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Cocaine

Toxicology

Cocaine (coke, snow) is an alkaloid (benzoecgonine methyl ester) of the coca bush (Erythroxylon coca), which grows primarily in the Andes. The leaves contain about 1% cocaine. Cocaine was first used as an anesthetic in 1884. It is chemically related to local anesthetics, but has only been proven to be of value for external use in treating eyes, ears, nose, and throat conditions. Crack is the free base of cocaine; Lhis is smoked.

Cocaine blocks the reuptake of noradrenaline and dopamine at the synapse, and in this way increases the catecholamine concentration. This leads to a sympathicomimetic and central stimulating cffect.

When cocaine is taken orally, it is absorbed very slowly becausc of its vasoconstrictive action and the hydrolytic breakdown in the stomach. It is metabolized in the liver within 2 hours to the ineffective primary metabolite, benzoecgonine. About 20% is excreted unchanged via the kidneys. Intranasal absorption occurs within 20 minutes (there is a delay as a result of vasoconstriction). Intravenous administration or crack smoking cause an effect within a few minutes.

In the USA, 4-20% of all pregnant women were said to have experience with cocaine (Fantel 1990). Until the beginning of the 1980s, cocaine was considered to be non-toxic prenatally. Since then, countless developmental disturbances have been attributed to repeated use of cocaine or crack during pregnancy. In the light of the available experience to date, sporadic use in early pregnancy when social relationships are intact and there is no additional damaging factor (such as alcohol, other drugs, infections, malnutrition, or trauma) does not seem to involve any noteworthy increased risk for birth defects.

Documented consequences of cocaine use itself - independent from other drugs - are placenta abruptio and premature rupture of the membranes (Addis 2001). An increased rate of miscarriage, prematurity, stillbirths, intrauterine growth restriction, and microcephaly could not be specifically attributed to cocaine. In addition, there have been reports of cerebral seizures, necrotizing enterocolitis in newborns, birth defects of the urogenital and skeletal systems, as well as intestinal atresia and infarction (Eyler 1998A, Hoyme 1990. Schaefer 1990, Mercado 1989, Chasnoff 1988). A typical "cocaine syndrome" cannot be defined (Little 1996). Furthermore, a meta-analysis covering 33 studies did not find higher risks of major malformations compared with children exposed to poly-drug use but no cocaine (Addis 2001). The wide spectrum of morphological changes that have been attributed to cocaine have been explained as a result of vasoconstriction with reduced circulation both in the area of the placcnta and in the fetal organs. As a result, (focal) differentiation and growth disturbances could be induced during all phases of pregnancy.

Cocaine and crack cause more severe heart, circulatory, and neurological effects in pregnant women than in those who are not pregnant. It has been discussed whether the damage to the embryo following decreased perfusion may not in fact be the direct consequence of oxygen deprivation, but rather may be causcd by a highly reactive toxic oxygen radical following reperfusion of the ischemic tissue. In the first trimester, the fetoplacental unit does not have sufficient protective antioxidants.

Cocaine is found in relatively high concentrations in the amniotic fluid and, due to limited clearance, the level decreases very slowly.

For this reason, the fetus can take in significant amounts of cocaine by swallowing and through its skin, which is quite permeable until the twenty-fourth week of pregnancy (Woods 1998).

The acute symptoms observed in the newborn are less marked than those associated with heroin, and are more apt to be of a toxic nature than related to withdrawal - for example, sleep disturbances, tremor, weak suck, hypertonia, vomiting, high-pitched crying, sneezing, tachypnea, soft stools, and fever. Beyond this, in some studies noticeable deviations from the norm were observed in neurological tests in newborns, EEC changes, and sudden infant death, as well as later behavioral deviations and (motor) developmental disturbances (Eyler 1998B). However, a review covering 36 publications concludcd that among children aged 6 years or younger there is no convincing evidence that prenatal cocaine exposure is associated with morphological and functional (e.g. language) developmental toxic effects that are independent from prenatal exposure to tobacco, marijuana or alcohol (Beeghly 2006, Schiller 2005, Bandstra 2004, 2002, Messinger 2004, Frank 2001).

Recommendation. Because cocaine has potentially toxic effects on development, it should not be used during pregnancy. However, cocaine use does not necessarily justify interruption of the pregnancy. In the case of repeated use, especially when living conditions are problematic, the normal development of the fetus should be confirmed with detailed ultrasound.

Amphetamines

Toxicology

Due to their vasoconstrictive effects in high doses, amphetamine derivatives such as in "speed" and "ecstasy" can, similar to cocaine, lead to lowered perfusion of the fetoplacental unit or of individual fetal organs. There has as yet been no consistent indication that sporadic use, when the living conditions are otherwise intact, increases the risk of congenital anomalies. However, some older publications from the 1970s describe birth defects in connection with the use of amphetamines during pregnancy (surveyed in Schardein 2000). In addition, in a prospectively collected series of cases of 136 pregnant women exposed to ecstasy (without a control group), 12 developmental anomalies were described among the 78 live-born babies. However, some of these were minor anomalies, (i.e. foot deformities). No typical pattern could be discerned. Just about half of the mothers had also consumed alcohol or other drugs in quantities that were not defined (McElhatton 1999). In a further study of 228

pregnant users, the rate of minor developmental anomalies was double that observed in an unexposed control group. There was an increase, in the newborn period, of neurological symptoms, including disturbances of muscle tone and hyperexcitability. The rate of spontaneous abortion was not increased, but there were three stillborn babies in the exposed group (Felix 2000). In this study, too, tobacco and alcohol and. to some extent, other drugs were also consumed. For an overview of developmental casuistics and maternal exposure to amphetamines, see Golub (2005).

Among 65 children followed-up until 14 years of age, a significant number had learning difficulties at school. However, a large percentage of the mothers not only abused amphetamines during their pregnancies, but also consumed opiates and alcohol, smoked more than 10 cigarettes a day, and were in problematic psychosocial situations. At the age 14 years, only 22% of the children still lived with their mothers (Cernerud 1996).

A Thai study of 47 newborns born to mothers who were metham-phetamine abusers during pregnancy concluded that such in utero exposure caused a wide variety of withdrawal symptoms and significantly smaller-for-date infants. No gross malformations were found (Chomchai 2004). Similar fetal growth restriction was noted in a US population (Smith 2006).

Recommendation. Pregnant women should avoid amphetamines under all circumstances. However, exposure does not justify interruption of the pregnancy. If there has been significant consumption during the first trimester, the normal development of the fetus should be monitored with detailed ultrasound.

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