COVID-19 Coagulopathy: Current knowledge and guidelines on anticoagulation

Abstract

COVID-19-associated coagulopathy (CAC) is a feature of COVID-19 that can lead to various thrombotic complications and death. In this review, we briefly highlight possible etiologies, including direct cytotoxicity caused by the SARS-CoV-2 virus, and the activation of proinflammatory molecules such as cytokines, underlying coagulopathy. Endothelial dysfunction has been highlighted as pivotal, irrespective of the mechanism involved in CAC. Specific features of CAC distinguishing it from disseminated intravascular coagulopathy and sepsis or ARDS-associated coagulopathy have been discussed. We have also highlighted some hematological parameters, such as elevated D-dimers and partial prothrombin and prothrombin times prolongation, which can guide the use of anticoagulation in critically ill patients. We conclude by highlighting the importance of prophylactic anticoagulation in all COVID-19 hospitalized patients and reiterate the need for institution-specific guidelines for anticoagulation COVID-19 patients since individual institutions have different patient populations.

Prevalence of Venous Thromboembolism in Critically Ill Patients With Coronavirus Disease 2019: A Meta-Analysis

“…The mechanisms of the vulnerability of critically ill patients with COVID-19 to VTE events remain undetermined. Several possible mechanisms have been suggested according to previous clinical and preclinical studies, including cytokine storm with activation of leukocytes, endothelium, and platelets resulting in upregulation of tissue factor, activation of coagulation, thrombin generation and fibrin formation, and deranged coagulation with imbalances in plasminogen activator inhibitor-1, tissue factor pathway inhibitor, and activated protein C that promotes fibrin generation and limits fibrinolysis, hypoxic vaso-occlusion, and direct viral effects with cell activation ( 49 – 52 ). Future studies are needed to determine whether these are specific to SARS-CoV-2 infection or a final common pathway in the thromboinflammatory response to viral infections and a marker of disease severity.…”

Coagulation and wound repair during COVID-19

“…1 C ). This tissue damage leads to cytokine production, stimulating increased expression of tissue factor on endothelial cells and exposure of TF to activate the coagulation pathway,leading to the cleavage of prothrombin to thrombin ( 37 , 38 ). Interestingly, while tissue factor protein levels are increased in COVID-19 patients, the transcripts are not elevated ( 39 , 40 ), indicating that regulation of SARS-CoV-2 induced thrombotic events is complex.…”

“…COVID-19 patients have been reported to have high levels of PAI-1 and D-dimers in their blood ( 49 , 50 ), consistent with the microthrombi observed in COVID-19 patient autopsies. Confoundingly, intra-alveolar hemorrhage has also been observed in COVID-19 lungs and elevated levels of pro-fibrinolytic uPA and tPA have been associated with reduced respiratory function and more severe disease ( 37 )). Excessive levels of uPA and tPA can lead to breakdown of fibrin before damaged areas have been sufficiently repaired ( Fig.…”

“…Retrospective studies have determined that lethal SARS-CoV-2 cases had higher D-dimer and fibrin degradation products in their blood ( 55 , 56 ). These patients also had longer prothrombin time and met criteria consistent with disseminated intravascular coagulopathy ( 37 ). Similarly, low platelet counts and prolonged activated partial thromboplastin time were associated with more severe disease ( 57 ).…”

Ophthalmic Outpatient and Inpatient Care Under Pandemic Conditions: Hygiene, Triage and New Challenges

“…vaskulitischen Ereignissen einhergehen können [48 -50]. Als mögliche Mechanismen werden hierbei eine direkte Zytotoxizität durch das SARS-CoV-2-Virus, die Aktivierung proinflammatorischer Zytokine ("Zytokinsturm") sowie eine endotheliale Dysfunktion diskutiert [51,52].…”