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ObjectiveTo assess whether length of hospital stay is decreased among moderately preterm infants weaned from incubator to crib at a lower vs higher weight.Study designThis trial was conducted in the Eunice Kennedy Shriver National Institute of Child Health and Human Development Neonatal Research Network. Infants with gestational ages 29-33 weeks, birthweight

Objective. Oxygen delivery through nasal cannulae to convalescent preterm infants is a common but largely unstudied practice. To learn more about current nasal cannula oxygen delivery practices, we examined the variations in oxygen delivery through nasal cannulae among the centers of the Neonatal Research Network, the frequency of prescription of low levels of oxygen, and the success of weaning to room air. We hypothesized that some infants treated with oxygen through nasal cannulae were receiving oxygen levels equivalent to those of room air. Methods. This was a descriptive, nested, cohort study of nasal cannula oxygen prescription among 187 infants with birth weights of Results. Fifty-two infants (27.8%) were receiving oxygen concentrations and flow rates through nasal cannulae that delivered an effective FI[O.sub.2] of Conclusions. Prescription of oxygen with combinations of flow rates and oxygen concentrations that delivered a low effective FI[O.sub.2] was common. We speculate that some of this, including the inadvertent prescription of an effective FI[O.sub.2] equivalent to that of room air, is related to lack of knowledge of the effective FI[O.sub.2]. Routine calculation of effective FI[O.sub.2] values may prompt earlier trials of room air and thus reduce unnecessary days of oxygen therapy. ABBREVIATIONS. FI[O.sub.2], fraction of inspired oxygen; STOP-ROP, Supplemental Therapeutic Oxygen for Prethreshold Retinopathy of Prematurity., Oxygen delivery through nasal cannulae to convalescent preterm infants is a common but largely unstudied practice. There are no existing criteria regarding when personnel attempt to wean infants from oxygen [...]

Objective: Examine the association between placental inflammation and neonatal infections, and 25OH vitamin D (25OH D) levels at birth among very low birth weight infants (VLBWI).Study Design: Serum 25OH D levels were measured in 89 VLBWI (≤1250 g) and 47 mothers on day one, and in 78 infants on day 21. Placentas were examined for maternal and fetal inflammation. Infants were divided into deficient (≤10 ng/ml) and adequate (>10 ng/ml) groups based on 25OH D levels on day 1.Results: Mean ± SD maternal levels of 25OH D (21 ± 9 ng/ml) correlated with infants' levels (15 ± 8 ng/ml), (p < .001). 25OH D levels were lower in deficient (32/89) than in adequate group (8 ± 2 versus 20 ± 7 ng/ml, p = .011). Infants' 25OH D levels rose significantly by day 21 (p < .001). Univariate analyses showed no differences between infant groups in maternal or fetal inflammation, or neonatal infections (p > .05). Logistic regression analyses revealed no association between deficient 25OH D levels and the odds of maternal or fetal inflammation or other infections. Levels of 25OH D did not correlate with severity of placental inflammation.Conclusions: Deficient levels of 25OH D at birth are not associated with the occurrence of placental inflammation or neonatal infections among VLBWI. [ABSTRACT FROM AUTHOR]

