Your browser doesn't support javascript.
Show: 20 | 50 | 100
Results 1 - 4 de 4
Add filters

Document Type
Year range
International Journal of Healthcare Management ; 2023.
Article in English | Scopus | ID: covidwho-2255085


Background: The coronavirus disease 2019 (COVID-19) pandemic contributed to intensified nurse burnout. Workplace factors influence burnout, requiring organizational-level action to mitigate this problem. Aim: To inform immediate and long-term organizational tactics, we created workforce-informed recommendations for addressing burnout by engaging our nursing workforce to identify and prioritize the factors driving their burnout. Methods: We creatively applied the participatory management LISTEN-SORT-EMPOWER model to gather nurse views on burnout, capturing data through focus group sessions and mobile app postings. We coded findings through thematic and sentiment analysis, and participants ranked these results to prioritize the factors of their burnout. Results: We collected 80 h of feedback and 603 app comments, resulting in 800,000+ words. Our analysis identified twelve drivers of burnout, including three themes: (1) Staffing shortages (660;43.8%);(2) Environment and culture (548;36.4%);(3) Total compensation (299;19.8%). Additionally, 1300+ nurses chose income, workload/stress injury, and work schedule as uppermost priorities for addressing their burnout. Conclusions: Through novel project methods, leaders embraced participatory management to actively partner with nurses in identifying the drivers of nurse burnout. Healthcare organizations can design relevant and effective interventions to lessen clinician burnout by directly engaging and partnering with those experiencing burnout. © 2023 Informa UK Limited, trading as Taylor & Francis Group.

American Journal of the Medical Sciences ; 365(Supplement 1):S204, 2023.
Article in English | EMBASE | ID: covidwho-2229639


Case Report: Protein losing enteropathy (PLE) occurs when proteins leak from the gastrointestinal (GI) system more rapidly than they are produced. Inflammation of the GI tract facilitates increased membrane permeability of gastric mucosa, leading to excess protein leakage. 1 PLE in children has been associated with CMV, rotavirus, COVID-19, HIV, C. difficile, and autoimmune diseases like Crohn's Disease. 2-6 Norovirus is a known cause of PLE in immunocompromised pediatric patients. 7-8 However, to our knowledge, there are no case reports about PLE precipitated by norovirus in immunocompetent pediatric patients. The purpose of this case report is to present a case of PLE precipitated by a norovirus infection in a 4- year-old previously healthy child. While the above gastrointestinal viruses have been proposed as precipitators for this disease, PLE precipitated by norovirus infection has not been well described. This case also highlights the importance of early diagnosis and management to avoid complications. Method(s): Our patient initially presented with two days of abdominal pain, diarrhea, emesis, reduced urine output, and swelling of the lower extremities. He was exposed to several sick family members-his sister had upper respiratory symptoms and his grandmother had gastrointestinal symptoms. Physical exam was notable for diminished breath sounds in the right lower lobe, abdominal distension with diffuse tenderness and dullness to percussion, significant scrotal and penile edema, and bilateral lower extremity pitting edema. Laboratory results revealed leukocytosis, hypoalbuminemia, hyponatremia, elevated aspartate aminotransferase (AST), and elevated serum alpha-1-antitrypsin, as well as low Immunoglobulins G and M. CD3 and CD4 levels were low reflecting cellular immune dysregulation seen in patients with PLE. IgA and Tissue Transglutaminase (TTF) were within normal limits. Ebstein Barr Virus and cytomegalovirus IgM antibodies were negative. COVID IgG was negative as well. His Polymerase chain reaction (PCR) gastrointestinal panel was positive for norovirus. A chest X-ray showed a large right pleural effusion. Abdominal CT revealed large ascites slightly more predominant in the upper abdomen, mesenteric lymphadenitis, and bilateral pleural effusions. Echocardiogram showed small anterior and apical pericardial effusions. Result(s): Based on the patient's elevated serum alpha-1 antitrypsin levels, hypoalbuminemia, low levels of immunoglobulins and lymphocytes, and clinical manifestations of ascites, bilateral pleural effusions, pericardial effusion, and dependent edema, along with a positive PCR for norovirus, the diagnosis of PLE secondary to Norovirus was made. Conclusion(s): This case demonstrates the importance of recognizing viruses like Norovirus as potential causes of PLE to avoid a delay in diagnosis and initiation of therapy, and to avoid unnecessary additional testing. Copyright © 2023 Southern Society for Clinical Investigation.

