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:This study was conducted to compare the efficacy and effects of dexmedetomidine and midazolam in preoperative sedation.Materials and Methods:A total of 125 patients in American Society of Anaesthesiologists (ASA) I-II were divided into three groups: Group I (n = 40) for controls, Group II (n = 40) for Dexmedetomidine (1 μg/kg), and group III was the midazolam group (n = 45). Group III was further divided into three subgroups according to the doses of midazolam: Group IIIA (n = 15) received 0.02 mg/kg, group IIIB (n = 15) received 0.04 mg/kg, and group IIIC (n = 15) received 0.06 mg/kg of midazolam. Drugs were infused over a 10-minute period with appropriate monitoring. Ramsay and visual analog scores, for sedation and anxiety, respectively, and mean arterial pressure, heart rate, and SpO2 measurement, including respiratory rates were recorded, every 5 minutes for 30 minutes following infusion.Results:There was marked sedation and a decrease in anxiety in groups II and IIIC (P < 0.01). Mean arterial pressure (MAP) and heart rate (HR) decreased significantly in group II (P < 0.01 and P < 0.05, respectively), but there was no associated hypotension (MAP <60 mm Hg) or bradycardia (HR <50 bpm) (P < 0.05). Respiratory rates and SpO2 values decreased in groups II, IIIA, IIIB, and IIIC. The differences in respiratory rates were not significant (P > 0.05); however, decrease in SpO2 was significant in group IIIC (P < 0.01).Conclusions:Dexmedetomidine was as effective as higher doses of midazolam in sedation. The hemodynamic and respiratory effects were minimal. Although dexmedetomidine caused significant decrease in the blood pressure and heart rate, it probably just normalized increased levels caused by preoperative stress.

Single-session hypnosis has never been evaluated as a premedication technique in patients undergoing coronary artery bypass grafting (CABG). The aim of the present study was to evaluate the beneficial effects of clinical hypnotherapy on perioperative anxiety, pain perception, sedation, and necessity for ventilator assistance in patients undergoing CABG. Double-blind, randomized, clinical trial was performed. Forty-four patients undergoing CABG surgery were randomized into two groups. The patients in group A received preprocedural hypnosis by an anesthesiologist. Patients in group B (control) had only information on the surgical intervention by the same anesthesiologist. State-Trait-Anxiety Index-I (STAI-I) and Beck Depression Inventory (BDI) were performed preoperatively in both groups. Visual analog scale (VAS) and Ramsay sedation scale (RSS) were evaluated on 0th, 1st, 2nd, 4th, 6th, 8th, 10th, 12th, and 24th hours, postoperatively. Postoperative anxiety level, analgesic drug consumption, and duration of ventilator assistance and intensive care unit (ICU) stay were also documented. When anxiety and depression levels were compared, significantly lower STA-I and BDI values were detected in group A after hypnotherapy ( = 0.001, = 0.001, respectively). Significantly less total doses of remifentanil (34.4 ± 11.4 vs. 50.0 ± 13.6 mg) and morphine (4.9 ± 3.3 vs. 13.6 ± 2.7 mg) were administered in group A in the postoperative period. Ventilator assistance duration (6.8 ± 2.0 vs. 8.9 ± 2.7 hours) was also shorter in group A when compared with that in group B ( = 0.007). Hypnosis session prior to surgery was an effective complementary method in decreasing presurgical anxiety, and it resulted in better pain control as well as reduced ventilator assistance following CABG surgery.

