No abstract

Background-Each year approximately 10 million babies do not breathe immediately at birth, of which about 6 million require basic neonatal resuscitation. The major burden is in low-income settings, where health system capacity to provide neonatal resuscitation is inadequate.Objective-To systematically review the evidence for neonatal resuscitation content, training and competency, equipment and supplies, cost, and key program considerations, specifically for resource-constrained settings.Results-Evidence from several observational studies shows that facility-based basic neonatal resuscitation may avert 30% of intrapartum-related neonatal deaths. Very few babies require advanced resuscitation (endotracheal intubation and drugs) and these newborns may not survive without ongoing ventilation; hence, advanced neonatal resuscitation is not a priority in settings without neonatal intensive care. Of the 60 million nonfacility births, most do not have access to resuscitation. Several trials have shown that a range of community health workers can perform neonatal resuscitation with an estimated effect of a 20% reduction in intrapartum-related neonatal deaths, based on expert opinion. Case studies illustrate key considerations for scale up.Conclusion-Basic resuscitation would substantially reduce intrapartum-related neonatal deaths. Where births occur in facilities, it is a priority to ensure that all birth attendants are

ABSTRACT. Objective. In recent years, gains in neonatal survival have been most evident among very low birth weight, preterm, and low birth weight (LBW) infants. Most of the improvement in neonatal survival since the early 1980s seems to be the consequence of decreasing birth weight-specific mortality rates, which occurred during a period of increasing preterm and LBW rates. Although the decline in neonatal mortality has been widely publicized in the United States, research suggests that clinicians may still underestimate the chances of survival of an infant who is born too early or too small and may overestimate the eventuality of serious disability. So that clinicians may have current and needed ethnic-and race-specific estimates of the "chances" of early survival for newborn infants, we examined birth weight/gestational age-specific neonatal mortality rates for the 3 largest ethnic/racial groups in the United States: non-Hispanic whites, Hispanics, and non-Hispanic blacks. Marked racial variation in birth weight and gestational age-specific mortality has long been recognized, and growing concerns have been raised about ongoing and increasing racial disparities in pregnancy outcomes. Our purpose for this investigation was to provide an up-to-date national reference for birth weight/ gestational age-specific neonatal mortality rates for use by clinicians in care decision making and discussions with parents.Methods. The National Center for Health Statistics linked live birth-infant death cohort files for 1995-1997 were used for this study. Singleton live births to US resident mothers with a reported maternal ethnicity/race of non-Hispanic white, non-Hispanic black, or Hispanic (n ‫؍‬ 10 610 715) were selected for analysis. Birth weight/ gestational age-specific neonatal mortality rates were calculated using 250 g/2-week intervals for each ethnic/racial group.Results. The overall neonatal mortality rates for whites, Hispanics, and blacks were 3.24, 3.45, and 8.16 neonatal deaths per 1000 live births, and the proportion of births <28 weeks was 0.35%, 0.45%, and 1.39%, respectively. Newborns who weighed <1500 g comprised <2.5% of all births in each racial/ethnic group but accounted for >50% of neonatal deaths. For whites, Hispanics, and blacks, >50% of newborns 24 to 25 weeks of gestational age survived. For most combinations of birth weights <3500 g and gestational ages of <37 weeks, the neonatal mortality rate was lowest among blacks, compared with whites or Hispanics. At these same gestational age/birth weight combinations, Hispanics have slightly lower mortality rates than whites. For combinations of birth weights >3500 g and gestational ages of 37 to 41 weeks, Hispanics had the lowest neonatal mortality rate. In these birth weight/gestational age combinations, where approximately two thirds of births occur, blacks had the highest neonatal mortality rate.Conclusions. Compared with earlier reports, these data suggest that a substantial improvement in birth weight/gestational age-specific neonatal mortality has o...

Fetal and neonatal inflammation is associated with several morbidities of prematurity. Its relationship to retinopathy of prematurity (ROP) has not been investigated. Our objective was to determine the relationship between cytokine levels and ROP in the first 3 postnatal wks. Data for this study were derived from the NICHD Cytokine Study. Dried blood spots (DBS) were obtained from infants Ͻ1000 g on days 0 -1, 3 Ϯ 1, 7 Ϯ 2, 14 Ϯ 3, and 21 Ϯ 3. Infants were classified into three groups-no, mild, and severe ROP. Multiplex Luminex assay was used to quantify 20 cytokines. Temporal profiles of cytokines were evaluated using mixed-effects models after controlling for covariates. Of 1074 infants enrolled, 890 were examined for ROP and 877 included in the analysis. ROP was associated with several clinical characteristics on unadjusted analyses. Eight cytokines remained significantly different across ROP groups in adjusted analyses. IL-6 and IL-17 showed significant effects in early time periods (D0 -3); TGF-␤, brain-derived neurotrophic factor (BDNF), and regulated on activation, normal T cell expressed and secreted (RANTES) in later time periods (D7-21) and IL-18, C-reactive protein (CRP), and neurotrophin-4 (NT-4) in both early and later time periods. We conclude that perinatal inflammation may be involved in the pathogenesis of ROP. (Pediatr Res 67: 394-400, 2010) R etinopathy of prematurity (ROP), a vasoproliferative disorder of the developing retina, is a major cause of blindness in infancy. ROP is a biphasic disease consisting of an initial phase of blunted vascular growth followed by a second phase of vasoproliferation that is recognized on ophthalmoscopy 4 to 6 wks after birth. Angiogenesis, the fundamental process involved in retinal vascular development, is tightly regulated by a complex network of cytokines, extracellular matrix components, and growth factors the action of which varies in a time-dependent fashion. Although inflammatory cytokines have the ability to modulate angiogenesis, their role in triggering the dysregulated angiogenesis in ROP has not been investigated (1). Abbreviations: BDNF, brain-derived neurotrophic factor; CRP, C-reactive protein; FIRS, fetal inflammatory response syndrome; GM-CSF, granulocyte-macrophage colony-stimulating factor; IVH, intraventricular hemorrhage; MCP-1, monocyte chemoattractant protein-1; MIP-1␣, macrophage inflammatory protein-1␣; MMP-9, matrix metalloproteinase-9; NEC, necrotizing enterocolitis; NT-4, neurotrophin-4; PVL, periventricular leukomalacia; RANTES, regulated upon activation, normal T cell expressed and secreted; ROP, retinopathy of prematurity; sIL-6R, soluble IL-6 receptor 0031-3998/10/6704-0394 PEDIATRIC RESEARCH

clinicaltrials.gov Identifier: NCT01875159.