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COVID-19 Curbside Consults

Update to coagulopathy in COVID-19: Manifestations and management

Simon R. Mucha, MD, Siddharth Dugar, MD, Keith McCrae, MD, Douglas Joseph, DO, John Bartholomew, MD, Gretchen L. Sacha, PharmD, RPh, BCCCP and Michael Militello, PharmD, RPh, BCPS
Cleveland Clinic Journal of Medicine June 2021, DOI: https://doi.org/10.3949/ccjm.87a.ccc024-up
Simon R. Mucha
Critical Care Medicine, Respiratory Institute, Cleveland Clinic; Clinical Instructor, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH
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Siddharth Dugar
Pulmonary Medicine, Cleveland Clinic; Clinical Assistant Professor, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH
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Keith McCrae
Hematology and Medical Oncology, and Cellular and Molecular Medicine, Cleveland Clinic; Professor, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH
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Douglas Joseph
Cardiovascular Medicine, Cleveland Clinic; Assistant Professor, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH
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John Bartholomew
Cardiovascular Medicine, Cleveland Clinic; Professor, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH
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  • For correspondence: [email protected]
Gretchen L. Sacha
Inpatient Pharmacy, Cleveland Clinic
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Michael Militello
Inpatient Pharmacy, Cleveland Clinic
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    Figure 1

    A short-axis view of the femoral vein (FV) and the femoral artery (FA) at the site of the saphenous vein (SV) inflow. Amorphous echogenicity in the femoral vein, greater than that of the adjacent femoral artery, is suggestive of slow venous flow. The vein was fully compressible, ruling out deep vein thrombosis at the site.

  • Figure 4
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    Figure 4

    Algorithm for preventing and treating COVID-19-associated coagulopathy.

    FEU = fibrinogen equivalent units

Tables

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    TABLE 1

    Cleveland Clinic approach to anticoagulation prophylaxis and management in COVID-19

    Category 1
    D-dimer < 3.0 μg/mL FEU Standard prophylaxis
    Category 2
    D-dimer ≥ 3.0 μg/mL FEU High-intensity prophylaxis
    Category 3
    Confirmed VTE Full anticoagulation
    StandardEnoxaparin 40 mg subcutaneously every 24 hoursEnoxaparin 40 mg subcutaneously every 12 hoursIV heparin per DVT/PE nomogram or enoxaparin 1 mg/kg subcutaneously every 12 hours
    Renal failureCrCl 10–30 mL/min: Enoxaparin 30 mg subcutaneously every 24 hours
    CrCl < 10 mL/min or AKIa: Unfractionated heparin 5,000 U subcutaneously every 12 hours
    CRRT: Unfractionated heparin 500 U/hour through circuit
    Circuit clotting: IV heparin per ACS nomograma
    CrCl < 30 mL/min or AKI: Enoxaparin 40 mg subcutaneously every 24 hours
    CrCl < 10 mL/min or AKIa: Unfractionated heparin 7,500 U subcutaneously every 12 hours
    CRRT: Unfractionated heparin 500 U/hour through circuit
    Circuit clotting: IV heparin per ACS nomograma
    IV heparin per DVT/VTE nomogram
    Obesity Standard> 100 kg: Enoxaparin 40 mg subcutaneously every 12 hours
    > 120 kg: Enoxaparin 60 mg subcutaneously every 12 hours
    > 100 kg: Enoxaparin 60 mg subcutaneously every 12 hours
    > 120 kg: Enoxaparin 80 mg subcutaneously every 12 hours
    IV heparin per DVT/PE nomogram
    or
    Enoxaparin 1 mg/kg subcutaneously every 12 hours, up to 150 mg
    Above 150 kg use unfractionated heparin
    Renal failure
    CrCl < 30 mL/ min or AKIb
    ≤ 120 kg: 7,500 U every 12 hours
    > 120 kg: 10,000 U every 12 hours
    CRRT: 500 U/h through circuit
    Circuit clotting: IV heparin per ACS nomograma
    ≤ 120 kg: 7,500 U every 8 hours
    > 120 kg: 10,000 U every 8 hours
    CRRT: 500 U/h through circuit
    Circuit clotting: IV heparin per ACS nomograma
    IV heparin per DVT/PE nomogram
    • ↵a IV heparin ACS nomogram: initial dose 60-U/kg bolus, then 12 U/kg/hour; target aPTT 49–67 seconds; target heparin anti-Xa 0.2–0.5 units/mL.

    • ↵b AKI definition: doubling of creatinine in 48 hours or anuria.

    • ACS = acute coronary syndrome; AKI = acute kidney injury; aPTT = activated partial thromboplastin time; CrCl = creatinine clearance; CRRT = continuous renal replacement therapy; DVT = deep vein thrombosis; FEU = fibrinogen equivalent units; IV = intravenous; PE = pulmonary embolism; VTE = venous thromboembolism

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  • Figure 2 (video). Another short-axis view of the femoral vein (center) and the femoral artery (bottom right) at the site of the saphenous vein inflow (top right). Swirling pattern of high echogenicity suggests low-flow state.

  • Figure 3 (video). Long-axis view of the femoral vein, with spontaneous echogenicity and slow flow.

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Cleveland Clinic Journal of Medicine: 92 (5)
Cleveland Clinic Journal of Medicine
Vol. 92, Issue 5
1 May 2025
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Update to coagulopathy in COVID-19: Manifestations and management
Simon R. Mucha, Siddharth Dugar, Keith McCrae, Douglas Joseph, John Bartholomew, Gretchen L. Sacha, Michael Militello
Cleveland Clinic Journal of Medicine Jun 2021, DOI: 10.3949/ccjm.87a.ccc024-up

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Update to coagulopathy in COVID-19: Manifestations and management
Simon R. Mucha, Siddharth Dugar, Keith McCrae, Douglas Joseph, John Bartholomew, Gretchen L. Sacha, Michael Militello
Cleveland Clinic Journal of Medicine Jun 2021, DOI: 10.3949/ccjm.87a.ccc024-up
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    • ABSTRACT
    • INTRODUCTION
    • A HIGHLY THROMBOTIC STATE
    • LABORATORY FINDINGS: ELEVATED D-DIMER
    • SEVERE LUNG DAMAGE FROM INFLAMMATION, THROMBOSIS
    • PATHOPHYSIOLOGY: INFLAMMATION PROMOTES THROMBOSIS
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