No abstract

Since 2004Since -2007, national guidelines and recommendations have been developed for the management of extremely preterm births in Sweden. If and how more uniform management has affected infant survival is unknown.

AimLittle is known about the amount of physical parent–infant closeness in neonatal intensive care units (NICUs), and this study explored that issue in six European countries.MethodsThe parents of 328 preterm infants were recruited in 11 NICUs in Finland, Estonia, Sweden, Norway, Italy and Spain. They filled in daily diaries about how much time they spent in the NICU, in skin‐to‐skin contact (SSC) and holding their babies in the first two weeks of their hospitalisation.ResultsThe parents' NICU presence varied from a median of 3.3 (minimum 0.7–maximum 6.7) to 22.3 (18.7–24.0) hours per day (p < 0.001), SSC varied from 0.3 (0–1.4) to 6.6 (2.2–19.5) hours per day (p < 0.001) and holding varied from 0 (0–1.5) to 3.2 (0–7.4) hours per day (p < 0.001). Longer SSC was associated with singleton babies and more highly educated mothers. Holding the baby for longer was associated with gestational age. The most important factor supporting parent–infant closeness was the opportunity to stay overnight in the NICU. Having other children and the distance from home to the hospital had no impact on parent–infant closeness.ConclusionParents spent more time in NICUs if they could stay overnight, underlining the importance that these facilities play in establishing parent–infant closeness.

Chorioamnionitis is associated with increased lung and brain injury in premature infants. Ureaplasma is the microorganisms most frequently associated with preterm birth. Whether Ureaplasma-induced antenatal inflammation worsens lung and brain injury is unknown. We developed a mouse model combining antenatal Ureaplasma infection and postnatal oxygen exposure. Intraamniotic Ureaplasma Parvum (UP) increased proinflammatory cytokines in placenta and fetal lungs. Antenatal exposure to UP or broth caused mild postnatal inflammation and worsened oxygen-induced lung injury. Antenatal UP exposure induced central microgliosis and disrupted brain development as detected by decreased number of calbindin-positive and calretinin-positive neurons in the neocortex. Postnatal oxygen decreased calretinin-positive neurons in the neocortex but combined with antenatal UP exposure did not worsen brain injury. Antenatal inflammation exacerbates the deleterious effects of oxygen on lung development, but the broth effects prohibit concluding that UP by itself is a compounding risk factor for bronchopulmonary dysplasia. In contrast, antenatal UP-induced inflammation alone is sufficient to disturb brain development. This model may be helpful in exploring the pathophysiology of perinatal lung and brain injury to develop new protective strategies.