Latent safety threat identification during in situ simulation debriefing: a qualitative analysis.

Background: Latent safety threats (LSTs) in healthcare are hazards or conditions that risk patient safety but are not readily apparent without system stress. In situ simulation (ISS), followed by post-scenario debriefing is a common method to identify LSTs within the clinical environment. The function of post-ISS debriefing for LST identification is not well understood. Objectives: This study aims to qualitatively characterise the types of LSTs identified during ISS debriefing. Methods: We conducted 12 ISS trauma scenarios followed by debriefing at a Canadian, Level 1 trauma centre. We designed the scenarios and debriefing for 15 and 20 min, respectively. Debriefings focused on LST identification, and each session was audio recorded and transcribed. We used an inductive approach with qualitative content analysis to code text data into an initial coding tree. We generated refined topics from the coded text data. Results: We identified five major topics: (1) communication and teamwork challenges, (2) system-level issues, (3) resource constraints, (4) positive team performance and (5) potential improvements to the current systems and processes. Conclusions: During simulation debriefing sessions for LST identification, participants discussed threats related to communication and interpersonal issues. Safety issues relating to equipment, processes and the physical space received less emphasis. These findings may guide health system leaders and simulation experts better understanding of the strengths and limitations of simulation debriefing for LST identification. Further studies are required to compare ISS-based LST identification techniques.

Characterizing the impact of snowfall on patient attendance at an urban emergency department in Toronto, Canada.

OBJECTIVES: We sought to determine whether addition of a snowfall variable improves emergency department (ED) patient volume forecasting. Our secondary objective was to characterize the magnitude of effect of snowfall on ED volume. METHODS: We used daily historical patient volume data and local snowfall records from April 1st, 2011 to March 31st, 2018 (2542 days) to fit a series of four generalized linear models: a baseline model which included calendar variables and three different snowfall models with an indicator variable for either any snowfall (>0 cm), moderate snowfall (≥1 cm), or large snowfall (≥5 cm). To evaluate model fit, we examined the Akaike Information Criterion (AIC) and Bayesian Information Criterion (BIC). Incident rate ratios were calculated to determine the effect of snowfall in each model. RESULTS: All three snowfall models demonstrated improved model fit compared to the model without snowfall. The best fitting model included a binary variable for snowfall (<1 cm vs. ≥1 cm). This model showed a statistically significant decrease in daily ED volume of 2.65% (95% CI: 1.23%-4.00%) on snowfall days. DISCUSSION: The addition of a snowfall variable results in improved model performance in short-term ED volume forecasting. Snowfall is associated with a modest, but statistically significant reduction in ED volume.

mTOR-Notch3 signaling mediates pulmonary hypertension in hypoxia-exposed neonatal rats independent of changes in autophagy.

BACKGROUND/AIM: Mammalian target of rapamycin (mTOR) is a pivotal regulator of cell proliferation, survival, and autophagy. Autophagy is increased in adult experimental chronic pulmonary hypertension (PHT), but its contributory role to pulmonary vascular disease remains uncertain and has yet to be explored in the neonatal animal. Notch is a major pro-proliferative pathway activated by mTOR. A direct relationship between autophagy and Notch signaling has not been previously explored. Our aim was to examine changes in mTOR-, Notch-, and autophagy-related pathways and the therapeutic effects of autophagy modulators in experimental chronic neonatal PHT secondary to chronic hypoxia. METHODS: Rat pups were exposed to normoxia or hypoxia (13% O2 ) from postnatal days 1-21, while receiving treatment with temsirolimus (mTOR inhibitor), DAPT (Notch inhibitor), or chloroquine (inhibitor of autophagic flux). RESULTS: Exposure to hypoxia up-regulated autophagy and Notch3 signaling markers in lung, pulmonary artery (PA), and PA-derived smooth muscle cells (SMCs). Temsirolimus prevented chronic PHT and attenuated PA and SMC signaling secondary to hypoxia. These effects were replicated by DAPT. mTOR or Notch inhibition also down-regulated smooth muscle content of platelet-derived growth factor ß-receptor, a known contributor to vascular remodeling. In contrast, chloroquine had no modifying effects on markers of chronic PHT. Knockdown of Beclin-1 in SMCs had no effect on hypoxia-stimulated Notch3 signaling. CONCLUSIONS: mTOR-Notch3 signaling plays a critical role in experimental chronic neonatal PHT. Inhibition of autophagy did not suppress Notch signaling and had no effect on markers of chronic PHT.