Background Policies for timing of cord clamping vary, with early cord clamping generally carried out in the first 60 seconds after birth, whereas later cord clamping usually involves clamping the umbilical cord greater than one minute after the birth or when cord pulsation has ceased. Objectives To determine the effects of different policies of timing of cord clamping at delivery of the placenta on maternal and neonatal outcomes. Search strategy We searched the Cochrane Pregnancy and Childbirth Group's Trials Register (December 2007). Selection criteria Randomised controlled trials comparing early and late cord clamping. Data collection and analysis Two review authors independently assessed trial eligibility and quality and extracted data. Main results We included 11 trials of 2989 mothers and their babies. No significant differences between early and late cord clamping were seen for postpartum haemorrhage or severe postpartum haemorrhage in any of the five trials (2236 women) which measured this outcome (relative risk (RR) for postpartum haemorrhage 500 mls or more 1.22, 95% confidence interval (CI) 0.96 to 1.55). For neonatal outcomes, our review showed both benefits and harms for late cord clamping. Following birth, there was a significant increase in infants needing phototherapy for jaundice (RR 0.59, 95% CI 0.38 to 0.92; five trials of 1762 infants) in the late compared with early clamping group. This was accompanied by significant increases in newborn haemoglobin levels in the late cord clamping group compared with early cord clamping (weighted mean difference 2.17 g/dL; 95% CI 0.28 to 4.06; three trials of 671 infants), although this effect did not persist past six months. Infant ferritin levels remained higher in the late clamping group than the early clamping group at six months. Authors' conclusions One definition of active management includes directions to administer an uterotonic with birth of the anterior shoulder of the baby and to clamp the umbilical cord within 30-60 seconds of birth of the baby (which is not always feasible in practice). In this review delaying clamping of the cord for at least two to three minutes seems not to increase the risk of postpartum haemorrhage. In addition, late cord clamping can be advantageous for the infant by improving iron status which may be of clinical value particularly in infants where access to good nutrition is poor, although delaying clamping increases the risk of jaundice requiring phototherapy.

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Effect of timing of umbilical cord clamping of term infants on maternal and neonatal outcomes

Intrauterine growth restriction (IUGR) is found in 1-10% of all pregnancies, and among women with risk factors even twice often. It is connected to worse obstetric results, and its complications can arise long time after delivery. In the paper we described etiology, diagnostics and monitoring of IUGR and its consequences for the child and for the course of neonatal periode.

Intrauterine growth restriction

Interferons and Proinflammatory Cytokines in Pregnancy and Fetal Development.

The steroid hormones progestagens, estrogens, androgens, and glucocorticoids as well as their precursor cholesterol are required for successful establishment and maintenance of pregnancy and proper development of the fetus The human placenta forms at the interface of maternal and fetal circulation It participates in biosynthesis and metabolism of steroids as well as their regulated exchange between maternal and fetal compartment This review outlines the mechanisms of human placental handling of steroid compounds Cholesterol is transported from mother to offspring involving lipoprotein receptors such as low-density lipoprotein receptor (LDLR) and scavenger receptor class B type I (SRB1) as well as ATP-binding cassette (ABC)-transporters, ABCA1 and ABCG1 Additionally, cholesterol is also a precursor for placental progesterone and estrogen synthesis Hormone synthesis is predominantly performed by members of the cytochrome P-450 (CYP) enzyme family including CYP11A1 or CYP19A1 and hydroxysteroid dehydrogenases (HSDs) such as 3β-HSD and 17β-HSD Placental estrogen synthesis requires delivery of sulfate-conjugated precursor molecules from fetal and maternal serum Placental uptake of these precursors is mediated by members of the solute carrier (SLC) family including sodium-dependent organic anion transporter (SOAT), organic anion transporter 4 (OAT4), and organic anion transporting polypeptide 2B1 (OATP2B1) Maternal-fetal glucocorticoid transport has to be tightly regulated in order to ensure healthy fetal growth and development For that purpose, the placenta expresses the enzymes 11β-HSD 1 and 2 as well as the transporter ABCB1 This article also summarizes the impact of diverse compounds and diseases on the expression level and activity of the involved transporters, receptors, and metabolizing enzymes and concludes that the regulatory mechanisms changing the physiological to a pathophysiological state are barely explored The structure and the cellular composition of the human placental barrier are introduced While steroid production, metabolism and transport in the placental syncytiotrophoblast have been explored for decades, few information is available for the role of placental-fetal endothelial cells in these processes With regard to placental structure and function, significant differences exist between species To further decipher physiologic pathways and their pathologic alterations in placental steroid handling, proper model systems are mandatory

