Misoprostol is an effective and safe agent for induction of labor in women with term premature rupture of membranes. When compared with oxytocin, the risk of contraction abnormalities and the rate of maternal and neonatal complications were similar among the 2 groups.

Animal and human studies show that in-utero exposure to preeclampsia alters fetal programming and results in long-term adverse cardiovascular outcomes in the offspring. Human epidemiologic data also suggest that offspring born to preeclamptic mothers are also at risk of adverse long term neurodevelopmental outcomes. Pravastatin, a hydrophilic lipid-lowering drug with pleiotropic properties, was found to prevent the altered cardiovascular phenotype of preeclampsia and restore fetal growth in animal models, providing biological plausibility for its use as a preventive agent for preeclampsia. In this study, we used a murine model of preeclampsia based on adenovirus over-expression of the anti-angiogenic factor soluble Fms-like tyrosine kinase 1, and demonstrated that adult offspring born to preeclamptic dams perform poorly on assays testing vestibular function, balance, and coordination, and that prenatal pravastatin treatment prevents impairment of fetal programming.

BACKGROUND: A leading cause of preventable maternal death is related to delayed response to clinical warning signs. Electronic surveillance systems may improve detection of maternal morbidity with automated notifications. This retrospective observational study evaluates the ability of an automated surveillance system and the Maternal Early Warning Criteria (MEWC) to detect severely morbid postpartum hemorrhage (sPPH) after delivery. METHODS: The electronic health records of adult obstetric patients of any gestational age delivering between April 1, 2017 and December 1, 2018 were queried to identify scheduled or unscheduled vaginal or cesarean deliveries. Deliveries complicated by sPPH were identified and defined by operative management of postpartum hemorrhage, transfusion of ≥4 units of packed red blood cells (pRBCs), ≥2 units of pRBCs and ≥2 units of fresh-frozen plasma, transfusion with >1 dose of furosemide, or transfer to the intensive care unit. The test characteristics of automated pages and the MEWC for identification of sPPH 24 hours after delivery were determined and compared using sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) and their 95% confidence intervals (CIs). McNemar test was used to compare these estimates for both early warning systems. RESULTS: The average age at admission was 30.7 years (standard deviation [SD] = 5.1 years), mean gestational age 38 weeks 4 days, and cesarean delivery accounted for 30.0% of deliveries. Of 7853 deliveries, 120 (1.5%) were complicated by sPPH. The sensitivity of automated pages for sPPH within 24 hours of delivery was 60.8% (95% CI, 52.1–69.6), specificity 82.5% (95% CI, 81.7–83.4), PPV 5.1% (95% CI, 4.0–6.3), and NPV 99.3% (95% CI, 99.1–99.5). The test characteristics of the MEWC for sPPH were sensitivity 75.0% (95% CI, 67.3–82.7), specificity 66.3% (95% CI, 65.2–67.3), PPV 3.3% (95% CI, 2.7–4.0), and NPV 99.4% (95% CI, 99.2–99.6). There were 10 sPPH cases identified by automated pages, but not by the MEWC. Six of these cases were identified by a page for anemia, and 4 cases were the result of vital signs detected by the bedside monitor, but not recorded in the patient’s medical record by the bedside nurse. Therefore, the combined sensitivity of the 2 systems was 83.3% (95% CI, 75.4–89.5). CONCLUSIONS: The automated system identified 10 of 120 deliveries complicated by sPPH not identified by the MEWC. Using an automated alerting system in combination with a labor and delivery unit’s existing nursing-driven early warning system may improve detection of sPPH.

ObjectiveUsing an animal model, we have previously shown that preeclampsia results in long-term adverse neuromotor outcomes in the offspring, and this phenotype was prevented by antenatal treatment with pravastatin. This study aims to localize the altered neuromotor programming in this animal model and to evaluate the role of pravastatin in its prevention.Materials and MethodsFor the preeclampsia model, pregnant CD-1 mice were randomly allocated to injection of adenovirus carrying sFlt-1 or its control virus carrying mFc into the tail vein. Thereafter they received pravastatin (sFlt-1-pra “experimental group”) or water (sFlt-1 “positive control”) until weaning. The mFc group (“negative control”) received water. Offspring at 6 months of age were sacrificed, and whole brains underwent magnetic resonance imaging (MRI). MRIs were performed using an 11.7 Tesla vertical bore MRI scanner. T2 weighted images were acquired to evaluate the volumes of 28 regions of interest, including areas involved in adaptation and motor, spatial and sensory function. Cytochemistry and cell quantification was performed using neuron-specific Nissl stain. One-way ANOVA with multiple comparison testing was used for statistical analysis.ResultsCompared with control offspring, male sFlt-1 offspring have decreased volumes in the fimbria, periaquaductal gray, stria medullaris, and ventricles and increased volumes in the lateral globus pallidus and neocortex; however, female sFlt-1 offspring showed increased volumes in the ventricles, stria medullaris, and fasciculus retroflexus and decreased volumes in the inferior colliculus, thalamus, and lateral globus pallidus. Neuronal quantification via Nissl staining exhibited decreased cell counts in sFlt-1 offspring neocortex, more pronounced in males. Prenatal pravastatin treatment prevented these changes.ConclusionPreeclampsia alters brain development in sex-specific patterns, and prenatal pravastatin therapy prevents altered neuroanatomic programming in this animal model.

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