Abstract
Title: Comparison of Clinical and Thrombotic Outcomes in SARS-CoV-2- Pneumonia versus Other Viral Pneumonia in an Urban Academic Medical Center
Objective: To compare clinical and thrombotic outcomes in SARS-CoV-2 pneumonia versus other viral pneumonias.
Introduction: Viral pneumonia (PNA) causes oxidative stress to the pulmonary vasculature, triggering endothelial dysfunction and activation of the coagulation cascade. Elevations in coagulation markers, including d-dimer and fibrinogen, have been observed. Recent studies indicate that SARS-CoV-2 infection causes endothelial cell injury, with activation of the coagulation cascade, and a high frequency of systemic thrombotic events. It remains unclear whether it is viral pneumonia itself, a specific viral strain (and/or viral load) that drives the clinical and thrombotic outcomes. Furthermore, limited data is available regarding clinical outcomes in a diverse patient population hospitalized with SARS-CoV-2 infection. This study is from a single urban medical center in Chicago, Illinois.
Study Design: A retrospective cohort study evaluating the medical records of hospitalized adult patients admitted to University of Illinois Hospital and Health Sciences System (UIHHSS) with SARS-CoV-2 pneumonia or other viral (H1N1 or H3N2) pneumonia between 10/01/2017 and 09/01/2020.
Methods: Patients were included if ≥18 years old, hospitalized, with a primary confirmed diagnosis of viral pneumonia (SARS-CoV-2, H1N1 or H3N2) based on ICD-10 code, viral diagnostic testing, diagnosis description, and appropriate clinical characteristics/imaging studies. Past medical history, inpatient medications, coagulation parameters, arterial/venous thrombotic outcomes, and other clinical outcomes (renal replacement therapy, mechanical ventilation, co-infection) were abstracted from UIHHSS electronic health record database.
Results: Medical records of 257 patient with a primary diagnosis of pneumonia were reviewed, 199 patients with SARS-CoV-2 PNA (95 male, average age 58 years, 52% Hispanic, 37% non-Hispanic Black) and 58 patients with other viral PNA (24 male, average age 63 years, 21% Hispanic, 55% non-Hispanic Black; 34 with H3N2, 24 with H1N1). Coagulation parameters (maximum D-dimer, fibrinogen, INR) were similar in both groups; average D-dimer was >3x ULN. Anticoagulation therapy was similarly prescribed in both groups (SARS-CoV-2, 95% vs 84%, H1N1 or H3N2), with prophylactic dose anticoagulation prescribed most frequently (73% vs 62%) and with high average compliance rates (89% vs 83%). Admission to the intensive care unit (ICU; 32% vs 29%) and the median length of stay (10 vs 4 days) was similar in both groups. Thrombotic events (n = 6, 3%) occurred only in SARS-CoV-2 PNA patients in the ICU: 3 pulmonary embolism (PE), 1 distal lower extremity deep vein thrombosis (DVT), 2 non-ST elevated myocardial infarctions (NSTEMI). There was a significantly higher incidence of use of renal replacement therapy (8.5% vs 0%, p=0.016) and mortality (15.6% vs 3.4%, p=0.048) in the SARS-CoV-2 PNA group compared to the H3N2/H1N1 PNA group. There were no differences in the rates of mechanical ventilation, the incidence of major bleeding or co-infection. In a multivariable logistic regression analysis, age (aOR 1.07), the presence of SARS-CoV-2 PNA (aOR 11.37), and ICU admission (aOR 41.95) were significantly associated with risk of mortality during hospitalization. Race and ethnicity were not associated with mortality.
Conclusion: The overall incidence of thrombotic events was low and occurred only in the SARS-CoV-2 PNA group. The low rate of venous thrombosis detected in this group, especially in the ICU setting, is likely related to the reduced use of diagnostic studies during the first COVID-19 pandemic in 2020 and to the high rates of anticoagulation prophylaxis orders and compliance. SARS-CoV-2 PNA was associated with a higher rate of renal failure and mortality compared to patients with H3N2/H1N1 viral pneumonia. There was no difference in mortality rates between Hispanic and non-Hispanic and between Black and non-Black patients. This study suggests that SARS-CoV-2 pneumonia leads to greater endothelial dysfunction than that observed in H3N2/H1N1 viral pneumonia and that race/ethnicity does not drive mortality outcomes.
Disclosures
Benken: BMS: Research Funding; CareDx: Research Funding; Transplant Genomics: Research Funding; Daiichi Sankyo: Research Funding; Verici Dx: Research Funding.
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