Perceived Impact of Digital Health Maturity on Patient Experience, Population Health, Health Care Costs, and Provider Experience: Mixed Methods Case Study.

BACKGROUND: Health care organizations understand the importance of new technology implementations; however, the best strategy for implementing successful digital transformations is often unclear. Digital health maturity assessments allow providers to understand the progress made toward technology-enhanced health service delivery. Existing models have been criticized for their lack of depth and breadth because of their technology focus and neglect of meaningful outcomes. OBJECTIVE: We aimed to examine the perceived impacts of digital health reported by health care staff employed in health care organizations across a spectrum of digital health maturity. METHODS: A mixed methods case study was conducted. The digital health maturity of public health care systems (n=16) in Queensland, Australia, was examined using the quantitative Digital Health Indicator (DHI) self-assessment survey. The lower and upper quartiles of DHI scores were calculated and used to stratify sites into 3 groups. Using qualitative methods, health care staff (n=154) participated in interviews and focus groups. Transcripts were analyzed assisted by automated text-mining software. Impacts were grouped according to the digital maturity of the health care worker's facility and mapped to the quadruple aims of health care: improved patient experience, improved population health, reduced health care cost, and enhanced provider experience. RESULTS: DHI scores ranged between 78 and 193 for the 16 health care systems. Health care systems in the high-maturity category (n=4, 25%) had a DHI score of ≥166.75 (the upper quartile); low-maturity sites (n=4, 25%) had a DHI score of ≤116.75 (the lower quartile); and intermediate-maturity sites (n=8, 50%) had a DHI score ranging from 116.75 to 166.75 (IQR). Overall, 18 perceived impacts were identified. Generally, a greater number of positive impacts were reported in health care systems of higher digital health maturity. For patient experiences, higher maturity was associated with maintaining a patient health record and tracking patient experience data, while telehealth enabled access and flexibility across all digital health maturity categories. For population health, patient journey tracking and clinical risk mitigation were reported as positive impacts at higher-maturity sites, and telehealth enabled health care access and efficiencies across all maturity categories. Limited interoperability and organizational factors (eg, strategy, policy, and vision) were universally negative impacts affecting health service delivery. For health care costs, the resource burden of ongoing investments in digital health and a sustainable skilled workforce was reported. For provider experiences, the negative impacts of poor usability and change fatigue were universal, while network and infrastructure issues were negative impacts at low-maturity sites. CONCLUSIONS: This is one of the first studies to show differences in the perceived impacts of digital maturity of health care systems at scale. Higher digital health maturity was associated with more positive reported impacts, most notably in achieving outcomes for the population health aim.

GSK137, a potent small-molecule BCL6 inhibitor with in vivo activity, suppresses antibody responses in mice.

B-cell lymphoma 6 (BCL6) is a zinc finger transcriptional repressor possessing a BTB-POZ (BR-C, ttk, and bab for BTB; pox virus and zinc finger for POZ) domain, which is required for homodimerization and association with corepressors. BCL6 has multiple roles in normal immunity, autoimmunity, and some types of lymphoma. Mice bearing disrupted BCL6 loci demonstrate suppressed high-affinity antibody responses to T-dependent antigens. The corepressor binding groove in the BTB-POZ domain is a potential target for small compound-mediated therapy. Several inhibitors targeting this binding groove have been described, but these compounds have limited or absent in vivo activity. Biophysical studies of a novel compound, GSK137, showed an in vitro pIC50 of 8 and a cellular pIC50 of 7.3 for blocking binding of a peptide derived from the corepressor silencing mediator for retinoid or thyroid hormone receptors to the BCL6 BTB-POZ domain. The compound has good solubility (128 µg/ml) and permeability (86 nM/s). GSK137 caused little change in cell viability or proliferation in four BCL6-expressing B-cell lymphoma lines, although there was modest dose-dependent accumulation of G1 phase cells. Pharmacokinetic studies in mice showed a profile compatible with achieving good levels of target engagement. GSK137, administered orally, suppressed immunoglobulin G responses and reduced numbers of germinal centers and germinal center B cells following immunization of mice with the hapten trinitrophenol. Overall, we report a novel small-molecule BCL6 inhibitor with in vivo activity that inhibits the T-dependent antigen immune response.

The development of highly potent and selective small molecule correctors of Z α1-antitrypsin misfolding.

