Risk Management and Treatment of Coagulation Disorders Related to COVID-19 Infection

Abstract

Coronavirus disease 2019 (COVID-19) is an emerging infectious disease. Bilateral pneumonia, acute respiratory failure, systemic inflammation, endothelial dysfunction and coagulation activation are key features of severe COVID-19. Fibrinogen and D-dimer levels are typically increased. The risk for venous thromboembolism is markedly increased, especially in patients in the intensive care unit despite prophylactic dose anticoagulation. Pulmonary microvascular thrombosis has also been described and the risk for arterial thrombotic diseases also appears to be increased while bleeding is less common than thrombosis, but it can occur. Evaluation for venous thromboembolism may be challenging because symptoms of pulmonary embolism overlap with COVID-19, and imaging studies may not be feasible in all cases. The threshold for evaluation or diagnosis of thromboembolism should be low given the high frequency of these events. Management and treatment are new challenges due to the paucity of high-quality evidence regarding efficacy and safety of different approaches to prevent or treat thromboembolic complications of the disease. All inpatients should receive thromboprophylaxis unless contraindicated. Some institutional protocols provide more aggressive anticoagulation with intermediate or even therapeutic dose anticoagulation for COVID-19 patients admitted to ICU. Therapeutic dose anticoagulation is always appropriate to treat deep venous thrombosis or pulmonary embolism, unless contraindicated. This article reviews evaluation and management of coagulation abnormalities in individuals with COVID-19.

Keywords: COVID-19; coagulopathy; deep vein thrombosis; pulmonary embolism; thromboprophylaxis; venous thromboembolism.

Figure 1

Computed tomography scan imaging of acute respiratory distress syndrome (ARDS) associated with COVID-19 and pulmonary emboli: pulmonary embolus across the bifurcation of the pulmonary trunk is noted, as indicated by the arrow.

Figure 2

(A) Extensive intra-alveolar hemorrhage, the alveolar spaces (alveolar septum yellow arrow) are filled by erythrocyte (green arrow) without fibrin and granulocytes (H&E 200 X) (B) Microvascular thrombi (H&E 100 X) in the arteriolar lumen (arteriole wall red arrow) there is microembolism consisting of fibrinous meshes that retain leukocytes and platelets (blue arrow).

Figure 3

(A) Macroscopic autopsy findings. Thrombi are noted in the lumen of the posterior tibial vein (blue arrow). (B) Histological examination (Masson’s trichrome 60 X), the antemortem thrombosis within the vein lumen (vein wall red arrow), which contain the so-called “lines of Zahn” (green arrow), representing the layerwise, alternating deposition of erythrocytes (yellow arrow), leukocytes and fibrin within the vessel lumen.