OBJECTIVES: To assess the optimal mode of delivery in women with, or carriers of, bleeding disorders.
SEARCH METHODS: We searched the Cochrane Cystic Fibrosis and Genetic Disorders Coagulopathies Trials Register, compiled from electronic database searches and handsearching of journals and conference abstract books. We also searched the Cochrane Pregnancy and Childbirth Group's Trials Register as well as trials registries and the reference lists of relevant articles and reviews.Date of last search of the Group's Trials Registers: 16 February 2017.
SELECTION CRITERIA: Randomised controlled trials and all types of controlled clinical trials investigating the optimal mode of delivery in women with, or carriers of, any type of bleeding disorder during pregnancy were eligible for the review.
DATA COLLECTION AND ANALYSIS: No trials matching the selection criteria were eligible for inclusion MAIN RESULTS: No results from randomised controlled trials were found.
AUTHORS' CONCLUSIONS: The review did not identify any randomised controlled trials investigating the safest mode of delivery and associated maternal and foetal complications during delivery in women with, or carriers of, a bleeding disorder. In the absence of high quality evidence, clinicians need to use their clinical judgement and lower level evidence (e.g. from observational trials, case studies) to decide upon the optimal mode of delivery to ensure the safety of both mother and foetus.Given the ethical considerations, the rarity of the disorders and the low incidence of both maternal and foetal complications, future randomised controlled trials to find the optimal mode of delivery in this population are unlikely to be carried out. Other high quality controlled studies (such as risk allocation designs, sequential design, and parallel cohort design) are needed to investigate the risks and benefits of natural vaginal and caesarean section in this population or extrapolation from other clinical conditions that incur a haemorrhagic risk to the baby, such as platelet alloimmunisation.
OBJECTIVE: To determine whether any association exists between the finding of an increased thickness of placenta, abnormal placenta shape, placental calcification, placental lake and abnormal cord insertion site at 20-22 and 30-32 weeks gestation with an increased risk of uteroplacental complications or a poor pregnancy outcome.
METHODOLOGY: A real-time ultrasound was used at the time of detail scan (at 20-22 weeks gestation) and at 30-32 weeks gestation to look for placenta appearance, fetal growth and anomaly. The main outcome measures were risk of hypertension disease in pregnancy, fetal growth restriction and poor fetal outcomes such as low Apgar score and low cord pH.
RESULT: The majority of the participants were Malay (77.9%). Abnormal placenta found at both gestations were placental lakes and thickness, and only one case had marginal cord insertion. Approximately 6% of the cases were confirmed placenta previa. No abnormal shape or abnormal calcification found at both gestations. About 10% patient developed hypertensive disease in pregnancy, 15% of the fetus was found to have growth restriction and another 16% have low umbilical cord pH. Majority of them delivered at term (90%) and via vaginal delivery (81%). There was no significance between presence of abnormal placental lake and thickness at both gestations with the maternal and fetal outcome.
CONCLUSION: Presence of abnormal placental thickness and lakes at 30-32 weeks scan associated with maternal hypertensive disease, fetal growth restriction and low umbilical cord pH, however these were not statistically significant.
METHODS: This was a cross-sectional study consisted of 21 pregnant women with hypertension and 23 without hypertension. The gestational age ranged from 28 to 39 weeks (hypertensive) and 32 to 40 weeks (normotensive). The paraffin embedded formalin fixed placenta tissue blocks were retrieved from the pathology archives. Endocan immunohistochemistry was performed on tissue sections of full thickness and maternal surface of the placenta. The endocan expression was determined in fetal endothelial cells, maternal endothelial cells, cytotrophoblasts, syncytiotrophoblasts and decidual cells. The differences in endocan expression in placenta between hypertensive and normotensive subjects were evaluated by Pearson chi-square test and t-test were used in the statistical analysis.
RESULTS: The endocan expression was significantly higher in fetal endothelial cells (P