Aortic Thromboembolism in Dogs and Cats

TL;DR. Aortic thromboembolism, commonly known as a saddle thrombus, is a sudden and life-threatening veterinary emergency where a blood clot blocks blood flow to a pet's hind limbs, causing severe pain and paralysis.

A saddle thrombus lodges at the aortic trifurcation, completely blocking blood flow to the hind limbs.

What is it?

Aortic thromboembolism (ATE)—often referred to as a "saddle thrombus" or feline aortic thromboembolism (FATE) in cats—is one of the most sudden, painful, and severe cardiovascular emergencies in veterinary medicine. The condition occurs when a blood clot (thrombus) forms inside the heart, breaks free, and travels down the main artery of the body (the aorta).

The aorta acts as the primary highway for oxygen-rich blood leaving the heart. As it travels toward the back of the body, it eventually splits into smaller branches that supply blood to each of the hind legs. This split is known as the aortic trifurcation. Because of the narrowing at this fork, a traveling blood clot frequently gets stuck right at the junction, straddling the split like a saddle. This blockage completely or partially cuts off the blood supply to one or both hind limbs, leading to a rapid and devastating lack of oxygen (ischemia) in the leg muscles and nerves.

When tissues are deprived of oxygen and glucose, a cascade of cellular damage begins. Within hours, muscle cells begin to die, a process known as rhabdomyolysis. This cellular breakdown releases dangerous levels of potassium and inflammatory proteins into the local tissues. At the same time, the sciatic and femoral nerves, which run down the hind limbs, are highly sensitive to oxygen deprivation. When their blood supply is cut off, they stop conducting electrical signals, leading to sudden paralysis (paresis) and a loss of reflexes.

For pet owners, understanding this condition is critical because it strikes without warning. A pet who appeared perfectly healthy moments before may suddenly collapse, lose the use of their back legs, and cry out in extreme distress. Immediate veterinary intervention is the only option to manage the intense pain and attempt to restore circulation.

Causes & risk factors

The vast majority of aortic thromboembolism cases are secondary to underlying heart disease. In cats, the primary culprit is hypertrophic cardiomyopathy (HCM), a disease that causes the heart muscle to become abnormally thick. When the heart muscle thickens, the left atrium (one of the upper chambers of the heart) often stretches and enlarges. This enlargement disrupts normal blood flow, causing blood to pool and stagnate in the chamber, which highly predisposes the cat to clot formation.

A leading veterinary internal medicine reference describes this risk:

"Marked LA enlargement is thought to magnify the risk for thromboembolus formation, although TE events occasionally occur in cats with relatively normal LA size. Neoplastic and systemic inflammatory disease are occasionally associated with systemic thromboemboli in cats. Hyperthyroidism may be a risk factor for TE disease in cats independent of its cardiac effects."

Male cats are statistically at a higher risk for developing thromboembolic disease, though this bias is primarily due to the higher prevalence of hypertrophic cardiomyopathy in male felines.

In dogs, the causes of systemic blood clots are often different and are frequently linked to conditions that create a "hypercoagulable state" (a tendency for the blood to clot too easily). These underlying triggers in dogs include:

• Cushing's disease (hyperadrenocorticism)
• Protein-losing kidney diseases (nephrotic syndrome)
• Immune-mediated hemolytic anemia (IMHA)
• Cancer (neoplasia)
• Sepsis or severe systemic infections
• Pancreatitis
• Severe trauma
• Hypothyroidism

Signs to watch for

The clinical signs of a saddle thrombus are dramatic and develop almost instantly. Recognizing these signs immediately can mean the difference between life and death for your pet.

Cardinal Signs (Emergency Red Flags)

• Severe, acute pain: Pets will often scream, howl, or pant heavily due to the sudden, excruciating pain of muscle ischemia.
• Posterior paresis or paralysis: The sudden inability to use one or both hind legs. Affected pets will often drag their back legs behind them.
• Absent arterial pulses: The femoral pulses (located in the inner thigh) will be weak or completely undetectable in the affected limbs.
• Acute limb weakness: A sudden onset of weakness in the legs, even if the pet can still slightly move them.

Common Signs

• Cool distal limbs: The hind paws and lower legs will feel noticeably cold to the touch compared to the rest of the body.
• Pale or cyanotic footpads and nailbeds: Because of the lack of blood flow, the skin of the footpads and the beds of the claws will look stark white, blue, or purple.
• Tachypnea (rapid breathing) and Dyspnea (labored breathing): While rapid breathing can indicate fluid in the lungs from concurrent heart failure, it is frequently a direct response to intense pain.
• Vocalization: Continuous crying out or groaning.
• Hypothermia: A dangerously low body temperature, often caused by poor systemic circulation.
• Azotemia: A buildup of nitrogenous waste products in the blood, indicating that the kidneys are suffering from poor blood perfusion or secondary damage.