α1-antitrypsin deficiency is characterised by the misfolding and intracellular polymerisation of mutant α1-antitrypsin protein within the endoplasmic reticulum (ER) of hepatocytes. Small molecules that bind and stabilise Z α1-antitrypsin were identified via a DNA-encoded library screen. A subsequent structure based optimisation led to a series of highly potent, selective and cellular active α1-antitrypsin correctors.

Design and development of a series of borocycles as selective, covalent kallikrein 5 inhibitors.

The connection between Netherton syndrome and overactivation of epidermal/dermal proteases, particularly Kallikrein 5 (KLK5) has been well established and it is expected that a KLK5 inhibitor would improve the dermal barrier and also reduce the pain and itch that afflict Netherton syndrome patients. One of the challenges of covalent protease inhibitors has been achieving selectivity over closely related targets. In this paper we describe the use of structural insight to design and develop a selective and highly potent reversibly covalent KLK5 inhibitor from an initial weakly binding fragment.

Impaired bone morphogenetic protein receptor II signaling in a transforming growth factor-ß-dependent mouse model of pulmonary hypertension and in systemic sclerosis.

RATIONALE: Up to 10% of patients with systemic sclerosis (SSc) develop pulmonary arterial hypertension (PAH). This risk persists throughout the disease and is time dependent, suggesting that SSc is a susceptibility factor. Outcome for SSc-PAH is poor compared with heritable or idiopathic forms, despite clinical and pathological similarities. Although susceptibility in heritable PAH and idiopathic PAH is strongly associated with gene mutations leading to reduced expression of bone morphogenetic protein receptor (BMPR) II, these mutations have not been observed in SSc-PAH. OBJECTIVES: To explore BMPRII expression and function in a mouse model of SSc (TßRIIΔk-fib) that is susceptible to developing pulmonary hypertension and in SSc lung. METHODS: BMPRII and downstream signaling pathways were profiled in lung tissue and fibroblasts from the TßRIIΔk-fib model, which develops pulmonary vasculopathy with pulmonary hypertension that is exacerbated by SU5416. Complementary studies examined SSc or control lung tissue and fibroblasts. MEASUREMENTS AND MAIN RESULTS: Our study shows reduced BMPRII, impaired signaling, and altered receptor turnover activity in a transforming growth factor (TGF)-ß-dependent mouse model of SSc-PAH. Similarly, a significant reduction in BMPRII expression is observed in SSc lung tissue and fibroblasts. Increased proteasomal degradation of BMPRII appears to underlie this and may result from heightened TGF-ß activity. CONCLUSIONS: We found reduced BMPRII protein in patients with SSc-PAH and a relevant mouse model associated with increased proteasomal degradation of BMPRII. Collectively, these results suggest that impaired BMP signaling, resulting from TGF-ß-dependent increased receptor degradation, may promote PAH susceptibility in SSc and provide a unifying mechanism across different forms of PAH.

An inhibitor of NADPH oxidase-4 attenuates established pulmonary fibrosis in a rodent disease model.

Idiopathic pulmonary fibrosis is a chronic progressive disease of increasing prevalence for which there is no effective therapy. Increased oxidative stress associated with an oxidant-antioxidant imbalance is thought to contribute to disease progression. NADPH oxidases (Nox) are a primary source of reactive oxygen species within the lung and cardiovascular system. We demonstrate that the Nox4 isoform is up-regulated in the lungs of patients with IPF and in a rodent model of bleomycin-induced pulmonary fibrosis and vascular remodeling. Nox4 is constitutively active, and therefore increased expression levels are likely to contribute to disease pathology. Using a small molecule Nox4/Nox1 inhibitor, we demonstrate that targeting Nox4 results in attenuation of an established fibrotic response, with reductions in gene transcripts for the extracellular matrix components collagen 1α1, collagen 3α1, and fibronectin and in principle pathway components associated with pulmonary fibrosis and hypoxia-mediated vascular remodeling: transforming growth factor (TGF)-ß1, plasminogen activator inhibitor-1, hypoxia-inducible factor, and Nox4. TGF-ß1 is a principle fibrotic mediator responsible for inducing up-regulation of profibrotic pathways associated with disease pathology. Using normal human lung-derived primary fibroblasts, we demonstrate that inhibition of Nox4 activity using a small molecule antagonist attenuates TGF-ß1-mediated up-regulation in expression of profibrotic genes and inhibits the differentiation of fibroblast to myofibroblasts, that is associated with up-regulation in smooth muscle actin and acquisition of a contractile phenotype. These studies support the view that targeting Nox4 may provide a therapeutic approach for attenuating pulmonary fibrosis.

