ABSTRACT
BACKGROUND: Human parechovirus genotype 3 (HPeV-3) has been linked to meningoencephalitis and sepsis-like disease in infants younger than 3 months. METHODS: We present clinical and phylogenetic characteristics of 15 infants who were admitted with HPeV-3 infections to 3 hospitals in Norway during a period of 7 months in 2011. RESULTS: Eleven patients had a sepsis-like disease, and meningoencephalitis was found in 10. Phylogenetic analyses of the viral protein (VP)3/VP1 region showed that all HPeV-3 isolates clustered closely and differentially from previously known HPeV-3 lineages. Fourteen of the 15 infants recovered after 1-3 weeks. One boy had widespread cerebral magnetic resonance imaging abnormalities, but at 1 year of age he had a normal psychomotor status. CONCLUSION: A new HPeV-3-strain caused sepsis-like disease and meningoencephalitis in 15 Norwegian infants. All but 1 recovered within a few weeks.
Subject(s)
Parechovirus/isolation & purification , Picornaviridae Infections/epidemiology , Picornaviridae Infections/pathology , Cluster Analysis , Female , Genotype , Hospitals , Humans , Infant , Infant, Newborn , Male , Meningoencephalitis/epidemiology , Meningoencephalitis/pathology , Meningoencephalitis/virology , Norway/epidemiology , Parechovirus/classification , Parechovirus/genetics , Phylogeny , RNA, Viral/genetics , Sepsis/epidemiology , Sepsis/pathology , Sepsis/virology , Treatment OutcomeABSTRACT
AIM: To show the potential for reversing acute intermediate to advanced phase bilirubin encephalopathy. METHODS: Case studies. RESULTS: Six extremely jaundiced infants had symptoms of intermediate to advanced phase acute bilirubin encephalopathy. The infants were treated aggressively. Two patients had brain magnetic resonance imaging showing increased signals in the globus pallidus. On follow-up, all infants are neurologically normal. CONCLUSIONS: Intermediate-to-advanced stage acute bilirubin encephalopathy may occasionally be reversible. These cases provide a strong argument in favour of rapid and aggressive intervention in infants presenting with extreme jaundice and neurological symptoms.
Subject(s)
Exchange Transfusion, Whole Blood , Immunoglobulins, Intravenous/therapeutic use , Jaundice, Neonatal/therapy , Kernicterus/therapy , Phototherapy , Acute Disease , Bilirubin/blood , Combined Modality Therapy , Female , Globus Pallidus/pathology , Humans , Infant, Newborn , Kernicterus/diagnosis , Magnetic Resonance Imaging , MaleABSTRACT
OBJECTIVE: To compare strategies with and without first-day of life pulse oximetry screening to detect critical congenital heart defects (CCHDs). STUDY DESIGN: Population based study including all live born infants in Norway in 2005 and 2006 (n = 116 057). Postductal (foot) arterial oxygen saturation (SpO(2)) was measured in apparently healthy newborns after transferral to the nursery, with SpO(2) < 95% as cut-off point. Out of 57 959 live births in the hospitals performing pulse oximetry screening, 50 008 (86%) were screened. RESULTS: A total of 136 CCHDs (1.2 per 1000) were diagnosed, 38 (28%) of these prenatally. Of the CCHDs detected after birth, 44/50 (88%) were detected before discharge in the population offered pulse oximetry screening (25 by pulse oximetry), compared to 37/48 (77%) in the non-screened population (p = 0.15). Median times for diagnosing CCHDs in-hospital before discharge were 6 and 16 h after birth respectively (p < 0.0001). In the screened population 6/50 (12%) CCHDs were missed and recognized after discharge because of symptoms. Two of the six missed cases failed the pulse oximetry screening, but were overlooked (echocardiography not performed before discharge). If these cases had been recognized, 4/50 (8%) would have been missed compared to 11/48 (23%) in the non-screened population (p = 0.05). Of the cases missed, 14/17 (82%) had left-sided obstructive lesions. CONCLUSION: First-day of life pulse oximetry screening provides early in-hospital detection of CCHDs and may reduce the number missed and diagnosed after discharge.
