Due to the clinically and technically demanding nature of breast x-ray imaging, mammography still remains one of the few essentially film-based radiological imaging techniques in modern medical imaging. There are a range of possible benefits available if a practical and economical direct digital imaging technique can be introduced to routine clinical practice. There has been much debate regarding the minimum specification required for direct digital acquisition. One such direct digital system available is computed radiography (CR), which has a modest specification when compared with modern screen-film mammography (SFM) systems. This paper details two psychophysical studies in which the detection of simulated microcalcifications with CR has been directly compared to that with SFM. The first study found that under scatter-free conditions the minimum detectable size of microcalcification was approximately 130 microns for both SFM and CR. The second study found that SFM had a 4.6% higher probability of observers being able to correctly identify the shape of 350 microns diameter test details; there was no significant difference for-either larger or smaller test details. From the results of these studies it has been demonstrated that the modest specification of CR, in terms of limiting resolution, does not translate into a dramatic difference in the perception of details at the limit of detectability. When judging the imaging performance of a system it is more important to compare the signal-to-noise ratio transfer spectrum characteristics, rather than simply the modulation transfer function.

The intervention was effective at achieving nearly universal early assessment and documentation of pain. This did not translate to an improvement in analgesic provision. Other means of changing behaviour need to be studied, possibly using the computerised record again to obligate analgesia provision.

Our large series of propofol sedations performed by emergency physicians supports the safety of this practice. The sentinel adverse event rate of 1% that we identify prompts review: we will in future emphasize adherence to the reduced 0.5 mg kg(-1) propofol dose in the elderly, and reconsider our use of metaraminol. We believe that our application of the World SIVA adverse event tool sets a benchmark for further 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...