COVID‐19 critical illness pathophysiology driven by diffuse pulmonary thrombi and pulmonary endothelial dysfunction responsive to thrombolysis. Issue 2 (5th June 2020)

• Record Type: Journal Article
• Authors: Poor, Hooman D.; Ventetuolo, Corey E.; Tolbert, Thomas; Chun, Glen; Serrao, Gregory; Zeidman, Amanda; Dangayach, Neha S.; Olin, Jeffrey; Kohli‐Seth, Roopa; Powell, Charles A.
• Is Part Of: Clinical and translational medicine. Volume 10:Issue 2(2020)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2020-06-05
• Subjects: COVID‐19 -- thrombolysis -- tissue plasminogen activator -- tPA; Clinical medicine -- Periodicals; Medicine, Experimental -- Periodicals; Medical innovations -- Periodicals; Molecular biology -- Periodicals; Pathology, Molecular -- Periodicals; 616.027
• DOI: 10.1002/ctm2.44
• Languages: English
• ISSNs: 2001-1326

Abstract

Abstract: Patients with severe COVID‐19 disease have been characterized as having the acute respiratory distress syndrome (ARDS). Critically ill COVID‐19 patients have relatively well‐preserved lung mechanics despite severe gas exchange abnormalities, a feature not consistent with classical ARDS but more consistent with pulmonary vascular disease. Many patients with severe COVID‐19 also demonstrate markedly abnormal coagulation, with elevated d ‐dimers and higher rates of venous thromboembolism. We present four cases of patients with severe COVID‐19 pneumonia with severe respiratory failure and shock, with evidence of markedly elevated dead‐space ventilation who received tPA. All showed post treatment immediate improvements in gas exchange and/or hemodynamics. We suspect that severe COVID‐19 pneumonia causes respiratory failure via pulmonary microthrombi and endothelial dysfunction. Treatment for COVID‐19 pneumonia may warrant anticoagulation for milder cases and thrombolysis for more severe disease.