Severe COVID-19 illness is associated with intense inflammation, leading to high rates of thrombotic complications that increase morbidity and mortality. Markedly elevated levels of D-dimer with normal fibrinogen levels are the hallmark laboratory findings of severe COVID-19– associated coagulopathy.
Prophylaxis against venous thromboembolism is paramount for all hospitalized patients, with more aggressive prophylaxis and screening recommended for patients with D-dimer levels above 3.0 μg/mL. Point-of-care ultrasonography is the imaging method of choice for patients at high risk, as it entails minimal risk of exposing providers to the virus.
Covid-19–associated coagulopathy (CAC) and disseminated intravascular coagulation are common in COVID-19 and are associated with severe illness and death. Critically ill patients without other risk factors for thrombosis can experience various thrombotic events, including microvascular thrombosis, venous and pulmonary thromboembolism, and acute arterial thrombosis.
This article discusses clinical manifestations of CAC, associated laboratory and histologic findings, recent evidence elucidating pathophysiologic mechanisms, and the way we manage it at Cleveland Clinic.
- We recommend measuring D-dimer, fibrinogen, prothrombin time, international normalized ratio, and activated partial thromboplastin time every 48 hours in hospitalized patients with COVID-19.
- Prophylaxis against venous thromboembolism is recommended for all COVID-19 patients on admission, using low-molecular-weight heparin, unfractionated heparin for those in renal failure, or fondaparinux for those with heparin-induced thrombocytopenia, even in the setting of thrombocytopenia as long as the platelet count is above 25 × 109/L.
- Patients with D-dimer levels 3.0 μg/mL or higher should undergo screening with point-of-care ultrasonography and receive more intensive prophylaxis.
A highly thrombotic state
The clinical presentation of CAC is that of a highly thrombotic state. Shared anecdotal experience from a variety of sources indicates that catheter-associated thrombosis and clotting of vascular access catheters are especially common problems. The need for catheter replacement and dialysis circuits that involve frequent interruption of continuous renal replacement therapy are other high-risk settings.
Two recent studies support the clinical impression that COVID-19 is highly thrombotic. Cui et al reported a 25% incidence of deep vein thrombosis in patients with severe coronavirus pneumonia. Klok et al found a 31% combined incidence of deep vein thrombosis, pulmonary embolism, and arterial thrombosis in critically ill patients with coronavirus. Of these events, 81% were pulmonary thromboembolic.
In Cleveland Clinic intensive care units, we are finding that point-of-care ultrasonography (POCUS) detects deep vein thrombosis at a rate of 25% to 30%, similar to rates in these studies. Another frequent finding is “slow venous flow.” This pattern, described as amorphous echogenicity in major veins, has been associated with a higher subsequent risk of deep vein thrombosis.