Venous thromboembolism (VTE) is a condition in which a blood clot forms in a vein. It affects up to 900,000 people in the United States each year and kills an estimated 60,000 to 100,000 of them. VTE is actually an umbrella term that covers two related problems: deep vein thrombosis (DVT), where a clot forms in a deep vein, and pulmonary embolism (PE), where a clot travels to the lungs.
How DVT and PE Are Connected
A DVT typically starts in the lower leg, thigh, or pelvis, though clots can also form in the arms. The clot itself may cause local symptoms, but the real danger comes when part of it breaks free and travels through the bloodstream to the lungs. That’s a pulmonary embolism, and it can be life-threatening. Not every DVT leads to a PE, and not every PE has an identifiable DVT that preceded it, but the two conditions are closely linked enough that doctors treat them as a single disease spectrum.
What Causes Blood Clots to Form
Three conditions drive clot formation: sluggish blood flow, damage to the blood vessel wall, and changes in the blood that make it clot more easily. When one or more of these factors is present, the risk of VTE rises. Sluggish flow is the most intuitive. Blood pooling in the legs during long stretches of immobility, whether from bed rest after surgery, a long-haul flight, or hospitalization, gives clots the opportunity to develop.
Beyond immobility, a long list of triggers can push the body toward clotting. Surgery, trauma, fractures, cancer, pregnancy, acute infections, and having a central IV line all count as provoking factors. Other contributors build risk more gradually: obesity, use of hormonal birth control or hormone therapy, older age, a sedentary lifestyle, and even corticosteroid use.
Genetics play a surprisingly large role. Roughly 50 to 60 percent of the variation in who gets VTE is attributed to genetic effects. The strongest known genetic risk factor is a mutation in one of the clotting genes (called Factor V Leiden), which makes a protein in the clotting pathway resistant to being switched off. Carrying one copy of this variant raises VTE risk two to seven times; carrying two copies raises it 15 to 20 times. Having a non-O blood type is another common inherited factor that modestly increases risk.
Symptoms of DVT
DVT often announces itself in one leg. You may notice swelling, pain or cramping that starts in the calf, skin that turns red or purple, and warmth over the affected area. Sometimes the symptoms are subtle enough to be dismissed as a muscle strain. In some cases, a DVT produces no noticeable symptoms at all, which is part of why VTE can be so dangerous. A clot you don’t know about can still break loose.
Symptoms of Pulmonary Embolism
PE symptoms tend to be more dramatic and harder to ignore. The hallmark is sudden shortness of breath that occurs even at rest and worsens with activity. Chest pain is common, often sharp and most noticeable when you breathe in deeply, cough, or bend over. Some people describe it as feeling like a heart attack. A rapid or irregular heartbeat is another frequent sign, and in severe cases, a sudden drop in heart rate or blood pressure can cause fainting.
The severity depends on the size of the clot and how much lung tissue it blocks. A small PE may cause mild breathlessness that’s easy to attribute to something else. A large one can be fatal within minutes. Any combination of sudden breathlessness, chest pain, and a racing heart warrants emergency evaluation.
How VTE Is Diagnosed
The two halves of VTE are diagnosed with different tools. For a suspected DVT, the standard test is a duplex ultrasound, which uses sound waves to visualize blood flow in the veins and spot blockages. It’s noninvasive and widely available. Doctors often pair it with a D-dimer blood test, which measures a substance released when a clot breaks down. A negative D-dimer result is useful for ruling VTE out. A positive result doesn’t confirm a clot on its own (inflammation and other conditions can raise D-dimer levels), but it tells clinicians to keep looking.
For a suspected PE, the gold standard is a CT pulmonary angiography (CTPA). This specialized CT scan involves injecting contrast dye into a vein and imaging the blood vessels in the lungs to look for clots directly.
Prevention in Hospitals
Hospitalized patients face elevated VTE risk from immobility, surgery, and acute illness, so prevention is a routine part of inpatient care. For patients at increased clot risk who aren’t likely to bleed, guidelines recommend blood-thinning medications during the hospital stay. For patients who are bleeding or at high risk of bleeding, mechanical options like inflatable compression sleeves on the legs are used instead. These devices squeeze the calves rhythmically to keep blood moving. Compression stockings are another option, though evidence that they reduce symptomatic clots is limited, and they can sometimes cause skin breakdown.
Outside the hospital, the same principles apply on a smaller scale. Moving regularly during long flights or car rides, staying active, maintaining a healthy weight, and discussing clot risk with a doctor before surgery or when starting hormonal medications all help reduce risk.
Long-Term Complications
Even after a clot is treated, VTE can leave lasting effects. Between 20 and 50 percent of people who have a DVT go on to develop post-thrombotic syndrome, a chronic condition caused by damage the clot inflicted on the vein and its valves. Symptoms include ongoing swelling, pain, heaviness, and skin changes in the affected leg. In about 5 percent of those cases, venous ulcers (open sores on the skin) develop over the following decade. Post-thrombotic syndrome has no simple fix and can significantly reduce quality of life.
PE carries its own long-term risk. A small percentage of people who survive a pulmonary embolism develop chronic thromboembolic pulmonary hypertension (CTEPH), a condition where unresolved clot material in the lungs permanently raises blood pressure in the pulmonary arteries. The incidence is estimated at around 1 percent within six months of a PE and roughly 3 percent by one year. It rarely appears more than two years after the initial event. CTEPH causes progressive shortness of breath and exercise intolerance, and it requires specialized treatment.