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Objective. To determine circadian variation in the onset of placental abruption. Methods. A retrospective study involving 115 placental abruptions, divided into four subgroups based on initial symptoms comprising abdominal pain, vaginal bleeding, both abdominal pain and bleeding, or other symptoms. The time of the initial symptom was considered the disease onset. We analyzed the frequency of disease onset and adverse perinatal outcome including perinatal death relative to the daily four 6-hour intervals. Results. Abdominal pain displayed significant circadian variation regarding the period of onset with higher levels from 0:00 AM to 6:00 AM (65%) compared with 0:00 PM to 6:00 PM (24%, p < 0.01). Vaginal bleeding did not display significant circadian variation (p = 0.45). Adverse perinatal outcome showed significant circadian variation with a higher occurrence of perinatal death from 0:00 AM to 6:00 AM (35%) compared with 0:00 PM to 6:00 PM (0%, p < 0.01). After adjustment using variables of abdominal pain and time period, both variables significantly affected perinatal death (odds ratio: 13.0 and 2.2, resp.). The risk of adverse perinatal outcome increased significantly when abdominal pain occurred, except for the period 0:00 PM to 6:00 PM (OR, 9.5). Conclusion. Placental abruption beginning with abdominal pain has circadian variation.

Aims Growth‐restricted fetuses have delayed rhythm formation in utero. The awake–sleep cycle of fetal heart rate pattern is thought to represent fetal rhythm. We aimed to study if the emergence of rhythm formation on fetal heart rate pattern delays in fetal growth restriction compared to appropriate‐for‐date fetuses. Methods This was a retrospective cohort study including 75, normal‐structured, singleton fetuses. Of them, 21 were fetal growth restriction and the remaining 54 were appropriate‐for‐date infants. We examined timing of emergence of rhythm formation on fetal heart rate pattern comparing between fetal growth restriction and appropriate‐for‐date fetuses after adjusting possible confounding factors as outcome measures. Results Rhythm formation was significantly delayed in fetal growth restriction (<10th percentile) compared to the appropriate‐for‐date subgroups (10–30, 30–50, 50–70 and 70–90th percentile) by 1–2 weeks. After adjusting confounding factors, growth restriction was the only independent variable to delay fetal rhythm formation. One infant for each group had neurodevelopmental disorder and the incidence did not reach statistically significant. Conclusion Based on fetal heart rate pattern analysis, growth‐restricted fetuses show 1–2 weeks delay in rhythm formation compared to appropriate‐for‐date fetuses.

Aims: Magnesium sulfate has neuroprotective effects in preterm infants. Whether other antepartum treatments interfere with the neuroprotective actions is not well known. This study aims to explore the impacts of antenatal administration of Magnesium sulfate or beta-2 adrenergic agonists as tocolytic agents on the developing brain in premature infants. Methods: This is a retrospective cohort study in four tertiary perinatal centers in Japan. We collected data of pregnant women and infants born between 28 and 36 weeks for tocolytic agents, gestational age, sex, antenatal corticosteroid, fetal growth restriction, pathological chorioamnionitis, low umbilical arterial pH values (<7.1), multiple pregnancy, mode of delivery and institutions after excluding clinical chorioamnionitis, non-reassuring fetal status or major anomalies. Tocolytic agents were categorized into four groups: no-tocolysis, magnesium sulfate, beta-2 adrenergic agonists and the combination of them. We conducted multiple comparisons with multivariate analyses using generalized linear regression models to compare the prevalence of a poor perinatal outcome defined as infant's death, brain damage, particularly cerebral palsy and developmental delay. Results: Among 1083 infants, 39% were no-tocolysis, 47% were magnesium sulfate, 41% were beta-2 adrenergic agonists and 27% were combination group, including the duplication. The incidence of poor perinatal outcome was decreased by magnesium sulfate (OR 0.27, 95% CI 0.10-0.72), but not changed significantly by beta-2 adrenergic agonists (OR 1.28, 95% CI 0.63-2.59) or the combination group (OR 2.24, 95% CI 0.67-7.54), compared with the no-tocolysis. Conclusion: The combination therapy for tocolysis with beta-2 adrenergic agonists diminished the magnesium sulfate neuroprotective action after adjusting for covariables.