Acute pulmonary embolism in COVID-19 related hypercoagulability
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Acute pulmonary embolism in COVID‑19 related hypercoagulability Cerruti Lorenzo1 · Boscaro Francesca1 · Poletto Francesco1 · Campello Elena1 · Spiezia Luca1 · Simioni Paolo1
© Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Since December 2019, a novel Coronavirus (SARS-CoV-2) was confirmed as the etiologic agent of a worldwide outbreak of a pneumonia that can result in severe respiratory failure. This clinical entity seems to be associated with a marked hypercoagulable state that causes both arterial and venous thromboembolic complications. Therefore, an adequate anti-thrombotic prophylaxis is recommended in hospitalized COVID-19 patients. Although rapidly worsening respiratory symptoms in a patient with SARS-CoV-2 respiratory infection may correlate with worsening pneumonia itself, it may also mask a pulmonary embolism. We report the case of a 50-year-old man affected by SARS-CoV-2 pneumonia, who developed acute pulmonary embolism. Keywords SARS-CoV-2 · COVID-19 · Coagulation · Interstitial pneumonia · Pulmonary embolism · Case report
Highlights • We reported a case of pulmonary embolism precipitating
worsening respiratory failure in a 50-year-old man with COVID-19 pneumonia. • Whole blood thromboelastometry profiles indicated that the patient was indeed in a severe hypercoagulable state. • Thromboelastometry could be a useful tool to screen for COVID-19 related hypercoagulability and to determine the optimal anticoagulant treatment.
Background Coronaviruses (CoVs) are enveloped, single-stranded RNA viruses that can cause respiratory, enteric and neurologic symptoms in humans [1]. In December 2019, a novel CoV caused an outbreak of severe pneumonia in Wuhan (China) Electronic supplementary material The online version of this article (https://doi.org/10.1007/s11239-020-02160-1) contains supplementary material, which is available to authorized users. * Spiezia Luca [email protected] 1
General Internal Medicine and Thrombotic and Haemorrhagic Diseases Unit, Department of Medicine, Padova University Hospital, Padua, Italy
and quickly spread worldwide soon thereafter. This clinical entity was later defined by the World Health Organization as Coronavirus Disease 2019 (COVID-19) and its etiologic agent was named Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) [2]. Zhou et al. identified that older age, D-dimer levels > 1 μg/mL, and higher SOFA score on admission were associated with higher odds of in-hospital death [3]. Our recent findings revealed that most severe COVID-19 patients—admitted to the Intensive Care Unit for respiratory failure—present a predominant hypercoagulable state that could lead to arterial and venous thromboembolic complications [4]. It has been reported that the infection causes endothelial dysfunction and an inflammatory state that results in increased thrombin generation and reduced fibrinolysis [5]. Furthermore, hypoxia from severe pneumonia may also promote thrombosis, resulting in higher blood viscosity [6]. The presence of occlus
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