Imatinib attenuates hypoxia-induced pulmonary arterial hypertension pathology via reduction in 5-hydroxytryptamine through inhibition of tryptophan hydroxylase 1 expression.

RATIONALE: Whether idiopathic, familial, or secondary to another disease, pulmonary arterial hypertension (PAH) is characterized by increased vascular tone, neointimal hyperplasia, medial hypertrophy, and adventitial fibrosis. Imatinib, a potent receptor tyrosine kinase inhibitor, reverses pulmonary remodeling in animal models of PAH and improves hemodynamics and exercise capacity in selected patients with PAH. OBJECTIVES: Here we use both imatinib and knockout animals to determine the relationship between platelet-derived growth factor receptor (PDGFR) and serotonin signaling and investigate the PAH pathologies each mediates. METHODS: We investigated the effects of imatinib (100 mg/kg) on hemodynamics, vascular remodeling, and downstream molecular signatures in the chronic hypoxia/SU5416 murine model of PAH. MEASUREMENTS AND MAIN RESULTS: Treatment with imatinib reduced all measures of PAH pathology observed in hypoxia/SU5416 mice. In addition, 5-hydroxytryptamine (5-HT) and tryptophan hydroxylase 1 (Tph1) expression were reduced compared with the normoxia/SU5416 control group. Imatinib attenuated hypoxia-induced increases in Tph1 expression in pulmonary endothelial cells in vitro via inhibition of the PDGFR-ß pathway. To better understand the consequences of this novel mode of action for imatinib, we examined the development of PAH after hypoxic/SU5416 exposure in Tph1-deficient mice (Tph1(-/-)). The extensive changes in pulmonary vascular remodeling and hemodynamics in response to hypoxia/SU5416 were attenuated in Tph1(-/-) mice and further decreased after imatinib treatment. However, imatinib did not significantly further impact collagen deposition and collagen 3a1 expression in hypoxic Tph1(-/-) mice. Post hoc subgroup analysis suggests that patients with PAH with greater hemodynamic impairment showed significantly reduced 5-HT plasma levels after imatinib treatment compared with placebo. CONCLUSIONS: We report a novel mode of action for imatinib, demonstrating TPH1 down-regulation via inhibition of PDGFR-ß signaling. Our data reveal interplay between PDGF and 5-HT pathways within PAH, demonstrating TPH1-dependent imatinib efficacy in collagen-mediated mechanisms of fibrosis.

Impact of digital health on the quadruple aims of healthcare: A correlational and longitudinal study (Digimat Study).

BACKGROUND: Digital healthcare aims to deliver on the quadruple aim: enhance patient experiences, improve population health, reduce costs and improve provider experiences. Despite large investments, it is unclear how advancing digital health enables these healthcare aims. OBJECTIVE: Our objectives were to: 1) measure the correlation between digital capability and health system outcomes mapped to the quadruple aim, and 2) measure the longitudinal impact of electronic medical record implementations upon health system outcomes. MATERIALS AND METHODS: We undertook two studies: 1) Digital health correlational study investigating the association among healthcare system capability and healthcare aims, and 2) Digital hospital longitudinal study investigating outcomes pre and post electronic medical record implementation. RESULTS: Digital health capability was associated with lower staff turnover. Digitising healthcare services was associated with decreased medication errors, decreased nosocomial infections, increased hospital activity, and a transient increase in staff leave. DISCUSSION: These results suggest positive impacts on the population health and healthcare costs aim, minimal impacts on the provider experience aim and no observed impacts to the patient experience aim. CONCLUSION: These findings should provide confidence to healthcare decision-makers investing in digital health.

Attenuation of leukocyte recruitment via CXCR1/2 inhibition stops the progression of PAH in mice with genetic ablation of endothelial BMPR-II.

Previous studies from our group have demonstrated that bone morphogenetic protein receptor-II (BMPR-II), expressed on pulmonary artery endothelial cells, imparts profound anti-inflammatory effects by regulating the release of proinflammatory cytokines and promoting barrier function by suppressing the transmigration of leukocytes into the pulmonary vessel wall. Here we demonstrate that, in mice with endothelial-specific loss of BMPR-II expression (L1Cre(+);Bmpr2(f/f)), reduction in barrier function and the resultant pulmonary hypertension observed in vivo are the result of increased leukocyte recruitment through increased CXCR1/2 signaling. Loss of endothelial expressed BMPR-II leads to elevated plasma levels of a wide range of soluble mediators important in regulating leukocyte migration and extravasation, including the CXCR1/2 ligand, KC. Treatment of L1Cre(+);Bmpr2(f/f) mice with the CXCR1/2 antagonist SCH527123 inhibits leukocyte transmigration into lung and subsequently reverses the pulmonary hypertension. Our data have uncovered a previously unrecognized regulatory function of BMPR-II, which acts to regulate the expression of CXCR2 on endothelial cells, suggesting that increased CXCR2 signaling may also be a feature of the human pathology and that CXCR1/2 pathway antagonists may represent a novel therapeutic approach for treating pulmonary hypertension because of defects in BMPR-II expression.

