Background: A considerable local variability in the rate of bronchopulmonary dysplasia (BPD) has been recorded previously. Objectives: The objectives of the present study were to describe regional differences in the rate of BPD in very preterm neonates from a European population-based cohort and to further delineate risk factors. Methods: 4,185 survivors to 36 weeks’ postmenstrual age of 4,984 live-born infants born at 24+0–31+6 weeks’ gestation in 2003 (the MOSAIC cohort) in 10 European regions were enrolled using predefined structured questionnaires. Results: Overall median gestational age of preterms without BPD was 30 weeks (range 23–31), median birth weight 1,320 g (range 490–3,150) compared with 27 weeks (23–31) and 900 g (370–2,460) in those with BPD. The region-specific crude rate of BPD ranged from 10.2% (Italian region) to 24.8% (UK Northern region). Maternal hypertension, immaturity, male gender, small for gestational age, Apgar <7 and region of care were associated with an increased incidence of BPD on multivariate analysis. Conclusion: A wide variability of BPD between European regions may be explained by different local practices; the strongest association however was with degree of immaturity.

No consensus exists in Europe about size or other criteria for NICUs. A better understanding of the characteristics associated with high-quality neonatal care is needed, given the high proportion of very preterm infants who are cared for in units that are considered small or less specialized by many recommendations.

Gestational diabetes mellitus (GDM) usually develops in the second half of pregnancy and, in order to address the impact of GDM on the conceptus, several issues must be raised: what are the immediate implications for the fetus and the neonate and why do they happen? What are the consequences for the offspring? What can be done? In a theoretical model the whole pathogenesis and spectrum of fetal and neonatal mortality and morbidity could primarily be attributed to the excessive transferal of glucose from mother of fetus, inducing fetal hyperglycemia, leading to fetal pancreatic islet hypertrophy and beta-cell hyperplasia with a consequent rise in insulin secretion. However, besides, and in addition to glucose, it is quite possible that other metabolic fuels, from amino acids to lipids, may also cross the placenta further contributing to the adverse intrauterine environment. Depending upon the time of gestation during critical developmental stages, the same metabolic fuels would have different effects upon the fetus, the neonate and quite possibly, upon the long-term outcome from neurological and psychosocial impairment to the adult development of metabolic and cardiovascular disorders. Based on clinical and experimental evidence that poor maternal homeostasis is at the core of the problem, it is of paramount importance to identify women at risk of GDM and to keep a tight metabolic control in order to avoid immediate and long-term consequences for their offspring.

Variation in the rate of very preterm delivery has a major influence on reported neonatal death rates.

CK-MB, mostly of muscle origin and reflecting labor stress or injury, is not to recommend as a measure of myocardial damage in the neonate. The rise in cTnI may be explained by a degree of myocardial involvement, albeit physiological. The initial rise and subsequent fall of NT-proBNP represents the physiological ventricular overload of transient birth adaptation.