Occasional Signs

• Contracture of affected muscles: Over the first 24 to 48 hours, the muscles of the hind legs (especially the calves) may become extremely hard, swollen, and painful to the touch due to muscle cell death.
• Heart murmurs, gallop sounds, or arrhythmias: Abnormal heart sounds detected by a veterinarian during an exam, indicating underlying cardiac disease.

Pale or bluish footpads and cold paws are classic clinical signs of a saddle thrombus.

How vets diagnose it

When you arrive at the emergency clinic, your veterinarian will perform a rapid physical examination focusing on the "five Ps" of vascular obstruction: Pain, Paresis (paralysis), Pulselessness, Pallor (paleness), and Poikilothermia (coldness). If these signs are present in the hind limbs, a presumptive diagnosis of aortic thromboembolism is made immediately, and pain management is started.

To confirm the diagnosis and evaluate the underlying cause, your vet will perform several key diagnostic tests:

• Echocardiography (Cardiac Ultrasound): This is the gold standard for identifying the underlying heart disease. The vet will look for left atrial enlargement and may even visualize an active, swirling clot (sometimes called "smoke" or spontaneous echo contrast) inside the heart.
• Abdominal Ultrasonography: An ultrasound of the abdomen allows the veterinarian to trace the aorta down to the split in the hind legs and directly visualize the blood clot blocking the vessel.
• Doppler Flow Studies: A Doppler probe is placed against the arteries of the hind paws to listen for the sound of rushing blood. In an affected limb, there will be complete silence, confirming a lack of blood flow.
• Thoracic Radiography (Chest X-rays): Because many of these pets have underlying heart disease, X-rays are vital to check for congestive heart failure (fluid in the lungs) before starting aggressive fluid therapy. A prominent veterinary critical care manual notes:

"It is important to note that patients who have suffered FATE often exhibit tachypnea that presumably is a manifestation of pain. In this patient population, tachypnea is inconsistently associated with congestion and it is therefore appropriate to obtain thoracic radiographs before administering diuretics to patients with FATE."

• Measurement of Muscle Enzymes: Blood tests will often show massive elevations in muscle enzymes like creatine kinase (CK) and aspartate aminotransferase (AST). These enzymes leak into the blood when muscle cells are severely damaged by a lack of oxygen.
• Thromboelastography (TEG): This specialized blood test measures the overall clotting efficiency of the blood, helping vets determine if the pet's body is in a hypercoagulable state.
• Angiography: This involves injecting a contrast dye into the bloodstream and taking rapid X-rays to map out exactly where the blood flow stops. While highly accurate, it has largely been replaced by non-invasive ultrasound techniques.

Echocardiography is the gold standard for identifying left atrial enlargement and active clot formation.

Treatment options

Treating an aortic thromboembolism is incredibly challenging and requires intensive, round-the-clock hospital care. The primary goals of treatment are to manage the pet's intense pain, prevent the clot from growing, support the cardiovascular system, and monitor for life-threatening complications.

First-Line Therapies (Anticoagulants & Platelet Inhibitors)

These medications do not dissolve the existing clot, but they are crucial for preventing the clot from getting larger and stopping new clots from forming:

• Unfractionated Heparin: An injectable anticoagulant administered in the hospital to quickly disrupt the clotting cascade.
• Low Molecular Weight Heparins (Dalteparin, Enoxaparin): Alternative injectable anticoagulants that offer more predictable activity and are often transitioned to for ongoing care.
• Clopidogrel: A highly effective oral medication that prevents platelets from clumping together. This is often the cornerstone of long-term preventative therapy.
• Aspirin: A nonsteroidal anti-inflammatory drug that also acts as a platelet aggregation reducer, sometimes used in combination with other therapies.

Second-Line Therapies

• Warfarin Sodium: A coumarin derivative anticoagulant that blocks the body's use of vitamin K to form clotting factors. Because it requires frequent, highly precise blood monitoring to prevent fatal bleeding complications, it is rarely used today and has largely been replaced by safer alternatives.

