Authors: Filipa Ribeiro Lucas, Emília Araújo, João Gigante, Soraia Silva, Yasar Yousafzai, Addisu Demeke Teklemariam, Anwar M. Hashem, Pedro Vieira, Maria Eugénia André, Steve Harakeh.
The emergence of the novel coronavirus, SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) has resulted in a major global pandemic posing various challenges to the worldwide health care systems. Clinical course of the infection, known as coronavirus disease of 2019 (COVID-19, ranges from mild subclinical disease to a life-threatening systemic illness. Common symptoms include a flu-like illness with fever and inflammation, and in severe cases pneumonia and systemic inflammation that results in morbidity and mortality. One of the complications of COVID-19 is its disruption of normal hemostasis resulting coagulopathy and thromboembolism. In this following review, we discuss present knowledge; summarize existing published information on the underlying mechanisms of action for COVID-19-associated coagulopathy; and propose algorithms for screening, management, and prevention of COVID-19 patients.
Many at-risk COVID-19 patients develop coagulopathies that can broadly be labelled as venous thromboembolism (VTE). These coagulopathies may occur separately or in combination, and include pulmonary embolism (PE), deep vein thrombosis (DVT) and acute large vessel occlusion resulting in stroke, myocardial infarction, ischemic and systemic arterial events. Laboratorybased testing is mandatory in the case of severely infected COVID-19 patients for screening of their coagulation status. Based on recent data, a major elevation in the levels of the D-dimer is used as a predictor of the adverse outcomes of the disease.
An imbalance between inflammation and coagulation may lead to a hypercoagulable state resulting in endothelial injury associated with a loss of dysregulation of fibrinolysis, excess thrombin generation, thrombi protective mechanisms, and thrombosis. Other involved mechanisms that may lead to an increased VTE risk, include the following: microvascular thrombosis, endothelial damage, leukocyte recruitment, systemic inflammation – the presence of the virus in endothelial cells, higher vascular permeability, destruction of cell membranes, platelet activation, and occlusion with ACE dysfunction, or even autoimmune mechanism. In all hospitalized COVID-19 patients, prophylaxis against thromboembolism is extremely important, especially in patients with elevated D-dimer levels and other coagulation abnormalities.
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