1,641 research outputs found

    BIS and spectral entropy monitoring during sedation with midazolam/remifentanil and dexmedetomidine/remifentanil

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    Haenggi and colleagues report considerable intra- and inter-individual variability in derived electroencephalogram (EEG) parameters (Bispectral Index (BIS), response entropy and state entropy) recorded in volunteers sedated with midazolam or dexmedetomidine infusions titrated to modified Ramsay scores of 2, 3 and 4, and a remifentanil infusion at a fixed target concentration. Possible explanations for the low, variable and fluctuating EEG parameters are that volunteers were intermittently asleep, and that remifentanil gave rise to a low amplitude, slowed EEG pattern despite maintained consciousness. BIS and entropy values should be interpreted in combination with clinical findings in patients sedated with these agents

    A taxonomy of parallel sorting

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    TR 84-601In this paper, we propose a taxonomy of parallel sorting that includes a broad range of array and file sorting algorithms. We analyze the evolution of research on parallel sorting, from the earliest sorting networks to the shared memory algorithms and the VLSI sorters. In the context of sorting networks, we describe two fundamental parallel merging schemes - the odd-even and the bitonic merge. Sorting algorithms have been derived from these merging algorithms for parallel computers where processors communicate through interconnection networks such as the perfect shuffle, the mesh and a number of other sparse networks. After describing the network sorting algorithms, we show that, with a shared memory model of parallel computation, faster algorithms have been derived from parallel enumeration sorting schemes, where keys are first ranked and then rearranged according to their rank

    Midline Shift is Unrelated to Subjective Pupillary Reactivity Assessment on Admission in Moderate and Severe Traumatic Brain Injury.

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    BACKGROUND: This study aims to determine the relationship between pupillary reactivity, midline shift and basal cistern effacement on brain computed tomography (CT) in moderate-to-severe traumatic brain injury (TBI). All are important diagnostic and prognostic measures, but their relationship is unclear. METHODS: A total of 204 patients with moderate-to-severe TBI, documented pupillary reactivity, and archived neuroimaging were included. Extent of midline shift and basal cistern effacement were extracted from admission brain CT. Mean midline shift was calculated for each ordinal category of pupillary reactivity and basal cistern effacement. Sequential Chi-square analysis was used to calculate a threshold midline shift for pupillary abnormalities and basal cistern effacement. Univariable and multiple logistic regression analyses were performed. RESULTS: Pupils were bilaterally reactive in 163 patients, unilaterally reactive in 24, and bilaterally unreactive in 17, with mean midline shift (mm) of 1.96, 3.75, and 2.56, respectively (p = 0.14). Basal cisterns were normal in 118 patients, compressed in 45, and absent in 41, with mean midline shift (mm) of 0.64, 2.97, and 5.93, respectively (p < 0.001). Sequential Chi-square analysis identified a threshold for abnormal pupils at a midline shift of 7-7.25 mm (p = 0.032), compressed basal cisterns at 2 mm (p < 0.001), and completely effaced basal cisterns at 7.5 mm (p < 0.001). Logistic regression revealed no association between midline shift and pupillary reactivity. With effaced basal cisterns, the odds ratio for normal pupils was 0.22 (95% CI 0.08-0.56; p = 0.0016) and for at least one unreactive pupil was 0.061 (95% CI 0.012-0.24; p < 0.001). Basal cistern effacement strongly predicted midline shift (OR 1.27; 95% CI 1.17-1.40; p < 0.001). CONCLUSIONS: Basal cistern effacement alone is associated with pupillary reactivity and is closely associated with midline shift. It may represent a uniquely useful neuroimaging marker to guide intervention in traumatic brain injury

    Dysnatremia and mortality: do sweat the small stuff...

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    Traumatic Axonal Injury: Mechanisms and Translational Opportunities.

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    Traumatic axonal injury (TAI) is an important pathoanatomical subgroup of traumatic brain injury (TBI) and a major driver of mortality and functional impairment. Experimental models have provided insights into the effects of mechanical deformation on the neuronal cytoskeleton and the subsequent processes that drive axonal injury. There is also increasing recognition that axonal or white matter loss may progress for years post-injury and represent one mechanistic framework for progressive neurodegeneration after TBI. Previous trials of novel therapies have failed to make an impact on clinical outcome, in both TBI in general and TAI in particular. Recent advances in understanding the cellular and molecular mechanisms of injury have the potential to translate into novel therapeutic targets.CSH is supported by a Wellcome Trust PhD for Clinicians. MPC is funded by the John and Lucille van Geest Foundation. DKM is supported by a Senior Investigator Award from the National Institute for Health Research, UK (NIHR), by the Acute Brain Injury and Repair theme of the Cambridge NIHR Biomedical Research Centre, and a Framework Program 7 grant from the European Union (CENTER-TBI; Grant No: 602150)This is the final version of the article. It first appeared from Elsevier via https://doi.org/ 10.1016/j.tins.2016.03.00

    Case mix, outcomes and comparison of risk prediction models for admissions to adult, general and specialist critical care units for head injury: a secondary analysis of the ICNARC Case Mix Programme Database

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    INTRODUCTION: This report describes the case mix and outcome (mortality, intensive care unit (ICU) and hospital length of stay) for admissions to ICU for head injury and evaluates the predictive ability of five risk adjustment models. METHODS: A secondary analysis was conducted of data from the Intensive Care National Audit and Research Centre (ICNARC) Case Mix Programme, a high quality clinical database, of 374,594 admissions to 171 adult critical care units across England, Wales and Northern Ireland from 1995 to 2005. The discrimination and calibration of five risk prediction models, SAPS II, MPM II, APACHE II and III and the ICNARC model plus raw Glasgow Coma Score (GCS) were compared. RESULTS: There were 11,021 admissions following traumatic brain injury identified (3% of all database admissions). Mortality in ICU was 23.5% and in-hospital was 33.5%. Median ICU and hospital lengths of stay were 3.2 and 24 days, respectively, for survivors and 1.6 and 3 days, respectively, for non-survivors. The ICNARC model, SAPS II and MPM II discriminated best between survivors and non-survivors and were better calibrated than raw GCS, APACHE II and III in 5,393 patients eligible for all models. CONCLUSION: Traumatic brain injury requiring intensive care has a high mortality rate. Non-survivors have a short length of ICU and hospital stay. APACHE II and III have poorer calibration and discrimination than SAPS II, MPM II and the ICNARC model in traumatic brain injury; however, no model had perfect calibration
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