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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% O2) or extrauterine (21% and 60% O2) atmospheres. Secretome data were compared with MSCs obtained from term umbilical cord tissues. The human fetal lung mesenchyme almost exclusively contains CD146pos. 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 in vitro 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.

Objective We previously reported the possible pathogenic role, among infants born ≤29 weeks, of transfusions in bronchopulmonary dysplasia. The present study examined this association in infants born >31 weeks. Study design Analysis of red blood cell (RBC) and platelet transfusions in five NICUs to infants born >31 weeks, and chronic neonatal lung disease (CNLD) at six-weeks of age. Results Seven-hundred-fifty-one infants born >31 weeks were still in the NICU when six-weeks of age. CNLD was identified in 397 (53%). RBC and platelet transfusions were independently associated with CNLD after controlling for potential confounders. For every transfusion, the adjusted odds of developing CNLD increased by a factor of 1.64 (95% CI, 1.38–2.02; p  < 0.001). Conclusions Among NICU patients born >31 weeks, transfusions received by six weeks are associated with CNLD incidence and severity. Though we controlled for known confounding variables in our regression models, severity of illness is an important confounder that limits our conclusions.

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.

Kernicterus spectrum disorder continues to occur in the USA, even after improvements in detecting and managing hyperbilirubinemia were brought about by the 2022 AAP revised guidelines. Three of eight new cases of kernicterus occurring in our state during the past 15 years were infants who were intentionally born at home following a low-risk term pregnancy where the AAP guidelines were not applied. Considering the number of births per year in each setting, infants born at home are 7 times more likely to develop kernicterus than infants born in a hospital. Herein, we report our most recent case. We then provide a practical recommendation for averting future cases of kernicterus following out-of-hospital births. Specifically, we recommend that hospital systems and/or health departments supply all midwives performing out-of-hospital births with the equipment and training necessary to comply with the AAP guidelines by quantitatively assessing hyperbilirubinemia on every neonate 24-48 h following birth. We propose that this noninvasive, simple, and rapid assessment should be free of charge to the midwife and to the family. We maintain that if this is done routinely after every out-of-hospital birth, it will identify the neonates who need phototherapy and who sometimes also need other medical care to prevent extreme hyperbilirubinemia. We believe that such a program will prevent acute bilirubin encephalopathy and kernicterus and that without such a program, the dreadful condition of kernicterus spectrum disorder will continue to occur among our population of infants born at home.

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.