Management of Thrombotic Complications in COVID-19: An Update

Abstract

Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV‑2), is now a global pandemic. This virus primarily affects the respiratory tract and causes lung injury characterized by acute respiratory distress syndrome. Although the pathophysiology of COVID-19 is not yet clear, the most widely accepted mechanism is systemic inflammation. A clinically significant effect of the inflammation is coagulopathy. As a result of this effect, patients are found to have a high risk of venous thromboembolism. Studies have reported a high incidence of thrombotic complications in critically ill patients with COVID-19. In this review, we discuss the most updated evidence on the pathophysiology, diagnosis, and treatment of the coagulopathy of COVID-19. Prophylactic anticoagulation is recommended for all in-patients with COVID-19. Those with a higher risk of developing thromboembolic events or who have already developed venous thromboembolism should be treated with therapeutic anticoagulation. We also discuss post-discharge prophylaxis for high-risk patients and some newly proposed treatments for the hypercoagulability that could improve the outcomes of the affected patients.

Fig. 1

Management of coronavirus disease 2019 (COVID-19)-associated coagulopathy [22, 23, 27]. Afib atrial fibrillation, ARDS acute respiratory distress syndrome, BID twice a day, BMI body mass index, CBC complete blood count, CK creatinine kinase, CPK creatinine phosphokinase, Crcl creatinine clearance, CTPA computed tomography pulmonary angiography, CUS compression ultrasonography, DDI drug–drug interaction, DOAC direct oral anticoagulant, DVT deep vein thrombosis, ECMO extracorporeal membrane oxygenation, HDI hemodynamic instability, HIT heparin induced thrombocytopenia, ICU intensive care unit, IMPROVE International Medical Prevention Registry on Venous Thromboembolism, LDH lactate dehydrogenase, LMWH low-molecular-weight heparin, N no, O₂ oxygen, OAC oral anticoagulation, PE pulmonary embolism, PT prothrombin time, PTT partial thromboplastin time, QD once a day, RRT renal replacement therapy, SC subcutaneous, tPA tissue plasminogen activator, UFH unfractionated heparin, VTE venous thromboembolism, Y yes. *Moderate COVID-19: evidence of lower respiratory illness by clinical assessment or imaging, with SpO₂ > 93% on room air at sea level. Severe COVID 19: SpO₂ ≤ 93% on room air at sea level, respiratory rate > 30, PaO₂/FiO₂ < 300, or lung infiltrates > 50%. Associated with ARDS, sepsis, and septic shock. Can progress to critical illness with cardiac, hepatic, renal, and central nervous system disease. **Risk stratification: VTE: PADUA/IMPROVE/Wells’ scoring systems. DIC: ISTH scoring system. ^If patient taking a DOAC or warfarin as an outpatient for routine indications (Afib, mechanical heart valves, recurrent VTE), switch to a therapeutic dose of LMWH (preferred to UFH as no PTT monitoring required) to decrease DDI. If patient is placed on UFH, monitor anti-Xa levels instead of PTT as latter shown to increase in severely ill patients with COVID-19 and confound results. ^¥If CUS/CTPA is not feasible, consider bedside point-of-care ultrasonography or bedside cardiac ultrasound for unexplained acute right ventricular strain or intra-cardiac thrombus. ^€Hematology consultation when required. ^#Cardiopulmonary deterioration due to PE