Coagulation Dysfunction

Abstract

Context: The coronavirus disease 2019 (COVID-19) is a highly contagious respiratory disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Coagulation dysfunction is a hallmark in patients with COVID-19. Fulminant thrombotic complications emerge as critical issues in patients with severe COVID-19. Objective: To present a review of the literature and discuss the mechanisms of COVID-19 underlying coagulation activation and the implications for anticoagulant and thrombolytic treatment in the management of COVID-19. Data Sources: We performed a systemic review of scientific papers on the topic of COVID-19, online available via the PubMed NCBI, medRxiv, and Preprints as of May 15, 2020. We also shared our experience on the management of thrombotic events in patients with COVID-19. Conclusions: COVID-19-associated coagulopathy ranges from mild laboratory alterations to disseminated intravascular coagulation (DIC) with a predominant phenotype of thrombotic/multiple organ failure. Characteristically, high D-dimer levels on admission and/or continuously increasing concentrations of D-dimer is associated with disease progression and poor overall survival. SARS-CoV-2 infection triggers the immune-hemostatic response. Drastic inflammatory responses including, but not limited to, cytokine storm, vasculopathy, and NETosis may contribute to an overwhelming activation of coagulation. Hypercoagulability and systemic thrombotic complications necessitate anticoagulant and thrombolytic interventions, which provide opportunities to prevent or reduce “excessive” thrombin generation, while preserving “adaptive” hemostasis and bring additional benefit via their anti-inflammatory effect in the setting of COVID-19.

Characteristics of coagulation alteration in patients with COVID-19

“…Compared with moderate patients, severe patients more frequently had dyspnea and lymphopenia, with markedly higher levels of IL-2R, IL-6, IL-10, and TNF-α [8]. The severe inflammatory state secondary to COVID-19 leads to severe derangement of hemostasis and prominent alternation of coagulation parameters [4,[9][10][11]. It is generally believed that deterioration of coagulation parameters during the disease course is closely associated with COVID-19 worsening and death.…”

Why Is COVID-19 More Severe in Patients With Diabetes? The Role of Angiotensin-Converting Enzyme 2, Endothelial Dysfunction and the Immunoinflammatory System

“…Pulmonary oedema occurs due to excess fluid seeping out of the blood vessels in the lungs, affecting the exchange of gas (oxygen and carbon dioxide), leading to decreased SpO 2 , respiratory failure and ICU admission. Coagulopathy, including microvascular thrombosis and disseminated intravascular coagulopathy (DIC) (76,77) and lymphopaenia could be a predictor of mortality in severe COVID-19 (78). Lung scarring and fibrosis, a hyper-inflammatory marker that suggests tissue damage due to overactive, dysregulated inflammation, occurs in survivors of severe disease.…”

COVID-19 pandemic effect on early pregnancy: are miscarriage rates altered, in asymptomatic women?

“…There is conflicting evidence of vertical transmission [5,6]. Evidence of coagulation disorders in COVID-19 patients are rising, which have the potential to adversely affect pregnancies [7,8], particularly when combined with the inherent hypercoagulability of gestation.…”