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Tran M, Sheth C, Bhandari R, et al. SARS-CoV-2 and pulmonary embolism: who stole the platelets?. Thromb J. 2020;18:16doi: 10.1186/s12959-020-00229-8.
Tran, M., Sheth, C., Bhandari, R., Cameron, S. J., & Hornacek, D. (2020). SARS-CoV-2 and pulmonary embolism: who stole the platelets?. Thrombosis journal, 1816. https://doi.org/10.1186/s12959-020-00229-8
Tran, Michael, et al. "SARS-CoV-2 and pulmonary embolism: who stole the platelets?." Thrombosis journal vol. 18 (2020): 16. doi: https://doi.org/10.1186/s12959-020-00229-8
Tran M, Sheth C, Bhandari R, Cameron SJ, Hornacek D. SARS-CoV-2 and pulmonary embolism: who stole the platelets?. Thromb J. 2020 Sep 03;18:16. doi: 10.1186/s12959-020-00229-8. eCollection 2020. PMID: 32905282; PMCID: PMC7467753.
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Thromb J. 2020 Sep 03;18:16. doi: 10.1186/s12959-020-00229-8. eCollection 2020.

SARS-CoV-2 and pulmonary embolism: who stole the platelets?.

Thrombosis journal

Michael Tran, Chirag Sheth, Rohan Bhandari, Scott J Cameron, Deborah Hornacek

Affiliations

  1. Heart Vascular and Thoracic Institute, Department of Cardiovascular Medicine, Section of Vascular Medicine, Cleveland Clinic Foundation, Desk J-35, Cleveland Clinic Foundation, Cleveland, OH 44195 USA.
  2. Department of Cardiovascular and Metabolic Sciences. Cleveland Clinic Lerner College of Medicine, Cleveland, OH 44195 USA.

PMID: 32905282 PMCID: PMC7467753 DOI: 10.1186/s12959-020-00229-8

Abstract

BACKGROUND: Patients infected with SARS-CoV-2 often develop venous and arterial thrombosis. The high patient mortality is partly attributed to thrombotic events. An emerging trend is the presence of immunological phenomena including antiphospholipid antibodies which may promote thrombosis. The mechanism for these observations is not clear though many patients with SARS-CoV-2 develop thrombocytopenia.

CASE PRESENTATION: We describe a patient with SARS-CoV-2 pneumonitis who presented with intermediate risk pulmonary embolism (PE). Careful attention to his daily platelet count suggested the possibility of immune mediated heparin-induced thrombocytopenia (HIT) which was confirmed by laboratory testing and resolved when anticoagulation was switched to a direct thrombin inhibitor.

CONCLUSIONS: Since excessive platelet activation and in situ thrombosis occur in HIT, this case underscores the need to consider that thrombocytopenia in patients with SARS-CoV-2-most of whom receive heparinoids-may be unrecognized HIT. A central role for the platelet in the etiology of thrombosis during the COVID-19 pandemic should be explored.

© The Author(s) 2020.

Keywords: COVID-19; HIT; Heparin; Pulmonary embolism; SARS-CoV-2; Thrombosis

Conflict of interest statement

Competing interestsNone.

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