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Indomethacin tocolysis and neurodevelopmental outcome.
Indian Journal of Pediatrics 2011 August
OBJECTIVE: To compare the neurodevelopmental outcomes, at 30-42 months adjusted age, between infants exposed to antenatal indomethacin and those unexposed to antenatal indomethacin.
METHODS: This was a retrospective cohort study. The study cohort consisted of all nonanomalous infants with birth weight ≤ 1250 g and/or gestational age ≤ 28 wks born between 2000 and 2003, who completed neurodevelopmental assessments between 30-42 months adjusted age. The authors compared the neurodevelopmental outcomes of infants exposed and unexposed to antenatal indomethacin.
RESULTS: Of the 321 infants, 75 infants (23%) exposed to antenatal indomethacin were lower in gestational age (26.4 vs 27.8 wks). In univariate analysis, infants exposed to antenatal indomethacin had significantly increased incidence of patent ductus arteriosus (PDA) (60% vs. 39%), surgical PDA ligation (40% vs. 18%) and bronchopulmonary dysplasia (81% vs. 60%). There was no significant difference in cerebral palsy, cognitive delay, deafness, blindness and major disability between the two groups. In multivariable logistic regression analysis, antenatal indomethacin exposure was not associated with cerebral palsy (OR, 0.70; 95% CI, 0.22-2.18), cognitive delay (OR, 0.56; 95% CI, 0.28-1.12) or neurodevelopmental disability (OR, 0.50; 95% CI, 0.21-1.19).
CONCLUSIONS: Neurodevelopmental outcome of preterm infants exposed to antenatal indomethacin is equivalent to those unexposed to antenatal indomethacin, despite being born earlier.
METHODS: This was a retrospective cohort study. The study cohort consisted of all nonanomalous infants with birth weight ≤ 1250 g and/or gestational age ≤ 28 wks born between 2000 and 2003, who completed neurodevelopmental assessments between 30-42 months adjusted age. The authors compared the neurodevelopmental outcomes of infants exposed and unexposed to antenatal indomethacin.
RESULTS: Of the 321 infants, 75 infants (23%) exposed to antenatal indomethacin were lower in gestational age (26.4 vs 27.8 wks). In univariate analysis, infants exposed to antenatal indomethacin had significantly increased incidence of patent ductus arteriosus (PDA) (60% vs. 39%), surgical PDA ligation (40% vs. 18%) and bronchopulmonary dysplasia (81% vs. 60%). There was no significant difference in cerebral palsy, cognitive delay, deafness, blindness and major disability between the two groups. In multivariable logistic regression analysis, antenatal indomethacin exposure was not associated with cerebral palsy (OR, 0.70; 95% CI, 0.22-2.18), cognitive delay (OR, 0.56; 95% CI, 0.28-1.12) or neurodevelopmental disability (OR, 0.50; 95% CI, 0.21-1.19).
CONCLUSIONS: Neurodevelopmental outcome of preterm infants exposed to antenatal indomethacin is equivalent to those unexposed to antenatal indomethacin, despite being born earlier.
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