Citations

AbstractRegistered nurses increasingly work in remote care and digital interaction roles, offering flexibility and expansion of their scope of practice. These roles may expose nurses to digital compassion fatigue, a phenomenon proposed to be characterized by the negative psychological and emotional impact of caring for patients remotely through the use of technology.The first objective of this work is to propose the phenomenon of “digital compassion fatigue” as a potentially further evolved and differentiated form of “compassion fatigue.” The second objective is to produce a comparative analysis of attributes, antecedents, and consequences through literature reviews.An evolutionary concept analysis approach was selected as a guide for exploring, discussing, and defining the new concept of digital compassion fatigue. Concept analysis was selected given the need for a framework that accounts for the dynamic nature of technology and practice. The process of conducting a concept analysis includes consideration of diverse and multidisciplinary perspectives. As a result, those in caring, educational, and/or support service roles (e.g., social work, counseling, and teaching) for which distance suffering and technostress could feasibly be present were also included in the literature searches and reviews. Health care-specific studies often included nurses in the sample but may not have differentiated their specific insights or data points in the results.The concept analysis explored the attributes, antecedents, and consequences of digital compassion fatigue, differentiating it from its evolutionary parent, compassion fatigue. Key antecedents included technostress, distant suffering, and the unique challenges of delivering care remotely. A major confounding variable was the COVID-19 pandemic, which may have heightened or introduced new technology-related stressors or highlighted the existence of digital compassion fatigue.Further defining and understanding digital compassion fatigue is crucial for developing effective strategies to support nurses who may experience it or who are at risk.

Background: Approximately 90% of patients who undergo arthroscopic rotator cuff repair (RCR) are satisfied with their pain levels and function after surgery. However, a subset of patients experience continued symptoms that warrant revision surgery. Preoperative risk factors for RCR failure requiring revision surgery have not been clearly defined. Purpose: To (1) determine the rate of RCR failure requiring revision surgery and (2) identify risk factors for revision surgery, which will help surgeons to determine patients who are at the greatest risk for RCR failure. Study Design: Systematic review and meta-analysis; Level of evidence, 4. Methods: A systematic review and meta-analysis in accordance with PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines were performed. The initial search resulted in 3158 titles, and 533 full-text articles were assessed for eligibility. A total of 10 studies met the following inclusion criteria: (1) human clinical studies, (2) arthroscopic RCR, (3) original clinical research, and (4) evaluation of preoperative risk factors for revision. Results: After a full-text review, a total of 16 risk factors were recorded and analyzed across 10 studies. Corticosteroid injection was the most consistent risk factor for revision surgery, reaching statistical significance in 4 of 4 studies, followed by workers’ compensation status (2/3 studies). Patients with corticosteroid injections had a pooled increased risk of revision surgery by 47% (odds ratio, 1.44 [95% CI, 1.36-1.52]). Patients with workers’ compensation had a pooled increased risk of revision surgery by 133% (odds ratio, 2.33 [95% CI, 2.09-2.60]). Age, smoking status, diabetes, and obesity were found to be risk factors in half of the analyzed studies. Conclusion: Corticosteroid injections, regardless of the frequency of injections, and workers’ compensation status were found to be significant risk factors across the literature based on qualitative analysis and pooled analysis. Surgeons should determine ideal candidates for arthroscopic RCR by accounting for corticosteroid injection history, regardless of the frequency, and insurance status of the patient.