SCL-mediated regulation of the cell-cycle regulator p21 is critical for murine megakaryopoiesis.

Megakaryopoiesis is a complex process that involves major cellular and nuclear changes and relies on controlled coordination of cellular proliferation and differentiation. These mechanisms are orchestrated in part by transcriptional regulators. The key hematopoietic transcription factor stem cell leukemia (SCL)/TAL1 is required in early hematopoietic progenitors for specification of the megakaryocytic lineage. These early functions have, so far, prevented full investigation of its role in megakaryocyte development in loss-of-function studies. Here, we report that SCL critically controls terminal megakaryocyte maturation. In vivo deletion of Scl specifically in the megakaryocytic lineage affects all key attributes of megakaryocyte progenitors (MkPs), namely, proliferation, ploidization, cytoplasmic maturation, and platelet release. Genome-wide expression analysis reveals increased expression of the cell-cycle regulator p21 in Scl-deleted MkPs. Importantly, p21 knockdown-mediated rescue of Scl-mutant MkPs shows full restoration of cell-cycle progression and partial rescue of the nuclear and cytoplasmic maturation defects. Therefore, SCL-mediated transcriptional control of p21 is essential for terminal maturation of MkPs. Our study provides a mechanistic link between a major hematopoietic transcriptional regulator, cell-cycle progression, and megakaryocytic differentiation.

Comparison of first-pass intubation success rates between two different videolaryngoscopes in an Australian prehospital and retrieval medicine service.

OBJECTIVE: To determine the effectiveness of the GlideScope Go videolaryngoscope (VL) in tracheal intubation in an Australian physician-staffed critical care prehospital and retrieval medicine service. METHODS: Our service has used VLs for several years, including the McGrath Mac, and from February 2019 the GlideScope Go. Clinicians may alternatively use direct laryngoscopy with a Macintosh laryngoscope. We conducted a non-inferiority trial comparing first-pass intubation success using the GlideScope Go VL with that using the McGrath Mac VL. We collected data on video intubation of all adult patients between February 2017 and December 2019, by our service. Comparison was also made with patients intubated using direct laryngoscopy with a Macintosh direct laryngoscope. RESULTS: One hundred and seventy-two patients were intubated with the aid of a VL. First-pass success rates (95% confidence interval [CI]) were 0.98 (0.92-0.99) and 0.92 (0.84-0.96), respectively, for the GlideScope Go and McGrath Mac, giving a difference (95% CI) in first-pass success rates of 0.06 (-0.01 to 0.13). First-pass success rate for the Macintosh laryngoscope was 0.88 (0.84-0.91). CONCLUSIONS: We demonstrated that first-pass success rates with the GlideScope Go are at least as good as our service had achieved with both the McGrath Mac and with direct laryngoscopy.

A Comparison Between the Rates of Radiation Oncologist and Urologist Consultations in Men Diagnosed With Prostate Cancer in Northern Ontario, Canada.

Purpose: Recommendations from Cancer Care Ontario stress the importance of multidisciplinary care from radiologists and urologists for prostate cancer treatment. The present study sought to examine what percentage of patients had a consultation with a radiation oncologist before undergoing a radical prostatectomy in Ontario, Canada, between 2010 and 2019. Methods and Materials: Administrative health care databases were used to analyze the number of consultations billed to the Ontario Health Insurance Plan from radiologists and urologists who treated men with a first prostate cancer diagnosis (n = 22,169). Results: In Ontario, 94.70% of Ontario Health Insurance Plan billings for patients with prostate cancer who had a prostatectomy within 1 year of a prostate cancer diagnosis were from urology, and 37.66% and 1.77% of billings were received from radiation oncology and medical oncology specialties, respectively. When sociodemographic variables were examined, having a lower neighborhood income (adjusted odds ratio [aOR], 0.69; confidence interval [CI], 0.62-0.76) and a rural residence (aOR, 0.72; CI, 0.65-0.79) were associated with lower odds of receiving a consultation from a radiation oncologist. When billings for consultations were examined geographically by region, Northeast Ontario (Local Health Integrated Network 13) had the lowest odds of receiving a radiation consultation compared with the rest of Ontario (aOR, 0.50; CI, 0.42-0.59). Conclusions: The results of this study show that differences in equitable access to multidisciplinary health care exist for men with a first prostate cancer diagnosis who reside in more northern and rural regions within Ontario, relative to the rest of the province. The reasons for these findings are likely multifactorial and may include factors such as patient treatment preference and distance/travel to receive treatment. However, as diagnosis year increased, so did the chances of receiving a radiation oncologist consultation, and this upward trend may reflect the implementation of Cancer Care Ontario guidelines.

