Mortality and Pulmonary Embolism in Acute Respiratory Distress Syndrome From COVID-19 vs. Non-COVID-19
There may be a difference in respiratory mechanics, inflammatory markers, and pulmonary emboli in COVID-19 associated ARDS vs. ARDS from other etiologies. Our purpose was to determine differences in respiratory mechanics, inflammatory markers, and incidence of pulmonary embolism in patients with and...
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Published in | Frontiers in medicine Vol. 9; p. 800241 |
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04.03.2022
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Abstract | There may be a difference in respiratory mechanics, inflammatory markers, and pulmonary emboli in COVID-19 associated ARDS vs. ARDS from other etiologies. Our purpose was to determine differences in respiratory mechanics, inflammatory markers, and incidence of pulmonary embolism in patients with and without COVID-19 associated ARDS admitted in the same period and treated with a similar ventilation strategy.
A cohort study of COVID-19 associated ARDS and non COVID-19 patients in a Saudi Arabian center between June 1 and 15, 2020. We measured respiratory mechanics (ventilatory ratio (VR), recruitability index (RI), markers of inflammation, and computed tomography pulmonary angiograms.
Forty-two patients with COVID-19 and 43 non-COVID patients with ARDS comprised the cohort. The incidence of "recruitable" patients using the recruitment/inflation ratio was slightly lower in COVID-19 patients (62 vs. 86%;
= 0.01). Fifteen COVID-19 ARDS patients (35.7%) developed a pulmonary embolism as compared to 4 (9.3%) in other ARDS patients (
= 0.003). In COVID-19 patients, a D-Dimer ≥ 5.0 mcg/ml had a 73% (95% CI 45-92%) sensitivity and 89% (95% CI 71-98%) specificity for predicting pulmonary embolism. Crude 60-day mortality was higher in COVID-19 patients (35 vs. 15%;
= 0.039) but three multivariate analysis showed that independent predictors of 60-day mortality included the ventilatory ratio (OR 3.67, 95% CI 1.61-8.35), PaO2/FIO2 ratio (OR 0.93; 95% CI 0.87-0.99), IL-6 (OR 1.02, 95% CI 1.00-1.03), and D-dimer (OR 7.26, 95% CI 1.11-47.30) but not COVID-19 infection.
COVID-19 patients were slightly less recruitable and had a higher incidence of pulmonary embolism than those with ARDS from other etiologies. A high D-dimer was predictive of pulmonary embolism in COVID-19 patients. COVID-19 infection was not an independent predictor of 60-day mortality in the presence of ARDS. |
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AbstractList | PurposeThere may be a difference in respiratory mechanics, inflammatory markers, and pulmonary emboli in COVID-19 associated ARDS vs. ARDS from other etiologies. Our purpose was to determine differences in respiratory mechanics, inflammatory markers, and incidence of pulmonary embolism in patients with and without COVID-19 associated ARDS admitted in the same period and treated with a similar ventilation strategy.MethodsA cohort study of COVID-19 associated ARDS and non COVID-19 patients in a Saudi Arabian center between June 1 and 15, 2020. We measured respiratory mechanics (ventilatory ratio (VR), recruitability index (RI), markers of inflammation, and computed tomography pulmonary angiograms.ResultsForty-two patients with COVID-19 and 43 non-COVID patients with ARDS comprised the cohort. The incidence of “recruitable” patients using the recruitment/inflation ratio was slightly lower in COVID-19 patients (62 vs. 86%; p = 0.01). Fifteen COVID-19 ARDS patients (35.7%) developed a pulmonary embolism as compared to 4 (9.3%) in other ARDS patients (p = 0.003). In COVID-19 patients, a D-Dimer ≥ 5.0 mcg/ml had a 73% (95% CI 45–92%) sensitivity and 89% (95% CI 71–98%) specificity for predicting pulmonary embolism. Crude 60-day mortality was higher in COVID-19 patients (35 vs. 15%; p = 0.039) but three multivariate analysis showed that independent predictors of 60-day mortality included the ventilatory ratio (OR 3.67, 95% CI 1.61–8.35), PaO2/FIO2 ratio (OR 0.93; 95% CI 0.87–0.99), IL-6 (OR 1.02, 95% CI 1.00–1.03), and D-dimer (OR 7.26, 95% CI 1.11–47.30) but not COVID-19 infection.ConclusionCOVID-19 patients were slightly less recruitable and had a higher incidence of pulmonary embolism than those with ARDS from other etiologies. A high D-dimer was predictive of pulmonary embolism in COVID-19 patients. COVID-19 infection was not an independent predictor of 60-day mortality in the presence of ARDS. There may be a difference in respiratory mechanics, inflammatory markers, and pulmonary emboli in COVID-19 associated ARDS vs. ARDS from other etiologies. Our purpose was to determine differences in respiratory mechanics, inflammatory