32 min

VTE rate, "COVID toes," and Virchow's triad: What you need to know about COVID and coagulation Blood & Cancer

    • Medicine

Adam C. Cuker, MD, joins host David H. Henry, MD, to discuss recent findings regarding coagulation in COVID-19 patients. Both Dr. Cuker and Dr. Henry both practice at the Hospital of the University of Pennsylvania in Philadelphia.
Dr. Cuker cited data suggesting at least 25%-30% of patients with COVID-19 develop venous thromboembolism (VTE), despite receiving prophylactic anticoagulation. Furthermore, COVID-19 patients have presented with “lots of different thrombotic manifestations,” he said. This includes stroke and “COVID toes syndrome,” a condition in which patients present with ischemic toes, which appears to have a thromboembolic etiology.
Dr. Cuker suggested that all three aspects of Virchow’s triad may be at play in patients with COVID-19 who have thrombotic manifestations, including:
Circulatory stasis (in patients who are immobilized/sedated/prone/paralyzed). Hypercoagulability (inflammation, high levels of factor VIII and fibrinogen, neutrophil extracellular traps). Endothelial injury (SARS-CoV-2 may infect endothelial cells via ACE2). Dr. Cuker notes that high D-dimer correlates with disease severity and prognosis in COVID-19 patients. He also compares COVID-19 to heparin-induced thrombocytopenia (HIT), noting that both are associated with venous and arterial thromboses. And, like HIT patients, those with COVID-19 may require therapeutic-intensity anticoagulation to prevent clots.
Dr. Cuker says his hospital’s recommendations for anticoagulation in COVID-19 patients are as follows:
Stable hospitalized patients should receive standard-intensity prophylaxis. ICU patients should receive intermediate- or therapeutic-intensity anticoagulation (at the discretion of the provider). On discharge, patients should receive low-dose rivaroxaban (Xarelto) at 10 mg daily for 30 days as prophylaxis. A nonhospitalized patient who has no risk factors for thrombotic events should not receive thromboprophylaxis. Dr. Cuker also discusses two recent publications on thrombosis and anticoagulation in COVID-19 patients. In one study, thrombotic events occurred in 31% of COVID-19 patients admitted to the ICU at three Dutch hospitals (Thromb Res. 2020 Apr 10. pii: S0049-3848(20)30120-1).
Another study suggested that systemic anticoagulation may improve outcomes of patients hospitalized with COVID-19 (J Am Coll Cardiol. 2020 May 5. pii: S0735-1097(20)35218-9).
Show notes by Emily Bryer, DO, resident in the department of internal medicine, University of Pennsylvania, Philadelphia.
Disclosures:
Dr. Henry has no financial disclosures relevant to this episode.
Dr. Cuker has served as a consultant for Synergy CRO. His institution has received research support on his behalf from Alexion, Bayer, Pfizer, Novo Nordisk, Sanofi, Spark, and Takeda.
*  *  * 
For more MDedge Podcasts, go to mdedge.com/podcasts
Email the show: podcasts@mdedge.com
Interact with us on Twitter: @MDedgehemonc
David Henry on Twitter: @davidhenrymd
 
 
 

Adam C. Cuker, MD, joins host David H. Henry, MD, to discuss recent findings regarding coagulation in COVID-19 patients. Both Dr. Cuker and Dr. Henry both practice at the Hospital of the University of Pennsylvania in Philadelphia.
Dr. Cuker cited data suggesting at least 25%-30% of patients with COVID-19 develop venous thromboembolism (VTE), despite receiving prophylactic anticoagulation. Furthermore, COVID-19 patients have presented with “lots of different thrombotic manifestations,” he said. This includes stroke and “COVID toes syndrome,” a condition in which patients present with ischemic toes, which appears to have a thromboembolic etiology.
Dr. Cuker suggested that all three aspects of Virchow’s triad may be at play in patients with COVID-19 who have thrombotic manifestations, including:
Circulatory stasis (in patients who are immobilized/sedated/prone/paralyzed). Hypercoagulability (inflammation, high levels of factor VIII and fibrinogen, neutrophil extracellular traps). Endothelial injury (SARS-CoV-2 may infect endothelial cells via ACE2). Dr. Cuker notes that high D-dimer correlates with disease severity and prognosis in COVID-19 patients. He also compares COVID-19 to heparin-induced thrombocytopenia (HIT), noting that both are associated with venous and arterial thromboses. And, like HIT patients, those with COVID-19 may require therapeutic-intensity anticoagulation to prevent clots.
Dr. Cuker says his hospital’s recommendations for anticoagulation in COVID-19 patients are as follows:
Stable hospitalized patients should receive standard-intensity prophylaxis. ICU patients should receive intermediate- or therapeutic-intensity anticoagulation (at the discretion of the provider). On discharge, patients should receive low-dose rivaroxaban (Xarelto) at 10 mg daily for 30 days as prophylaxis. A nonhospitalized patient who has no risk factors for thrombotic events should not receive thromboprophylaxis. Dr. Cuker also discusses two recent publications on thrombosis and anticoagulation in COVID-19 patients. In one study, thrombotic events occurred in 31% of COVID-19 patients admitted to the ICU at three Dutch hospitals (Thromb Res. 2020 Apr 10. pii: S0049-3848(20)30120-1).
Another study suggested that systemic anticoagulation may improve outcomes of patients hospitalized with COVID-19 (J Am Coll Cardiol. 2020 May 5. pii: S0735-1097(20)35218-9).
Show notes by Emily Bryer, DO, resident in the department of internal medicine, University of Pennsylvania, Philadelphia.
Disclosures:
Dr. Henry has no financial disclosures relevant to this episode.
Dr. Cuker has served as a consultant for Synergy CRO. His institution has received research support on his behalf from Alexion, Bayer, Pfizer, Novo Nordisk, Sanofi, Spark, and Takeda.
*  *  * 
For more MDedge Podcasts, go to mdedge.com/podcasts
Email the show: podcasts@mdedge.com
Interact with us on Twitter: @MDedgehemonc
David Henry on Twitter: @davidhenrymd
 
 
 

32 min