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Coronavirus disease 2019 (COVID-19): Hypercoagulability

Coronavirus disease 2019 (COVID-19): Hypercoagulability


Coronavirus disease 2019 (COVID-19): Hypercoagulability


covid-19 hypercoagulability and cautiousness with convalescent plasma what is convalescent plasma covid 19 does convalescent plasma help covid

Hypercoagulable state: In COVID-19 disease a hypercoagulable state can be observed that usually associates acute inflammatory alteration & lab findings that’re different from that of acute disseminated intravascular coagulation (DIC), save for those with very severe disease. Fibrinogen & D-dimer levels are usually elevated, with typically only modest prolongation of PT & aPTT & mild thrombocytosis or thrombocytopenia. The finding of a lupus anticoagulant (LA) is common in subjects with a prolonged aPTT. Pathogenesis of these alterations is not completely understood, and there may be many contributing agents related to the acute inflammatory response to COVID-19.  


Risk of Thrombosis: The incidence of venous thromboembolism (VTE) is markedly elevated, particularly in ICU ptns, with case series findings of prevalence of about  25-43 % in ICU ptns, in the presence of prophylactic-dose anti-coagulation. Pulmonary microvascular thrombosis is also prevalent. In addition, the risk of arterial thrombotic events e.g. stroke, MI, and ischemic limbs have been also prevalent.


Lab testing: All ptns hospitalized with COVID-19 should have a basal profile of CBC with platelet count, PT, aPTT, fibrinogen, & D-dimer. Repeating these profile is performed according to ptn's clinical situation. OPD ptns do not require coagulation tests. The main target of profile is to provide prognostic interpretation that may be reflected on the level of ptn’s care.  


Imaging: Imaging tests are appropriately indicated for a suspected cases of VTE if available. If the standard diagnostic examinations are not available, other therapeutic options (e.g. compression ultrasonography) may be applied. Atypical lab alterations for COVID-19 should be further assessed.  


Management: Management is challenging due to the acuity of the illness and a paucity of high-quality evidence regarding efficacy and safety of different approaches to prevent or ttt thromboembolic complications of the disease. The following:

1)    Thromboprophylaxis: All hospitalized ptns should commence the thrombo-prophylaxis therapy unless there is contraindication. LMW is of choice, but unfractionated heparin may be used if LMW heparin is not available or if renal function is highly compromised. Some institutional regimens involve more aggressive form of anticoagulation with intermediate or even therapeutic-doses of anticoagulation for thrombo-prophylaxis. Ptns with no VTE are not currently provided thrombo-prophylaxis after discharge. An appropriate period of thrombo-prophylaxis after hospital discharge may be advised in selected cases.  

2)    VTE ttt: Therapeutic-dosage (full-dose) of anticoagulation therapy is warranted to ttt DVT & pulmonary embolism (PE), unless there’s clear contraindication. This regimen should be continued for minimum 3 mo.  

3)    Bleeding: Bleeding is less commonly observed than thrombosis but can be seen. If occurs, ttt is the same as in non-COVID-19 ptns that include [blood/plasma transfusion, anticoagulant reversing techniques, or particular products specified for an underlying bleeding disorder].  

4)    Areas of uncertainty: Participation in clinical trials is encouraged in order to improve understanding of the most effective and safest means of preventing and ttt thrombotic sequelae of COVID-19. Investigational disease-specific therapy may affect the thrombotic incidence, but the impact of these therapies on hemostasis in this cohort still uncertain.  



1.    Teuwen LA, Geldhof V, Pasut A, Carmeliet P. COVID-19: the vasculature unleashed. Nat Rev Immunol 2020; 20:389.

2.    Lowenstein CJ, Solomon SD. Severe COVID-19 Is a Microvascular Disease. Circulation 2020; 142:1609.

3.    Libby P, Lüscher T. COVID-19 is, in the end, an endothelial disease. Eur Heart J 2020; 41:3038.

4.    Middleton EA, He XY, Denorme F, et al. Neutrophil extracellular traps contribute to immunothrombosis in COVID-19 acute respiratory distress syndrome. Blood 2020; 136:1169.

5.    Hidalgo A. A NET-thrombosis axis in COVID-19. Blood 2020; 136:1118.

6.    Begbie M, Notley C, Tinlin S, et al. The Factor VIII acute phase response requires the participation of NFkappaB and C/EBP. Thromb Haemost 2000; 84:216.

7.    Magro C, Mulvey JJ, Berlin D, et al. Complement associated microvascular injury and thrombosis in the pathogenesis of severe COVID-19 infection: A report of five cases. Transl Res 2020; 220:1.

8.    Yu J, Yuan X, Chen H, et al. Direct activation of the alternative complement pathway by SARS-CoV-2 spike proteins is blocked by factor D inhibition. Blood 2020; 136:2080.

9.    Panigada M, Bottino N, Tagliabue P, et al. Hypercoagulability of COVID-19 patients in intensive care unit: A report of thromboelastography findings and other parameters of hemostasis. J Thromb Haemost 2020; 18:1738.

10.  Ranucci M, Ballotta A, Di Dedda U, et al. The procoagulant pattern of patients with COVID-19 acute respiratory distress syndrome. J Thromb Haemost 2020; 18:1747.




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fedo: Coronavirus disease 2019 (COVID-19): Hypercoagulability
Coronavirus disease 2019 (COVID-19): Hypercoagulability
Coronavirus disease 2019 (COVID-19): Hypercoagulability
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