markers, and incidence of pulmonary embolism in patients with and without COVID-19 associated ARDS admitted in the same period and treated with a similar ventilation strategy. A cohort study of COVID-19 associated ARDS and non COVID-19 patients in a Saudi Arabian center between June 1 and 15, 2020. We measured respiratory mechanics (ventilatory ratio (VR), recruitability index (RI), markers of inflammation, and computed tomography pulmonary angiograms. Forty-two patients with COVID-19 and 43 non-COVID patients with ARDS comprised the cohort. The incidence of "recruitable" patients using the recruitment/inflation ratio was slightly lower in COVID-19 patients (62 vs. 86%; = 0.01). Fifteen COVID-19 ARDS patients (35.7%) developed a pulmonary embolism as compared to 4 (9.3%) in other ARDS patients ( = 0.003). In COVID-19 patients, a D-Dimer ≥ 5.0 mcg/ml had a 73% (95% CI 45-92%) sensitivity and 89% (95% CI 71-98%) specificity for predicting pulmonary embolism. Crude 60-day mortality was higher in COVID-19 patients (35 vs. 15%; = 0.039) but three multivariate analysis showed that independent predictors of 60-day mortality included the ventilatory ratio (OR 3.67, 95% CI 1.61-8.35), PaO2/FIO2 ratio (OR 0.93; 95% CI 0.87-0.99), IL-6 (OR 1.02, 95% CI 1.00-1.03), and D-dimer (OR 7.26, 95% CI 1.11-47.30) but not COVID-19 infection. COVID-19 patients were slightly less recruitable and had a higher incidence of pulmonary embolism than those with ARDS from other etiologies. A high D-dimer was predictive of pulmonary embolism in COVID-19 patients. COVID-19 infection was not an independent predictor of 60-day mortality in the presence of ARDS. Purpose There may be a difference in respiratory mechanics, inflammatory markers, and pulmonary emboli in COVID-19 associated ARDS vs. ARDS from other etiologies. Our purpose was to determine differences in respiratory mechanics, inflammatory markers, and incidence of pulmonary embolism in patients with and without COVID-19 associated ARDS admitted in the same period and treated with a similar ventilation strategy. Methods A cohort study of COVID-19 associated ARDS and non COVID-19 patients in a Saudi Arabian center between June 1 and 15, 2020. We measured respiratory mechanics (ventilatory ratio (VR), recruitability index (RI), markers of inflammation, and computed tomography pulmonary angiograms. Results Forty-two patients with COVID-19 and 43 non-COVID patients with ARDS comprised the cohort. The incidence of “recruitable” patients using the recruitment/inflation ratio was slightly lower in COVID-19 patients (62 vs. 86%; p = 0.01). Fifteen COVID-19 ARDS patients (35.7%) developed a pulmonary embolism as compared to 4 (9.3%) in other ARDS patients ( p = 0.003). In COVID-19 patients, a D-Dimer ≥ 5.0 mcg/ml had a 73% (95% CI 45–92%) sensitivity and 89% (95% CI 71–98%) specificity for predicting pulmonary embolism. Crude 60-day mortality was higher in COVID-19 patients (35 vs. 15%; p = 0.039) but three multivariate analysis showed that independent predictors of 60-day mortality included the ventilatory ratio (OR 3.67, 95% CI 1.61–8.35), PaO2/FIO2 ratio (OR 0.93; 95% CI 0.87–0.99), IL-6 (OR 1.02, 95% CI 1.00–1.03), and D-dimer (OR 7.26, 95% CI 1.11–47.30) but not COVID-19 infection. Conclusion COVID-19 patients were slightly less recruitable and had a higher incidence of pulmonary embolism than those with ARDS from other etiologies. A high D-dimer was predictive of pulmonary embolism in COVID-19 patients. COVID-19 infection was not an independent predictor of 60-day mortality in the presence of ARDS. |
Author | Balhamar, Abdullah Alqahtani, Saleh A Papanikolaou, John Memish, Ziad A Kutsogiannis, Demetrios J Faqihi, Fahad Karakitsos, Dimitrios Brindley, Peter G Alharthy, Abdulrahman Brochard, Laurent |
AuthorAffiliation | 2 Critical Care Department, King Saud Medical City , Riyadh , Saudi Arabia 7 Institute of Medical Science, University of Toronto , Toronto, ON , Canada 4 Research and Innovation Center, King Saud Medical City , Riyadh , Saudi Arabia 3 Department of Medicine, The Johns Hopkins University Hospital , Baltimore, MD , United States 6 Interdepartmental Division of Critical Care Medicine, Institute of Medical Science, University of Toronto , Toronto, ON , Canada 8 Department of Internal Medicine, University of South Carolina, School of Medicine , Columbia, SC , United States 1 Department of Critical Care Medicine, Faculty of Medicine and Dentistry, The University of Alberta , Edmonton, AB , Canada 9 Critical Care Department, Keck School of Medicine, University of Southern California , Los Angeles, CA , United States 5 Department of Critical Care, Keenan Research Center and Li Ka Shing Institute, St. Michael's Hospital , Toronto , ON , Canada |
