Long peripheral catheters in neonates: filling the gap between short peripheral catheters and epicutaneous-caval catheters?

INTRODUCTION: Non-critically ill neonates at times require venous access to provide peripherally compatible infusions for a limited period (more than 3 days). In such a situation, short peripheral cannulas are not appropriate as their average duration is about 2 days, while-on the other hand-epicutaneous-caval catheters may be too invasive. In these patients, insertion of long peripheral cannulas may be an effective option. METHODS: In this observational retrospective study, we revised all "long" peripheral catheters (4 and 6 cm long) inserted by direct Seldinger technique in our neonatal intensive care unit when peripheral venous access was required for more than 3 days. RESULTS: We inserted 52 2Fr polyurethane catheters, either 4 cm long (n = 25) or 6 cm long (n = 27) in 52 patients. Mean dwelling time was 4.17 days (range 1-12). Most devices were inserted in the cephalic vein (n = 18, 35%), and the rest in the saphenous vein (n = 11, 21%) and other superficial veins. There was no significant correlation between the duration of the device and type of infusion (p = 0.40). The main complications were infiltration (n = 16, 31%) and phlebitis (n = 8, 15%). The rate of removal due to complications was significantly higher (p < 0.01) in neonates with bodyweight <2000 g at the time of insertion. CONCLUSION: In our experience, 2 Fr 4-6 cm long peripheral catheters may be a valid option for neonates requiring peripherally compatible infusions for more than 3 days. The limits of this study are the necessity of training in the technique of insertion and the small size of our sample. The longest dwell was observed in neonates weighing >2000 g at the time of LPC insertion.

Possible Coronavirus Disease 2019 Pandemic and Pregnancy: Vertical Transmission Is Not Excluded.

Coronavirus disease 2019 outbreak has a growing impact on global health; vertical transmission of severe acute respiratory syndrome coronavirus 2 infection is still controversial. In this article, we describe a case of vertical transmission of severe acute respiratory syndrome coronavirus 2 in a newborn with respiratory and gastrointestinal symptoms.

Galactosialidosis: review and analysis of CTSA gene mutations.

BACKGROUND: Mutations in the CTSA gene, that encodes the protective protein/cathepsin A or PPCA, lead to the secondary deficiency of ß-galactosidase (GLB1) and neuraminidase 1 (NEU1), causing the lysosomal storage disorder galactosialidosis (GS). Few clinical cases of GS have been reported in the literature, the majority of them belonging to the juvenile/adult group of patients. METHODS: The correct nomenclature of mutations for this gene is discussed through the analysis of the three PPCA/CTSA isoforms available in the GenBank database. Phenotype-genotype correlation has been assessed by computational analysis and review of previously reported single amino acid substitutions. RESULTS: We report the clinical and mutational analyses of four cases with the rare infantile form of GS. We identified three novel nucleotide changes, two of them resulting in the missense mutations, c.347A>G (p.His116Arg), c.775T>C (p.Cys259Arg), and the third, c.1216C>T, resulting in the p.Gln406* stop codon, a type of mutation identified for the first time in GS. An Italian founder effect of the c.114delG mutation can be suggested according to the origin of the only three patients carrying this mutation reported here and in the literature. CONCLUSIONS: In early reports mutations nomenclature was selected according to all CTSA isoforms (three different isoforms), thus generating a lot of confusion. In order to assist physicians in the interpretation of detected mutations, we mark the correct nomenclature for CTSA mutations. The complexity of pathology caused by the multifunctions of CTSA, and the very low numbers of mutations (only 23 overall) in relation to the length of the CTSA gene are discussed.In addition, the in silico functional predictions of all reported missense mutations allowed us to closely predict the early infantile, late infantile and juvenile phenotypes, also disclosing different degrees of severity in the juvenile phenotype.