AbstractPurposeThe low exposures, unique x‐ray beam geometry, and scanning design in dual‐energy x‐ray absorptiometry (DXA) make measurement and quality‐control strategies different from traditional x‐ray equipment. This study examines the dependence of measured entrance‐air‐kerma (EAK) on both dose sensor type and scan length. The feasibility of using EAK to compare scanner output between different scan modes, individual scanners, and scanner platforms was also established. Finally, the congruence between measured and vendor‐reported EAK was analyzed.MethodsFour Hologic DXA scanners at two institutions and all four available scan modes were tested. EAK was measured directly by three types of Radcal dose sensors: 60‐cc pancake ion‐chamber (IC), 180‐cc pancake IC, and solid‐state detector. The coefficient of variation (COV) was used to assess the dependence of EAK on scan length. Variations in EAK between the types of dose sensors as well as measured versus vendor‐reported values were evaluated using Bland–Altman analysis: mean ±95% prediction interval (PI): 1.96σ.ResultsDose sensor variations in EAK were minimal, with a −3.5 ± 3.5% (mean ±95% PI) percent difference between the two sizes of IC's. The solid‐state detector produced highly similar measurements to the 180‐cc IC. These small differences were consistent across all scanners and all scan modes tested. Neither measured nor vendor‐reported EAK values were found to show relevant dependence on scan length, with all COV values ≤4%. Differences between measured and reported EAK were higher at −6 ± 48%. Likely errors in vendor‐reported EAK calculations were also identified.ConclusionIt is feasible to quantify DXA scanner stability using EAK as a quality‐control metric with a variety of solid‐state and IC dose sensors, and the scan length used is not critical. Although vendor‐reported EAK was consistent among scanners of the same platform, measured EAK varied significantly from scanner to scanner. As a result, measured and reported EAK may not always be comparable.

Abstract Background Hemocompatibility‐related adverse events (HRAE) negatively influence survival. However, no study has examined the impact of these events on health‐related quality of life (HRQOL) and functional outcomes following continuous‐flow left ventricular assist device implantation (CF‐LVAD). We assessed the impact of HRAE events on HRQOL and hypothesized that HRAE's adversely impact HRQOL and functional outcomes. Methods INTERMACS database identified patients undergoing primary CF‐LVAD implantation from 2008 to 2017. HRAEs included stroke, non‐surgical bleeding, hemolysis, and pump thrombosis and were identified as defined in the literature. HRAEs were further stratified as Tier 1–2 and disabling stroke events. Time‐series analysis was executed for HRAE patients with values pre‐HRAE, post‐HRAE, and closest to 12 months follow up. Local polynomial regression curves modeling individual patients were superimposed into “spaghetti” plots. Results All HRQOL and functional metrics improved in patients over time, despite HRAE complications. However, these patient metrics were significantly reduced compared to the non‐HRAE cohort. Advanced data visualization techniques noted a decline after experiencing an HRAE with a subsequent recovery to baseline levels or higher. Six‐minute walk test (6MWT) was noted to be most affected in the post‐HRAE period but recovered similar to other metrics. Conclusions The burden of HRAE following CF‐LVAD implantation did not negatively impact the quality of life. However, the 6MWT did not increase in the post‐HRAE period in all HRAE patients. Improvement of heart failure symptoms after CF‐LVAD coupled with optimal management following the HRAE act to preserve the enhanced quality of life.

Purpose To develop and internally validate a machine‐learning algorithm to reliably predict cost after anterior cruciate ligament reconstruction (ACLR). Methods A retrospective review of the New York State Ambulatory Surgery and Services database was performed to identify patients who underwent elective ACLR from 2015 to 2016. Features included in initial models consisted of patient characteristics (age, sex, insurance status, income, medical comorbidities as classified by the Clinical Classifications Software diagnosis code) as well as intraoperative variables (type of anesthesia and procedure‐specific factors). Models were generated to predict total charges using 4 algorithms: random forest, extreme gradient boost, elastic net penalized regression, and support vector machines with radial kernels. Training was performed with 10‐fold cross‐validation followed by internal validation via 0.632 bootstrapping. Model discriminative performance was assessed by area under the receiver operating characteristic curve, calibration, and the Brier score. Decision curve analysis was performed to demonstrate the net benefit of using the final model in practice. Results In total, 7,311 patients undergoing ambulatory ACLR were included. The random forest model demonstrated the best performance assessed via internal validation (area under the curve = 0.85), calibration, and the Brier score (0.208). Cost incurred was influenced by anesthesia type, operating room time, and number of chronic comorbidities. Decision curve analysis revealed a net benefit for use of the random forest model and the model was integrated into a web‐based open‐access application. Conclusions The random forest model predicted cost after ambulatory ACLR using a large, statewide database with good performance. The top variables found to predict increased charges were general anesthesia, operating room time, meniscal repair, self‐pay insurance, patient neighborhood characteristics, and number of chronic conditions. Level of Evidence III, retrospective cohort study.

