Emergency physicians' perceptions of critical appraisal skills: a qualitative study.

BACKGROUND: Critical appraisal of medical research is a valuable skill set that emergency physicians must learn in order to become competent clinicians. Despite the need for effective critical appraisal skills training, these skills have remained difficult to teach and assess. This study aimed to explore emergency physicians' perceptions of the barriers and motivations for learning critical appraisal skills in order to develop more successful critical appraisal training methods for Emergency Medicine (EM) residents. METHODS: This qualitative study involved in-depth, semi-structured interviews with emergency physicians interested in education and administration at an urban academic hospital. Transcribed interviews were descriptively coded by three main reviewers. A coding template was developed after coding an initial set of interviews and used to code the remaining transcripts. A thematic analysis of the codes was conducted to create a summary report which was given to the interviewees as part of a member checking process to further solidify themes. RESULTS: Fourteen emergency physicians participated in the study. They described time limitations, perceived difficulty, and disinterest as major barriers to learning critical appraisal. Physicians noted patient care as well as professional identity goals of being a good educator or researcher as motivations for developing critical appraisal skills. CONCLUSION: There remain significant challenges to learning critical appraisal skills as well as an increasing need to build these skills during residency. Educational theories and a greater emphasis on professional identity formation during residency can be incorporated to create a more effective approach to teaching critical appraisal skills despite these barriers.

The time-sensitive challenge of diagnosing spinal epidural abscess in the emergency department.

Spinal epidural abscess (SEA) is a rare but devastating condition. Entry of infectious contents into the epidural space occurs via contiguous infected tissue, hematogenous spread, or iatrogenic inoculation. Traditionally, emergency providers are taught to assess for the "classic triad" of spinal pain, fever, and neurological deficits, but this constellation of findings is seen in only 10-15% of cases. Delays in diagnosis and treatment of this condition directly correspond to worse, and often debilitating, outcomes for these patients. This review will demonstrate the challenges of diagnosing SEA, describe key diagnostic pitfalls, and present a model and framework for its evaluation. The authors conducted a systematic review in PubMed and Google Scholar for articles describing the emergency medicine evaluation and management of spinal epidural abscess dating from 1996 to 2016. Of the initial 219 articles found, 18 articles were selected based on their relevancy to emergency medicine. Lower back pain is a common chief complaint, whereas SEA is a rare condition and may not be anticipated. The "classic triad" of SEA symptoms presents infrequently. Moreover, the early symptoms of back pain and fever are non-specific, and patients seek medical attention at varying stages of disease progression. Once the more conspicuous and wide-ranging neurological symptoms develop, they are often irreversible. In fact, final outcomes correlate with the severity and duration of symptoms before surgery. Furthermore, discovering these late neurological symptoms can be particularly difficult in bed-bound and chronically ill patients. MRI is the best diagnostic imaging tool for SEA. Early diagnosis is the major prognostic factor for favorable outcome of SEA, and yet, making this diagnosis in the emergency department (ED) has proved challenging. Shifting from a "classic triad" screening to a risk factor-based model of evaluation represents the current optimal strategy for diagnosing SEA. An algorithm incorporating the most recent data is provided.

Regulation of AMP-activated protein kinase by multisite phosphorylation in response to agents that elevate cellular cAMP.

The AMP-activated protein kinase (AMPK) and cAMP signaling systems are both key regulators of cellular metabolism. In this study, we show that AMPK activity is attenuated in response to cAMP-elevating agents through modulation of at least two of its alpha subunit phosphorylation sites, viz. alpha-Thr(172) and alpha1-Ser(485)/alpha2-Ser(491), in the clonal beta-cell line INS-1 as well as in mouse embryonic fibroblasts and COS cells. Forskolin, isobutylmethylxanthine, and the glucose-dependent insulinotropic peptide inhibited AMPK activity and reduced phosphorylation of the activation loop alpha-Thr(172) via inhibition of calcium/calmodulin-dependent protein kinase kinase-alpha and -beta, but not LKB1. These agents also enhanced phosphorylation of alpha-Ser(485/491) by the cAMP-dependent protein kinase. AMPK alpha-Ser(485/491) phosphorylation was necessary but not sufficient for inhibition of AMPK activity in response to forskolin/isobutylmethylxanthine. We show that AMPK alpha-Ser(485/491) can be a site for autophosphorylation, which may play a role in limiting AMPK activation in response to energy depletion or other regulators. Thus, our findings not only demonstrate cross-talk between the cAMP/cAMP-dependent protein kinase and AMPK signaling modules, but also describe a novel mechanism by which multisite phosphorylation of AMPK contributes to regulation of its enzyme activity.