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This article delves into standardised patients' (SP) roles in healthcare education, using role-play and in-person methodology for realistic scenario simulation and learner technical and non-technical skill enhancement. Key to the success of the SP programme are phases like recruitment, onboarding, training and continuous quality improvement, cultivating a qualified pool of engaged SPs. Sustained SP engagement involves strategies such as tailored training sessions, quizzes, just-in-time videos and anaesthesia-specific self-assessment tools. The benefits of sessions led by SPs lie in their flexibility, providing anaesthesia learners with a controlled, experiential learning environment, where they can safely learn from mistakes. Addressing challenges in launching SP programmes for training, the article underscores clear objectives, strategic resource allocation, curriculum integration and specialised SP training. Implementing technology, quality assurance and ongoing evaluations are vital for dynamic SP programmes. The article advocates holistic SP programme implementation and optimisation, with continuous improvement for acquiring skills by anaesthesia professionals.
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Internado y Residencia , Niño , Humanos , Estados Unidos , Educación de Postgrado en Medicina , Acreditación , Competencia ClínicaRESUMEN
There is a paucity of literature regarding administrative approvals required for clinical studies during a pandemic. We aimed to evaluate variation in duration of administrative approvals within the Viral Infection and Respiratory illness Universal Study (VIRUS): A Global COVID-19 Registry. DESIGN SETTING AND SUBJECTS: Survey analysis of 188 investigators who participated in the VIRUS: COVID-19 registry, a prospective, observational global registry database of 287 sites. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: For each study site approved through December 8, 2020, we assessed the duration in days: 1) from institutional review board (IRB) submission to IRB approval, 2) from IRB approval to Research Electronic Data Capture (REDCap) access, 3) from REDCap access to first patient data entry in REDCap, and 4) total duration from IRB submission to first patient data entry in REDCap. Analysis of variance and Wilcoxon rank-sum test were used to compare time durations. Of 287 sites, 188 sites (United States = 155, non-United States = 33) provided complete administrative data. There was considerable variability in duration from IRB submission to first patient data entry with median (interquartile range) of 28 days (16-50 d), with differences not significantly different by country (United States: 30 [17-50] vs non-United States: 23 d [8-46 d]; p = 0.08) or previous "multisite trial experience" (experienced: 27 [15-51] vs not experienced: 29 d [13-47 d]; p = 0.67). The U.S. sites had a higher proportion of female principal investigators (n = 77; 50%), compared with non-U.S. sites (n = 7; 21%; p = 0.002). Non-U.S. sites had a significantly shorter time to first patient data entry after REDCap access: 7 (1-28) versus 3 days (1-6 d) (p = 0.02). CONCLUSIONS: In this Society of Critical Care Medicine global VIRUS: COVID-19 Registry, we identified considerable variability in time from IRB submission to first patient data entry with no significant differences by country or prior multicenter trial experience. However, there was a significant difference between US and non-U.S. sites in the time from REDCap access to first data entry.
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BACKGROUND: Sinus node (SN) dysfunction is observed in some long-QT syndrome (LQTS) patients, but has not been studied as a function of LQTS genotype. LQTS6 involves mutations in the hERG ß-subunit MiRP1, which also interacts with hyperpolarization-activated, cyclic nucleotide gated (HCN) channels-the molecular correlate of SN pacemaker current (If ). An LQTS registry search identified a 55-year male with M54T MiRP1 mutation, history of sinus bradycardia (39-56 bpm), and prolonged QTc. OBJECTIVE: We tested if LQTS6 incorporates sinus bradycardia due to abnormal If . METHODS: We transiently co-transfected neonatal rat ventricular myocytes (to study currents in a myocyte background) with human HCN4 (hHCN4, primary SN isoform) or human HCN2 (hHCN2) and one of the following: empty vector, wild-type hMiRP1 (WT), M54T hMiRP1 (M54T). Current amplitude, voltage dependence, and kinetics were measured by whole cell patch clamp. RESULTS: M54T co-expression decreased HCN4 current density by 80% compared to hHCN4 alone or with WT, and also slowed HCN4 activation at physiologically relevant voltages. Neither WT nor M54T altered HCN4 voltage dependence. A computer simulation predicts that these changes in HCN4 current would decrease rate and be additive with published effects of M54T mutation on hERG kinetics on rate. CONCLUSIONS: We conclude that M54T LQTS6 mutation can cause sinus bradycardia through effects on both hERG and HCN currents. Patients with other LQTS6 mutations should be examined for SN dysfunction, and the effect on HCN current determined.
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Relojes Biológicos/genética , Bradicardia/diagnóstico , Bradicardia/genética , Mutación/genética , Canales de Potasio con Entrada de Voltaje/genética , Animales , Animales Recién Nacidos , Células Cultivadas , Técnicas de Cocultivo , Regulación hacia Abajo/genética , Humanos , Masculino , Persona de Mediana Edad , Canales de Potasio con Entrada de Voltaje/antagonistas & inhibidores , Ratas , Ratas WistarRESUMEN
OBJECTIVE: We describe the coagulopathy and hemorrhagic complications associated with fulminant, secondary hemophagocytic lymphohistiocytosis in a cohort of patients with Epstein-Barr virus-associated T-cell lymphoproliferative disorder. PATIENTS AND METHODS: Institutional Review Board-approved retrospective review of all patients at our children's hospital over 3 years (2008-2010) with hemophagocytic lymphohistiocytosis secondary to acute Epstein-Barr virus-associated T-cell lymphoproliferative disorder. RESULTS: Four males (2, 3, 17, and 20 yr old) presented with fever, hepatosplenomegaly, and pancytopenia with elevated serum ferritin, and all met clinical and laboratory criteria for secondary hemophagocytic lymphohistiocytosis. d-dimer on admission was elevated in all patients and remained extremely elevated during hospitalization, while the median prothrombin and activated partial thromboplastin times as well as fibrinogen were all in the normal range. Within a few weeks to months following admission, all patients developed multiorgan system failure with episodes of severe, life-threatening hemorrhage; in all four patients, hemorrhage was not associated with a nadir in platelet count. There were no survivors beyond 4 months from diagnosis. CONCLUSIONS: A coagulopathy characterized by persistent, extreme elevations in plasma d-dimer and severe, life-threatening hemorrhage was noted in association with hemophagocytic lymphohistiocytosis secondary to Epstein-Barr virus-associated T-cell lymphoproliferative disorder. We speculate that this coagulopathy is a marker of severe hemophagocytic lymphohistiocytosis in this setting.