Critical Care 2017, 21(Suppl 1):P349 Introduction Imbalance in cellular energetics has been suggested to be an important mechanism for organ failure in sepsis and septic shock. We hypothesized that such energy imbalance would either be caused by metabolic changes leading to decreased energy production or by increased energy consumption. Thus, we set out to investigate if mitochondrial dysfunction or decreased energy consumption alters cellular metabolism in muscle tissue in experimental sepsis. Methods We submitted anesthetized piglets to sepsis (n = 12) or placebo (n = 4) and monitored them for 3 hours. Plasma lactate and markers of organ failure were measured hourly, as was muscle metabolism by microdialysis. Energy consumption was intervened locally by infusing ouabain through one microdialysis catheter to block major energy expenditure of the cells, by inhibiting the major energy consuming enzyme, N+/K + -ATPase. Similarly, energy production was blocked infusing sodium cyanide (NaCN), in a different region, to block the cytochrome oxidase in muscle tissue mitochondria. Results All animals submitted to sepsis fulfilled sepsis criteria as defined in Sepsis-3, whereas no animals in the placebo group did. Muscle glucose decreased during sepsis independently of N+/K + -ATPase or cytochrome oxidase blockade. Muscle lactate did not increase during sepsis in naïve metabolism. However, during cytochrome oxidase blockade, there was an increase in muscle lactate that was further accentuated during sepsis. Muscle pyruvate did not decrease during sepsis in naïve metabolism. During cytochrome oxidase blockade, there was a decrease in muscle pyruvate, independently of sepsis. Lactate to pyruvate ratio increased during sepsis and was further accentuated during cytochrome oxidase blockade. Muscle glycerol increased during sepsis and decreased slightly without sepsis regardless of N+/K + -ATPase or cytochrome oxidase blocking. There were no significant changes in muscle glutamate or urea during sepsis in absence/presence of N+/K + -ATPase or cytochrome oxidase blockade. ConclusionsThese results indicate increased metabolism of energy substrates in muscle tissue in experimental sepsis. Our results do not indicate presence of energy depletion or mitochondrial dysfunction in muscle and should similar physiologic situation be present in other tissues, other mechanisms of organ failure must be considered. , and long-term follow up has shown increased fracture risk [2]. It is unclear if these changes are a consequence of acute critical illness, or reduced activity afterwards. Bone health assessment during critical illness is challenging, and direct bone strength measurement is not possible. We used a rodent sepsis model to test the hypothesis that critical illness causes early reduction in bone strength and changes in bone architecture. Methods 20 Sprague-Dawley rats (350 ± 15.8g) were anesthetised and randomised to receive cecal ligation and puncture (CLP) (50% cecum length, 18G needle single pass through anterior and posterior wa...

Background: Diabetes mellitus (DM) causes debilitating complications and, as a result, diabetics frequently require intensive care. Although lungs are not thought to be affected primarily by DM, an increasing number of studies indicate physiological and structural abnormalities in diabetic lungs. Objectives: Pyrrolidine dithiocarbamate (PDTC) is a metal chelator and a potent inhibitor of NF-ĸB. Keeping in mind that NF-ĸB activation may be crucial in end-organ injury due to DM, we studied the role of PDTC on the inhibition of NF-ĸB activation and its effects on possible lung injury in rats with streptozotocin-induced DM. Methods: 36 Sprague-Dawley rats were allocated into 4 groups: diabetes, diabetes + PDTC, control and control + PDTC. At the end of 10 weeks, rats were sacrificed and their lungs were taken for histopathological and immunohistochemical evaluation [for NF-ĸB (p65) and endothelial nitric oxide (eNOS) immunoreactivities]. Protein carbonyl content (PCC), superoxide dismutase (SOD) and reduced glutathione (GSH) activities were measured. Results: Histopathologically, basal membranes were thickened and there was intense inflammatory reaction in diabetic lungs. However, the PDTC group, in which there were poor positive expressions of eNOS and p65 activity compared to diabetes group, revealed fewer inflammatory changes. PCC levels in diabetic lungs were higher, but SOD and GSH activities were lower. However, measurements of these parameters in the PDTC group and controls gave similar results. Conclusion: Lungs are exposed to changes induced by oxidative stress in diabetes through NF-ĸB activation and PDTC seems to be useful to prevent diabetic lung injury.