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  • Article: Interrater Reliability of the Bedside Shivering Assessment Scale.
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    ABSTRACT: Background Since its early development, the Bedside Shivering Assessment Scale (BSAS) has had only initial psychometric testing. Before this instrument is incorporated into routine practice, its interrater reliability should be explored in a diverse group of practitioners. Methods This prospective nonrandomized study used a panel of 5 observers who completed 100 paired assessments. Observers independently scored patients for shivering by using the BSAS. Kappa statistics were determined by using SAS version 9.4 with BSAS scores treated as ordinal data. Results A weighted kappa value of 0.48 from 100 paired observations of 22 patients indicates moderate agreement of the BSAS scores. Most of the BSAS scores were 0 or 1; dichotomizing shivering as little or no shivering versus significant shivering resulted in a kappa of 0.66 (substantial agreement). No relationship was found between timing of assessment or the role of the practitioner and the likelihood of both observers assigning the same BSAS score. Conclusion The BSAS has adequate interrater reliability to be considered for use among a diverse group of practitioners.
    American Journal of Critical Care 01/2013; 22(1):70-74. · 1.66 Impact Factor
  • Article: ApolipoproteinE mimetic peptides improve outcome after focal ischemia.
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    ABSTRACT: Growing clinical evidence implicates isoform-specific effects of apoliporotein E (apoE) in reducing neuroinflammation and mediating adaptive responses following ischemic and traumatic brain injury. However, the intact apoE holoprotein does not cross the blood-brain barrier and thus has limited therapeutic potential. We have created a small peptide, COG1410 (acetyl-AS-Aib-LRKL-Aib-KRLL-amide), derived from the apoE receptor-binding region. COG1410 retains the anti-inflammatory and neuroprotective biological properties of the intact holoprotein and penetrates the blood-brain barrier. In the current study, we utilized a murine model of transient focal cerebral ischemia and reperfusion to demonstrate that intravenous (IV) administration of COG1410 reduces infarct volume and radiographic progression of infarct, and improves functional outcome as assessed by Rotarod when delivered up to 4 hours after ischemia onset.
    Experimental Neurology 12/2012; · 4.70 Impact Factor
  • Article: Xenon Neuroprotection in Experimental Stroke: Interactions with Hypothermia and Intracerebral Hemorrhage.
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    ABSTRACT: BACKGROUND:: Xenon has been proven to be neuroprotective in experimental brain injury. The authors hypothesized that xenon would improve outcome from focal cerebral ischemia with a delayed treatment onset and prolonged recovery interval. METHODS:: Rats were subjected to 70 min temporary focal ischemia. Ninety minutes later, rats were treated with 0, 15, 30, or 45% Xe for 20 h or 0 or 30% Xe for 8, 20, or 44 h. Outcome was measured after 7 days. In another experiment, after ischemia, rats were maintained at 37.5° or 36.0°C for 20 h with or without 30% Xe. Outcome was assessed 28 days later. Finally, mice were subjected to intracerebral hemorrhage with or without 30% Xe for 20 h. Brain water content, hematoma volume, rotarod function, and microglial activation were measured. RESULTS:: Cerebral infarct sizes (mean ± SD) for 0, 15, 30, and 45% Xe were 212 ± 27, 176 ± 55, 160 ± 32, and 198 ± 54 mm, respectively (P = 0.023). Neurologic scores (median ± interquartile range) followed a similar pattern (P = 0.002). Infarct size did not vary with treatment duration, but neurologic score improved (P = 0.002) at all xenon exposure durations (8, 20, and 44 h). Postischemic treatment with either 30% Xe or subtherapeutic hypothermia (36°C) had no effect on 28-day outcome. Combination of these interventions provided long-term benefit. Xenon improved intracerebral hemorrhage outcome measures. CONCLUSION:: Xenon improved focal ischemic outcome at 7, but not 28 days postischemia. Xenon combined with subtherapeutic hypothermia produced sustained recovery benefit. Xenon improved intracerebral hemorrhage outcome. Xenon may have potential for clinical stroke therapy under carefully defined conditions.
    Anesthesiology 11/2012; · 5.36 Impact Factor
  • Article: Guilty by association?*.
    Gary E Macy, Michael L James
    Critical care medicine 07/2012; 40(7):2230-1. · 6.37 Impact Factor
  • Article: Correlation of leukocytosis with early neurological deterioration following supratentorial intracerebral hemorrhage.
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    ABSTRACT: Intracerebral hemorrhage (ICH) is a devastating and common admitting diagnosis to intensive care units in the USA. Despite advances in critical care, patients with ICH often experience early neurological deterioration (END) in the first 72 hours after admission due to a variety of factors, including hematoma and cerebral edema evolution. The purpose of this study was to determine factors associated with END after ICH. Using the Duke University Hospital Neuroscience Critical Care Unit Database, we retrospectively identified patients with an admitting diagnosis of supratentorial ICH from January to December 2010, verified by CT imaging. END was defined as a decrease in the Glasgow Coma Scale score of ≥3 or death within the first 72 hours after hemorrhage. The chi-squared or t-test analysis was used to compare the groups, as appropriate. Multiple logistical regression modeling was performed to test for associations between likely predictors of END. Of the 89 subjects admitted with supratentorial ICH, we included 83 in the analysis based on complete datasets. Of these, 31 experienced END within 72 hours after onset of symptoms. ICH score, presence of midline shift on imaging, and white blood cell (WBC) count were used in a regression model for predicting END. WBC count demonstrated the greatest association with END. Patients with ICH are prone to END within the first few days after hemorrhage. Elevated WBC count appears predictive of deterioration. These data demonstrate that heightened inflammatory state after ICH may be related to early deterioration after injury.
    Journal of Clinical Neuroscience 06/2012; 19(8):1096-100. · 1.25 Impact Factor

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