OBJECTIVES. Craniosynostosis is a devastating disorder characterized by premature closure of the cranial plates before or shortly after birth. This results in an abnormally shaped skull, face, and brain. Little is known about hearing disorders in such patients, and nothing has been published about their auditory brainstem responses. Our objective was to evaluate such patients for auditory brainstem response and hearing disorders with the long-term goal of improving patient evaluation and management. PATIENTS AND METHODS. We evaluated the auditory brainstem responses, hearing, and brain images of children with fibroblast growth factor receptor 2 craniosynostosis (n = 11). RESULTS. Prolongation of the auditory brainstem response I-to-III interpeak latency was a frequent characteristic of fibroblast growth factor receptor 2 craniosynostosis, occurring in 91% of our patients. Prolongation of the III-to-V interpeak latency was an occasional characteristic, occurring in 27% of our patients. Whenever the I-to-III interpeak latency was prolonged, wave II was always abnormal. Associated morbidities included sensorineural hearing loss (27%), recurrent otitis media (100%), and Arnold-Chiari malformation (27%). Cranial decompression improved the interpeak latencies of 2 children. CONCLUSIONS. These previously undocumented auditory brainstem response abnormalities reflect abnormal neural transmission, which could cause peripheral and central auditory processing disorders. We speculate that the major pathogenic basis of the I-to-III interpeak latency and wave II abnormalities is compression of the auditory nerve as it passes through the internal auditory meatus and posterior fossa, which would explain the auditory nerve hearing loss, tinnitus, and vertigo that affect these children. Awareness of these abnormalities could lead to important advancements in the auditory and neurosurgical assessment and management of this overlooked patient group. We provide recommendations for the improved assessment and management of these patients. In particular, we recommend that auditory brainstem response diagnostics become standard clinical care for this patient group as the best way to detect auditory nerve compression. KEYWORDS. Apert syndrome, Arnold-Chiari malformation, auditory brainstem response, central auditory processing disorder, conductive hearing loss, craniosynostosis, Crouzon syndrome, fibroblast growth factor receptor, Jackson-Weiss syndrome, Pfeiffer syndrome, recurrent otitis media, sensorineural hearing loss, tinnitus, vertigo. PEDIATRICS 2007;119:e1351-e1360. URL: www.pediatrics.org/cgi/doi/10.1542/peds.2006-3009

To the Editor.-- Bronchopulmonary dysplasia (BPD) is a chronic lung disease (CLD) that occurs in preterm infants receiving respiratory support with mechanical ventilation or prolonged oxygen supplementation. However, the molecular [...]

Background. Preterm infants with bronchopulmonary dysplasia (BPD) exhibit prolonged elevation of inflammatory indices in their tracheal aspirates. Tumor necrosis factor-[alpha] (TNF-[alpha]) is a central mediator of the inflammatory response. The adenine-containing alleles of TNF-[alpha]-308 and lymphotoxin-[alpha]+250 have been associated with increased levels of TNF-[alpha], whereas the adenine allele of TNF-[alpha]-238 produces lower levels of TNF-[alpha] after stimulation. High levels of TNF-[alpha] may promote chronic inflammation by overwhelming counter-regulatory mechanisms and may lead to the development of BPD. Low levels of TNF-[alpha] may decrease the risk and/or severity of BPD. Objective. To determine whether alleles of TNF-[alpha] play a role in the susceptibility and/or severity of BPD among very low birth weight infants. Methods. Infants with birth weights of [lesser than or equal to] 1250 g were included. Genotypic analyses (polymerase chain reaction-restriction fragment length polymorphism assays) were performed with DNA extracted from whole-blood samples. Results. Infants who developed BPD (fraction of inspired oxygen at postconceptional age of 36 weeks of >0.21, n = 51) had a younger gestational age (mean [+ or -] SD: 27 [+ or -] 4 vs 29 [+ or -] 2 weeks) and lower birth weight (853 [+ or -] 184 vs 997 [+ or -] 193 g) than did infants without BPD (n = 69). The genotypic distributions of lymphotoxin-[alpha]+250 and TNF-[alpha]-308 were comparable among the groups of infants. However, the AA and GA TNF-[alpha]-238 genotypes were much less likely to occur among infants with BPD than among infants without BPD. The adenine allele of TNF-[alpha]-238 was absent among infants with severe BPD and occurred significantly less often among infants with moderate or severe BPD, compared with infants with mild BPD. The number of adenine alleles of TNF-[alpha]-238 was correlated inversely with the severity of BPD (r = -.341). Conclusion. The adenine allele of TNF-[alpha]-238 may reduce the risk and severity of BPD. Pediatrics 2004;114:e243-e248. URL: http://www.pediatrics.org/cgi/ content/full/114/2/e243; tumor necrosis factor-[alpha], cytokines, bronchopulmonary dysplasia, polymorphism, low birth weight infants.