Cooling can be considered for infants with neonatal encephalopathy following postnatal collapse or preterm birth, those with underlying surgical or cardiac conditions, and infants starting cooling >6 postnatal hours.

Our regional clinical cohort had lower mortality and comparable rates of CP compared with historical outcomes in TH trials. In contrast to historical cohorts, only one-third of the 18 children with CP were severely affected and 12 were mildly affected, all of whom were independently ambulant by 24 months.

BackgroundBreathing the inert gas Xenon (Xe) enhances hypothermic (HT) neuroprotection after hypoxia-ischemia (HI) in small and large newborn animal models. The underlying mechanism of the enhancement is not yet fully understood, but the combined effect of Xe and HT could either be synergistic (larger than the two effects added) or simply additive. A previously published study, using unilateral carotid ligation followed by hypoxia in seven day old (P7) rats, showed that the combination of mild HT (35°C) and low Xe concentration (20%), both not being neuroprotective alone, had a synergistic effect and was neuroprotective when both were started with a 4 h delay after a moderate HI insult. To examine whether another laboratory could confirm this finding, we repeated key aspects of the study.Design/MethodsAfter the HI-insult 120 pups were exposed to different post-insult treatments: three temperatures (normothermia (NT) NT37°C, HT35°C, HT32°C) or Xe concentrations (0%, 20% or 50%) starting either immediately or with a 4 h delay. To assess the synergistic potency of Xe-HT, a second set (n = 101) of P7 pups were exposed to either HT35°C+Xe0%, NT+Xe20% or a combination of HT35°C+Xe20% starting with a 4 h delay after the insult. Brain damage was analyzed using relative hemispheric (ligated side/unligated side) brain tissue area loss after seven day survival.ResultsImmediate HT32°C (p = 0.042), but not HT35°C significantly reduced brain injury compared to NT37°C. As previously shown, adding immediate Xe50% to HT32°C increased protection. Neither 4 h-delayed Xe20%, nor Xe50% at 37°C significantly reduced brain injury (p>0.050). In addition, neither 4 h-delayed HT35°C alone, nor HT35°C+Xe20% reduced brain injury. We found no synergistic effect of the combined treatments in this experimental model.ConclusionsCombining two treatments that individually were ineffective (delayed HT35°C and delayed Xe20%) did not exert neuroprotection when combined, and therefore did not show a synergistic treatment effect.

Background The WHO's Vision 2020 global initiative against blindness, launched in 2000, prioritises children. Progress has been hampered by the global paucity of epidemiological data about childhood visual disability. The British Childhood Visual Impairment and Blindness Study 2 (BCVIS2) was undertaken to address this evidence gap. Methods UK-wide prospective population-based observational study of all those aged under 18 years newly diagnosed with visual impairment or blindness between Oct 1, 2015 and Nov 1 2016. Eligible children were notified simultaneously but independently by their managing ophthalmologists and paediatricians via the two national active surveillance schemes, the British Ophthalmic and Paediatric Surveillance Units. Standardised detailed data were collected at diagnosis and one year later. Incidence estimates and relative rates by key sociodemographic factors were calculated. Descriptive analyses were undertaken of underlying ophthalmic disorders and nonophthalmic comorbidities. FindingsOf 784 cases, 72% had additional non-ophthalmic impairments/disorders and 4% died within the year. Annual incidence was highest in the first year of life, 5•2 per 10,000 (95% CI 4•7-5•7) with cumulative incidence by 18 years of 10•0 per 10,000 (95% CI 9•4 to 10•8). Rates were higher for those from any ethnic minority group, the lowest quintile of socio-economic status, born preterm or with low birthweight. Only 44% had a single ophthalmic condition: disorders of the brain/visual pathways affected 48% overall. Prenatal or perinatal aetiological factors accounted for 84% of all conditions. InterpretationBCVIS2 provides a contemporary snapshot of the heterogeneity, multi-morbidity and vulnerability associated with childhood visual disability in a high income country, and the arising complex needs. These findings will facilitate developing and delivering healthcare and planning interventional research. They highlight the importance of including childhood visual disability as a sentinel event and metric in global child health initiatives.

Postnatal phenobarbital for the prevention of intraventricular haemorrhage in preterm infants (Review)

No abstract

Xenon delivery during ambulance retrieval was feasible, reduced starting delays, and used very little gas.

Neonatal hypoxic‐ischemic encephalopathy (HIE) is associated with alterations in cerebral blood flow (CBF) as a result of perinatal asphyxia. The extent to which CBF changes contribute to injury, and whether treatments that ameliorate these changes might be neuroprotective, is still unknown. Higher throughput techniques to monitor CBF changes in rodent models of HIE can help elucidate the underlying pathophysiology. We developed a laser speckle imaging (LSI) technique to continuously monitor CBF in six postnatal‐day 10 (P10) rats simultaneously before, during, and after unilateral hypoxia‐ischemia (HI, ligation of the left carotid artery followed by hypoxia in 8% oxygen). After ligation, CBF to the ligated side fell by 30% compared to the unligated side (P < 0.0001). Hypoxia induced a bilateral 55% reduction in CBF, which was partially restored by resuscitation. Compared to resuscitation in air, resuscitation in 100% oxygen increased CBF to the ligated side by 45% (P = 0.033). Individual variability in CBF response to hypoxia between animals accounted for up to 24% of the variability in hemispheric area loss to the ligated side. In both P10 and P7 models of unilateral HI, resuscitation in 100% oxygen did not affect hemispheric area loss, or hippocampal CA1 pyramidal neuron counts, after 1‐week survival. Continuous CBF monitoring using LSI in multiple rodents simultaneously can screen potential treatment modalities that affect CBF, and provide insight into the pathophysiology of HI.