Anticoagulation in COVID-19
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Describing the background rationale, and evidence based indications for the use of anticoagulation in COVID-19 disease
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Anticoagulation in COVID-19
- 1. Khaled M. Taema Ass. Professor of Critical Care Medicine Cairo University
- 12. 31 %
- 13. 0.0% 5.0% 10.0% 15.0% 20.0% 25.0% 30.0% 35.0% Pneumonia ARDS Cardiac arrhythmias DIC AKI Septic shock Acute liver injury Myocarditis Endocarditis Bleeding The Egyptian experience Percent of complication
- 18. Infection
- 23. Lupus Anticoagulant Negative 55% Lupus Anticoagulant positive 45%
- 25. 0.0% 5.0% 10.0% 15.0% 20.0% 25.0% 30.0% 35.0% 28-Day mortality 30.3% 29.7% Heparin users Heparin non-users
- 29. Retrospective study > 18 Years old PCR positive for COVID-19 Mechanically ventilated CTPA done
- 30. 18 pts24 pts40 pts Standard dose thromboprophylaxis High dose thromboprophylaxis 0% 5% 10% 15% 20% 25% 30% 35% 40% 45% 50% 50 % 11 %
- 34. We previously reported markedly increased mortality after GAS infection in mice genetically engineered to carry human PLG, and showed that this increased susceptibility was dependent on the species-specific interaction of SK with PLG.10 Our data further suggested that local fibrin formation was critical to the host defense against microbial spread and that SK served to coopt the host fibrinolytic system to overcome fibrin-related immune surveillance mechanisms and barrier function. The current study confirms and extends these findings and demonstrates the critical role of thrombin generation in the host defense against GAS. Our findings identify important contributions from both the platelet and plasma FV pools to this process and suggest that the primary function of thrombin in this setting is focused on the generation of the fibrin matrix.
- 36. Pharmacologic VTE prophylaxis for all hospitalized patients with confirmed or highly suspected COVID-19 is recommended For all non-critically ill hospitalized patients (non-ICU) with confirmed or highly suspected COVID-19, standard dose VTE prophylaxis is recommended For critically ill patients (i.e., in an ICU) with confirmed or highly suspected COVID-19, increased doses of VTE prophylaxis (e.g., enoxaparin 40 mg subcutaneous twice daily, enoxaparin 0.5 mg/kg subcutaneous twice daily may be given For patients that are improving and transferring out of the ICU to the medical ward, it is reasonable to deescalate to standard VTE prophylaxis dosing
- 38. What? No studies compared different anticoagulants for thromboprophylaxis in acutely ill hospitalized patients with COVID-19 Studies on non COVID pts UFH LMWH Fondaparinux DOACs No in PE risk Bleeding risk
- 42. Managing Coagulopathy in Patients with COVID-19 What drug? Chronic anticoagulant users Outpatient Hospitalized patients
- 43. Hospitalized patients VTE prophylaxis, unless contraindicated (e.g., a patient has active hemorrhage or severe thrombocytopenia), should be prescribed using the recommendations for patients who have been admitted to a hospital for other indications Patients with COVID-19 who experience an incident thromboembolic event or who are highly suspected to have thromboembolic disease at a time when imaging is not possible should be managed with therapeutic doses of anticoagulant therapy. There are currently insufficient data to recommend either for or against using therapeutic doses of antithrombotic agents for COVID-19 in patients who are admitted to a hospital
- 44. Hospitalized patients Patients with COVID-19 who require extracorporeal membrane oxygenation or continuous renal replacement therapy or who have thrombosis of catheters or extracorporeal filters should be treated with therapeutic anticoagulation.
- 45. Post Discharge Routine post-discharge VTE prophylaxis is not recommended for patients with COVID-19. The benefits of post-discharge prophylaxis for certain high-risk patients may be warranted (rivaroxaban 10 mg daily for 31 to 39 days) • Modified IMPROVE-VTE score ≥4; or • Modified IMPROVE-VTE score ≥2 and D-dimer level >2 times the upper limit of normal; or • Age ≥75 years; or • Age >60 years and D-dimer level >2 times the upper limit of normal; or • Age 40 to 60 years, D-dimer level >2 times the upper limit of normal, and previous VTE event or cancer. High-risk patients
Editor's Notes
- The story started with the early autopsy studies that revealed microvascular thrombosis
- The cumulative incidence of thrombotic events were 31 %, The main form is the presence of Pulmonary embolism. All patients in this study received prophylactic anticoagulation with different protocols
- DIC was the 4th common complication in our series
- The significant correlation between IL6 and fibrinogen confirm the link between inflammation and procoagulant changes
- This endotheliopathy was previously described in sepsis patients
- Infection (whether its source) cause disruption of the Glycocalyx layer of the endothelium which cause leucocyre activation and thrombus formation.
- There is an evidence of direct invasion of the SARS-COV2 to the vascular endothelial cells. There is widescale expression of ACE2 receptors within the vascular endothelial cells.
- Another proposed mechanism for co-agulopathy included the activation of factor seven by the extracellular RNA
- A retrospective study including 449 patients
- Despite that there was no mortality difference with the use of anticoagulation in the whole population,
- There was mortality benefit with the anticoagulation use in patients with sepsis induced coagulopathy > 4 and those with D dimer > 6 upper limit of normal
- Study that evaluated 2773 patients
- Even rTPA was tried in a 3 cases series that revealed initial improvement in PF ratio yet then redecreased