Supervising Students During a Global Pandemic: Clinical Educators' Perceptions of a Student-Led Telerehabilitation Service During Covid-19

Scope: In March 2020, COVID-19 restrictions prompted services delivered by student-led clinics in the university sector to transition to telehealth. This provided a unique opportunity to explore the challenges and opportunities faced by clinical educators when supervising students to deliver telehealth. Methodology: Semi-structured interviews were conducted with allied health clinical educators who supervised students on clinical placement who were required to provide services via telehealth. Clinical educators across the disciplines of audiology, occupational therapy, physiotherapy, and speech pathology were asked to reflect on their experiences and perceptions of the rapid transition to a telehealth model for student clinical placements. A content analysis approach was used to analyse qualitative data. Conclusions: From the perspective of clinical educators, student-led telehealth services can effectively meet client needs while achieving student learning outcomes. This study highlights many opportunities for student learning via telehealth in the clinical education environment and the role of the clinical educator in the learning experience.

Postacute Rehabilitation for Survivors of COVID-19 in an Inpatient Rehabilitation Setting: A Case Series

Research Objectives To investigate the rehabilitation outcomes of patients with COVID-19, admitted to an in-hospital inpatient rehabilitation unit. Design Case series method. All patients were followed up by phone call six months after discharge. Setting In-hospital Inpatient Rehabilitation Unit. Participants Subjects included three male patients in the age range of 55-65 with underlying medical conditions after COVID-19 infection with a mean acute hospital stay of 39 days. Interventions All three patients received services from an interdisciplinary team led by a physical medicine and rehabilitation specialist. Interventions were focused on managing ongoing medical issues, weaning off of supplemental oxygen, restorative and compensatory training to improve independence with functional mobility, activities of daily living, assessment and treatment of dysphagia, speech/voice, and cognitive-communication deficits. Main Outcome Measures Six-minute Walk Test, 10-meter Walk Test, GG codes, Berg Balance Scale, MRC sum score, Montreal Cognitive Asessment, Dynamometry and 9-hole Peg Test. Results The average length of stay at the rehabilitation unit was 21 days. The distance on six-minute walk has improved from being unable to walk for six minutes on admission to an average of 921 feet at a speed of 1.05m/s. Two out of three patients remained at medium risk of falls requiring use of assistive devices for mobility. Persisting dysphagia and dependence on supplemental oxygen was an issue for one patient. All three patients discharged home with support from family members and no episode of readmission to hospital within six months after discharge. Conclusions Ongoing fatigue, cognitive impairment and reduced endurance demonstrates the impact of COVID-19 on multiple organ systems in the body. Intensive inpatient rehabilitation is beneficial to accelerate recovery process, while managing ongoing medical issues. Author(s) Disclosures Russell ME: Speakers Bureau for Allergan and Merz. LIjo, Hamilton, Wren: Nothing to disclose.

SARS-CoV-2 infects blood monocytes to activate NLRP3 and AIM2 inflammasomes, pyroptosis and cytokine release (preprint)

SARS-CoV-2 causes acute respiratory distress that can progress to multiorgan failure and death in a minority of patients. Although severe COVID-19 disease is linked to exuberant inflammation, how SARS-CoV-2 triggers inflammation is not understood. Monocytes and macrophages are sentinel immune cells in the blood and tissue, respectively, that sense invasive infection to form inflammasomes that activate caspase-1 and gasdermin D (GSDMD) pores, leading to inflammatory death (pyroptosis) and processing and release of IL-1 family cytokines, potent inflammatory mediators. Here we show that expression quantitative trait loci (eQTLs) linked to higher GSDMD expression increase the risk of severe COVID-19 disease (odds ratio, 1.3, p<0.005). We find that about 10% of blood monocytes in COVID-19 patients are infected with SARS-CoV-2. Monocyte infection depends on viral antibody opsonization and uptake of opsonized virus by the Fc receptor CD16. After uptake, SARS-CoV-2 begins to replicate in monocytes, as evidenced by detection of double-stranded RNA and subgenomic RNA and expression of a fluorescent reporter gene. However, infection is aborted, and infectious virus is not detected in infected monocyte supernatants or patient plasma. Instead, infected cells undergo inflammatory cell death (pyroptosis) mediated by activation of the NLRP3 and AIM2 inflammasomes, caspase-1 and GSDMD. Moreover, tissue-resident macrophages, but not infected epithelial cells, from COVID-19 lung autopsy specimens showed evidence of inflammasome activation. These findings taken together suggest that antibody-mediated SARS-CoV-2 infection of monocytes/macrophages triggers inflammatory cell death that aborts production of infectious virus but causes systemic inflammation that contributes to severe COVID-19 disease pathogenesis.

SARS-CoV-2 infects blood monocytes to activate NLRP3 and AIM2 inflammasomes, pyroptosis and cytokine release (preprint)

SARS-CoV-2 causes acute respiratory distress that can progress to multiorgan failure and death in some patients. Although severe COVID-19 disease is linked to exuberant inflammation, how SARS-CoV-2 triggers inflammation is not understood. Monocytes are sentinel blood cells that sense invasive infection to form inflammasomes that activate caspase-1 and gasdermin D (GSDMD) pores, leading to inflammatory death (pyroptosis) and processing and release of IL-1 family cytokines, potent inflammatory mediators. Here we show that ~10% of blood monocytes in COVID-19 patients are dying and infected with SARS-CoV-2. Monocyte infection, which depends on antiviral antibodies, activates NLRP3 and AIM2 inflammasomes, caspase-1 and GSDMD cleavage and relocalization. Signs of pyroptosis (IL-1 family cytokines, LDH) in the plasma correlate with development of severe disease. Moreover, expression quantitative trait loci (eQTLs) linked to higher GSDMD expression increase the risk of severe COVID-19 disease (odds ratio, 1.3, p<0.005). These findings taken together suggest that antibody-mediated SARS-CoV-2 infection of monocytes triggers inflammation that contributes to severe COVID-19 disease pathogenesis.