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Platelet transfusions are life-saving treatments for specific populations of neonates. However, recent evidence indicates that liberal prophylactic platelet transfusion practices cause harm to premature neonates. New efforts to better balance benefits and risks are leading to the adoption of more restrictive platelet transfusion guidelines in neonatal intensive care units (NICU). Although restrictive guidelines have the potential to improve outcomes, implementation barriers exist. We postulate that as neonatologists become more familiar with the data on the harm of liberal platelet transfusions, enthusiasm for restrictive guidelines will increase and barriers to implementation will decrease. Thus, we focused this educational review on; (1) the adverse effects of platelet transfusions to neonates, (2) awareness of platelet transfusion “refractoriness” in thrombocytopenic neonates and its association with poor outcomes, and (3) the impetus to find alternatives to transfusing platelets from adult donors to NICU patients.

Exogenous mesenchymal stromal cells (MSCs) ameliorate experimental bronchopulmonary dysplasia. Moreover, data from term-born animal models and human tracheal aspirate-derived cells suggest altered mesenchymal signaling in the pathophysiology of neonatal lung disease. We hypothesized that hyperoxia, a factor contributing to the development of bronchopulmonary dysplasia, perturbs human lung-resident MSC function. Mesenchymal cells were isolated from human fetal lung tissue (16-18 wk of gestation), characterized and cultured in conditions resembling either intrauterine (5% O ) or extrauterine (21% and 60% O ) atmospheres. Secretome data were compared with MSCs obtained from term umbilical cord tissues. The human fetal lung mesenchyme almost exclusively contains CD146 MSCs expressing SOX-2 and OCT-4, which secrete elastin, fibroblast growth factors 7 and 10, vascular endothelial growth factor, angiogenin, and other lung cell-protecting/-maturing proteins. Exposure to extrauterine atmospheres leads to excessive proliferation, reduced colony-forming ability, alterations in the cell's surface marker profile, decreased elastin deposition, and impaired secretion of factors important for lung growth. Conversely, umbilical cord-derived MSCs abundantly secreted factors that impaired lung MSCs are unable to produce. Oxygen-impaired human fetal lung MSC function may contribute to disrupted repair capacity and arrested lung growth. Exogenous MSCs may act by triggering the signaling pathways lost by impaired endogenous lung mesenchymal cells.

Objectives To assess the feasibility of drawing, processing, safety-testing, and banking term umbilical cord blood to meet the packed red blood cell transfusion (RBC Tx) needs of extremely-low-gestational-age neonates (ELGANs). Design (1) Retrospectively analyze all ELGANs RBC Tx over the past three years, (2) Estimate local cord blood availability, (3) Assess interest in this project, and implementation barriers, through stakeholder surveys. Results In three years we cared for 266 ELGANs; 165 (62%) received ≥1 RBC Tx. Annual RBC Tx averaged 197 (95% CI, 152–243). If 10% of our 10,353 annual term births had cord blood drawn and processed, and half of those tested were acceptable for Tx, collections would exceed the 95th % upper estimate for need by >four-fold. Interest exceeded 97%. Identified barriers included FDA approval, training to collect cord blood, and cost. Conclusion RBC Tx needs of ELGANS could be met by local cord blood collection.

Rat or human lung samples are enzymatically digested, and CD31-expressing cells are positively selected using magnetic-activated cell sorting before plating in endothelial-specific growth conditions. Blood vessels are crucial for the normal development, lifelong repair and homeostasis of tissues. Recently, vascular progenitor cell–driven 'postnatal vasculogenesis' has been suggested as an important mechanism that contributes to new blood vessel formation and organ repair. Among several described progenitor cell types that contribute to blood vessel formation, endothelial colony-forming cells (ECFCs) have received widespread attention as lineage-specific 'true' vascular progenitors. Here we describe a protocol for the isolation of pulmonary microvascular ECFCs from human and rat lung tissue. Our technique takes advantage of an earlier protocol for the isolation of circulating ECFCs from the mononuclear cellular fraction of peripheral blood. We adapted the earlier protocol to isolate resident ECFCs from the distal lung tissue. After enzymatic dispersion of rat or human lung samples into a cellular suspension, CD31-expressing cells are positively selected using magnetic-activated cell sorting and plated in endothelial-specific growth conditions. The colonies arising after 1–2 weeks in culture are carefully separated and expanded to yield pure ECFC cultures after a further 2–3 weeks. The resulting cells demonstrate the defining characteristics of ECFCs such as (i) 'cobblestone' morphology of cultured cell monolayers; (ii) acetylated low-density lipoprotein uptake and Ulex europaeus lectin binding; (iii) tube-like network formation in Matrigel; (iv) expression of endothelial cell–specific surface markers and the absence of hematopoietic or myeloid surface antigens; (v) self-renewal potential displayed by the most proliferative cells; and (vi) contribution to de novo vessel formation in an in vivo mouse implant model. Assuming typical initial cell adhesion and proliferation rates, the entire procedure can be completed within 4 weeks. Isolation and culture of lung vascular ECFCs will allow assessment of the functional state of these cells in experimental and human lung diseases, providing newer insights into their pathophysiological mechanisms.

