Although both transfusion programs were well tolerated, our finding of more frequent major adverse neurologic events in the restrictive RBC-transfusion group suggests that the practice of restrictive transfusions may be harmful to preterm infants.

Background: Serum ferritin measurements are used in clinical populations to estimate total body iron stores and the risk of subsequent iron deficiency or overload. The lack of normative newborn serum ferritin concentration data between 23 and 41 weeks has led to difficulty in establishing the incidence and degree of abnormal iron status in the neonatal period. Objectives: The primary objective of this review was to summarize the maternal and gestational factors that determine ferritin concentrations in full-term and pre-term newborn infants and to generate comprehensive reference values. The secondary objective was to assess serum ferritin concentrations in newborn infants at risk for abnormal fetal iron metabolism, including maternal diabetes mellitus, intrauterine growth restriction and maternal smoking during pregnancy. Methods: Serum ferritin and gestational age data at birth from 457 low-risk pre-term and term infants of 23–41 weeks gestation obtained from 35 published studies reviewed from a period of 25 years and from recently collected data from our centers were assessed by regression analysis. Slopes and intercepts of the high-risk groups were compared with the standard curve. Results: Umbilical cord serum ferritin concentrations increased with advancing gestational age, from a mean of 63 µg/l at 23 weeks to 171 µg/l at 41 weeks gestation (p < 0.001). The infants of diabetic mothers had a lower intercept than the control infants (p < 0.001). Conclusions: Iron deficiency and overload have been implicated in neurodevelopmental impairments. Normative cord serum ferritin data may permit a more precise assessment of infants who are at risk for abnormal iron status at birth.

BACKGROUND-Safe, accurate methods permitting simultaneous and/or repeated measurement of red blood cell (RBC) survival (RCS) are important to investigate pathophysiology and therapy of anemia. Methods using chromium 51 ( 51 Cr) -labeled RBCs are unacceptable for infants, children, and pregnant women. We report RCS measured in vivo using RBCs labeled with several densities of biotin (BioRBCs).

This review summarizes the current thinking about the causes of anemia universally experienced by preterm infants in the early postnatal weeks. In addition to describing developmentally determined physiologic processes contributing to anemia of prematurity, this review discusses clinically important nonphysiologic contributors to anemia experienced by preterm infants during the neonatal period. Chief among these and an important contributor to the need for red blood cell transfusions is the heavy laboratory phlebotomy loss sustained shortly after birth, when neonatal cardiorespiratory illness is most severe. Understanding and recognizing the physiologic and nonphysiologic processes contributing to anemia encountered in early postnatal life is important in knowing which treatment and prevention modalities are likely to be most effective in different clinical situations. The evaluation of rare and uncommon acquired and genetic causes of anemia in newborns are not covered in this review.

Red cell survival can be measured accurately in humans using enumeration of biotinylated red cells. The method is practical and does not expose the patient to radiation.

As long as an umbilical artery catheter is available for blood sampling with an in-line blood gas and chemistry monitor, significant reductions in neonatal RBC transfusions can be achieved. The patients most likely to benefit from monitor use are the smallest, most critically ill newborns.

Tissue hypoxia is the major stimulus of erythropoietin (EPO) synthesis in fetuses and adults. Since EPO does not cross the placenta and is not stored, fetal plasma and amniotic fluid levels indicate EPO synthesis and elimination. Acutely, the rate and magnitude of the increase in plasma EPO levels correlate with the intensity of hypoxia. Amniotic fluid EPO levels correlate with cord plasma levels in normal and abnormal pregnancies, with fetal plasma EPO levels in humans averaging 2.6 times higher than the corresponding amniotic fluid EPO levels. Recent experimental and clinical studies demonstrate that EPO has neuroprotective effects related to its anti-apoptotic and vascular growth-promoting properties. Although under basal conditions the fetal kidneys are the main site of EPO production, during hypoxia recent experimental data indicate an important role of the placenta. Amniotic fluid EPO levels have been shown to increase exponentially during fetal hypoxia in preeclamptic, diabetic and Rh-immunized pregnancies, to correlate inversely with cord blood pH, pO₂ and base excess and to predict neonatal morbidities and NICU admission. As an indicator of chronic intrauterine hypoxia, fetal EPO measurements have increased our knowledge about the pathogenesis and importance of intrauterine growth restriction, macrosomia, diabetic pregnancy, prolonged pregnancy, meconium staining, fetal hemorrhage, fetal anemia, maternal smoking and alcohol consumption, abnormal fetal heart rate and abnormal Doppler flow patterns. While the clinical utility of fetal amniotic fluid and plasma EPO measurements in the management of high-risk pregnancies and their offspring is promising, adequately powered clinical trials are urgently needed.

Significant volumes of blood loss are attributable to overdraw for laboratory testing. This occurrence likely exacerbates the anemia of prematurity and may increase the need for transfusions in some infants. Attempts should be made to correct the factors involved. Common sense suggests that blood samples drawn in tubes with fill-lines marked on the outside would more closely approximate the volumes requested than those without. Conversely, the use of unmarked tubes could lead to phlebotomy overdraw because phlebotomists may overcompensate to avoid having to redraw the sample because of an insufficient volume for analysis. We were surprised to observe that the lightest and most critically ill infants experienced the greatest blood overdraw. (ABSTRACT TRUNCATED)