4.6 Article

Association between maternal labour epidural analgesia and autistic traits in offspring

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JOURNAL OF CLINICAL ANESTHESIA
卷 89, 期 -, 页码 -

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ELSEVIER SCIENCE INC
DOI: 10.1016/j.jclinane.2023.111162

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This is an observational study investigating the association between maternal epidural analgesia (MEA) and autism spectrum disorder (ASD) in children. The study found no significant association between MEA and the development of ASD and autistic traits. This study is important for assessing the impact of maternal epidural analgesia on child health.
Study objective: Studies investigating associations between maternal epidural analgesia (MEA) and autism spectrum disorder (ASD) in the offspring are conflicting and lack prospective neurobehavioral follow-up assessments for autistic traits. We aim to prospectively investigate associations between MEA and autistic traits in the offspring. Design: Prospective neurobehavioral observational cohort study. Setting: Singaporean tertiary healthcare institutions. Patients: Participants recruited were singleton non-IVF children, >36 weeks gestation, delivered via normal vaginal delivery by mothers >18 years of age, delivered in Singapore from June 2009-September 2010 and followed up over 7 years. Interventions: Exposure to maternal epidural analgesia during delivery. Measurements: The primary outcome is an abnormal Social Responsiveness Scale (SRS) T score at 7 years (=60 points). Secondary outcomes include the diagnosis of ASD and abnormal scores for autistic traits assessed via a neurobehavioral battery comprising: CBCL (child behavioural checklist), Q-CHAT (Quantitative Checklist for Autism in Toddlers), and Bayley-III. Multivariable analyses adjusting for maternal and offspring characteristics were performed. Main results: 704 out of 769 mother-child dyads recruited fulfilled the criteria for analysis. 365/704 mothers received MEA. The incidence of an abnormal SRS score at 7 years in offspring exposed to MEA was 19.9%, and 26.1% in non-exposed offspring (p = 0.154). Multivariable analysis did not demonstrate a significant association between MEA and abnormal SRS scores at 7 years (O.R.0.726, 95% C.I. 0.394-1.34, p = 0.305). After adjustment for maternal and fetal demographics, exposure to MEA was not significantly associated with an abnormal screen in all other tests for autistic traits. The clinical incidence of ASD was 1.76% in children without exposure to MEA, and 2.32% in children with MEA exposure (p = 0.506). Conclusions: MEA is not significantly associated with the development of ASD and autistic traits in offspring, assessed over 7 years. Results should be taken into perspective given our wide confidence intervals and small cohort size.

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