Making electronic prescribing alerts more effective: scenario-based experimental study in junior doctors

Objective

Expert authorities recommend clinical decision support systems to reduce prescribing error rates, yet large numbers of insignificant on-screen alerts presented in modal dialog boxes persistently interrupt clinicians, limiting the effectiveness of these systems. This study compared the impact of modal and non-modal electronic (e-) prescribing alerts on prescribing error rates, to help inform the design of clinical decision support systems.

Design

A randomized study of 24 junior doctors each performing 30 simulated prescribing tasks in random order with a prototype e-prescribing system. Using a within-participant design, doctors were randomized to be shown one of three types of e-prescribing alert (modal, non-modal, no alert) during each prescribing task.

Measurements

The main outcome measure was prescribing error rate. Structured interviews were performed to elicit participants'' preferences for the prescribing alerts and their views on clinical decision support systems.

Results

Participants exposed to modal alerts were 11.6 times less likely to make a prescribing error than those not shown an alert (OR 11.56, 95% CI 6.00 to 22.26). Those shown a non-modal alert were 3.2 times less likely to make a prescribing error (OR 3.18, 95% CI 1.91 to 5.30) than those not shown an alert. The error rate with non-modal alerts was 3.6 times higher than with modal alerts (95% CI 1.88 to 7.04).

Conclusions

Both kinds of e-prescribing alerts significantly reduced prescribing error rates, but modal alerts were over three times more effective than non-modal alerts. This study provides new evidence about the relative effects of modal and non-modal alerts on prescribing outcomes.     

全自动加样处理系统数据传导错误原因分析及排除

目的查找导致全自动加样处理系统（EVO）数据传导错误的原因。方法逐项排除导致数据传导错误可能的原因。结果全自动加样处理系统的微机主板电池老化,使加样器的微机时间与酶免处理分析系统的时间存在差异,导致加样信息数据传导错误而致实验失败。结论应及时更换与EVO（或FAME）相连的微机主板电池,平日注重仪器的保养维护,加强开机时对微机时间的观察,确保仪器的正常运行,保证实验室的正常工作。     

Enhanced sphingosine-1-phosphate receptor 2 expression underlies female CNS autoimmunity susceptibility

Multiple sclerosis (MS) is an inflammatory disease of the CNS that is characterized by BBB dysfunction and has a much higher incidence in females. Compared with other strains of mice, EAE in the SJL mouse strain models multiple features of MS, including an enhanced sensitivity of female mice to disease; however, the molecular mechanisms that underlie the sex- and strain-dependent differences in disease susceptibility have not been described. We identified sphingosine-1-phosphate receptor 2 (S1PR2) as a sex- and strain-specific, disease-modifying molecule that regulates BBB permeability by destabilizing adherens junctions. S1PR2 expression was increased in disease-susceptible regions of the CNS of both female SJL EAE mice and female patients with MS compared with their male counterparts. Pharmacological blockade or lack of S1PR2 signaling decreased EAE disease severity as the result of enhanced endothelial barrier function. Enhanced S1PR2 signaling in an in vitro BBB model altered adherens junction formation via activation of Rho/ROCK, CDC42, and caveolin endocytosis-dependent pathways, resulting in loss of apicobasal polarity and relocation of abluminal CXCL12 to vessel lumina. Furthermore, S1PR2-dependent BBB disruption and CXCL12 relocation were observed in vivo. These results identify a link between S1PR2 signaling and BBB polarity and implicate S1PR2 in sex-specific patterns of disease during CNS autoimmunity.     

Murine Epsins Play an Integral Role in Podocyte Function

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