SARS-CoV-2 and pulmonary embolism: who stole the platelets?
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CASE REPORT
Open Access
SARS-CoV-2 and pulmonary embolism: who stole the platelets? Michael Tran1*, Chirag Sheth1, Rohan Bhandari1, Scott J. Cameron2
and Deborah Hornacek1
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. Keywords: Pulmonary embolism, HIT, SARS-CoV-2, COVID-19, Thrombosis, Heparin
Background Critically ill patients with COVID-19 infection often have multiple abnormalities in hemostasis and thrombosis. Recent literature documents hematologic derangements including mild thrombocytopenia [1], elevated d-dimer [2], prolonged activated partial-thromboplastin time (aPTT), and disseminated intravascular coagulation (DIC) [3]. It is unclear whether these changes reflect SARS-CoV-2 infection, or an inflammatory state of acute illness. The recent medical literature reports multiple anticoagulation strategies to prevent thrombotic events in patients infected with SARS-CoV-2. Emerging reports suggest the possibility of HIT developing in SARS-CoV-2 patients receiving heparin anticoagulation [4, 5]. This case was a diagnostic * Correspondence: [email protected] 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 Full list of author information is available at the end of the article
dilemma since both thrombocytopenia and in situ pulmonary thrombosis are common features of SARS-CoV-2 infection [6], making less common diagnoses, such as HIT, which shares similar features, more challenging to diagnose.
Case presentation A 62-year-old man with type 2 diabetes mellitus presented to the emergency department (ED) with 4-day history fever, cough, and dyspnea. The patient’s vitals in the ED were as follows: Temperature 39.2 °C (102.6 °F), blood pressure 167/67 mmHg, heart rate 135 beats per min, respiratory rate 22 breaths per minute, oxygen saturation 74% on room air. The SaO2 improved to 96% wi
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