Cocaine
Drugs and Chemicals Associated with Birth Defects
Cocaine (street names “coke;’ “snow;’ “lady;’ and “gold dust”) use is a major public health concern. Use of cocaine in the 1970s was primarily limited to the intranasal route. In the 1980s, a decrease in the street cost and wider availability of cocaine resulted in an increasing prevalence of intravenous and smoked (”free-base” or “crack”) routes of use. Consequently, the prevalence of cocaine-associated medical complications has increased. Cocaine is commonly used intranasally (”snorting”), by injection, and by smoking the free alkaloid form (crack). Crack (named after the cracking or popping sound that is made when the crystals are ignited in a pipe while smoking the drug) is a highly purified form of free alkaloid cocaine. In a survey of a number of urban hospitals nationwide, positive urine toxicology for cocaine metabolites was detected among 10-48% of pregnant women. The crack form of cocaine is believed to be more addictive than other forms. Administered systemically, cocaine blocks the presynaptic reuptake of neurotransmitters (norepinephrine and dopamine), causing these neurotransmitters to accumulate at postsynaptic receptor sites, resulting in intense vasoconstriction, acute arterial hypertension, and tachycardia.
The drug is metabolized primarily by plasma and hepatic cholinesterases to water-soluble metabolites (benzoylecgonine and ecgonine methyl ester). The most commonly used urine test detects benzoylecgonine at a sensitivity of 300 ng/mL. The elimination half-life of the parent drug is approximately 4-5 hours. Cocaine metabolites can be detected in urine for 24-48 hours. Pharmacokinetics of peri-natal cocaine use are poorly studied, but cocaine is known to cross the placenta readily. It is thought that urine tests in neonates exposed to cocaine in utero may be positive for a similar time as they are in an adult, although benzoylecgonine has been detected in neonatal urine for up to 4 days.
Potentially lethal medical complications associated with cocaine use, directly or indirectly, seem attributable to the intense sympathomimetic effects of the drug. They include acute myocardial infarction, cardiac arrhythmias, rupture of the ascending aorta, cerebrovascular accidents, seizures, bowel ischemia, and hyperthermia.
Use or abuse of cocaine during pregnancy is a major risk factor for the mother and her unborn child. Most pregnant cocaine users are patients with unplanned pregnancies of uncertain gestational age who seek prenatal care late (if at all) and have poor nutrition. They also tend to be abusers of multiple drugs, including tobacco and alcohol. It seems clear that there is, at minimum, a risk of 25% for preterm birth and 20% for infants that are small for gestational age, but studies are confounded by the effects of poor health and use of other substances of abuse. Studies have indicated as much as a 10-fold increase in the risk of abruption, suggesting an increase from 0.1% among all pregnancies to a 1% risk among cocaine-exposed pregnancies. Neurobehavioral abnormalities in neonates exposed to cocaine in utero are well documented, especially the tendency for hyperirritability and an inability to respond appropriately to stimulation. A purported increased incidence of sudden infant death syndrome among cocaine-exposed infants was suggested but has not been confirmed. An increased frequency of certain congenital anomalies among cocaine-exposed neonates has been reported. These anomalies include congenital heart disease, intestinal atresias, cerebral infarction, brain cavitation defects, and genitourinary defects.
It is thought that the increased risk of congenital anomalies among cocaine-exposed infants is associated with cocaine-induced vasoconstriction, which may cause infarction, severe hypoxemia, and hypoperfusion that may interrupt normal morphogenesis. A pattern of anomalies termed the vascular disruption syndrome has been described. The mechanism of vascular disruption is supported by animal studies that showed dose-dependent decreases in uterine blood flow and marked fetal hypoxemia, hypertension, hypoperfusion, and tachycardia in experimental animals that were administered cocaine intravenously.
Clinical evaluation of obstetric patients should incorporate the following protocol, which the clinician should consider for both medical and legal reasons:
• All pregnant women should be asked about previous and current drug use at the time of the first prenatal visit.
• The life-threatening implications of cocaine use during pregnancy for the patient and for her infant should be clearly explained to the pregnant woman admitting to cocaine use. She should be offered support services to aid in her abstinence.
• Continued abstinence from the use of cocaine should be reinforced and encouraged. Periodic urine testing for metabolites of cocaine is one way to discourage relapse in a pregnant woman admitting to cocaine use before or during pregnancy. The requirements for consent may vary from state to state.
• Urine testing of the mother, the neonate, or both may be useful in some clinical situations, such as unexplained fetal growth restriction, unexpected prematurity, or abruption in a woman not known to have hypertensive disease, even when cocaine abuse has not been previously suspected. The mother’s consent may need to be obtained before testing.
• Physicians should be familiar with their own state laws regarding consent for drug screening of pregnant women and newborns.
• Some state laws consider in utero drug exposure a form of child abuse or neglect and require the reporting of positive drug tests in pregnant women and newborns. Physicians should be familiar with state laws regarding testing and reporting.
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