Table of contentsP001 - Sepsis impairs the capillary response within hypoxic capillaries and decreases erythrocyte oxygen-dependent ATP effluxR. M. Bateman, M. D. Sharpe, J. E. Jagger, C. G. EllisP002 - Lower serum immunoglobulin G2 level does not predispose to severe flu.J. Solé-Violán, M. López-Rodríguez, E. Herrera-Ramos, J. Ruíz-Hernández, L. Borderías, J. Horcajada, N. González-Quevedo, O. Rajas, M. Briones, F. Rodríguez de Castro, C. Rodríguez GallegoP003 - Brain protective effects of intravenous immunoglobulin through inhibition of complement activation and apoptosis in a rat model of sepsisF. Esen, G. Orhun, P. Ergin Ozcan, E. Senturk, C. Ugur Yilmaz, N. Orhan, N. Arican, M. Kaya, M. Kucukerden, M. Giris, U. Akcan, S. Bilgic Gazioglu, E. TuzunP004 - Adenosine a1 receptor dysfunction is associated with leukopenia: A possible mechanism for sepsis-induced leukopeniaR. Riff, O. Naamani, A. DouvdevaniP005 - Analysis of neutrophil by hyper spectral imaging - A preliminary reportR. Takegawa, H. Yoshida, T. Hirose, N. Yamamoto, H. Hagiya, M. Ojima, Y. Akeda, O. Tasaki, K. Tomono, T. ShimazuP006 - Chemiluminescent intensity assessed by eaa predicts the incidence of postoperative infectious complications following gastrointestinal surgeryS. Ono, T. Kubo, S. Suda, T. Ueno, T. IkedaP007 - Serial change of c1 inhibitor in patients with sepsis – A prospective observational studyT. Hirose, H. Ogura, H. Takahashi, M. Ojima, J. Kang, Y. Nakamura, T. Kojima, T. ShimazuP008 - Comparison of bacteremia and sepsis on sepsis related biomarkersT. Ikeda, S. Suda, Y. Izutani, T. Ueno, S. OnoP009 - The changes of procalcitonin levels in critical patients with abdominal septic shock during blood purificationT. Taniguchi, M. OP010 - Validation of a new sensitive point of care device for rapid measurement of procalcitoninC. Dinter, J. Lotz, B. Eilers, C. Wissmann, R. LottP011 - Infection biomarkers in primary care patients with acute respiratory tract infections – Comparison of procalcitonin and C-reactive proteinM. M. Meili, P. S. SchuetzP012 - Do we need a lower procalcitonin cut off?H. Hawa, M. Sharshir, M. Aburageila, N. SalahuddinP013 - The predictive role of C-reactive protein and procalcitonin biomarkers in central nervous system infections with extensively drug resistant bacteriaV. Chantziara, S. Georgiou, A. Tsimogianni, P. Alexandropoulos, A. Vassi, F. Lagiou, M. Valta, G. Micha, E. Chinou, G. MichaloudisP014 - Changes in endotoxin activity assay and procalcitonin levels after direct hemoperfusion with polymyxin-b immobilized fiberA. Kodaira, T. Ikeda, S. Ono, T. Ueno, S. Suda, Y. Izutani, H. ImaizumiP015 - Diagnostic usefullness of combination biomarkers on ICU admissionM. V. De la Torre-Prados, A. Garcia-De la Torre, A. Enguix-Armada, A. Puerto-Morlan, V. Perez-Valero, A. Garcia-AlcantaraP016 - Platelet function analysis utilising the PFA-100 does not predict infection, bacteraemia, sepsis or outcome in critically ill patientsN. Bolton, J. Dudziak, S. Bonney, A. Tridente, P. NeeP017 - Extracellular histone H3 levels are in...

