Infection with the SARS-CoV-2 virus, which causes COVID-19, has been linked to an increased risk of developing blood clots, a condition known as coagulopathy. This connection is well-established, particularly among patients experiencing severe illness or requiring hospitalization. Deep Vein Thrombosis (DVT) is a serious form of blood clotting that occurs in the body’s deep veins. Its occurrence is notably higher in people affected by COVID-19 than in the general population, involving a complex interplay between the virus and the body’s vascular and immune systems.
Deep Vein Thrombosis: A Basic Overview
Deep Vein Thrombosis (DVT) is the formation of a blood clot within a deep vein, most commonly in the legs, thighs, or pelvis. These clots can partially or completely block blood flow, leading to symptoms like swelling, pain, and warmth in the affected limb. The greatest danger of DVT lies in its potential to cause a Pulmonary Embolism (PE).
A PE occurs if a fragment of the clot breaks away and travels through the bloodstream, lodging in the arteries of the lungs. This blockage impedes blood flow and oxygen exchange, quickly becoming life-threatening and requiring emergency medical care. DVT and PE are collectively referred to as Venous Thromboembolism (VTE).
How COVID-19 Triggers Clot Formation
The SARS-CoV-2 virus promotes clot formation through several distinct biological pathways that create a state of “thromboinflammation.”
Endothelial Dysfunction
One primary mechanism is Endothelial Dysfunction, where the virus attacks the endothelial cells lining the blood vessels, causing damage and inflammation. This direct injury disrupts the vessel wall’s natural anti-clotting properties and triggers the coagulation cascade.
Cytokine Storm and Hypercoagulability
COVID-19 also induces a powerful, exaggerated immune response often referred to as a cytokine storm. Pro-inflammatory molecules like Interleukin-6 (IL-6) and Interleukin-8 (IL-8) are released in large quantities, which directly activate platelets and clotting factors. This systemic inflammation creates a hypercoagulable state.
Neutrophil Extracellular Traps (NETs)
The heightened inflammatory environment leads to the formation of Neutrophil Extracellular Traps (NETs). These are web-like structures released by immune cells to trap pathogens. NETs, along with activated platelets, accelerate the clotting process and contribute to the dense microthrombi often observed in the lungs of severely ill patients.
Identifying Risk Factors and Warning Signs
The likelihood of developing DVT during a COVID-19 infection is strongly influenced by patient factors and illness severity. Advanced age is an independent risk factor, with risk increasing significantly for those in their sixties and beyond. Pre-existing conditions such as obesity, diabetes, and cardiovascular disease also increase the vulnerability to clotting events.
The most significant risk factor is the severity of the COVID-19 infection itself, especially for patients requiring hospitalization, ICU admission, or mechanical ventilation. Prolonged immobility due to severe illness, whether in the hospital or at home, further compounds the risk by slowing blood flow in the deep veins. Elevated levels of the blood marker D-dimer, which indicates the breakdown of blood clots, are also highly associated with DVT in COVID-19 patients.
DVT Warning Signs
Recognizing the physical warning signs of DVT is important for early diagnosis. Symptoms typically affect only one leg and include sudden or gradual swelling, pain or tenderness that feels like a cramp, and skin that is warm to the touch. The affected area may also appear red or discolored.
Pulmonary Embolism (PE) Symptoms
If a DVT progresses to a PE, the symptoms become more urgent. These can include sudden shortness of breath, sharp chest pain that worsens with deep breathing, and a rapid heart rate. Other emergency signs are coughing up blood, feeling faint, or experiencing dizziness. Any of these signs should prompt immediate medical attention, as a PE is a life-threatening emergency.
Treatment and Prevention Strategies
For hospitalized COVID-19 patients, a standard preventative strategy involves the use of prophylactic anticoagulants, or blood thinners, unless there is a high risk of bleeding. Low-molecular-weight heparin (LMWH) is the preferred agent for this preventive measure, administered to reduce the chance of clot formation during the acute phase of illness. The level of anticoagulation may be intensified for critically ill patients due to their high risk.
Another important preventative measure is early and consistent physical mobilization for patients who are able. Even small movements help to maintain blood flow and prevent venous stasis, or pooling of blood, that contributes to clot formation. For patients who are unable to move, mechanical devices such as intermittent pneumatic compression may be used to help circulate blood in the legs.
When a DVT or PE is confirmed through imaging, the standard treatment shifts to therapeutic anticoagulation. This involves higher doses of blood thinners to dissolve the existing clot and prevent new ones. The initial treatment often involves injectable medications like LMWH. Following the acute phase, patients are typically transitioned to oral anticoagulants for a minimum duration of three months to ensure full resolution of the clot and reduce the risk of recurrence.