Objectives The aims of this study were to evaluate the prevalence, complications, and mortality of hypernatremic dehydration in neonates and to compare the effect of correction rate at 48 hours on mortality and on neurological outcome in the short term. Methods This retrospective study was conducted between January 2007 and 2011 in the neonatal intensive care unit. Term neonates were included. The patients were grouped as follows: group 1 = 150 to 160 mmol/L, group 2 = 161 to 170 mmol/L and group 3 = 171 to 189 mmol/L. Results Among 4280 neonates, 81 cases (1.8%) had hypernatremic dehydration. Groups 1, 2, and 3 consisted of 55, 23, and 3 patients, respectively. Mortality rates were as follows: 3.6%, 17.3%, and 66.6%. Mean serum sodium (Na) correction rates at 0 to 24 hours and 24 to 48 hours were 0.48 ± 0.2 versus 0.38 ± 0.31 mmol/L per hour (group 1) and 0.49 ± 0.21 versus 0.52 ± 0.28 mmol/L per hour (group 2), respectively. In 32 patients (58.1%) from group 1 and in 13 patients (56.5%) from group 2, correction rate of 0.5 mmol/L per hour or less was achieved. Twenty-two patients developed convulsions, which was the most common complication during therapy. Serum Na greater than 160 mmol/L at admission (odds ratio, 1.9; 95% confidence interval, 1.3–3.7) and serum Na correction rate of greater than 0.5 mmol/L per hour (odds ratio, 4.3; 95% confidence interval, 1.2–6.5) were independent risk factors for death or convulsion. There was a significant difference between groups 1 and 2 in Denver Developmental Screening Test II results (64.1% vs 30.7 %, P = 0.001). Conclusion Hypernatremic dehydration is an important problem that should be managed properly to avoid adverse outcomes.

Neonatal thrombocytopenia is one of the most common hematologic disorders in neonatal intensive care units (NICUs). The purpose of this study was to determine the prevalence of thrombocytopenia and whether thrombocytopenia has an effect on the occurrence of intraventricular hemorrhage (IVH) ≥ grade 2 and on mortality rate. This study was carried out retrospectively in neonates admitted to NICU of Cumhuriyet University in Sivas, Turkey, between 2009 and 2012. Among 2218 neonates evaluated, 208 (9.4%) developed thrombocytopenia. The prevalence of IVH ≥ grade 2 was more in infants with thrombocytopenia (7.2%) than in those without thrombocytopenia (4.4%), although this was not statistically significant (P = .08). In univariate analysis, IVH ≥ grade 2 was higher in cases with very severe thrombocytopenia (35.7%, n = 5) than in those with mild (2.1%, n = 2), moderate (4.7%, n = 3), and severe thrombocytopenia (15.2%, n = 5) (P = .04). Multivariate logistic regression analysis showed that birth weight <1500 g (OR 6.2, 95% CI 3.4–9.8; P = .0001), gram-negative sepsis (OR 2.5, 95% CI 1.8–4.2; P = .01), very severe thrombocytopenia (OR 1.3, 95% CI 1.1–2.1; P = .03), and platelet transfusion ≥2 (OR 7.3, 95% CI 4.1–12.1; P = .001) were significant risk factors for mortality. The results of our study suggest that outcomes of neonates with thrombocytopenia depend not only on platelet count but also on decreased gestational age or birth weight, prenatal factors, and sepsis.

Apoptosis is a main regulator in responses of cellular immunity throughout systemic viral infections. Perforin, soluble Fas ligand, caspase-3 and caspase-cleaved cytokeratin-18 (M-30) are mediators of apoptosis. The aim of this study is the evaluation of Crimean-Congo hemorrhagic fever (CCHF) disease changes in the levels of these apoptotic markers and the relation of these changes with disease severity. Forty-nine hospitalized children with CCHF and 36 healthy controls were enrolled in this prospective study. The CCHF patients were classified into 2 groups based on disease severity (severe group and nonsevere group). Demographic characteristics and clinical and laboratory findings of all patients were recorded on admission. Serum perforin, caspase-3 and soluble Fas ligand levels were found to be significantly higher both in the severe and nonsevere CCHF groups than the healthy control group (P < 0.05), but there was no significant difference in these apoptotic markers between severe and nonsevere CCHF groups (P > 0.05). In addition, serum M-30 levels did not differ significantly among all groups (P > 0.05). There was a positive correlation between serum values for perforin, caspase-3 and M-30 and the disease’s severity criteria such as aspartate aminotransferase and/or alanine aminotransferase. The serum levels of all these markers were negatively correlated with disease severity criteria such as the platelet count. In this study, we concluded that the interactions of cytolytic granules containing perforin and caspase cascade and Fas-FasL may play an important role in the pathogenesis of CCHF in children.