Alternate lineage restriction and B cell fate commitment require the transcription factor Pax5, but the functions of EBF, in these processes remain largely unexplored. In the absence of EBF, expandable and clonal lymphoid progenitors retain considerable myeloid potential. Conversely, ectopic expression of EBF in multipotential progenitors directs B cell generation at the expense of myeloid cell fates. EBF induces Pax5 and antagonizes expression of C/EBPα , PU.1 and Id2 . Importantly, sustained expression of EBF in Pax5 −/− hematopoietic progenitors is sufficient to block their myeloid and T lineage potentials in vivo . Furthermore, in Pax5 −/− pro‐B cells increased EBF expression represses alternate lineage genes. Thus, EBF can restrict alternate lineage choice and promote B cell fate commitment independently of Pax5.

Abstract Prothrombin complex concentrate (PCC) administration has increased among cardiac surgery patients in recent years; however, use in LVAD implantation/exchange is not widespread due to the fear of thrombotic complications. The purpose of this study was to compare the clinical outcomes of patients undergoing LVAD implantation/exchange with intraoperative PCC administration versus traditional transfusion practices alone. Adult LVAD implants/exchanges at our institution between 2015 and 2018 were included. Patients were categorized as receiving intraoperative PCC or no‐PCC (traditional). The primary outcome was the need for allogenic transfusion and transfusion volume at 48 hours after initial intensive care unit (ICU) admission. Secondary outcomes included metrics of morbidity and mortality. A total of 160 patients (39 PCC, 121 traditional) were analyzed. In unadjusted analysis, patients in the PCC group received lower intraoperative transfusion volumes compared to the traditional group although not statistically significant (1464 mL [IQR 796, 4876] vs. 2568 mL [IQR 1292, 3606]; P value .37). In the fully adjusted analysis, patients in the PCC group had increased odds of transfusion within 48 hours of ICU admission (OR 4.06, 95% CI: 1.35‐12.20; P < .01); however, there was no significant difference in transfusion volumes ( P = .09). Patients receiving PCCs had higher incidence of deep vein thrombosis (10.3% vs. 0%; P < .01) and 30‐day mortality (17.9% vs. 4.1%; P < .01). LVAD pump thrombosis occurred in 2.6% versus 0.8% in the PCC and traditional groups, respectively; P = .98. Patients undergoing LVAD implantation and exchange represent a complex surgical cohort. The results of this study suggest that the intraoperative PCC use during LVAD implant/exchange was associated with reduced intraoperative transfusions. Intraoperative PCC use was, however, associated with higher odds of postoperative transfusion, although transfusion volumes were not significantly different. While the deep vein thrombosis and 30‐day mortality rates were higher in the PCC group, these results are likely related to the degree of surgical and patient complexity rather than PCC use itself. Further studies are needed to assess PCC use in this surgical cohort.

Parkinson’s disease (PD) is thought to be caused by a combination of genetic and environmental factors. Bacterial or viral infection has been proposed as a potential risk factor, and there is supporting although not entirely consistent epidemiologic and basic science evidence to support its role. Encephalitis caused by influenza has included parkinsonian features. Epidemiological evidence is most compelling for an association between PD and hepatitis C virus. Infection with Helicobacter pylori may be associated not only with PD risk but also response to levodopa. Rapidly evolving knowledge regarding the role of the microbiome also suggests a role of resident bacteria in PD risk. Biological plausibility for the role for infectious agents is supported by the known neurotropic effects of specific viruses, particular vulnerability of the substantia nigra and even the promotion of aggregation of alpha-synuclein. A common feature of implicated viruses appears to be production of high levels of cytokines and chemokines that can cross the blood-brain barrier leading to microglial activation and inflammation and ultimately neuronal cell death. Based on multiple avenues of evidence it appears likely that specific bacterial and particularly viral infections may increase vulnerability to PD. The implications of this for PD prevention requires attention and may be most relevant once preventive treatments for at-risk populations are developed.