Following the introduction of these guidelines, fewer babies in Norway receive phototherapy, and no cases of chronic kernicterus have been reported during this period.

BackgroundRSV is recognized as the most important cause of serious lower respiratory tract illness in infants and young children worldwide leading to hospitalisation in a great number of cases, especially in certain high-risk groups. The aims of the present study were to identify risk groups, outcome and incidences of hospitalisation for RSV bronchiolitis in Norwegian children under two years of age and to compare the results with other studies.MethodsWe performed a population-based retrospective survey for the period 1993–2000 in children under two years of age hospitalised for RSV bronchiolitis.Results822 admissions from 764 patients were identified, 93% had one hospitalisation, while 7% had two or more hospitalisations. Mean annual hospitalisation incidences were 21.7 per 1.000 children under one year of age, 6.8 per 1.000 children at 1–2 years of age and 14.1 per 1.000 children under two years of age. 77 children (85 admissions) belonged to one or more high-risk groups such as preterm birth, trisomy 21 and congenital heart disease. For preterm children under one year of age, at 1–2 years of age and under two years of age hospitalisation incidences per 1.000 children were 23.5, 8.7 and 16.2 respectively. The incidence for children under two years of age with trisomy 21 was 153.8 per 1.000 children.ConclusionWhile the overall hospitalisation incidences and outcome of RSV bronchiolitis were in agreement with other studies, hospitalisation incidences for preterm children were lower than in many other studies. Age on admission for preterm children, when corrected for prematurity, was comparable to low-risk children. Length of hospitalisation and morbidity was high in both preterm children, children with a congenital heart disease and in children with trisomy 21, the last group being at particular high risk for severe disease.

BPD remains a severe complication of extreme prematurity in spite of prenatal steroids and surfactant treatment. Whether associations with surfactant and PDA treatment simply reflect severity of early lung disease or have causal relationships should probably be studied in randomized controlled trials.

ABSTRAm. The acute effects of normoxemic hypocarbia and hypercarbia were examined in six newborn piglets. Brain blood flow was maintained during hypocarbia until extremely low Paco2 ( 4 5 mm Hg) levels were achieved at which time total brain and cerebral blood flow decreased significantly from baseline values. Blood flow to the thalamus, cerebellum and brain stem was unchanged from baseline conditions during hypocarbia. This suggests that the newborn brain is relatively insensitive to moderate degrees of hypocarbia. Extreme hypocarbia (Paco, e l 5 mm Hg) was associated with a significant increase in heart rate, accompanied by a significant decrease in mean arterial blood pressure; however, cardiac output was not significantly different from baseline determinations. Hypercarbia with normoxemia was associated with significant increases in total brain blood flow, with greater blood flow to the brain stem, cerebellum, and thalamus than to the cerebrum. The percentage of cardiac output received by the brain was also significantly increased, although total cardiac output was unchanged. This demonstrates that the newborn cerebral vasculature is sensitive to hypercarbia and that regional differences in sensitivity may account for the greater increments in blood flow to the caudal portions of the brain than that to the cerebrum. (Pediatr Res 18:1132-1136, 1984) Hyperventilation to extremely low Paco2 levels has been advocated as a form of therapy for pulmonary vasospasm in the human neonate (7,22). Hyperventilation has also been used in adults as a method of restoring autoregulation of the brain blood flow following brain injury (21). In the adult, there is no further reduction in cerebral blood flow below carbon dioxide tensions of approximately 20 mm Hg, presumably because ischemia induces metabolic changes in the brain that ovemde the C02 control of the cerebral vasculature (3,10,26 species whose brain maturation differs significantly from that of the term human neonate. The maturation of the newborn piglet brain is comparable to a human infant of 36-38 wk gestation (6, 23). Therefore, we utilized the newborn piglet to assess the acute effects of variations in Paco2 on brain blood flow and cardiac output, with a comparison of regional blood flow within the brain and the percentage of cardiac output received by the brain during hypo-and hypercarbia. MATERIALS AND METHODSSix, 1-to 4-day-old farm-bred piglets were subjects of this study. All piglets remained with the sows until the morning of the study. The weight of the piglets was 1.52 & 0.42 kg (mean +. SD).surgical procedures. All surgical procedures were performed under nitrous oxide inhalation anesthesia with local anesthesia using 1% xylocaine. A tracheotomy was performed and the piglets were ventilated with a pressure-limited Amsterdam infant ventilator using a gas mixture of 70% nitrous oxide and 30% oxygen. Polyvinyl catheters (OD127 ID86) were placed in the left axillary artery, abdominal aorta via the femoral artery and inferior vena cava via the femoral ...

No abstract

No abstract

ABSTRACT. The mechanisms by which bilirubin causes neurotoxicity in newborns have not been well defined, but an involvement in synaptic transmission appears possible. Herein we present evidence for an inhibitory effect of bilirubin on both basal and depolarization-induced (50 mM KCl) phosphorylation of synapsin I, a synaptic vesicleassociated protein that may play a role in neurotransmitter release. Synaptosomes from rat cerebral cortices, prelabeled with 32P in vitro to label the intraterminal ATP pool, were incubated with or without bilirubin and bovine serum albumin (added as a stabilizer) at varying doses and for different time intervals. Some preparations were also depolarized by high KC1 concentrations to induce Ca++ influx. The phosphorylation of synapsin I was monitored. Our results show that addition of bilirubin to the medium significantly decreases 32P incorporation into synapsin I, both under basal and depolarizing conditions, in a timeand dose-dependent manner, significant effects being observed already at 10 pM bilirubin after 120-min incubation of the synaptosomes. Separate analysis of the multiple phosphorylation sites in synapsin I showed that the phosphorylation of both the "head" and "tail" regions of the protein was decreased by bilirubin. Removal of the bilirubin-containing incubation medium retarded the decrease in synapsin I 32P content, indicating that the effect observed may be reversible. The nontoxic pyrrole biliverdin had no effect on synapsin I phosphorylation under the experimental conditions used, indicating that the effect was specific to bilirubin. Our results thus suggest that bilirubin may achieve some of its reversible effects on the brain through inhibition of the phosphorylation of the synapsic vesicleassociated protein synapsin I. (Pediatr Res 23: 219-223, 1988)

No abstract