A Cancer Care Ontario Consensus-Based Organizational Guideline for the Planning and Delivery of Spine Stereotactic Body Radiation Therapy Treatment in Ontario.

The proposed recommendations are primarily based on the consensus opinion and in-field experience of the Ontario Health/Cancer Care Ontario stereotactic body radiation therapy (SBRT) for Spine Metastasis Guideline Development Group and published literature when available. Primary consideration was given to the perceived benefits for patients and the small likelihood of harm arising from recommendation implementation. Apart from the magnetic resonance imaging (MRI) follow-up strategy, all evidence was considered indirect and was provided by the working group in conjunction with their collective expertise in the field of SBRT. The application of an SBRT program requires a multidisciplinary team consisting of a radiation oncologist, spine surgeon, neuroradiologist, medical physicist, medical dosimetrist, and radiation therapist. In Canada, linear accelerators are the most used treatment delivery units and should follow technology-specific quality assurance procedures. Immobilization technique is location dependant. Treatment planning MRI sequences should be acquired no more than 14 days from the date of treatment. In the case of epidural disease, simulation MRI should be completed no more than 7 days from the date of treatment. After treatment, patients should be followed with routine clinical visits every 3 months for the first year, every 3 to 6 months during years 2 and 3, and every 4 to 6 months thereafter. The recommendations enclosed provide a framework for the minimum requirements for a cancer center in Ontario, Canada to offer SBRT for spine metastases.

Knockout or inhibition of USP30 protects dopaminergic neurons in a Parkinson's disease mouse model.

Mutations in SNCA, the gene encoding α-synuclein (αSyn), cause familial Parkinson's disease (PD) and aberrant αSyn is a key pathological hallmark of idiopathic PD. This α-synucleinopathy leads to mitochondrial dysfunction, which may drive dopaminergic neurodegeneration. PARKIN and PINK1, mutated in autosomal recessive PD, regulate the preferential autophagic clearance of dysfunctional mitochondria ("mitophagy") by inducing ubiquitylation of mitochondrial proteins, a process counteracted by deubiquitylation via USP30. Here we show that loss of USP30 in Usp30 knockout mice protects against behavioral deficits and leads to increased mitophagy, decreased phospho-S129 αSyn, and attenuation of SN dopaminergic neuronal loss induced by αSyn. These observations were recapitulated with a potent, selective, brain-penetrant USP30 inhibitor, MTX115325, with good drug-like properties. These data strongly support further study of USP30 inhibition as a potential disease-modifying therapy for PD.

The Impact of a Cyberattack at a Radiation Oncology Department: Immediate Response and Future Preparedness.

Cyberattacks are increasing year after year and many organizations, including hospitals, are becoming targets. Radiation oncology is especially vulnerable because of the reliance on computer and network capabilities to transfer relevant patient information for safe and effective patient treatment. In early 2019, our institution was hit by a ransomware attack that brought down our oncology information system (OIS). Although we were not fully prepared for such an attack, a total of 69 treatment fractions occurred without our OIS thanks to the quick development of a contingency plan and the ability to restore the patients' records. The OIS was recovered by the manufacturer 4 days after the attack. We also have developed a contingency plan and outline important considerations for institutions trying to prepare for unexpected downtime such as a cyberattack.

Evaluating Digital Health Capability at Scale Using the Digital Health Indicator.

