Background

Rounds are a foundational practice in patient care and education in the inpatient healthcare environment, but increased demands on inpatient teams have led to dissatisfaction with inefficient, ineffective rounds. In this study, we describe the design, implementation, and evaluation of a novel rounding framework ("NET Rounding") that provides behaviorally-based strategies to inpatient teams to achieve efficient rounds while preserving patient safety and education.

Methods

NET Rounding consists of nine recommendations divided into three categories: Novel rounding strategies, shared Expectations, and Time management. This framework was introduced as a bundled intervention at a single-site, quaternary-care, academic hospital from March-May 2021. Eighty-three residents and 64 attendings rotated on the inpatient teaching service during the intervention period. Participants were surveyed before, during, and after their rotation about rounding's contribution to educational value, patient safety, resident duty hour violations and rotation experience. Additionally, rounding duration was recorded daily by team attendings.

Results

Thirty-two residents (38.5%) and 45 attendings (70%) completed post-intervention surveys. Rounding duration was recorded on 529/626 rounding days (80.6%) and resulted in achieving efficient rounds on 412/529 days (77.9%). Residents reported improvement in perceived patient safety (54 to 84%, p = 0.0131) and educational value of rounds (38 to 69%, p = 0.0213) due to NET Rounding; no change was observed amongst attendings in these areas (79 to 84% and 70 to 80%, p = 0.7083 and 0.4237, respectively). Overall, 29/32 residents (91%) and 33/45 attendings (73%) reported a positive impact on rotation experience.

Conclusions

NET Rounding enabled inpatient teaching teams to complete rounds more efficiently while preserving patient safety and education.

Acquired drug resistance to anticancer targeted therapies remains an unsolved clinical problem. Although many drivers of acquired drug resistance have been identified^1-4, the underlying molecular mechanisms shaping tumour evolution during treatment are incompletely understood. Genomic profiling of patient tumours has implicated apolipoprotein B messenger RNA editing catalytic polypeptide-like (APOBEC) cytidine deaminases in tumour evolution; however, their role during therapy and the development of acquired drug resistance is undefined. Here we report that lung cancer targeted therapies commonly used in the clinic can induce cytidine deaminase APOBEC3A (A3A), leading to sustained mutagenesis in drug-tolerant cancer cells persisting during therapy. Therapy-induced A3A promotes the formation of double-strand DNA breaks, increasing genomic instability in drug-tolerant persisters. Deletion of A3A reduces APOBEC mutations and structural variations in persister cells and delays the development of drug resistance. APOBEC mutational signatures are enriched in tumours from patients with lung cancer who progressed after extended responses to targeted therapies. This study shows that induction of A3A in response to targeted therapies drives evolution of drug-tolerant persister cells, suggesting that suppression of A3A expression or activity may represent a potential therapeutic strategy in the prevention or delay of acquired resistance to lung cancer targeted therapy.