Developing EMR-based algorithms to Identify hospital adverse events for health system performance evaluation and improvement: Study protocol.

BACKGROUND: Measurement of care quality and safety mainly relies on abstracted administrative data. However, it is well studied that administrative data-based adverse event (AE) detection methods are suboptimal due to lack of clinical information. Electronic medical records (EMR) have been widely implemented and contain detailed and comprehensive information regarding all aspects of patient care, offering a valuable complement to administrative data. Harnessing the rich clinical data in EMRs offers a unique opportunity to improve detection, identify possible risk factors of AE and enhance surveillance. However, the methodological tools for detection of AEs within EMR need to be developed and validated. The objectives of this study are to develop EMR-based AE algorithms from hospital EMR data and assess AE algorithm's validity in Canadian EMR data. METHODS: Patient EMR structured and text data from acute care hospitals in Calgary, Alberta, Canada will be linked with discharge abstract data (DAD) between 2010 and 2020 (n~1.5 million). AE algorithms development. First, a comprehensive list of AEs will be generated through a systematic literature review and expert recommendations. Second, these AEs will be mapped to EMR free texts using Natural Language Processing (NLP) technologies. Finally, an expert panel will assess the clinical relevance of the developed NLP algorithms. AE algorithms validation: We will test the newly developed AE algorithms on 10,000 randomly selected EMRs between 2010 to 2020 from Calgary, Alberta. Trained reviewers will review the selected 10,000 EMR charts to identify AEs that had occurred during hospitalization. Performance indicators (e.g., sensitivity, specificity, positive predictive value, negative predictive value, F1 score, etc.) of the developed AE algorithms will be assessed using chart review data as the reference standard. DISCUSSION: The results of this project can be widely implemented in EMR based healthcare system to accurately and timely detect in-hospital AEs.

Validated algorithms for identifying timing of second event of oropharyngeal squamous cell carcinoma using real-world data.

BACKGROUND: Understanding occurrence and timing of second events (recurrence and second primary cancer) is essential for cancer specific survival analysis. However, this information is not readily available in administrative data. METHODS: Alberta Cancer Registry, physician claims, and other administrative data were used. Timing of second event was estimated based on our developed algorithm. For validation, the difference, in days between the algorithm estimated and the chart-reviewed timing of second event. Further, the result of Cox-regression modeling cancer-free survival was compared to chart review data. RESULTS: Majority (74.3%) of the patients had a difference between the chart-reviewed and algorithm-estimated timing of second event falling within the 0-60 days window. Kaplan-Meier curves generated from the estimated data and chart review data were comparable with a 5-year second-event-free survival rate of 75.4% versus 72.5%. CONCLUSION: The algorithm provided an estimated timing of second event similar to that of the chart review.

Breast reconstruction after therapeutic or prophylactic mastectomy for breast cancer: A comparison of guideline recommendations.

BACKGROUND: The purpose of this article is to illuminate differences in published clinical practice guideline recommendations for breast reconstruction after prophylactic and therapeutic mastectomy. METHODS: Ten guidelines were identified through a systematic search of websites and databases of reputable oncology guideline developers, and key differences and gaps in recommendations were noted. Quality assessment of the guidelines was conducted by three reviewers using the AGREE II tool, focusing on breast reconstruction specific documents rather than the general breast cancer guidelines. RESULTS: The most comprehensive guidelines were published by Alberta Health Services, Cancer Care Ontario, the American Society of Plastic Surgeons, and the Association of Breast Surgery/British Association of Plastic Reconstructive and Aesthetic Surgeons. AGREE II scores in the domains of "Scope and Purpose" and "Clarity and Presentation" were ranked relatively high for all four guidelines while "Applicability" and "Editorial Independence" were ranked relatively low. The Alberta and Ontario guidelines were the overall highest ranked guidelines across all domains. CONCLUSION: Overall, these guidelines provide consistent recommendations on who should receive breast reconstruction education, who is a candidate for postmastectomy breast reconstruction, and the appropriate timing of reconstruction and extent of mastectomy. Future updates from all should focus on expanding to include alloplastic and autologous forms of reconstruction and should include a broad scope of relevant questions.

Smoothelin-like 1 deletion enhances myogenic reactivity of mesenteric arteries with alterations in PKC and myosin phosphatase signaling.

The role of the smoothelin-like 1 (SMTNL1) protein in mediating vascular smooth muscle contractile responses to intraluminal pressure was examined in resistance vessels. Mesenteric arterioles from wild type (WT) and SMTNL1 global knock-out (KO) mice were examined with pressure myography. SMTNL1 deletion was associated with enhanced myogenic tone in vessels isolated from male, but not female, mice. Intraluminal pressures greater than 40 mmHg generated statistically significant differences in myogenic reactivity between WT and KO vessels. No overt morphological differences were recorded for vessels dissected from KO animals, but SMTNL1 deletion was associated with loss of myosin phosphatase-targeting protein MYPT1 and increase in the myosin phosphatase inhibitor protein CPI-17. Additionally, we observed altered contractile responses of isolated arteries from SMTNL1 KO mice to phenylephrine, KCl-dependent membrane depolarization and phorbol 12,13-dibutyrate (PDBu). Using pharmacological approaches, myogenic responses of both WT and KO vessels were equally affected by Rho-associated kinase (ROCK) inhibition; however, augmented protein kinase C (PKC) signaling was found to contribute to the increased myogenic reactivity of SMTNL1 KO vessels across the 60-120 mmHg pressure range. Based on these findings, we conclude that deletion of SMTNL1 contributes to enhancement of pressure-induced contractility of mesenteric resistance vessels by influencing the activity of myosin phosphatase.