AuthorAffiliation_xml | – name: 4 Research and Innovation Center, King Saud Medical City , Riyadh , Saudi Arabia – name: 6 Interdepartmental Division of Critical Care Medicine, Institute of Medical Science, University of Toronto , Toronto, ON , Canada – name: 9 Critical Care Department, Keck School of Medicine, University of Southern California , Los Angeles, CA , United States – name: 3 Department of Medicine, The Johns Hopkins University Hospital , Baltimore, MD , United States – name: 1 Department of Critical Care Medicine, Faculty of Medicine and Dentistry, The University of Alberta , Edmonton, AB , Canada – name: 2 Critical Care Department, King Saud Medical City , Riyadh , Saudi Arabia – name: 7 Institute of Medical Science, University of Toronto , Toronto, ON , Canada – name: 5 Department of Critical Care, Keenan Research Center and Li Ka Shing Institute, St. Michael's Hospital , Toronto , ON , Canada – name: 8 Department of Internal Medicine, University of South Carolina, School of Medicine , Columbia, SC , United States |
Author_xml | – sequence: 1 givenname: Demetrios J surname: Kutsogiannis fullname: Kutsogiannis, Demetrios J organization: Department of Critical Care Medicine, Faculty of Medicine and Dentistry, The University of Alberta, Edmonton, AB, Canada – sequence: 2 givenname: Abdulrahman surname: Alharthy fullname: Alharthy, Abdulrahman organization: Critical Care Department, King Saud Medical City, Riyadh, Saudi Arabia – sequence: 3 givenname: Abdullah surname: Balhamar fullname: Balhamar, Abdullah organization: Critical Care Department, King Saud Medical City, Riyadh, Saudi Arabia – sequence: 4 givenname: Fahad surname: Faqihi fullname: Faqihi, Fahad organization: Critical Care Department, King Saud Medical City, Riyadh, Saudi Arabia – sequence: 5 givenname: John surname: Papanikolaou fullname: Papanikolaou, John organization: Critical Care Department, King Saud Medical City, Riyadh, Saudi Arabia – sequence: 6 givenname: Saleh A surname: Alqahtani fullname: Alqahtani, Saleh A organization: Department of Medicine, The Johns Hopkins University Hospital, Baltimore, MD, United States – sequence: 7 givenname: Ziad A surname: Memish fullname: Memish, Ziad A organization: Research and Innovation Center, King Saud Medical City, Riyadh, Saudi Arabia – sequence: 8 givenname: Peter G surname: Brindley fullname: Brindley, Peter G organization: Department of Critical Care Medicine, Faculty of Medicine and Dentistry, The University of Alberta, Edmonton, AB, Canada – sequence: 9 givenname: Laurent surname: Brochard fullname: Brochard, Laurent organization: Institute of Medical Science, University of Toronto, Toronto, ON, Canada – sequence: 10 givenname: Dimitrios surname: Karakitsos fullname: Karakitsos, Dimitrios organization: Critical Care Department, Keck School of Medicine, University of Southern California, Los Angeles, CA, United States |
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Copyright | Copyright © 2022 Kutsogiannis, Alharthy, Balhamar, Faqihi, Papanikolaou, Alqahtani, Memish, Brindley, Brochard and Karakitsos. Copyright © 2022 Kutsogiannis, Alharthy, Balhamar, Faqihi, Papanikolaou, Alqahtani, Memish, Brindley, Brochard and Karakitsos. 2022 Kutsogiannis, Alharthy, Balhamar, Faqihi, Papanikolaou, Alqahtani, Memish, Brindley, Brochard and Karakitsos |
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Keywords | COVID-19 recruitment inflation ratio respiratory mechanics ventilatory ratio acute respiratory distress syndrome pulmonary embolism interleukin-6 (IL-6) |
Language | English |
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Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Reviewed by: Claudio Rabec, Centre Hospitalier Regional Universitaire De Dijon, France; Jorge Moisés, Hospital Clínic de Barcelona, Spain This article was submitted to Pulmonary Medicine, a section of the journal Frontiers in Medicine Edited by: Daniel Rodenstein, Cliniques Universitaires Saint-Luc, Belgium |
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Snippet | There may be a difference in respiratory mechanics, inflammatory markers, and pulmonary emboli in COVID-19 associated ARDS vs. ARDS from other etiologies. Our... Purpose There may be a difference in respiratory mechanics, inflammatory markers, and pulmonary emboli in COVID-19 associated ARDS vs. ARDS from other... PurposeThere may be a difference in respiratory mechanics, inflammatory markers, and pulmonary emboli in COVID-19 associated ARDS vs. ARDS from other... |
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Title | Mortality and Pulmonary Embolism in Acute Respiratory Distress Syndrome From COVID-19 vs. Non-COVID-19 |
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