Background and objectives AKI is a major clinical problem and predictor of outcome in hospitalized patients. In 2013, the Kidney Disease: Improving Global Outcomes (KDIGO) group published the third consensus AKI definition and classification system after the Risk, Injury, Failure, Loss of Kidney Function, and End-Stage Kidney Disease (RIFLE) and the Acute Kidney Injury Network (AKIN) working group systems. It is unclear which system achieves optimal prognostication in hospital patients.Design, setting, participants, & measurements A retrospective observational study using hospital laboratory, admission, and discharge databases was performed that included adult patients admitted to a teaching hospital in Tokyo, Japan between April 1, 2008, and October 31, 2011. AKI occurring during each hospital stay was identified, and discriminative ability of each AKI classification system based on serum creatinine for the prediction of hospital mortality was assessed. The receiver operating characteristic curve, a graphical measure of test performance, and the area under the curve were used to evaluate how classifications preformed on the study population.Results In total, 49,518 admissions were studied, of which 11.0% were diagnosed with RIFLE criteria and 11.6% were diagnosed with KDIGO criteria, but only 4.8% were diagnosed with AKIN criteria. Overall hospital mortality was 3.0%. AKI staging and hospital mortality were closely correlated in all systems. Discrimination for hospital mortality was similar for RIFLE and KDIGO criteria (area under the curve=0.77 versus 0.78; P=0.02), whereas AKIN discrimination was inferior (area under the curve=0.69 versus RIFLE [P,0.001] versus KDIGO [P,0.001]).Conclusion Among hospital patients, KDIGO and RIFLE criteria achieved similar discrimination, but the discrimination of AKIN was inferior.

BackgroundAtrial fibrillation (AF) is a common arrhythmia in the ICU. The aim of this review is to summarize relevant information on new-onset AF in non-cardiac critical illness with respect to epidemiology, prevention, and treatment.MethodsWe conducted a PubMed search in June 2014 and included studies describing the epidemiology, prevention, and treatment of new-onset AF and atrial flutter during ICU stay in non-cardiac adult patients. Selected studies were divided into the three categories according to the extracted information. The methodological quality of selected studies was described according to the Grading of Recommendations Assessment, Development and Evaluation system.ResultsWe identified 1,132 citations, and after full-text-level selection, we included 10 studies on etiology/outcome and five studies on treatment. There was no study related to prevention. Overall quality of evidence was mostly low or very low due to their observational study designs, small sample sizes, flawed diagnosis of new-onset AF, and the absence of mortality evaluation. The incidence of new-onset AF varied from 4.5% to 15.0%, excluding exceptional cases (e.g., septic shock). Severity scores of patients with new-onset AF were higher than those without new-onset AF in eight studies, in four of which the difference was statistically significant. Five studies reported risk factors for new-onset AF, all of which used multivariate analyses to extract risk factors. Multiple risk factors are reported, e.g., advanced age, the white race, severity scores, organ failures, and sepsis. Hospital mortality in new-onset AF patients was higher than that of patients without AF in all studies, four of which found statistical significance. Among the five studies on treatment, only one study was randomized controlled, and various interventions were studied.ConclusionsNew-onset AF occurred in 5%–15% of the non-cardiac critically ill patients. Patients with new-onset AF had poor outcomes compared with those without AF. Despite the high incidence of new-onset AF in the general ICU population, currently available information for AF, especially for management (prevention, treatment, and anticoagulation), is quite limited. Further research is needed to improve our understanding of new-onset AF in critically ill patients.

BackgroundIn vasopressor-dependent patients who had undergone cardiovascular surgery, we examined whether those with progression of acute kidney injury (AKI) had a greater difference (deficit) between premorbid and within-ICU hemodynamic pressure-related parameters compared to those without AKI progression.MethodsWe assessed consecutive adults who underwent cardiovascular surgery and who stayed in our ICU for at least 48 hours and received vasopressor support for more than 4 hours. We obtained premorbid and vasopressor-associated, time-weighted average values for hemodynamic pressure-related parameters (systolic [SAP], diastolic [DAP], and mean arterial pressure [MAP]; central venous pressure [CVP], mean perfusion pressure [MPP], and diastolic perfusion pressure [DPP]) and calculated deficits in those values. We defined AKI progression as an increase of at least one Kidney Disease: Improving Global Outcomes stage.ResultsWe screened 159 patients who satisfied the inclusion criteria and identified 76 eligible patients. Thirty-six patients (47 %) had AKI progression. All achieved pressure-related values were similar between patients with or without AKI progression. However, deficits in DAP (P = 0.027), MPP (P = 0.023), and DPP (P = 0.002) were significantly greater in patients with AKI progression.ConclusionsPatients with AKI progression had greater DAP, MPP, and DPP deficits compared to patients without AKI progression. Such deficits might be modifiable risk factors for the prevention of AKI progression.