Our data demonstrate that S-(+)-ketamine possesses anti-inflammatory potential. Anaesthesia with S-(+)-ketamine may have beneficial effects in attenuating the CPB-induced systemic inflammatory response.

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IntroductionIn recent years, critical incident (CI) reporting has increasingly been regarded as part of ongoing quality management. CI databanks also aim to improve health and safety issues for patients as well as staff. The aim of this study was to identify frequent causes of adverse events in critical care with the potential to harm patients, staff or visitors by analysing data from a voluntary and optionally anonymous critical incident reporting system.MethodsThe study includes all critical incidents reported during a 90-month period in a 13-bed adult general intensive care unit (ICU). Reporting of incidents was performed via an electronic reporting system or by a manual critical incident report. All CIs were classified in the following main categories: equipment, administration, pharmaceuticals, clinical practice, and health & safety hazards. The overall distribution of incidents within the different categories was compared with the regional database of ICUs in the Cheshire and Mersey region of northwest England for 2008.ResultsA total of 1127 CIs were reported during the study period. The frequencies within the main categories were: equipment 338 (30%), clinical practice 257 (22.8%), pharmaceuticals 238 (21.1%), administration 213 (18.9%), health and safety hazards 81 (7.2%). The regional database had a similar frequency of critical incidents within the different categories, suggesting that our results may reflect a general distribution pattern of CIs in intensive care.ConclusionsCritical incident reporting helps to identify frequent causes of adverse events in critical care. Improvements in quality of care following implementation of preventative strategies such as introduction of regular equipment training sessions will have to be assessed further in future studies.

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...

The P/F ratio was a better predictor of need for mechanical ventilation than STSS. The P/F ratio is a simple and accepted determinant of hypoxaemia and should be used if secondary triaging becomes necessary during future influenza pandemics.