BackgroundWhile rates of postpartum haemorrhage (PPH) have continued to rise, it is not clear if the association with other morbidity and transfusion has changed over time. This study explores the recent trend in postpartum haemorrhage and whether postpartum haemorrhage is associated with increased transfusions or adverse outcomes over time.MethodsLinked birth and hospital data were used to examine ICD-10 AM coded PPH and outcomes in maternal birth admission records, 2003-–2011 in hospitals in New South Wales (NSW), Australia (N = 818,965 pregnancies). Trends were calculated on the whole population, and among subgroups, and tested using the Cochran Armitage test for trend. Logistic regression models were developed separately for vaginal and caesarean births, and for a maternal morbidity composite indicator (excluding transfusion) and red cell transfusion. Adjusted odds ratios (aOR) for each year relative to 2003 and 95 % confidence intervals (CI) are presented with adjustment for maternal (eg. age, country of birth) and pregnancy factors (eg. parity, interventions, pregnancy complications).ResultsOverall, there was a significant increase in the PPH rate, from 6.1 % in 2003 to 8.3 % in 2011 (p < 0.0001). Crude rates of postpartum haemorrhage with transfusion increased from 0.75 % (n = 636) to 1.21 % (n = 1145) (p < 0.0001) while crude rates of postpartum haemorrhage with maternal morbidity increased from 0.18 % (n = 149) to 0.23 % (n = 221) (p = 0.02). Having accounted for maternal and pregnancy factors, there were significant overall decreases in the odds of morbidity among women with a PPH delivering vaginally (in 2006, 2007 and 2010, aORs were 0.70 (95 % CI 0.52, 0.96) 0.69 (0.51, 0.94) and 0.64 (0.47, 0.87) relative to 2003; p < 0.05), and no significant decrease among women delivered by caesarean section (aOR 0.87 (0.58, 1.29) in 2011; p = 0.37). Among women with a PPH delivering vaginally, there was a trend towards a non-linear increase in the adjusted odds of transfusion by birth year. Compared to women who had vaginal births with PPH in 2003, the adjusted odds for transfusion was between 1.1 and 1.2 fold higher for those with a PPH delivering vaginally in 2007, 2009, 2010 and 2011. However there was no significant trend amongst caesarean births (aOR 0.84 (0.66, 1.06) in 2011; p = 0.29).ConclusionsPPH has become more frequent, however this has not been associated with a clear pattern of increased severe maternal morbidity. This suggests that the increase in PPH may represent fewer severe haemorrhages, better management of severe haemorrhage or better recording of PPH. The increase in transfusions following vaginal births with PPH warrants further investigation.Electronic supplementary materialThe online version of this article (doi:10.1186/s12884-015-0788-5) contains supplementary material, which is available to authorized users.

Identification and subsequent treatment of GDM in twin pregnancy demonstrates a similar risk of adverse perinatal outcomes compared with non-GDM twin pregnancies.

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Background: Fetuses affected by placental insufficiency do not receive adequate nutrients and oxygenation, become growth restricted and acidemic, and can demise. Preterm fetal growth restriction is a severe form of placental insufficiency with a high risk of stillbirth. We set out to identify maternal circulating mRNA transcripts that are differentially expressed in preterm pregnancies complicated by very severe placental insufficiency, in utero fetal acidemia, and are at very high risk of stillbirth. Methods: We performed a cohort study across six hospitals in Australia and New Zealand, prospectively collecting blood from 128 pregnancies complicated by preterm fetal growth restriction (delivery < 34 weeks' gestation) and 42 controls. RNA-sequencing was done on all samples to discover circulating mRNAs associated with preterm fetal growth restriction and fetal acidemia in utero. We used RT-PCR to validate the associations between five lead candidate biomarkers of placental insufficiency in an independent cohort from Europe (46 with preterm fetal growth restriction) and in a third cohort of pregnancies ending in stillbirth.

