COVID-19 Associated Coagulopathy and Thrombotic Complications

Abstract

The SARS-CoV-2 virus caused a global pandemic within weeks, causing hundreds of thousands of people infected. Many patients with severe COVID-19 present with coagulation abnormalities, including increase D-dimers and fibrinogen. This coagulopathy is associated with an increased risk of death. Furthermore, a substantial proportion of patients with severe COVID-19 develop sometimes unrecognized, venous, and arterial thromboembolic complications. A better understanding of COVID-19 pathophysiology, in particular hemostatic disorders, will help to choose appropriate treatment strategies. A rigorous thrombotic risk assessment and the implementation of a suitable anticoagulation strategy are required. We review here the characteristics of COVID-19 coagulation laboratory findings in affected patients, the incidence of thromboembolic events and their specificities, and potential therapeutic interventions.

Extensive Arterial Thrombus Following Discharge after a Covid-19 Infection

“…The proinflammatory cytokines that increase over the course of infection activate the coagulation cascade by multiple mechanisms, including increased expression of tissue factor and endothelial activation. 2 , 3 Critical patients are more prone to thromboembolic complications, while patients treated in the general wards are also under risk. Lodigiani et al.…”

“…The novel coronavirus pandemic is associated with coagulopathy and an increased risk of thromboembolic events. 1 , 2 Most reports of thromboembolism are venous; however, severe arterial thrombi are reported and can worsen the prognosis of Covid-19 patients. Below described is a case of an extensive arterial thrombus in the left leg of a patient that occurred after discharge from Covid-19 pneumonia.…”

Systemic arterio-venous thrombosis in COVID-19: A pictorial review

“…CAC is postulated to be one of the significant causes for sudden deaths in this pandemic especially those occurring out of hospitals[ 2 ]. Literature is still emerging regarding the epidemiology and pathophysiology behind CAC with reported incidence of venous and arterial thromboembolism between 10%-25% among the COVID-19 admitted patients, with increase in incidence up to 31%-59% amongst those in intensive care[ 3 - 5 ]. The pro-coagulant state has been attributed to macrophage and endothelial cell mediated processes culminating in the acceleration of fibrin synthesis and suppression of its degradation[ 2 ].…”

A case report of multisite arterial thrombosis in a patient with coronavirus disease 2019 (COVID-19)

“…Different theories have been considered to explain this manifestation, such as the increase in the vasoconstrictor angiotensin II, the decrease in the vasodilator angiotensin, and the sepsis-induced release of cytokines. 3 …”