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Haemostatic abnormalities are associated with mortality in COVID-19

Presented By
Dr Yu Hu, Wuhan Union Hospital, China
EHA 2021

COVID-19 causes a variety of abnormalities in thrombosis and haemostasis. Several studies have demonstrated that the severity grade of coagulopathies is significantly associated with the severity of COVID-19 disease progression and mortality.

COVID-19 is a systemic infectious disease affecting various organ systems and thus causing a broad variety of symptoms, including haematological abnormalities, such as thrombosis, embolism, and petechiae [1]. In a single-centre, retrospective cohort study (n=380) looking at complications of 55 non-survivors, acute respiratory distress syndrome was present in 69%, septic shock in 20%, disseminated intravenous coagulation (DIC) in 15% and venous thromboembolism (VTE) in 5% [2]. Dr Yu Hu (Wuhan Union Hospital, China) discussed coagulopathies in COVID-19 in further detail [3].

Dr Hu noted that patients with fatal COVID-19 had a significantly higher level of D-dimer compared with COVID-19-survivors, as well as increased activated partial thromboplastin time (aPTT), increased prothrombin time (PT), and decreased fibrinogen levels. Results from a meta-analysis evaluating 24 studies demonstrated that PT values at baseline were significantly associated with risk stratification and prognosis. D-dimer at baseline was associated with stratification [4]. Platelet count was significantly decreased in patients who died from COVID-19 (P<0.001). The incidence of thrombocytopenia in non-survivors (n=55) was 63.6% versus 15.3% in survivors (n=176).

Three studies from China indicated that nadir platelet count was associated with the risk of in-hospital death (P<0.05), with 92.1% mortality in patients with 0–50 x 109 platelets/L and 61.2% mortality in patients with 50–100 x 109 platelets/L at nadir platelet count [5–7]. Thrombotic microangiopathy was confirmed by histopathology from autopsy, thrombi mostly being red thrombi formed by fibrin network and red blood cells.

The incidence of DIC has also been associated with disease severity and mortality, but numbers differed markedly between studies, ranging from 0.1–2.7% in survivors and from 14.6–71.4% in non-survivors [4,8,9]. Dr Hu hypothesised that the discrepancies in DIC incidence may be due to a lack of recognition of COVID-19-associated DIC at the beginning of the outbreak, the complexity of both COVID-19 and DIC, and the lack of a golden standard for DIC diagnosis.

Mechanisms of COVID-19-associated coagulopathy include systematic inflammation, endothelial dysfunction (by direct infection and secondary damage), and platelet activation (SARS-CoV-2 directly binds and enhances platelet activation in vitro).

In summary, coagulopathy is one of the important causes of death in COVID-19 patients and should be closely monitored by clinicians. Given the various haematological abnormalities in COVID-19, timely therapeutic intervention with anticoagulant therapy could improve prognosis.

    1. Gupta A, et al. Nat Med 2020;26(7):1017–32.
    2. Liao D, et al. Lancet Haematology 2020:7(9)e671–8.
    3. Hu Y. Abnormalities in thrombosis and haemostasis in patients with COVID-19. P214-1, EHA 2021 Virtual Congress, 9–17 June.
    4. Luo L, et al. Aging 2020:12(16):15918–37.
    5. Yang X, et al. J Thromb Haemost. 2020;18(6):1469–72.
    6. Liu Y, et al. Platelets 2020;31(4):490–6.
    7. Zhao X, et al. EPMA Journal 2020;11(2):139–
    8. Helms J, et al. Intensive Care Med 2020;46(6):1089–98.
    9. Tang N, et al. J Thromb Haemost. 2020;18(4):844–7.


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