The DAGMAR Score: D-dimer assay-guided moderation of adjusted risk. Improving specificity of the D-dimer for pulmonary embolism

We generated a novel scoring system to improve the test characteristics of D-dimer in patients with suspected PE (pulmonary emboli).Electronic Medical Record data were retrospectively reviewed on Emergency Department (ED) patients 18?years or older for whom a D-dimer and imaging were ordered between June 4, 2012 and March 30, 2016. Symptoms (dyspnea, unilateral leg swelling, hemoptysis), age, vital signs, medical history (cancer, recent surgery, medications, history of deep vein thrombosis or PE, COPD, smoking), laboratory values (quantitative D-dimer, platelets, and mean platelet volume (MPV)), and imaging results (CT, VQ) were collected.Points were designated to factors that were significant in two multiple regression analyses, for PE or positive D-dimer. Points predictive of PE were designated positive values and points predictive of positive D-dimer, irrespective of presence of PE, were designated negative values.The DAGMAR (D-dimer Assay-Guided Moderation of Adjusted Risk) score was developed using age and platelet adjustment and points for factors associated with PE and elevated D-dimer.Of 8486 visits reviewed, 3523 were unique visits with imaging, yielding 2253 (26.5%) positive D-dimers. 3501 CT scans and 156 VQ scans were completed, detecting 198 PE.In our cohort, a DAGMAR Score?<?2 equated to overall PE risk?<?1.2%. Specificity improved (38% to 59%) without compromising sensitivity (94% to 96%). Use of the DAGMAR Score would have reduced CT scans from 2253 to 1556 and lead to fewer false negative results.By considering factors that affect D-dimer and also PE, we improved specificity without compromising sensitivity.     

Predictors of Short Intensive Care Unit Stay for Patients with Diabetic Ketoacidosis Using a Novel Emergency Department–Based Resuscitation and Critical Care Unit

Background

The resuscitation and critical care unit is a novel emergency department–intensive care unit designed to provide early critical care to emergency department patients for ≤24 h.

Dexamethasone potentiates in vitro blood-brain barrier recovery after primary blast injury by glucocorticoid receptor-mediated upregulation of ZO-1 tight junction protein

Owing to the frequent incidence of blast-induced traumatic brain injury (bTBI) in recent military conflicts, there is an urgent need to develop effective therapies for bTBI-related pathologies. Blood-brain barrier (BBB) breakdown has been reported to occur after primary blast exposure, making restoration of BBB function and integrity a promising therapeutic target. We tested the hypothesis that treatment with dexamethasone (DEX) after primary blast injury potentiates recovery of an in vitro BBB model consisting of mouse brain endothelial cells (bEnd.3). DEX treatment resulted in complete recovery of transendothelial electrical resistance and hydraulic conductivity 1 day after injury, compared with 3 days for vehicle-treated injured cultures. Administration of RU486 (mifepristone) inhibited effects of DEX, confirming that barrier restoration was mediated by glucocorticoid receptor signaling. Potentiated recovery with DEX treatment was accompanied by stronger zonula occludens (ZO)-1 tight junction immunostaining and expression, suggesting that increased ZO-1 expression was a structural correlate to BBB recovery after blast. Interestingly, augmented ZO-1 protein expression was associated with specific upregulation of the α⁺ isoform but not the α⁻ isoform. This is the first study to provide a mechanistic basis for potentiated functional recovery of an in vitro BBB model because of glucocorticoid treatment after primary blast injury.