Abstract
Hypercoagulability and thrombosis remain a challenge to diagnose and treat in severe COVID-19 infection. The ability of conventional global coagulation tests to accurately reflect in vivo hypo- or hypercoagulability is questioned. The currently available evidence suggests that markedly increased D-dimers can be used in identifying COVID-19 patients who may need intensive care unit (ICU) admission and close monitoring or not. Viscoelastic methods (VMs), like thromboelastography (TEG) and rotational thromboelastometry (ROTEM), estimate the dynamics of blood coagulation. The evaluation of coagulopathy by VMs in severe COVID-19 infection seems an increasingly attractive option. Available evidence supports that COVID-19 patients with acute respiratory failure suffer from severe hypercoagulability rather than consumptive coagulopathy often associated with fibrinolysis shutdown. However, the variability in definitions of both the procoagulant profile and the clinical outcome assessment, in parallel with the small sample sizes in most of these studies, do not allow the establishment of a clear association between the hypercoagulable state and thrombotic events. VMs can effectively provide insight into the pathophysiology of coagulopathy, detecting the presence of hypercoagulability in critically ill COVID-19 patients. However, it remains unknown whether the degree of coagulopathy can be used in order to predict the outcome, establish a diagnosis or guide anticoagulant therapy.
Highlights
Ill coronavirus disease 2019 (COVID-19) patients are at risk of developing hypoxia and excessive inflammation but, frequent thrombotic manifestations [1].Hypercoagulability and thrombosis remain a challenge to diagnose and treat in severe COVID-19 infections [2].Diagnostics 2020, 10, 817; doi:10.3390/diagnostics10100817 www.mdpi.com/journal/diagnosticsIn sepsis, the disturbance between components of the coagulation and fibrinolytic system leads to a variable clinical picture, tilting from an initial hypercoagulability towards a subsequent hypocoagulable disease state, depending on the phase of septic coagulopathy [3]
Bleeding complications are rare in severe COVID-19 patients, suggesting that disseminated intravascular coagulation (DIC) and consumption coagulopathy are not common complications of COVID-19, while pulmonary microthrombosis seems to be partially related with the pathophysiological mechanism of COVID-19-related acute respiratory distress syndrome (ARDS) [4]
Our search strategy combined terms or keywords that are related to COVID-19 infection (COVID-19, etc.) with those related to the viscoelastic methods for the identification of relevant articles
Summary
Ill coronavirus disease 2019 (COVID-19) patients are at risk of developing hypoxia and excessive inflammation but, frequent thrombotic manifestations [1].Hypercoagulability and thrombosis remain a challenge to diagnose and treat in severe COVID-19 infections [2].Diagnostics 2020, 10, 817; doi:10.3390/diagnostics10100817 www.mdpi.com/journal/diagnosticsIn sepsis, the disturbance between components of the coagulation and fibrinolytic system leads to a variable clinical picture, tilting from an initial hypercoagulability towards a subsequent hypocoagulable disease state, depending on the phase of septic coagulopathy [3]. Ill coronavirus disease 2019 (COVID-19) patients are at risk of developing hypoxia and excessive inflammation but, frequent thrombotic manifestations [1]. Hypercoagulability and thrombosis remain a challenge to diagnose and treat in severe COVID-19 infections [2]. The disturbance between components of the coagulation and fibrinolytic system leads to a variable clinical picture, tilting from an initial hypercoagulability towards a subsequent hypocoagulable disease state, depending on the phase of septic coagulopathy [3]. Bleeding complications are rare in severe COVID-19 patients, suggesting that disseminated intravascular coagulation (DIC) and consumption coagulopathy are not common complications of COVID-19, while pulmonary microthrombosis seems to be partially related with the pathophysiological mechanism of COVID-19-related acute respiratory distress syndrome (ARDS) [4]. The resultant enhanced procoagulant activity, in association with suppressed plasmin activity by the reduced urokinase-type plasminogen activator and increased plasminogen activator inhibitor-1 [5], contributes to fibrin deposition, forming localized/disseminated microthrombi and worse clinical outcomes [6,7]
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