Open Forum Infectious Diseases ; 9(Supplement 2):S474, 2022.
Article in English | EMBASE | ID: covidwho-2189766


Background. Peak SARS-CoV-2 viral replication occurs in the upper respiratory tract in presymptomatic and early symptomatic phases. Administration of a monoclonal antibody may be most beneficial in the early time period immediately after symptom onset. Here we describe the effect of early therapy on efficacy in patients receiving ADI. Methods. High risk patients with mild or moderate COVID-19 were enrolled in the ADI treatment study (STAMP), with primary endpoint of COVID-19 related hospitalization or all-cause death through Day 29 in patients with disease due to confirmed or suspected SARS-CoV-2 variants other than Omicron. Patients were randomized 1:1 to receive ADI or placebo administered by a single intramuscular (IM) injection. For this subgroup analysis, patients that had received therapy within 3 days of symptom onset were evaluated. Results. In the overall population, the study met the primary endpoint demonstrating 66% relative risk reduction of COVID-19 hospitalization or all cause death in 336 patients. Among 261 patients receiving therapy within 3 days of symptom onset (n=133 ADI, n=128 placebo), ADI was associated with a statistically significant reduction in the risk of COVID-19-related hospitalization or all-cause death through Day 29 compared with placebo (4 [3%] vs. 15 [11.7%], standardized risk difference -8%, 95% CI: -14.11, -1.86, p=0.0106), demonstrating a 72% standardized relative risk reduction in favor of ADI. When given as early therapy, ADI provided a greater reduction in viral load from baseline to Day 5 compared with placebo as assessed by saliva samples, with an adjusted least-squares mean difference of -0.97 log10 copies/mL (95% CI: -1.540, -0.391;p=0.0011). No study drug related SAEs, including deaths, and no hypersensitivity reactions were reported. Conclusion. Early therapy with a single dose of ADI 300 mg IM provided a 72% reduction in the risk of COVID-19 related hospitalization and all-cause death compared to placebo in high-risk ambulatory patients with mild to moderate COVID-19. Therapy within the first 3 days also led to a greater reduction in viral load compared to placebo and favorable outcomes in patients who are at high risk for progression of disease.

Topics in Antiviral Medicine ; 29(1):248-249, 2021.
Article in English | EMBASE | ID: covidwho-1250702


Background: Individuals hospitalized with COVID-19 exhibit a wide spectrum of disease. There is growing evidence that racial and ethnic minorities bear a disproportionate burden from COVID-19. Temporal changes in the pandemic epidemiology require careful study to identify determinants of poor outcomes. We assessed patient socio-demographics, comorbidities, baseline severity, treating hospital and pandemic month as independent risk factors for mortality and time to discharge. Methods: We analyzed 2500 individuals hospitalized with PCR-confirmed COVID-19 in 5 hospitals in the University of Pennsylvania Health System between March and September 2020, using electronic health records to assess outcomes through 8 weeks post-admission. Hospital discharge and mortality were analyzed as competing risks using a multivariable cause-specific hazards model. Results: Patients were 50.9% Black, 39.4% White and 9.7% other race;11% were Hispanic. Mortality decreased markedly over time, with cumulative incidence (95% CI) 30 days post-admission of 19.1% (17.2, 21.3) in March- April versus 6.3% (4.3, 8.9) in July-September;19% of deaths occurred after discharge. During this time, average age (SD) at admission declined from 62.7 (17.6) to 53.4 (20.6), ICU level care at admission increased from 16.5% to 18.6%, mechanical ventilation declined from 9.4% to 2.9%. Compared to Caucasian, Black race was associated with more severe disease at admission, a higher rate of co-morbidities and residence in low income zip code. In multivariable models, there were no detectable differences in mortality risk by race;while admitting hospital, increasing age, admission early in the pandemic, and severe disease and low blood pressure at admission were associated with increased mortality hazard (Figure 1). Mortality appeared similar between sexes, though males tended to have longer hospital stays (discharge hazard ratio 0.82 (95% CI: 0.75, 0.90)). Hispanic ethnicity was associated with fewer baseline co-morbidities and lower mortality hazard (0.57, 95% CI: 0.37, .087). Conclusion: We found that morbidity and mortality for hospitalized COVID-19 patients substantially decreased over time but post-discharge mortality remained non-trivial. Black race was associated with more risk factors for morbidity and with treatment at hospitals with lower mortality. In multivariable models, there were no detectable race differences in hospital outcomes. Future work is needed to better understand the identified betweenhospital differences in mortality.