Search

Introduction Rapid response team (RRT) and code activation events occur relatively commonly in inpatient settings. RRT systems have been the subject of a significant amount of analysis, although this has been largely focused on the impact of RRT system implementation and RRT events on patient outcomes. There is reason to believe that the structured assessment of RRT and code events may be an effective way to identify opportunities for system improvement, although no standardised approach to event analysis is widely accepted. We developed and refined a protocolised system of RRT and code event review, focused on sustainable, timely and high value event analysis meant to inform ongoing improvement activities.Methods A group of clinicians with expertise in process and quality improvement created a protocolised analytic plan for rapid response event review, piloted and then iteratively optimised a systematic process which was applied to all subsequent cases to be reviewed.Results Hospitalist reviewers were recruited and trained in a methodical approach. Each reviewer performed a chart review to summarise RRT events, and collect specific variables for each case (coding). Coding was then reviewed for concordance, at monthly interdisciplinary group meetings and ‘Action Items’ were identified and considered for implementation. In any 12-month period starting in 2021, approximately 12–15 distinct cases per month were reviewed and coded, offering ample opportunities to identify trends and patterns.Conclusion We have developed an innovative process for ongoing review of RRT-Code events. The review process is easy to implement and has allowed for the timely identification of high value improvement opportunities.

The human cytomegalovirus (HCMV) infects fibroblasts via an interaction of its envelope glycoprotein gO with the cellular platelet-derived growth factor receptor alpha (PDGFRα), and soluble derivatives of this receptor can inhibit viral entry. We aimed to select mutants with resistance against PDGFRα-Fc and the PDGFRα-derived peptides GT40 and IK40 to gain insight into the underlying mechanisms and determine the genetic barrier to resistance. An error-prone variant of strain AD169 was propagated in the presence of inhibitors, cell cultures were monitored weekly for signs of increased viral growth, and selected viruses were tested regarding their sensitivity to the inhibitor. Resistant virus was analyzed by DNA sequencing, candidate mutations were transferred into AD169 clone pHB5 by seamless mutagenesis, and reconstituted virus was again tested for loss of sensitivity by dose-response analyses. An S48Y mutation in gO was identified that conferred a three-fold loss of sensitivity against PDGFRα-Fc, a combination of mutations in gO, gH, gB and gN reduced sensitivity to GT40 by factor 4, and no loss of sensitivity occurred with IK40. The resistance-conferring mutations support the notion that PDGFRα-Fc and GT40 perturb the interaction of gO with its receptor, but the relatively weak effect indicates a high genetic barrier to resistance.