ObjectiveBuilding on our previous study, showing a correlation between ferritin in serum and urine, we conducted a feasibility evaluation, measuring urinary ferritin as a potential noninvasive screening test for iron deficiency among NICU patients.Study designThis was a prospective analysis of paired serum/urine ferritin levels. We defined iron-limited erythropoiesis by a RET-He <5th percentile lower reference interval (<28 pg).ResultsWe obtained 49 paired serum/urine samples from neonates judged as at-risk for iron deficiency. Urine ferritin (“corrected” for urine creatinine and specific gravity) correlated with serum ferritin (correlation coefficient of log10-transformed values 0.44). A corrected urine ferritin <12 ng/mL had a sensitivity of 82% (95% CI, 67–93%) and a specificity of 100% (CI, 66–100%) for detecting iron-limited erythropoiesis, with a positive predictive value of 100% (CI, 89–100%).ConclusionsMeasuring urinary ferritin in NICU patients is feasible. Since low values identify iron-limitation, this could become a useful noninvasive screen.

ObjectiveTo assess the feasibility and safety of one dose of Darbepoetin alpha (Darbe) administered to neonates ≥34 weeks with mild neonatal encephalopathy (NE).MethodsRandomized, masked, placebo-controlled study including neonates ≥34 weeks gestation with mild NE. Neonates were randomized to receive one dose of Darbe (10 μg/kg IV) or placebo. Clinical and laboratory maternal and newborn data were collected. The Bayley Scales of Infant and Toddler Development, third edition (Bayley-III) and a standardized neurological examination at 8–12 months of corrected age were assessed.ResultsThere were no differences in baseline characteristics of the 21 infants randomized (9 Darbe, 12 placebo). Adverse events were not reported at any time. Bayley-III scores were average in both Darbe and placebo groups.ConclusionThis study demonstrates that a randomized, masked, placebo-controlled trial is safe and feasible. A large, randomized trial is warranted to assess the effect of Darbe in this population.

ObjectivePlacental abruption can cause maternal blood loss and maternal anemia. It is less certain whether abruption can cause fetal blood loss and neonatal anemia.Study designRetrospective multi-hospital 24-month analysis of women with placental abruption and their neonates.ResultsOf 55,111 births, 678 (1.2%) had confirmed abruption; 83% of these neonates (564) had one or more hemoglobins recorded in the first day. Four-hundred-seventy (83.3%) had a normal hemoglobin (≥5th% reference interval) while 94 (16.7%) had anemia, relative risk 3.26 (95% CI, 2.66–4.01) vs. >360,000 neonates from previous reference interval reports. The relative risk of severe anemia (<1st% interval) was 4.96 (3.44–7.16). When the obstetrician identified the abruption as “small” or “marginal” the risk of anemia was insignificant.ConclusionsMost abruptions do not cause neonatal anemia but approximately 16% do. If an abruption is not documented as small, it is important to surveille the neonate for anemia.

A transfusion-requiring “late anemia” can complicate the management of neonates convalescing from hemolytic disease of the fetus and newborn (HDFN). This anemia can occur in any neonate after HDFN but is particularly prominent in those who received intrauterine transfusions and/or double-volume exchange transfusions. Various reports describe this condition as occurring based on ongoing hemolysis , either due to passive transfer of alloantibody through breast milk or persistence of antibody not removed by exchange transfusion. However, other reports describe this condition as the result of inadequate erythrocyte production . Both hypotheses might have merit, because perhaps; (1) some cases are primarily due to continued hemolysis, (2) others are primarily hypoproductive, and (3) yet others result from a mixture of these two mechanisms. We propose prospective collaborative studies that will resolve this issue by serially quantifying end-tidal carbon monoxide. Doing this will better inform the assessment and treatment of neonates recovering from HDFN.