Pulmonary embolism in dogs is almost always caused by an underlying disease rather than occurring on its own. A blood clot forms elsewhere in the body, travels through the bloodstream, and lodges in the arteries of the lungs, blocking blood flow. The most common triggers include immune-mediated hemolytic anemia, Cushing’s disease, kidney disease that causes protein loss, heartworm infection, cancer, and sepsis.
How Blood Clots Form and Reach the Lungs
Three conditions set the stage for a clot to develop: sluggish blood flow, damage to blood vessel walls, and blood that clots too easily. In veterinary medicine, these are the same three factors (known collectively as Virchow’s triad) that explain clot formation in humans. Most dogs that develop pulmonary embolism have at least one underlying illness pushing their blood toward a hypercoagulable state, meaning the normal balance between clotting and clot-dissolving tips heavily toward clotting.
Once a clot forms, typically in a deep vein of the legs or abdomen, it can break free and travel through the right side of the heart into the pulmonary arteries. A large clot can block a major artery and cause sudden cardiovascular collapse. Smaller clots may lodge in branch arteries, reducing oxygen exchange in the lungs more gradually.
Immune-Mediated Hemolytic Anemia (IMHA)
IMHA is one of the most dangerous triggers for pulmonary embolism in dogs. In this condition, the immune system attacks and destroys the dog’s own red blood cells. That destruction activates the clotting system in two ways: it releases clotting factors directly, and fragments of destroyed red blood cells clump together, forming aggregates that can seed clots. In one retrospective study of 72 dogs with IMHA, thromboemboli were found in 20 of 25 dogs that underwent postmortem examination, and the overall mortality rate was 58%. Blood clots, including those in the lungs, are the leading cause of death in dogs with IMHA.
Risk factors that made thromboembolism more likely in those dogs included severe drops in platelet count, elevated bilirubin (a marker of red blood cell destruction), and low albumin levels. Anticlotting therapy is now considered a critical part of IMHA treatment specifically because of how frequently these dogs develop emboli.
Cushing’s Disease
Dogs with hyperadrenocorticism, commonly called Cushing’s disease, produce excessive amounts of cortisol. That hormone excess creates a perfect storm for clotting. Cortisol increases the production of several clotting factors, suppresses the body’s natural clot-dissolving system (fibrinolysis), and lowers antithrombin activity. Antithrombin is one of the body’s key brakes on clot formation, so when its levels drop, clots form more readily.
Research has shown that even dogs given the steroid prednisone (a synthetic form of cortisol) develop measurably lower antithrombin levels. This means dogs on long-term steroid therapy for other conditions also carry an elevated clotting risk, not just dogs with naturally occurring Cushing’s. The hypercoagulable state in Cushing’s disease involves multiple overlapping mechanisms, which is part of why it’s such a significant risk factor.
Protein-Losing Kidney Disease
When a dog’s kidneys are damaged in a way that allows protein to leak into the urine, a condition called protein-losing nephropathy (PLN), the risk of blood clots rises substantially. The traditional explanation is that the kidneys lose antithrombin along with albumin, tipping the balance toward excessive clotting. However, a 2024 study of 150 dogs with kidney-related protein loss found that antithrombin was below the reference range in only 1 of 7 dogs that developed clots, suggesting the full mechanism is more complex than antithrombin loss alone.
Low albumin levels themselves were associated with clotting events in these dogs. The relationship between protein loss and thrombosis likely involves several disrupted pathways, but the clinical takeaway is clear: dogs diagnosed with PLN are at meaningful risk for pulmonary embolism and are often placed on preventive anticlotting medication.
Other Common Underlying Causes
Several additional diseases are well-documented triggers:
- Heartworm disease. Adult heartworms living in the pulmonary arteries cause direct damage to vessel walls and chronic inflammation, both of which promote local clot formation. Dead or dying worms after treatment can also trigger acute emboli.
- Cancer. Many tumors release substances that activate the clotting cascade. Certain cancers, particularly hemangiosarcoma and carcinomas, are especially prone to causing a body-wide clotting disorder called disseminated intravascular coagulation (DIC), which can send clots to the lungs.
- Sepsis. Severe infection causes widespread inflammation that damages blood vessel walls and activates clotting throughout the body.
- Protein-losing enteropathy. Similar to kidney-based protein loss, this intestinal condition causes proteins (including clotting regulators) to leak from the gut, shifting the balance toward hypercoagulability.
- Trauma and surgery. Physical injury to blood vessels, combined with reduced mobility and blood flow during recovery, can trigger clot formation.
- Blood transfusions and certain chemotherapy drugs. Both are recognized risk factors, likely through activation of clotting pathways or vessel wall damage.
Signs That Suggest a Pulmonary Embolism
Dogs with pulmonary embolism typically show sudden respiratory distress. The onset is often acute, developing over hours rather than days. In one case series, the median time from first symptom to full respiratory crisis was just one day. Common signs include rapid or labored breathing, coughing, exercise intolerance, weakness, and collapse. Gums may appear pale or bluish due to poor oxygen delivery. Some dogs show no warning signs before a sudden collapse, particularly when a large clot blocks a major pulmonary artery.
These symptoms overlap with many other respiratory and cardiac conditions, which makes pulmonary embolism notoriously difficult to diagnose without imaging. A blood test measuring D-dimer levels (a protein fragment released when clots break down) can help screen for the condition. In dogs, a D-dimer level above 0.3 mg/L has shown 100% sensitivity for detecting pulmonary embolism, meaning it catches essentially all true cases. However, specificity is only about 71%, so elevated D-dimer can also occur with other conditions. It’s a useful rule-out test: a normal result makes PE very unlikely, but an elevated result needs confirmation.
How Pulmonary Embolism Is Confirmed
CT angiography is the most definitive diagnostic tool available in veterinary medicine. It involves injecting contrast dye and taking rapid CT images of the chest to visualize blood flow through the pulmonary arteries. Veterinarians look for complete blockage of a pulmonary artery or filling defects, areas where contrast dye flows around a clot rather than through the vessel normally. Both central clots in the main arteries and smaller peripheral clots in branch vessels can be identified this way. CT angiography requires anesthesia and specialized equipment, so it’s typically performed at veterinary specialty or emergency hospitals.
Treatment and Outlook
Treatment centers on two goals: dissolving or preventing further growth of existing clots, and treating the underlying disease that triggered the embolism. Anticoagulant therapy is the mainstay. Injectable heparin is commonly used in the hospital setting for immediate clot prevention, though it requires repeated injections that are difficult for owners to manage at home. Newer oral anticoagulants are being studied for longer-term use in dogs, with early research suggesting certain doses can achieve blood-thinning levels comparable to what works in humans.
Oxygen support is critical for dogs in respiratory distress. Many require hospitalization with supplemental oxygen until their breathing stabilizes. Dogs with DIC or severe underlying disease may need plasma transfusions to replenish natural clotting regulators.
Prognosis depends heavily on the underlying cause and how much lung tissue is affected. Dogs with IMHA-related pulmonary embolism face particularly high mortality. Dogs whose underlying condition can be controlled, such as those with treatable Cushing’s disease or heartworm infection, generally have a better chance of recovery. Early recognition of risk and preventive anticoagulant therapy in high-risk patients, like those with IMHA or protein-losing diseases, is one of the most effective strategies for improving outcomes.