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...

We observed a significant decrease in mean wait times after implementing our intervention. This decrease led to increased staff productivity and cost savings. Once wait times became a measurable metric, we were able to identify causes for delays and improve our operations, which can be performed in any patient care facility.

No abstract

235 Background: The MD Anderson Clinical and Translational Research Center (CTRC) focuses on Phase I and early Phase II clinical trials and is managing approximately 156 studies annually. This 18-room combined treatment and laboratory unit manages an average of 12,500 research pharmacologic time points and over 3,000 individual shipments yearly. In FY12, 74% of shipments were done on the day of collection (DOC), whereas 26% of the shipments were shipped periodically as required by the corresponding protocol. All studies are monitored at each step for errors - minor (simple DOC label corrections) or major (improper or missed specimen). Activity is analyzed and reported monthly. Methods: In 2010, to ensure accuracy of timing, collection method, proper storage, specimen condition, and destination accuracy, we developed a robust proprietary Oracle-based laboratory tracking system (LabTracker). In addition, we designed an Advanced Research Management and Data Analysis interface (ARMADA) which provides daily step by step protocol guidance using an innovative color-icon touch-screen display of all required protocol activities for patients in the CTRC. LabTracker contains all auditable items required in the clinical trial and markedly reduces work duplication and handwritten data transcription. We hypothesized that this input system would help decrease errors and improve research quality. Results: In FY10 there were 2,506 DOC shipments with an overall error rate of 3.07%. In FY12 errors decreased to 1.31% out of 3,128 DOC shipments. In FY10, there were 14,507 timepoints with 28 major errors (0.19%). In 2012, with 13,490 timepoints, major errors decreased to 19 (0.076%). LabTracker database also supports billing and has catalogued over 275,000 samples. This system provides real-time accounting and has revolutionized the quality control system of the CTRC as well as the research finance component with 98% charge capture efficiency within 30 days. Conclusions: The LabTracker/ARMADA systems are high volume phase I protocol management tools which have improved quality, decreased redundant work, and support a real time financial management system for complex phase I clinical trials.