and L. Gilstrap. 1989. Cocaine abuse during pregnancy: Maternal and fetal implications. Obstet Gynecol. 75157-60. 13. Woods, J., M. Plessinger, and K. Clark. 1987. Effect of cocaine on uterine blood flow and fetal oxygenation. JAMA. 257:957-61.
14. Moore, T., J. Sort, L. Miller, T. Key, and R. Resnik. 1986. Hemodynamic effects of intravenous cocaine on the pregnant ewe and fetus. Am.] Obstet Gynecol. 155:88388. 15. Chasnoff, I., K. Burns, and W. Burns. 1987. Cocaine use in pregnancy: Perinatal morbidity and mortality. Neurotoxicol Teratol. 9:291-93. 16. Hadeed, A,, and S. Siefel. 1989. Maternal cocaine use during pregnancy: Effect on the newborn infant. Pediatrics. 84:205-10. 17. Mahahk, M., R. Gautieri, and D. Mann. 1980. Teratogenic potential of cocaine hydrochloride in CF-1 mice. J %arm Sci. 69:703-6. 18. Madden, J., T. Payne, and S. Miller. 1986. Maternal cocaine abuse and effect on the newborn. Pediatrics. 77~209-11, 19. Oro, A,, and S . Dixon. 1987. Perinatal cocaine and methamphetamine exposure: Maternal and neonatal correlates. J Pediatr. 111:571-78. 20. Doberczak, T., S. Shanzer, R. Senie, and S. Kandall. 1988. Neonatal neurologic and electroencephalographic effects of intrauterine cocaine exposure. J Pediatr. 115354-58. 21. Chasnoff, I., D. Griffith, S . MacGregor, K. Dirkes, and K. Burns. 1988. Temporal patterns of cocaine use in pregnancy. JAMA. 261:1741-44. 22. Chouteau, M., P. Namerow, and P. Leppart. 1988. The effect of cocaine abuse on birth weight and gestational age. Obstet Gynecol. 72351-54. 23. Teske, M., and M. Trese. 1987. Retinopathyofprematurity-like fundus and persistent hyperplastic primaryvitreous associated with maternal cocaine use. Am JOpbtbalmol. 105719-20. Address for correspondence: Heather Peters, RN, MSN, 10322 S. Austin, Chicago Ridge, IL 60415.
Heather Peters is a graduate student in the Maternal Child Program at Rush University, College of Nursing, Chicago, Illtnots. She currently works at the Unlversity of Illinols in labor and deltvery and for Women’s Health Ltd., a home birth service in Chicago. Ms. Peters is a member of the Illinois Nurses Association, the Midwives’ Alltance of North Amertca, and Sigma Theta Tau. Catherine Jursich Theorell is a practtttoner-teacher at Rush University, College of Nursing, Chicago, Illinots, and 1s a neonatal nurse practitioner in the Special Care Nursery. Ms. Theorell b a member of Alpha Sigma Nu, the National Associatton of Neonatal Nurses, and Sigma Theta Tau.
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