The OneTogether collaborative approach to reduce the risk of surgical site infection: identifying the challenges to assuring best practice

Background: Surgical site infections (SSI) account for 16% of healthcare associated infections, and are associated with considerable morbidity, mortality and increased costs of care. Ensuring evidence-based practice to prevent SSI is incorporated across the patient’s surgical journey is complex. OneTogether is a quality improvement collaborative of infection prevention and operating department specialists, formed to support the spread and adoption of best practice to prevent SSI. This paper describes the findings of an expert workshop on infection prevention in operating departments. Methods: A total of 84 delegates from 75 hospitals attended the workshop, comprising 46 (55%) theatre nurses/operating department practitioners; 16 (19%) infection control practitioners and 22 (26%) other healthcare practitioners. Discussion focused on evidence, policy implementation and barriers to best practice. Responses were synthesised into a narrative review. Results: Delegates reported significant problems in translating evidence-based guidance into everyday practice, lack of local polices and poor compliance. Major barriers were lack of leadership, poorly defined responsibilities, and lack of knowledge/training. Conclusions: This workshop has provided important insights into major challenges in assuring compliance with best practice in relation to the prevention of SSI. The OneTogether partnership aims to support healthcare practitioners to improve the outcomes of patients undergoing surgery by reducing the risk of SSI

Interleukin-6 signaling drives fibrosis in unresolved inflammation

Fibrosis in response to tissue damage or persistent inflammation is a pathological hallmark of many chronic degenerative diseases. By using a model of acute peritoneal inflammation, we have examined how repeated inflammatory activation promotes fibrotic tissue injury. In this context, fibrosis was strictly dependent on interleukin-6 (IL-6). Repeat inflammation induced IL-6-mediated T helper 1 (Th1) cell effector commitment and the emergence of STAT1 (signal transducer and activator of transcription-1) activity within the peritoneal membrane. Fibrosis was not observed in mice lacking interferon-γ (IFN-γ), STAT1, or RAG-1. Here, IFN-γ and STAT1 signaling disrupted the turnover of extracellular matrix by metalloproteases. Whereas IL-6-deficient mice resisted fibrosis, transfer of polarized Th1 cells or inhibition of MMP activity reversed this outcome. Thus, IL-6 causes compromised tissue repair by shifting acute inflammation into a more chronic profibrotic state through induction of Th1 cell responses as a consequence of recurrent inflammation