Diabetes Care 2017;40:e98-e100 | https://doi.org/10.2337/dc17-0626Fetal exposure to hyperglycemia is a major determinant of large-for-gestationalage (LGA; birth weight .90th centile for gender) neonates (1), yet targets for glycemic control beyond the first trimester in type 1 diabetes (T1D) pregnancy remain controversial. As HbA 1c represents a summary measure of glycemic control, it might not adequately reflect acute glucose fluctuations or glycemic variability (GV) that contributes to excess fetal growth. Moreover, neonates born to women who attain HbA 1c ,6% (42 mmol/mol) in the third trimester of pregnancy have an LGA prevalence of 25% (2), with associated adverse perinatal outcomes (3). In contrast to HbA 1c , continuous glucose monitoring (CGM) allows precise observation of GV. Several studies have demonstrated an association between higher GV and increased birth weight (1,4,5). The capability of GV compared with HbA 1c to identify women likely to have LGA neonates is, however, unclear. We evaluated the association between various measures of GV, HbA 1c , and LGA neonates in T1D pregnancy.Twenty-one pregnant women with T1D were recruited over a 2-year period, and measurements of HbA 1c and GV (EasyGV, University of Oxford, Oxford, U.K.) using CGM (Medtronic, Macquarie Park, New South Wales, Australia) were carried out at three time points: 14-18, 24-28, and 32-36 weeks' gestation. The study was approved by the local ethics committee (Northern Sydney Local Health District Human Research Ethics Committee), and all participants gave written informed consent.The mean 6 SD gestational age at delivery was 37.5 6 1.4 weeks, and birth weight was 3,454 6 576 g, with eight neonates born LGA. HbA 1c at each time point was 6.1 6 0.9%, 6.0 6 0.8%, and 6.2 6 1.0%, respectively. The LGA group had significantly higher mean glucose and GV indices than the non-LGA group at 24-28 weeks' gestation ( Fig. 1A-D) and higher HbA 1c at each time point (Fig. 1E).Linear regression demonstrated a significant association between birth weight centile and each of the glycemic measures at 24-28 weeks of gestation. Because the GV indices demonstrated significant colinearity, we included the J-index alone in subsequent analyses, as it was most strongly correlated with birth weight centile (r 5 0.853; P , 0.0001). Using univariate linear modeling, J-index at 24-28 weeks maintained a significant independent association with birth weight centile (r 2 5 0.229; P , 0.05), whereas HbA 1c did not (r 2 5 0.008; P 5 0.713). The combination of J-index and HbA 1c at this time point resulted in a greater association with birth weight centile (r 2 5 0.477; P , 0.01), with mean values of 31.7% and 5.95%, respectively. Furthermore, using cutoffs of HbA 1c .6% and J-index .30 identified all neonates that were born LGA (receiver operating characteristic curve analysis, data not shown).Despite attaining close to recommended HbA 1c target levels for T1D in pregnancy (HbA 1c #6%), our cohort of women demonstrated an ;40% incidence of LGA neonates, which conc...

BackgroundAsthma exacerbations are common during pregnancy and associated with an increased risk of adverse perinatal outcomes. Adjusting asthma treatment based on airway inflammation rather than symptoms reduces the exacerbation rate by 50 %. The Breathing for Life Trial (BLT) will test whether this approach also improves perinatal outcomes.Methods/designBLT is a multicentre, parallel group, randomised controlled trial of asthma management guided by fractional exhaled nitric oxide (FENO, a marker of eosinophilic airway inflammation) compared to usual care, with prospective infant follow-up. Women with physician-diagnosed asthma, asthma symptoms and/or medication use in the previous 12 months, who are 12–22 weeks gestation, will be eligible for inclusion. Women randomised to the control group will have one clinical assessment of their asthma, including self-management education. Any treatment changes will be made by their general practitioner. Women randomised to the intervention group will have clinical assessments every 3–6 weeks during pregnancy, and asthma treatments will be adjusted every second visit based on an algorithm which uses FENO to adjust inhaled corticosteroid (ICS) dose (increase in dose when FENO >29 parts per billion (ppb), decrease in dose when FENO <19 ppb, and no change when FENO is between 19 and 29 ppb). A long acting beta agonist (LABA) will be added when symptoms remain uncontrolled. Both the control and intervention groups will report on exacerbations at a postpartum phone interview. The primary outcome is adverse perinatal outcome (a composite measure including preterm birth, intrauterine growth restriction, neonatal hospitalisation at birth or perinatal mortality), assessed from hospital records. Secondary outcomes will be each component of the primary outcome, maternal exacerbations requiring medical intervention during pregnancy (both smokers and non-smokers), and hospitalisation and emergency department presentation for wheeze, bronchiolitis or croup in the first 12 months of infancy. Outcome assessment and statistical analysis of the primary outcome will be blinded. To detect a reduction in adverse perinatal outcomes from 35 % to 26 %, 600 pregnant women with asthma per group are required.DiscussionThis trial will provide evidence for the effectiveness of a FENO-based management strategy in improving perinatal outcomes in pregnant women with asthma. If successful, this would improve the management of pregnant women with asthma worldwide.Trial registrationAustralian New Zealand Clinical Trials Registry ACTRN12613000202763.

Introduction: Extremes of fetal growth are associated with increased perinatal mortality and morbidity and a higher prevalence of cardiovascular disease, obesity and diabetes in later life. We aimed to identify changes in placental gene expression in pregnancies with evidence of growth dysfunction and candidate genes that may be used to identify abnormal patterns of growth prior to delivery. Methods: Growth-restricted (n = 4), macrosomic (n = 6) and normal term (n = 5) placentas were selected from a banked series (n = 200) collected immediately after caesarean section. RNA was extracted prior to microarray analysis using Affymetrix HG-U219 arrays to determine variation in gene expression. Genes of interest were confirmed using qRT-PCR. Results: 338 genes in the growth-restricted and 41 genes in the macrosomic group were identified to be significantly dysregulated (>2-fold change; p < 0.05). CPXM2 and CLDN1 were upregulated and TXNDC5 and LRP2 downregulated in fetal growth restriction. In macrosomia, PHLDB2 and CLDN1 were upregulated and LEP and GCH1 were downregulated. Discussion: Dysfunctional growth is associated with differential placental gene expression and affects genes with a whole spectrum of developmental and cellular functions. Better elucidation of these pathways may allow the development of biomarkers to identify growth abnormalities and effective prenatal intervention.