Audit of a computerized version of the Manchester triage system and a SIRS-based system for the detection of sepsis at triage in the emergency department.

BACKGROUND AND IMPORTANCE: Different triage systems can be used to screen for sepsis and are often incorporated into local electronic health records. Often the design and interface of these digitalizations are not audited, possibly leading to deleterious effects on screening test performance. OBJECTIVE: To audit a digital version of the MTS for detection of sepsis during triage in the ED. DESIGN: A single-center retrospective study SETTINGS AND PARTICIPANTS: Patients (n=29766) presenting to an ED of a tertiary-care center who received formal triage were included. OUTCOME MEASURES AND ANALYSIS: Calculated performance measures included sensitivity, specificity, likelihood ratios, and AUC for the detection of sepsis. Errors in the application of the specific sepsis discriminator of the MTS were recorded. MAIN RESULTS: A total of 189 (0.7%) subjects met the Sepsis-3 criteria, with 47 cases meeting the criteria for septic shock. The MTS had a low sensitivity of 47.6% (95% CI 40.3 to 55.0) for allocating sepsis patients to the correct triage category. However, specificity was high at 99.4% (95% CI 99.3 to 99.5).

Role of oxidative stress, angiogenesis and chemo-attractant cytokines in the pathogenesis of ischaemic protection induced by remote ischaemic conditioning: Study of a human model of ischaemia-reperfusion induced vascular injury.

AIMS: We explored the effect of remote ischaemic conditioning (RIC) on endothelial function and on circulating mediators. METHODS AND RESULTS: In 20 healthy male volunteers (mean age 31 ± 10 years), flow-mediated dilation (FMD) was measured before and after 20 min of arm ischaemia, followed by reperfusion. Remote ischaemic conditioning (RIC) was performed by applying 3 cycles of 5 min of ischaemia of the leg at the onset of index arm ischaemia. Each volunteer underwent the IR-induced vascular injury protocol with and without RIC in a crossover study design. In the control group, IR significantly reduced FMD (5.9 ± 2.9% before IR vs. 2.2 ± 3.7% after IR; p < 0.001). This effect was significantly attenuated by performing RIC (FMD of 5.5 ± 3.1% before IR vs. 4.0 ± 3.4% % after IR; p for interaction = 0.01). Serum levels of SOD and ADMA increased significantly whereas MCP-1 and VEGF levels decreased significantly. Only changes in SOD levels were significantly related to the degree of RIC induced protection (r² = 0.34; p = 0.018). CONCLUSION: RIC has protective effects against endothelial IR injury. Our biomarker study suggests that anti-oxidative stress mediators, such as SOD, seem to be more involved in the pathogenesis of RIC-induced protection in humans than angiogenesis factors or chemo-attractant cytokines.