A pulmonary embolism (PE) is a sudden blockage in one of the pulmonary arteries, usually caused by a blood clot (thrombus) that traveled from a deep vein, often in the leg. Since the pandemic began, medical professionals have recognized that SARS-CoV-2 infection significantly increases the risk of developing this life-threatening complication. This heightened risk has made the prevention and management of blood clots a central focus in the care of people with COVID-19.
The Confirmed Link: COVID-19 and Blood Clots
Studies consistently demonstrate that COVID-19 infection is an independent risk factor for developing blood clots, including deep vein thrombosis and pulmonary embolism. The virus causes hypercoagulability, meaning the blood becomes unusually prone to clotting, an effect more pronounced than in other severe viral pneumonias. This is particularly evident in individuals with severe illness requiring hospital care.
The incidence of pulmonary embolism in people hospitalized with COVID-19 has been reported to be around 7.1% in large studies. This risk is substantially higher for those admitted to the Intensive Care Unit (ICU), where the incidence of PE can rise to approximately 13.7% in critically ill patients. Developing a PE is associated with a greater risk of severe events, including respiratory failure and increased mortality. Furthermore, the infection can cause widespread microthrombi, or tiny clots, to form within the small blood vessels of the lungs.
How COVID-19 Triggers Clot Formation
The increased clotting risk is driven by the virus’s ability to trigger a massive inflammatory response, often termed “thromboinflammation.” The SARS-CoV-2 virus can directly damage the endothelium, the specialized layer of cells lining the inside of blood vessels. This damage causes the vessel surface to shift from a smooth, non-stick lining to a rough, pro-clotting surface.
The systemic inflammatory state, or “cytokine storm,” releases high levels of signaling molecules, such as interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α). These cytokines activate the coagulation cascade, promoting the formation of fibrin, the protein mesh that forms the structural basis of a clot. This immune activation also primes white blood cells to release Neutrophil Extracellular Traps (NETs), web-like structures that serve as scaffolds for clot formation.
The infection also causes activation and dysfunction of platelets, the cell fragments responsible for initiating blood clotting. Platelets in people with COVID-19 become hyperreactive and release procoagulant microvesicles, enhancing the body’s clotting ability. This combined effect of inflammation, endothelial injury, and platelet overdrive creates an environment where blood clots form easily, contributing directly to pulmonary embolism.
Identifying High-Risk Factors
Certain clinical characteristics and pre-existing conditions place individuals at a greater risk of developing a pulmonary embolism during or shortly after a COVID-19 infection. The most significant predictor is the severity of the illness, with those requiring intensive care or mechanical ventilation facing the highest risk. The degree of inflammation and clotting activity can be measured by monitoring the blood marker D-dimer; an elevated D-dimer level indicates increased risk for PE.
Advanced age and specific underlying health issues also contribute to susceptibility to clotting complications. Conditions such as obesity, cardiovascular disease, and diabetes are linked to poor outcomes in COVID-19 and increase the likelihood of PE. Prolonged immobility or bed rest, common during severe illness, compounds the risk by slowing blood flow and encouraging the formation of deep vein thrombi that can travel to the lungs.
Prevention and Treatment Approaches
To mitigate the risk of pulmonary embolism, standard medical practice involves administering prophylactic anticoagulants, or blood thinners, to individuals hospitalized with COVID-19. This preventative treatment typically involves low-molecular-weight heparin or similar agents, given in low doses to reduce clot formation without significantly increasing the risk of major bleeding. For high-risk patients with extremely elevated clotting markers, such as D-dimer, physicians may consider increasing the dose to a full therapeutic level, even if a clot has not yet been confirmed.
When a pulmonary embolism is diagnosed, acute treatment focuses on therapeutic anticoagulation, using higher doses of blood thinners to stop the clot from growing and allow the body to break it down naturally. In severe cases where the PE is large or causes hemodynamic instability (meaning it significantly affects the heart and blood pressure), physicians may use thrombolytic drugs. These “clot-busting” medications rapidly dissolve the existing clot and restore blood flow to the lungs. Vaccination remains important, as reducing the severity of the initial COVID-19 infection inherently lowers the risk of developing a serious clotting complication like PE.