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Tytuł:
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COVID-19 critical illness pathophysiology driven by diffuse pulmonary thrombi and pulmonary endothelial dysfunction responsive to thrombolysis.
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Autorzy:
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Poor HD; Division of Pulmonary, Critical Care, and Sleep Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
Ventetuolo CE; Department of Medicine and Health Services, Policy and Practice, Alpert Medical School of Brown University, Providence, Rhodes Island, USA.
Tolbert T; Division of Pulmonary, Critical Care, and Sleep Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
Chun G; Division of Pulmonary, Critical Care, and Sleep Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
Serrao G; Division of Cardiology, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
Zeidman A; Division of Nephrology, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
Dangayach NS; Departments of Neurosurgery and Neurology, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
Olin J; Division of Cardiology, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
Kohli-Seth R; Department of Surgery, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
Powell CA; Division of Pulmonary, Critical Care, and Sleep Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
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Źródło:
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Clinical and translational medicine [Clin Transl Med] 2020 Jun; Vol. 10 (2), pp. e44. Date of Electronic Publication: 2020 Jun 05.
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Typ publikacji:
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Journal Article
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Język:
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English
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Imprint Name(s):
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Publication: 2020- : [Hoboken, NJ] : Wiley
Original Publication: Heidelberg : Springer-Verlag
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References:
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Clin Transl Med. 2020 Jun;10(2):e44. (PMID: 32508062)
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Grant Information:
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R01 HL141268 United States HL NHLBI NIH HHS
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Contributed Indexing:
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Keywords: COVID-19; tPA; thrombolysis; tissue plasminogen activator
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Entry Date(s):
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Date Created: 20200609 Latest Revision: 20210110
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Update Code:
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20240104
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PubMed Central ID:
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PMC7288983
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DOI:
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10.1002/ctm2.44
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PMID:
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32508062
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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.
(© 2020 The Authors. Clinical and Translational Medicine published by John Wiley & Sons Australia, Ltd on behalf of Shanghai Institute of Clinical Bioinformatics.)
Update of: medRxiv. 2020 Apr 21;:. (PMID: 32511632)
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