BACKGROUND: Health service providers must understand their digital health capability if they are to drive digital transformation in a strategic and informed manner. Little is known about the assessment and benchmarking of digital maturity or capability at scale across an entire jurisdiction. The public health care system across the state of Queensland, Australia has an ambitious 10-year digital transformation strategy. OBJECTIVE: The aim of this research was to evaluate the digital health capability in Queensland to inform digital health strategy and investment. METHODS: The Healthcare Information and Management Systems Society Digital Health Indicator (DHI) was used via a cross-sectional survey design to assess four core dimensions of digital health transformation: governance and workforce; interoperability; person-enabled health; and predictive analytics across an entire jurisdiction simultaneously. The DHI questionnaire was completed by each health care system (n = 16) within Queensland in February to July 2021. DHI is scored 0 to 400 and dimension score is 0 to 100. RESULTS: The results reveal a variation in DHI scores reflecting the diverse stages of health care digitization across the state. The average DHI score across sites was 143 (range 78-193; SD35.3) which is similar to other systems in the Oceania region and global public systems but below the global private average. Governance and workforce was on average the highest scoring dimension (x̅= 54), followed by interoperability (x̅ = 46), person-enabled health (x̅ = 36), and predictive analytics (x̅ = 30). CONCLUSION: The findings were incorporated into the new digital health strategy for the jurisdiction. As one of the largest single simultaneous assessments of digital health capability globally, the findings and lessons learnt offer insights for policy makers and organizational managers.

Apolipoprotein E Genotype Moderation of the Association Between Physical Activity and Brain Health. A Systematic Review and Meta-Analysis.

INTRODUCTION: Possession of one or two e4 alleles of the apolipoprotein E (APOE) gene is associated with cognitive decline and dementia risk. Some evidence suggests that physical activity may benefit carriers of the e4 allele differently. METHOD: We conducted a systematic review and meta-analysis of studies which assessed APOE differences in the association between physical activity and: lipid profile, Alzheimer's disease pathology, brain structure and brain function in healthy adults. Searches were carried out in PubMed, SCOPUS, Web of Science and PsycInfo. RESULTS: Thirty studies were included from 4,896 papers screened. Carriers of the e4 allele gained the same benefit from physical activity as non-carriers on most outcomes. For brain activation, e4 carriers appeared to gain a greater benefit from physical activity on task-related and resting-state activation and resting-state functional connectivity compared to non-carriers. Post-hoc analysis identified possible compensatory mechanisms allowing e4 carriers to maintain cognitive function. DISCUSSION: Though there is evidence suggesting physical activity may benefit e4 carriers differently compared to non-carriers, this may vary by the specific brain health outcome, perhaps limited to brain activation. Further research is required to confirm these findings and elucidate the mechanisms.

Responding to the COVID-19 pandemic: The experiences of South Australia's Rescue, Retrieval and Aviation Services.

COVID-19 poses significant challenges to pre-hospital and retrieval medicine (PHRM) clinicians - and many are unique to this area of clinical practice. We share the experiences of the South Australian Ambulance Service (SAAS) MedSTAR Emergency Medical Retrieval Service in preparing for the COVID-19 pandemic in the pre-hospital and retrieval setting - including the role of a multidisciplinary leadership team; challenges and potential approaches to screening for COVID-19; personal protective equipment for pre-hospital and aeromedical taskings; issues arising with interstate retrievals; and the role of telehealth. Although novel solutions allowed SAAS MedSTAR to continue to deliver high-quality care, considering the resource implications involved in undertaking the transfer of patients with COVID-19, it is clear that significant community disease transmission threatens to overwhelm any PHRM service. Should Australia face a significant future outbreak, it is conceivable that some PHRM operations may need to be reduced or suspended entirely.

The Operation of Canada's Only Virtually Operated Radiation Oncology Service During the COVID-19 Pandemic.

PURPOSE: Our institution operates a remote radiation oncology service in Northern Ontario, Canada. Since the start of the coronavirus disease 2019 pandemic, this center has operated without radiation oncologists on site owing to safety precautions, and this study seeks to understand the effect of this shift. METHODS AND MATERIALS: Departmental level data reports were used to investigate differences in metrics between April to May of 2019 and April to May 2020. These metrics include the total number of referrals received, average wait time from referral to consult, the number of cases that underwent peer review before beginning treatment, the total number of fractions given over each period, patient-reported outcomes, and patient satisfaction. We also examined the importance of physical examinations and the use of SABR treatment. RESULTS: There was an observed decrease in the number of referrals received, total number of fractions administered, and number of patients providing patient-reported outcomes. We observed no change in patient wait times, cases undergoing peer review before commencing treatment, or overall patient satisfaction. Challenges were identified in the collection of patient- reported outcomes and the conduction of physical examinations. CONCLUSIONS: This paper provides proof of concept that a radiation clinic can function entirely virtually in the short term without sacrificing patient satisfaction, efficiency, or safety.