RESUMO
Background: Research suggests that quantitative metric reports can improve the clinical performance of emergency physicians; however, few studies have examined their effects on physicians in training. The primary study objective was to assess the effects of providing emergency medicine (EM) residents with individualized throughput metrics with regard to emergency department (ED) disposition times. Methods: We performed a single-center, retrospective, observational study from January 2021 to December 2022 examining ED disposition times before and after providing upper-level EM residents individualized throughput metrics. Residents received monthly reports of three specific metrics averaged over the preceding 6 months: (1) median time from room to discharge order (Rm2Dc), (2) median time from return of all results to discharge order (Rlts2Dc), and (3) median time from room and to consult order for hospitalization (Rm2Hosp). Overall mean values of the three metrics before and during metric sharing were compared via independent t-test and stratified by level of training and time of year. Adjusted analysis was performed to control for temporal differences between study periods. Testing was conducted at α = 0.05 level of significance. Results: A total of 35 unique residents were included in the analysis. Overall, mean disposition times were not significantly different before and during reporting of metrics: Rm2Dc (154.8 min vs. 148.9 min, p = 0.109), Rslt2Dc (46.5 min vs. 45.1 min, p = 0.522), and Rm2Hosp (141.7 min vs. 135.7 min, p = 0.257). Subgroup analysis yielded similar results, aside from a significant decrease in mean Rm2Hosp in the postgraduate year-3 (PGY-3) group (145.8 min vs. 124.1 min, p = 0.004). Analysis with adjusted means yielded results similar to those observed with unadjusted data. Conclusions: Overall, individualized throughput metrics were not correlated with decreased average times to ED disposition for upper-level EM residents; however, in the subset of hospitalized patients seen by PGY-3 residents, we observed a mean decrease of 21.7 min to consultation.
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BACKGROUND: The HEART score for risk stratifying chest pain patients in the emergency department (ED) has been widely adopted in clinical practice, but is often employed with nonconformant serial troponin measurements. OBJECTIVE: The primary objective of this study was to examine the utility of obtaining a second conventional 3-h troponin I (TnI) level in ED patients presenting with potential acute coronary syndrome (ACS), stratified by HEART score and duration of symptoms. METHODS: This was a retrospective cohort study of consecutive adult ED patients with a complete HEART score. We assessed the utility of repeat TnI measurement by examining the positivity rate of ΔTnI = [Second TnI] - [Initial TnI] stratified by HEART score and time elapsed since onset or resolution of symptoms. Major adverse cardiac events (MACE) within 6 weeks of index visit were assessed. RESULTS: A total of 944 patients were included with 433 (45.9%) assigned a low risk HEART score 0-3. Of the 268 (61.9%) low risk HEART score patients receiving a second TnI, only 3 (1.1%, [0.2-3.2%]) resulted in a positive ΔTnI, one of which occurred in the setting of an elevated initial TnI. Overall, patients presenting within 3 h of symptoms were more likely to experience positive ΔTnI, index MACE and MACE at 6 weeks compared to patients presenting ≥3 h since symptoms onset/resolution and patients with unknown timing of symptoms (15.9% vs 11.0% vs 10.3%, p < 0.001; 10.0% vs 5.3% vs 4.6%, p = 0.021; 12.7% vs 6.6% vs 6.4%, p = 0.047). CONCLUSION: Our data suggest serial measurement of conventional troponin provides limited added benefit in low risk HEART score patients, regardless of duration and timing of symptoms. Conversely, serial troponin measurement may confer utility in moderate/high risk HEART score patients, particularly those presenting within 3 h of symptoms.
Assuntos
Síndrome Coronariana Aguda , Infarto do Miocárdio , Adulto , Humanos , Infarto do Miocárdio/diagnóstico , Estudos Retrospectivos , Medição de Risco/métodos , Síndrome Coronariana Aguda/diagnóstico , Troponina I , Dor no Peito/diagnóstico , Dor no Peito/etiologia , Serviço Hospitalar de Emergência , BiomarcadoresRESUMO
Human monocytic ehrlichiosis (HME) is a potentially life-threatening tick-borne rickettsial disease (TBRD) caused by the obligate intracellular Gram-negative bacteria, Ehrlichia. Fatal HME presents with acute ailments of sepsis and toxic shock-like symptoms that can evolve to multi-organ failure and death. Early clinical and laboratory diagnosis of HME are problematic due to non-specific flu-like symptoms and limitations in the current diagnostic testing. Several studies in murine models showed that cell-mediated immunity acts as a "double-edged sword" in fatal ehrlichiosis. Protective components are mainly formed by CD4 Th1 and NKT cells, in contrast to deleterious effects originated from neutrophils and TNF-α-producing CD8 T cells. Recent research has highlighted the central role of the inflammasome and autophagy as part of innate immune responses also leading to protective or pathogenic scenarios. Recognition of pathogen-associated molecular patterns (PAMPS) or damage-associated molecular patterns (DAMPS) triggers the assembly of the inflammasome complex that leads to multiple outcomes. Recognition of PAMPs or DAMPs by such complexes can result in activation of caspase-1 and -11, secretion of the pro-inflammatory cytokines IL-1ß and IL-18 culminating into dysregulated inflammation, and inflammatory cell death known as pyroptosis. The precise functions of inflammasomes and autophagy remain unexplored in infections with obligate intracellular rickettsial pathogens, such as Ehrlichia. In this review, we discuss the intracellular innate immune surveillance in ehrlichiosis involving the regulation of inflammasome and autophagy, and how this response influences the innate and adaptive immune responses against Ehrlichia. Understanding such mechanisms would pave the way in research for novel diagnostic, preventative and therapeutic approaches against Ehrlichia and other rickettsial diseases.