Effect of delayed versus early umbilical cord clamping on neonatal outcomes and iron status at 4 months: a randomised controlled trial. (25/42)

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A randomized, masked study of weekly erythropoietin dosing in preterm infants. (26/42)

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The effects of malaria and intermittent preventive treatment during pregnancy on fetal anemia in Malawi. (27/42)

BACKGROUND: Fetal anemia is common in malarious areas and is a risk factor for infant morbidity and mortality. Malaria during pregnancy may cause decreased cord hemoglobin (Hb) and fetal anemia among newborns. Intermittent preventive treatment during pregnancy (IPTp) with sulfadoxine-pyrimethamine (SP) is protective against malaria but may also affect hematopoiesis and contribute to fetal anemia. METHODS: Peripheral, placental, and cord blood were examined for malaria parasitemia and Hb concentration in a cross-section of 3848 mothers and infants delivered at Queen Elizabeth Central Hospital in Blantyre, Malawi between 1997 and 2006. Unconditional linear and logistic regressions were performed with multiple imputation for missing covariates to assess the associations between malaria, IPTp with SP, and fetal anemia. RESULTS: The overall prevalence of fetal anemia was 7.9% (n = 304). Malaria parasitemia at delivery was associated with an adjusted decrease in cord Hb of -0.24 g/dL (95% confidence interval [CI], -.42 to -.05). The adjusted prevalence odds ratio for the effect of malaria on fetal anemia was 1.41 (95% CI, 1.05-1.90). Primigravidae who did not take IPTp had infants at highest risk for fetal anemia, and density of parasitemia was correlated with the decrease in cord Hb. There was no significant association between SP use and cord Hb or fetal anemia. CONCLUSIONS: Malaria during pregnancy, but not IPTp, decreases cord Hb and is a risk factor for fetal anemia in Malawi. Intermittent preventive treatment during pregnancy with SP may continue to be safe and effective in preventing malaria during pregnancy and fetal anemia despite development of SP resistance.  (+info)

Nonpharmacological, blood conservation techniques for preventing neonatal anemia--effective and promising strategies for reducing transfusion. (28/42)

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International survey of transfusion practices for extremely premature infants. (29/42)

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Effects of anaemia on haemodynamic and clinical parameters in apparently stable preterm infants. (30/42)

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Doppler middle cerebral artery peak systolic velocity for diagnosis of neonatal anemia. (31/42)

OBJECTIVES: The peak systolic velocity (PSV) of the middle cerebral artery was found to be predictive of fetal anemia and is routinely applied in the treatment of such fetuses. Our objective was to determine whether a correlation exists between the PSV in the neonatal middle cerebral artery and hemoglobin levels for possible future implementation in clinical practice. METHODS: A prospective study on 151 neonates was conducted, examining their middle cerebral artery PSV concomitantly with their hemoglobin level during the first 36 hours after delivery. The study population included 122 normocythemic, 24 anemic, and 5 polycythemic neonates. An analysis of variance between normocythemic, anemic, and polycythemic neonates was performed, and a regression analysis of the PSV versus hemoglobin levels was conducted. RESULTS: The normocythemic neonates had a mean middle cerebral artery PSV +/- SD of 41.3 +/- 11.4 cm/s, whereas the anemic neonates had a significantly higher PSV (63.8 +/- 28.5 cm/s), and the polycythemic neonates had a significantly lower PSV (26.8 +/- 7.4 cm/s; P < .001). A statistically significant correlation was found between hemoglobin levels and the middle cerebral artery PSV (P < .01). CONCLUSIONS: Neonatal anemia and polycythemia can be rapidly diagnosed at the bedside by examining the middle cerebral artery PSV. This technique can be used as an ancillary measure to promptly diagnose acute neonatal blood volume changes for an immediate intervention.  (+info)

A mathematical modeling approach to quantify the role of phlebotomy losses and need for transfusions in neonatal anemia. (32/42)

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