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Physiology and Pathophysiology of Steroid Biosynthesis, Transport and Metabolism in the Human Placenta

Fetal growth restriction (FGR) continues to be a leading cause of preventable stillbirth and poor neurodevelopmental outcomes in offspring, and furthermore is strongly associated with the obstetrical complications of iatrogenic preterm birth and pre-eclampsia. The terms small for gestational age (SGA) and FGR have, for too long, been considered equivalent and therefore used interchangeably. However, the delivery of improved clinical outcomes requires that clinicians effectively distinguish fetuses that are pathologically growth-restricted from those that are constitutively small. A greater understanding of the multifactorial pathogenesis of both early- and late-onset FGR, especially the role of underlying placental pathologies, may offer insight into targeted treatment strategies that preserve placental function. The new maternal blood biomarker placenta growth factor offers much potential in this context. This review highlights new approaches to effective screening for FGR based on a comprehensive review of: etiology, diagnosis, antenatal surveillance and management. Recent advances in novel imaging methods provide the basis for stepwise multi-parametric testing that may deliver cost-effective screening within existing antenatal care systems.

Screening for fetal growth restriction and placental insufficiency.

Fetal growth restriction (FGR) is a condition that affects 5–10% of pregnancies and is the second most common cause of perinatal mortality. This review presents the most recent knowledge on FGR and focuses on the etiology, classification, prediction, diagnosis, and management of the condition, as well as on its neurological complications. The Pubmed, SCOPUS, and Embase databases were searched using the term “fetal growth restriction”. Fetal growth restriction (FGR) may be classified as early or late depending on the time of diagnosis. Early FGR (<32 weeks) is associated with substantial alterations in placental implantation with elevated hypoxia, which requires cardiovascular adaptation. Perinatal morbidity and mortality rates are high. Late FGR (≥32 weeks) presents with slight deficiencies in placentation, which leads to mild hypoxia and requires little cardiovascular adaptation. Perinatal morbidity and mortality rates are lower. The diagnosis of FGR may be clinical; however, an arterial and venous Doppler ultrasound examination is essential for diagnosis and follow-up. There are currently no treatments to control FGR; the time at which pregnancy is interrupted is of vital importance for protecting both the mother and fetus. Early diagnosis of FGR is very important, because it enables the identification of the etiology of the condition and adequate monitoring of the fetal status, thereby minimizing risks of premature birth and intrauterine hypoxia.

Fetal growth restriction: current knowledge.

The present study aimed to evaluate the performance of QuantusFLM software, which performs quantitative analysis of lung tissue texture through ultrasound images, in predicting lung maturity in fetal growth restriction (FGR). We included patients with singleton gestations between 34 and 38 6/7 wk and divided them into two groups: FGR and control (appropriate for gestational age [AGA]). The images were captured by ultrasound according to a specific protocol up to 48 h before delivery and analyzed with QuantusFLM software. The main clinical outcome evaluated was lung maturity (i.e., the absence of neonatal respiratory morbidity). We included 111 patients; one was excluded because of low image quality, leaving 55 patients in each group. The FGR group had a lower birth weight (2207 g vs. 2891 g, p

Jaqueline Brandão Mazzola

Papers

Fetal growth restriction: current knowledge.

Prediction of Lung Maturity in Fetuses with Growth Restriction through Quantitative Ultrasound Analysis

evaluation Of Fetal Red Blood Cells For Passage Of The Maternal Circulation During Afterbirth By Kleihauer Betke Test : 187 | oral | obstetrics