PHENCYCLIDINE

Fetal Risk Summary

Phencyclidine (PCP) is an illicit drug used for its hallucinogenic effects. Transfer to the fetus has been demonstrated in humans with placental metabolism of the drug (1,2,3,4,5,6 and 7) . Qualitative analysis of the urine from two newborns revealed phencyclidine levels of 75 ng/mL or greater up to 3 days after birth (2). In 24 (12%) of 200 women evaluated at a Los Angeles hospital, cord blood PCP levels ranged from 0.10 to 5.80 ng/mL (3). Cord blood concentrations were twice as high as maternal serum–1215 vs. 514 pg/mL in one woman who allegedly consumed her last dose approximately 53 days before delivery (4). PCP in the newborn's urine was found to be 5841 pg/mL (4).

Relatively few studies have appeared on the use of phencyclidine during pregnancy, but fetal exposure may be more common than this lack of reporting indicates. During a 9-month period of 1980–1981 in a Cleveland hospital, 30 of 519 (5.8%) consecutively screened pregnant patients were discovered to have PCP exposure (8). In a subsequent report from this same hospital, 2,327 pregnant patients were screened for PCP exposure between 1981 and 1982 (6). Only 19 patients (0.8%) had positive urine samples, but up to 256 (11%) or more may have tested positive with more frequent checking (6). In the Los Angeles study cited above, 12% were exposed (3). However, the specificity of the chemical screening methods used in this latter report have been questioned (7).

Most pregnancies in which the mother used phencyclidine apparently end with healthy newborns (3,4,9). However, case reports involving four newborns indicate that the use of this agent may result in long-term damage (2,9,10): Depressed at birth, jittery, hypertonic, poor feeding (2) (2 infants) Irritable, poor feeding and sucking reflex (9) (1 infant) Triangular-shaped face with pointed chin, narrow mandibular angle, antimon-   goloid slanted eyes, poor head control, nystagmus, inability to track visually,   respiratory distress, hypertonic, jitteriness (10) (1 infant) Irritability, jitteriness, hypertonicity, and poor feeding were common features in the affected infants. In three of the neonates, most of the symptoms had persisted at the time of the report. In the case with the malformed child, no causal relationship with PCP could be established. Marijuana was also taken, and it is a known teratogen in some animal species (11). However, marijuana is not considered to be a human teratogen (see Marijuana).

A study published in 1992 described the effects of PCP on human fetal cerebral cortical neurons in culture (12). High levels of the drug caused progressive degeneration and death of the neurons whereas sublethal concentrations inhibited axonal outgrowth. Because the fetal central nervous system can concentrate and retain PCP, these results suggested that PCP exposure during pregnancy could produce profound functional impairments (12).

Abnormal neurobehavior in the newborn period was observed in nine infants delivered from mothers who had used PCP during pregnancy (13). The abnormality was significantly more than that observed in control infants and those exposed in utero to opiates, sedative/stimulants, or the combination of pentazocine and tripelennamine (i.e., T's and blue's). However, by 2 years of age, the mental and psychomotor development of all of the drug-exposed infants, including those exposed to PCP, were similar to controls.

Breast Feeding Summary

Phencyclidine (PCP) is excreted into breast milk (14). One lactating mother, who took her last dose 40 days previously, excreted 3.90 ng/mL in her milk. In animal studies, milk concentrations of PCP were 10 times those of plasma (1). Women consuming PCP should not breast-feed. The American Academy of Pediatrics considers the drug to be contraindicated during breast feeding (15).

References

1. Nicholas JM, Lipshitz J, Schreiber EC. Phencyclidine: its transfer across the placenta as well as into breast milk. Am J Obstet Gynecol 1982;143:143–6.
2. Strauss AA, Modanlou HD, Bosu SK. Neonatal manifestations of maternal phencyclidine (PCP) abuse. Pediatrics 1981;68:550–2.
3. Kaufman KR, Petrucha RA, Pitts FN Jr, Kaufman ER. Phencyclidine in umbilical cord blood: preliminary data. Am J Psychiatry 1983;140:450–2.
4. Petrucha RA, Kaufman KR, Pitts FN. Phencyclidine in pregnancy: a case report. J Reprod Med 1982;27:301–3.
5. Rayburn WF, Holsztynska EF, Domino EF. Phencyclidine: biotransformation by the human placenta. Am J Obstet Gynecol 1984;148:111–2.
6. Golden NL, Kuhnert BR, Sokol RJ, Martier S, Bagby BS. Phencyclidine use during pregnancy. Am J Obstet Gynecol 1984;148:254–9.
7. Lipton MA. Phencyclidine in umbilical cord blood: some cautions. Am J Psychiatry 1983;140:449.
8. Golden NL, Sokol RJ, Martier S, Miller SI. A practical method for identifying angel dust abuse during pregnancy. Am J Obstet Gynecol 1982;142:359–61.
9. Lerner SE, Burns RS. Phencyclidine use among youth: history, epidemiology, and acute and chronic intoxication. In Petersen R, Stillman R, eds. Phencyclidine (PCP) Abuse: An Appraisal. National Institute on Drug Abuse Research Monograph No. 21, US Government Printing Office, 1978.
10. Golden NL, Sokol RJ, Rubin IL. Angel dust: possible effects on the fetus. Pediatrics 1980;65:18–20.
11. Persaud TVN, Ellington AC. Teratogenic activity of cannabis resin. Lancet 1968;2:406–7.
12. Mattson MP, Rychlik B, Cheng B. Degenerative and axon outgrowth-altering effects of phencyclidine in human fetal cerebral cortical cells. Neuropharmacology 1992;31:279–91.
13. Chasnoff IJ, Burns KA, Burns WJ, Schnoll SH. Prenatal drug exposure: effects on neonatal and infant growth and development. Neurobehavior Toxicol Teratol 1986;8:357–62.
14. Kaufman KR, Petrucha RA, Pitts FN Jr, Weekes ME. PCP in amniotic fluid and breast milk: case report. J Clin Psychiatry 1983;44:269–70.
15. Committee on Drugs, American Academy of Pediatrics. The transfer of drugs and other chemicals into human milk. Pediatrics 1994;93:137–50.