Improving Treatment for Drug-Exposed Infants
Treatment Improvement Protocol (TIP) Series 5

Effects of Cocaine Exposure on the Neonate

The abuse of cocaine became an alarming problem during the last decade. It is estimated that up to 8 million Americans use cocaine regularly and 30 to 40 percent of cocaine addicts are women. Cocaine use by pregnant women has multiple adverse influences on the mother's health, pregnancy outcome, and the well-being of the infants as discussed in recent review articles (Bandstra and Burkett, 1991; Dixon and Bejar, 1989; Dixon, Bresnahan, and Zuckerman, 1990; and Kandall, 1991, a and b). These effects are summarized in Exhibit 5, and are discussed in detail below.

As with heroin addiction, adverse effects may be due to the life circumstances and behavior of the mother as well as to the pharmacologic properties of cocaine itself.

Lack of prenatal care, poor nutrition, medical problems, and abuse of other drugs and alcohol pose significant risk to the mother and the fetus. In addition, cocaine use increases the possibility of the mother's engaging in behaviors such as unprotected sex that place her at risk for contracting HIV.

The pharmacologic action of cocaine inhibits uptake of norepinephrine in the synaptic cleft, thus leading to vasoconstriction, hypertension, and tachycardia. In animal models, cocaine increases uterine vascular resistance and decreases uterine blood flow with resulting fetal hypoxemia.

Therefore, cocaine may play an etiologic role in causation of abruptio placentae, premature labor, intrauterine growth retardation, and fetal vascular disruption. Cocaine exposure causes a direct neurotoxicity manifested by neurobehavioral disturbances that are usually less striking than those associated with opiate abstinence syndrome.

These neurobehavioral disturbances may be transient, and usually do not require treatment. An encephalopathic syndrome - including irritability, tremulousness, lethargy, somnolence, labile state, decreased habituation, and visual tracking difficulties - has been described in cocaine-exposed newborn infants by many investigators. In addition to clinical signs of cocaine-induced neurotoxicity, transient encephalographic abnormalities can be demonstrated in this population of infants. Besides clinical and encephalographic abnormalities, echoencephalographic abnormalities are found in some cocaine-exposed infants (Dixon and Bejar, 1989). Lesions varying from ischemic injury with cavitation to intraventricular hemorrhage and ventricular dilation are observed in 8-14 percent of the study population. Cerebral infarctions have also been described in other reports. In some infants, physiologic dysfunction is indicated by alterations in vital signs including tachycardia and hypertension, and cardiac arrhythmias. The risk of sudden infant death syndrome in this population of infants may be increased, but large epidemiologic studies are needed in order to differentiate between effects of cocaine and other factors, such as low socioeconomic status, polydrug abuse, and smoking.

Long-term effects of intrauterine cocaine exposure, as well as poly-drug exposure, are described in anecdotal reports, and include attention deficits, flat apathetic moods, decreased fantasy play, and other observations. However, long-term followup studies of cocaine-exposed children are scarce at present (Chasnoff et al., 1992).

Subtle neurobehavioral aberrations may persist beyond the neonatal period. Cocaine may produce long-term neurodysfunction, which is now being described anecdotally among the first cohort of babies exposed to crack in utero as they enter nursery school. The biologic vulnerability of infants exposed to crack in utero is modulated by the environment. The poor psychosocial, nutritional, medical, and socioeconomic status of the mother can all contribute to long-term neurodysfunctional sequelae in the infant (Mayes et al., 1992; Zuckerman and Frank, 1992). Additional risk factors - including intrauterine growth retardation, CNS pathology, prolonged hospitalization, and lack of intellectual nurturing - must be taken into consideration in evaluation of long-term neurobehavioral outcome of cocaine-exposed infants.

Treatment for Cocaine-Exposed Neonates

Treatment for the neonate demands an appropriate nursery environment, comprehensive assessments, pharmacologic intervention, and clinical diagnostic studies.

1. Optimal Nursery Environment - Such an environment features sound primary nursing care, gentle handling by as few caretakers as possible, and an avoidance of stimuli such as light and noise that will irritate the baby. To facilitate and promote optimal infant growth and development, nursery personnel should carefully monitor feeds, initiate strategies to facilitate intake for those infants experiencing feeding difficulties, observe for feeding intolerance or necrotizing enterocolitis, provide opportunities to interact with parents and environment as the infant is able to tolerate them, and provide primary nursing to facilitate parent-infant interactions.
2. Brazelton Neonatal Behavioral Assessment Scale - Use of the Brazelton Neonatal Behavioral Assessment Scale (Brazelton, 1984) is encouraged. This scale has been used extensively to evaluate newborn behavior such as habituation and responsivity to stimuli (faces, voices, light, bell, rattle, etc.); state (sleeping, alertness); characteristics of changes in state (irritability, inconsolability); and neurological and motor development. Although clinical expertise is demanded to administer the Brazelton Scale, programs will find it useful in evaluating infants exposed to drugs (Finnegan, 1986).
3. Neonatal Neurotoxicity Assessment - While asymptomatic infants do not need to be systematically assessed for neonatal neurotoxicity, consideration should be given to developing scoring criteria for those infants who are symptomatic. In the presence of significant withdrawal symptoms, other etiologies, including polydrug and alcohol exposure and metabolic problems, should be explored.
4. Pharmacotherapy - If irritability persists in an infant, a short course of phenobarbital is recommended.
5. Central Nervous System Imaging - Cranial sonograms are not routinely recommended, but recent literature is suggestive of CNS abnormalities, including hemorrhagic ischemic lesions in some drug-exposed infants. (Dixon and Bejar, 1989; Heier et al., 1991 a and b). As yet, evidence is insufficient to support a mandate for cranial sonograms in all cocaine-exposed infants. However, special consideration should be given to specific neuroimaging of cocaine-exposed preterm infants, infants whose head circumference falls below the 10th percentile on standardized fetal growth curves, and infants with abnormal neurologic signs, neurobehavioral dysfunction, or seizure activity.
6. Assessment for Congenital Malformations / Vascular Disruptions - Clinicians should have a heightened awareness of the possibility of uncommon but significant congenital malformations or vascular disruptions reported in cocaine-exposed neonates. Systems that may be affected include the genitourinary tract, cardiovascular system (congenital heart malformations), gastrointestinal tract, and skeletal system. Echocardiography and abdominal ultrasound are not currently recommended as routine assessments in cocaine-exposed infants, but should be performed based on clinical indications.
7. Sudden Infant Death Syndrome - As indicated earlier, SIDS is a multifactorial problem, and opiate exposure is known to increase the neonate's risk of SIDS. There is some controversy over the incidence of SIDS in cocaine-exposed infants, but crack cocaine does appear to raise the risk slightly over controls. Data also suggest that cocaine-exposed infants may exhibit respiratory dysfunction. There are no indications that apnea monitoring decreases the incidence of SIDS. Routine home apnea monitoring for drug-exposed infants is therefore not recommended.