Younger age, neutropenia, hematologic malignancy and longer catheterization are important risk factors for CLABSI, but further research is required for the prevention of catheter-related infection in children with malignancy.

Sepsis is a dysregulated host response to infection related to devastating outcomes. Recently, interest has been shifted towards apoptotic and antiapoptotic pathobiology. Apoptosis is executed through the activation of caspases regulated by a number of antiapoptotic proteins, such as survivin. The survivin and caspases’ responses to sepsis have not yet been elucidated. This is a multicenter prospective observational study concerning patients with sepsis (n = 107) compared to patients with traumatic systemic inflammatory response syndrome (SIRS) (n = 75) and to healthy controls (n = 89). The expression of survivin was quantified through real-time quantitative polymerase chain reaction for the different survivin splice variants (wild type-WT, ΔEx3, 2B, 3B) in peripheral blood leukocytes. The apoptotic or antiapoptotic tendency was specified by measuring survivin-WT, caspase-3, and -9 serum protein concentrations through enzyme-linked immunosorbent assay. The survivin-WT, -2B, -ΔΕx3 mRNA, survivin protein, and caspases showed an escalated increase in SIRS and sepsis, whereas survivin-3B was repressed in sepsis (p < 0.05). Survivin correlated with IL-8 and caspase-9 (p < 0.01). For discriminating sepsis, caspase-9 achieved the best receiver operating characteristic curve (AUROC) of 0.95. In predicting mortality, caspase-9 and survivin protein achieved an AUROC of 0.70. In conclusion, specific apoptotic and antiapoptotic pathways might represent attractive targets for future research in sepsis.

The ratio of tidal volume to functional residual capacity (FRC), defined as "volumetric" strain, causes physical lung deformation. The corresponding change in transpulmonary pressure at end inspiration, defined as stress, is directly applied to the alveolus [1]. Both stress and strain may cause global or local lung deformation and microscopic or macroscopic tissue damage, representing significant determinants of ventilator-induced lung injury [1]. A modified nitrogen washout/washin technique, measuring end-expiratory lung volume (EELV), correlated well with computed tomography and was proposed as a valuable tool to optimize ventilator settings, improving lung protective ventilation [2]. The aim of this study was to evaluate the effect of positive end-expiratory pressure (PEEP) on EELV, compliance of the respiratory system (Crs), and stress/strain in children with acute respiratory distress syndrome (ARDS), and compare it with children "at risk of ARDS" and those with no lung injury using the modified nitrogen washout/washin technique (see electronic supplementary material). To monitor the effects of the disease evolution on the PEEP-induced increases in lung stress/strain, measurements were repeated at predetermined time points. We hypothesized that PEEP escalation increases EELV, Crs, strain, and stress in mechanically ventilated children, potentially influenced by disease severity and timing. A total of 700 measurements were recorded in 25 mechanically ventilated critically ill children (ARDS, n = 8; at risk of ARDS, n = 5; without lung injury, n = 12). ARDS patients had higher oxygenation index (OI > 4) and PaCO 2 , lower PaO 2 /FiO 2 , PaO 2 , and prolonged length of

Oxidative stress is considered pivotal in the pathophysiology of sepsis. Oxidants modulate heat shock proteins (Hsp), interleukins (IL), and cell death pathways, including apoptosis. This multicenter prospective observational study was designed to ascertain whether an oxidant/antioxidant imbalance is an independent sepsis discriminator and mortality predictor in intensive care unit (ICU) patients with sepsis (n = 145), compared to non-infectious critically ill patients (n = 112) and healthy individuals (n = 89). Serum total oxidative status (TOS) and total antioxidant capacity (TAC) were measured by photometric testing. IL-6, -8, -10, -27, Hsp72/90 (ELISA), and selected antioxidant biomolecules (Ζn, glutathione) were correlated with apoptotic mediators (caspase-3, capsase-9) and the central anti-apoptotic survivin protein (ELISA, real-time PCR). A wide scattering of TOS, TAC, and TOS/TAC in all three groups was demonstrated. Septic patients had an elevated TOS/TAC, compared to non-infectious critically ill patients and healthy individuals (p = 0.001). TOS/TAC was associated with severity scores, procalcitonin, IL-6, -10, -27, IFN-γ, Hsp72, Hsp90, survivin protein, and survivin isoforms -2B, -ΔΕx3, -WT (p < 0.001). In a propensity probability (age-sex-adjusted) logistic regression model, only sepsis was independently associated with TOS/TAC (Exp(B) 25.4, p < 0.001). The AUCTOS/TAC (0.96 (95% CI = 0.93–0.99)) was higher than AUCTAC (z = 20, p < 0.001) or AUCTOS (z = 3.1, p = 0.002) in distinguishing sepsis. TOS/TAC, TOS, survivin isoforms -WT and -2B, Hsp90, IL-6, survivin protein, and repressed TAC were strong predictors of mortality (p < 0.01). Oxidant/antioxidant status is impaired in septic compared to critically ill patients with trauma or surgery and is related to anti-apoptotic, inflammatory, and innate immunity alterations. The unpredicted TOS/TAC imbalance might be related to undefined phenotypes in patients and healthy individuals.