Supportive Care and Monitoring

• Pain Management: This is the most critical immediate step. High doses of strong opioid medications are required to keep the pet comfortable.
• Fluid Therapy: Intravenous fluids are used to support blood pressure, expand vascular volume, and correct electrolyte imbalances. However, veterinarians must balance fluid therapy with extreme caution, as pets with concurrent heart failure can easily be pushed into fluid overload.
• Oxygen Therapy: Many of these pets are in congestive heart failure simultaneously, requiring supplemental oxygen via an oxygen cage or nasal cannula.
• Monitoring for Reperfusion Injury: This is a highly dangerous phenomenon that occurs when blood flow begins to return to the damaged limbs. As oxygenated blood re-enters the tissue, it washes accumulated toxins, inflammatory proteins, and potassium out of the dying muscles and into the general circulation. High potassium levels (hyperkalemia) can cause the heart rate to slow down dangerously or stop entirely. Vets must monitor blood potassium levels constantly during recovery and may use emergency medications like calcium gluconate, insulin, or dextrose to drive potassium back into the cells.
• Supportive Nursing Care: Because these pets are paralyzed and painful, they cannot move themselves. They require frequent turning to prevent pressure sores (decubital ulcers), physical therapy (passive range of motion) once the acute clot phase has stabilized, and assistance with urination if they cannot walk.

Surgical and Interventional Options

In some cases, physical removal of the clot may be considered, though success rates vary significantly by species:

"Thromboembolus removal using an embolectomy catheter has not been effective in cats but might be more successful in dogs of larger size. Arterial stenting has been used successfully in some dogs with aortic thromboembolism."

Prognosis

The prognosis for pets suffering from an aortic thromboembolism is unfortunately poor. The condition carries a high mortality rate, with approximately 30% of patients dying or failing to survive the initial hospitalization period due to heart failure, severe tissue damage, or the effects of reperfusion injury.

Additionally, approximately 30% of cases result in euthanasia during the acute phase. This decision is often made due to the severe, unmanageable pain the pet experiences, the high financial cost of multi-day intensive care, or the poor long-term outlook for the underlying heart disease.

For pets that do survive the initial crisis and regain use of their limbs, the long-term outlook remains guarded. It can take weeks to months for nerve function to return, and some pets may have permanent deficits, such as "knuckling" (walking on the tops of their paws) or a permanent limp. Because the underlying heart disease or systemic clotting disorder is still present, repeated thromboembolic events are very common. Lifelong medication, frequent veterinary rechecks, and careful home monitoring are required to give these pets the best possible quality of life.

Prevention

Because aortic thromboembolism is almost always a consequence of an underlying, silent disease, true prevention relies on early detection.

For cats, routine veterinary exams that identify a heart murmur or an abnormal heart rhythm should always be followed up with an echocardiogram. If a veterinary cardiologist detects significant left atrial enlargement before a clot forms, they will typically prescribe preventative medications like clopidogrel to reduce the risk of a future saddle thrombus.

For dogs, managing underlying conditions that cause hypercoagulability—such as treating Cushing's disease or closely monitoring protein-losing kidney diseases—is the most effective way to prevent systemic clots.

When to call your vet

Aortic thromboembolism is an absolute, Category 5 veterinary emergency. If you suspect your pet is experiencing a saddle thrombus, do not wait to see if they improve. Drive to the nearest open veterinary hospital or emergency clinic immediately.

Call ahead to let the clinic know you are on your way with a suspected saddle thrombus so they can prepare emergency pain management and oxygen therapy. Watch for these critical red flags:

• Sudden loss of use of the hind legs (dragging the legs)
• Sudden, intense crying out, howling, or screaming in pain
• Hind paws that feel cold to the touch
• Pale, blue, or purple footpads or nailbeds
• Rapid, shallow, or open-mouthed breathing

For specific breeds

While any dog or cat can develop a blood clot, certain breeds have documented predispositions to the underlying conditions that cause them.

In cats, breeds prone to hypertrophic cardiomyopathy—such as Maine Coons, Ragdolls, Persians, and Sphynxs—are at a higher risk for FATE.

In dogs, specific breeds have been identified with a higher risk of thromboembolic events:

• Greyhounds: Known to have unique clotting and fibrinolytic profiles that can predispose them to vascular complications.
• Labrador Retrievers: Prone to certain systemic inflammatory and neoplastic conditions that can trigger hypercoagulability.
• Cavalier King Charles Spaniels: This breed is highly prone to degenerative mitral valve disease. Furthermore, they have a specific risk for clots in the lungs:

"PTE [Pulmonary thromboembolism] has also been reported in Cavalier King Charles, with and without underlying mitral valve disease."

If you own one of these predisposed breeds, regular veterinary checkups and proactive screening for cardiac and systemic diseases are essential steps in protecting your pet.

Sources

• Small Animal Critical Care Medicine, 2nd Edition, p. 253
• Textbook of Veterinary Internal Medicine, 5th Edition, pp. 235, 236, 244