Risk of intracranial hemorrhage and other adverse outcomes after cocaine exposure in a cohort of 323 very low birth weight infants
1993; Elsevier BV; Volume: 122; Issue: 3 Linguagem: Inglês
10.1016/s0022-3476(05)83438-9
ISSN1097-6833
AutoresAnna M. Dusick, Robert Covert, Michael D. Schreiber, Gloria T. Yee, Susan P. Browne, Christine Moore, Ian R. Tebbett,
Tópico(s)Neonatal and fetal brain pathology
ResumoWe conducted a prospective cohort study of 323 consecutively born very low birth weight infants (≤1499 gm) to determine any association between prenatal cocaine exposure and (1) intracranial ultrasonographic abnormalities and (2) other adverse perinatal outcomes. The infants were assigned to either a cocaine-exposed group (n=86) or a cocaine-nonexposed group (n=146) on the basis of combined detection methods for prenatal maternal cocaine abuse including matermal history, matermal and infant urine immunoassay (Emit), and meconium analysis (high-performance liquid chromatography and gas chromatography-mass spectrometry). Ninety-one infants were not assigned because of early death before complete testina (n=80) or missed tests (n=11). The detected incidence of cocaine exposure in the assigned population was 37% (86/232). Meconlum testing with high-performance liquid chromatography and gas chromatography-mass spectrometry was the sole means of detection In 30% (26/86) of cases. The cocaine-nonexposed infants did not differ from the cocaine-exposed infants in the incidence of intraventricular hemorrhage (36% vs 35%), grades III and IV intraventricular hemorrhage (14% vs 14%), or periventricular leukomalacla (4% vs 2%). Adverse outcomes increased by cocaine exposure were abruptio placentae (8% vs 18%; p=0.046), surgical ligation of a patent ductus arteriosus (1% vs 7%; p=0.02), and seizures (5% vs 17%; tP=0.004). We conclude that prenatal cocalne exposure does not increase the incidence or severity of intracranial hemorrhage or periventricular leukomalacla but does increase the risk of abruptio placentae, surgical ligation of a patent ductus arteriosus and selzures in very low birth weight infants. We conducted a prospective cohort study of 323 consecutively born very low birth weight infants (≤1499 gm) to determine any association between prenatal cocaine exposure and (1) intracranial ultrasonographic abnormalities and (2) other adverse perinatal outcomes. The infants were assigned to either a cocaine-exposed group (n=86) or a cocaine-nonexposed group (n=146) on the basis of combined detection methods for prenatal maternal cocaine abuse including matermal history, matermal and infant urine immunoassay (Emit), and meconium analysis (high-performance liquid chromatography and gas chromatography-mass spectrometry). Ninety-one infants were not assigned because of early death before complete testina (n=80) or missed tests (n=11). The detected incidence of cocaine exposure in the assigned population was 37% (86/232). Meconlum testing with high-performance liquid chromatography and gas chromatography-mass spectrometry was the sole means of detection In 30% (26/86) of cases. The cocaine-nonexposed infants did not differ from the cocaine-exposed infants in the incidence of intraventricular hemorrhage (36% vs 35%), grades III and IV intraventricular hemorrhage (14% vs 14%), or periventricular leukomalacla (4% vs 2%). Adverse outcomes increased by cocaine exposure were abruptio placentae (8% vs 18%; p=0.046), surgical ligation of a patent ductus arteriosus (1% vs 7%; p=0.02), and seizures (5% vs 17%; tP=0.004). We conclude that prenatal cocalne exposure does not increase the incidence or severity of intracranial hemorrhage or periventricular leukomalacla but does increase the risk of abruptio placentae, surgical ligation of a patent ductus arteriosus and selzures in very low birth weight infants.
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