Ultrasound diagnosis of fetal anomalies associated with in utero cocaine exposure: further support for cocaine-induced vascular disruption teratogenesis

• Published in: Fetal diagnosis and therapy Vol. 9; no. 4; p. 239
• Main Authors: Hume, Jr, R F, Gingras, J L, Martin, L S, Hertzberg, B S, O'Donnell, K, Killam, A P
• Format: Journal Article
• Language: English
• Published: Switzerland 01-07-1994
• Subjects: Abnormalities, Drug-Induced - diagnostic imaging; Abnormalities, Drug-Induced - epidemiology; Adolescent; Adult; Cocaine - adverse effects; Female; Fetal Diseases - chemically induced; Humans; Maternal-Fetal Exchange; Pregnancy; Risk Factors; Ultrasonography, Prenatal; Vascular Diseases - chemically induced
• ISSN: 1015-3837
• DOI: 10.1159/000263940

The dramatic increase in cocaine use over the past decade has led to a concern about its possible teratogenicity. We have identified 6 structural fetal anomalies which we postulate may have cocaine-induced vascular accidents as the teratogenic mechanism: 2 complex choroid plexus cysts, gastroschisis, meconium peritonitis, urethral stenosis, and radial hypoplasia. Two additional anomalous neonates were born to perinatal cocaine users. Eight of 51 (15.7%) cocaine-exposed perinates exhibited anomalies versus 120 of 2,194 (5.4%) perinates without known cocaine exposure during this time period. This represents a 3-fold relative risk (RR = 2.87, OR = 3.22, chi square = 9.68, p < 0.005) for the cocaine-exposed fetus. Subjects were all identified as cocaine users prior to ultrasound-detected anomaly and ultrasonologists were blinded to maternal drug history. The vascular disruption model as the plausible mechanism for cocaine-associated teratogenesis is supported by the type of anomalies reported. In addition, cocaine use was prospectively determined to have occurred at the critical developmental period in each case.