Current Medical Issues

: 2021  |  Volume : 19  |  Issue : 4  |  Page : 303--305

Is coagulopathy a prognosis determining factor in COVID-19?

Muhammed Jasim Abdul Jalal 
 Department of Internal Medicine and Rheumatology, VPS Lakeshore Hospital, Kochi, Kerala, India

Correspondence Address:
Dr. Muhammed Jasim Abdul Jalal
Department of Internal Medicine and Rheumatology, VPS Lakeshore Hospital, Nettoor P. O., Maradu, NH 47 – Byepass, Kochi - 682 040, Kerala

How to cite this article:
Jalal MJ. Is coagulopathy a prognosis determining factor in COVID-19?.Curr Med Issues 2021;19:303-305

How to cite this URL:
Jalal MJ. Is coagulopathy a prognosis determining factor in COVID-19?. Curr Med Issues [serial online] 2021 [cited 2022 May 27 ];19:303-305
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Full Text

Dear Sir,

Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2). It has become a global public health issue with regard to its high transmissibility likely airborne, and rapid spread to nearly all countries. It may lead to coagulopathy and disseminated intravascular coagulation (DIC) making the prognosis worse and increasing the mortality rate.[1] The rate of COVID-19 complicated by DIC has been reported as 0.6% for survivors and 71.4% for nonsurvivors.[1] The management of COVID-19 is challenging when it comes to coagulopathy and DIC.[2] In this article, I am trying to highlight coagulopathy in COVID-19.

Severe COVID-19 can be considered sepsis with regard to the third International Consensus Definitions as it is a viral infection affecting the respiratory system causing pneumonia and acute respiratory distress syndrome.[3],[4] Prolonged bed rest in severe COVID-19 patients increases the risk of venous thromboembolism (VTE).[2] Thromboembolism is associated with increased mortality in severe COVID-19.[2] This explains the need for anticoagulation in severe COVID-19 patients.[5],[6]

Zhang et al. studied seven patients with COVID-19 who had significant extremity ischemia and suggested that hypercoagulable state of severe COVID-19 patients requires immediate care as it affects the overall prognosis.[7] These seven patients had elevated D-dimer and fibrinogen degradation products. This trial with elevated D-dimer possibly points to increased thromboembolic events which results in severe COVID. However, the elevated D-dimer may also be due to systemic inflammation such as C-reactive protein.

Wang et al. studied the clinical characteristics of 138 hospitalized patients with 2019, novel coronavirus-infected pneumonia in Wuhan, China. They retrospectively demonstrated a significant difference in D-dimer levels of 138 patients between those with and without the need of intensive care unit (ICU).[8] Elevated D-dimer and fibrinogen degradation products are linked with the formation of multiple microthrombi in the body and are associated with mortality outcomes in severe COVID-19.[2]

Fox et al. published the first autopsy series from New Orleans demonstrating pulmonary and cardiac pathology in COVID-19. Vascular congestion along with vascular endothelial and intimal injury in the cardiovascular system, alveolar septal edema, thrombus in capillaries, and microthrombus in hepatic portal region were some of their autopsy findings.[9] These results show that in a few patients with critical COVID-19 who died had evidence of endothelial activation and microthrombi in the lung which could possibly be one of the pathogenic mechanisms in COVID-19 severe illness.

Vascular endothelial cells and immune system tissues have angiotensin-converting enzyme 2 (ACE2). SARS-CoV-2 may directly attack vascular endothelial cells through ACE2.[10] Vascular endothelial injury results in cytokine storm damaging microvascular system and activates coagulation system by inhibiting fibrinolysis.

Severe COVID-19 causes hypoxia which increase blood viscosity and induce thrombosis. A hypoxia-inducible transcription factor-dependent signaling pathway is responsible for this hypoxia-induced thrombosis.[11]

Tang et al. studied the effect of anticoagulation on mortality in severe COVID-19. They compared 28-day mortality between cases receiving and not receiving heparin. The mortality was found lower in severe COVID-19 patients with coagulopathy who received anticoagulation. Thus, anticoagulation had a better prognosis in severe COVID-19 patients with coagulopathy.[1]

In conclusion, D-dimer and fibrinogen degradation products do have a role in determining the prognosis of COVID-19. Elevated D-dimer and fibrinogen degradation products increase the mortality rate in COVID-19 and are associated with poor prognosis. Thus, coagulopathy should be monitored in COVID-19 patients. Thrombosis prophylaxis should be given to all COVID-19 patients depending on the severity of COVID-19, body mass index, and creatinine clearance (CrCl) to prevent coagulopathy-associated complications in COVID-19 [Table 1].[12]{Table 1}

Among patients admitted to the ICU with COVID-19, intermediate-dose prophylactic anticoagulation, compared with standard-dose prophylactic anticoagulation, did not result in a significant difference in the primary outcome of venous or arterial thrombosis, treatment with extracorporeal membrane oxygenation, or mortality within 30 days.[6]

Parenteral anticoagulants are indicated in any acutely ill hospitalized patients. Hence, it is indicated in moderate, severe, and critical disease. Low-molecular-weight heparin (LMWH)/fondaparinux is preferred over unfractionated heparin (UFH), due to lesser patient contact of health-care staff and no need of activated partial thromboplastin time (aPTT) monitoring (necessitating patient contacts). Enoxaparin is the most preferred LMWH.

Dosing of anticoagulation:[13]

Standard weight-adjusted prophylactic dose in moderate disease (standard risk patient): (e.g., enoxaparin 40 mg once daily for a 70 kg adult with CrCl >30 mL/min)Intermediate dose LMWH in severe and critical disease (high-risk patient: requiring invasive ventilation/continuous positive airway pressure/noninvasive ventilation/high-flow nasal oxygen): (enoxaparin 40 mg two times per day for a 70 kg adult with CrCl >30 mL/min)Therapeutic dose in diagnosed/highly suspected macrothrombosis (PE/deep vein thrombosis): (enoxaparin 1 mg/kg 12 hourly subcutaneous or 1.5 mg/kg subcutaneously once daily)Enoxaparin with dose reduction is the preferred over other LMWH drugs/fondaparinux in renal insufficiency. UFH with aPTT monitoring indicated at estimated glomerular filtration rate <15 mL/min.

Anticoagulation in moderate to severe and critical cases of COVID-19 is advisable. Enoxaparin is the preferred LMWH for anticoagulation in acute phase of VTE. Postdischarge prophylaxis may be considered in patients with high risk of thromboembolic events after assessing the bleeding risk. Rivaroxaban and apixaban are preferred for postdischarge prophylaxis.

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Conflicts of interest

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