Case Studies In Small Animal

Cardiovascular Medicine

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Case 21

Systemic Thromboembolism Section from "Small Animal Cardiovascular Medicine" On-Line

Text from "Small Animal Cardiovascular Medicine"


Systemic arterial thromboembolism (STE) is a relatively common and usually very serious sequel to feline cardiac disease. Although systemic thromboembolism can occur in dogs and can also occur in cats that do not have cardiac disease, >90% of cases seen in veterinary small animal practice are in cats with cardiac disease. The vast majority of these cats have left atrial enlargement when examined using echocardiography. The left atrium is usually the site of thrombus formation. Systemic thromboembolism used to be a common complication of dilated cardiomyopathy in cats. Because the incidence of this disease has decreased dramatically, the incidence of STE has decreased. However, STE is still a common complication of hypertrophic cardiomyopathy and the unclassified or restrictive forms of feline cardiac disease. It occasionally occurs in cats with hyperthyroidism.

Most cats (approximately 90%) presented with STE have the thromboembolus lodged at the terminal abdominal aorta (the aortic trifurcation). This type of thromboembolus commonly extends down the external iliac arteries, giving it the appearance of a saddle. Consequently, these are commonly called saddle thromboemboli. Thromboembolism of the terminal aorta produces acute caudal limb paresis/paralysis and pain with a loss of the femoral pulses and pale or cyanotic pads (pain, paralysis, pulselessness, and pallor). Some cats, however, have smaller thromboemboli that lodge in one femoral artery, a brachial artery, or another smaller artery. Occasionally, a large thromboembolus lodges more proximally in the aorta, above the renal arteries, resulting in acute renal failure. In other cats, a very large thromboembolus lodges in the mitral valve orifice, the left ventricle, or the proximal aorta at the region of the brachiocephalic trunk, causing sudden death.


A thrombus is an aggregation of platelets and fibrin with entrapped blood cells. Systemic arterial thromboembolism occurs when a thrombus forms in some region of the left heart or systemic circulation and then breaks loose to become an embolus and travel to a distal region of the systemic circulation. Here it lodges and partially or completely occludes blood flow distal to the thromboembolus. Intravascular thrombus formation is an unusual event and requires predisposing factors to allow it to occur. Thrombus formation in cats usually occurs in the left atrium, most commonly in the left auricle.

Intravascular Thrombus Formation

Reasons for intravascular thrombus formation include sluggish blood flow, endothelial damage, and increased blood coagulability. One study has documented increased platelet aggregability in some cats with cardiomyopathy. A specific reason for this finding has not been elucidated. When observed at a postmortem examination, atria from cats with cardiac disease and thromboembolism are very large and may be somewhat fibrotic. Usually no evidence of endothelial damage or other factors that might stimulate thrombus formation are present. The left atrium is usually enlarged in cats with STE. In one study it was severely enlarged in 57%, moderately enlarged in 14%, and mildly enlarged in 22% of cats with STE. Only 5% had a normal left atrial size.

The most plausible explanation for thrombus formation in cats is sluggish blood flow in the left atrium. The amount of blood that flows through the left atrium in cats with cardiomyopathy is normal to low. Normal to low blood flow through an enlarged chamber results in a lower than normal blood flow velocity. An analogy to explain why blood flow velocity is low in an enlarged left atrium would be a canoe floating down a river that is a fixed width and a fixed depth with a water flow velocity of 1 foot per second. As you float down the river in your canoe, it will also move at 1 foot/second. If the Army Corps of Engineers comes in and widens one section of the river you will notice that the velocity (speed) at which your canoe travels will slow down in the area where the river is wider because the same amount of water is coming into a larger area. The same is true for the left atrium. This is especially true in regions like the left auricle. An analogy for flow in the left auricle would be a cove along one bank of a river. Here flow would be slower than the rest of the river because of its semi-isolation. Only small eddy currents would exist that would have very low flow velocities.

When blood flow slows to a certain velocity, red cells and other blood factors clump together. This can be easily demonstrated by ultrasounding the heart of an animal during euthanasia. When the heart stops beating, the cardiac chambers fill with a hazy, amorphous density as blood cells clump. A similar density is often observed in an enlarged left atrium in cats with severe cardiac disease. This abnormality is also recognized in humans with cardiomyopathies, atrial fibrillation, or mitral stenosis and is termed spontaneous echocardiographic contrast (also known euphemistically as "smoke"). In the living animal or human, this contrast swirls in the left atrium. In humans, spontaneous echo contrast is associated with increased left atrial size and with reduced left atrial blood flow velocity. It is the factor most strongly associated with left auricular thrombus formation and with systemic embolic events. No studies have been performed in veterinary medicine. However, in our experience, finding a thrombus in the left atrium or left auricle in a cat with spontaneous echo contrast on an echocardiogram is common. Sometimes they are obvious. At other times one must search for them, especially when they are confined to the left auricle. The stasis of blood also allows activated coagulation factors to accumulate and intermittent movement of viscous blood may induce platelet activation. If low blood flow velocity is such an important factor, one might also expect dogs with dilated cardiomyopathy to be prone to left atrial thrombus formation. Systemic thromboembolism is rare in dogs with dilated cardiomyopathy. The reason for this discrepancy may be due to species differences in erythrocyte aggregability. One study has documented that normal cat red cells are more aggregable than those of dogs, rats, rabbits, humans, and gerbils. Cats’ platelets are also more reactive than other species. Feline platelets undergo spontaneous aggregation in vitro and are more responsive to serotonin-induced aggregation than are platelets from other species. Cats also have a greater volume of platelets per body weight than other species.


Once a left atrial thrombus has formed, it can do one of three things: 1) it can remain static and cause no problem; 2) it can dislodge and become an embolus; or 3) it can grow very large and occlude intracardiac blood flow. The incidence of the first and third outcomes is unknown. If a thrombus causes no clinical abnormalities, the thrombus usually goes undetected. If it occludes intracardiac flow, it causes death and if a postmortem examination is not done, the cause of death is never known. Only the second scenario results in clinical signs for which the owners commonly seek medical attention for their pet.

The clinical signs produced depend primarily on the site occluded by the thromboembolus, whether the occlusion is total or partial, and the amount of collateral circulation. Bilateral renal embolization can cause renal failure. Embolization of the cerebral arteries causes central nervous system signs. Embolization of a brachial artery causes forelimb pain and paresis. Most left atrial thrombi apparently become quite large before they dislodge. These thromboemboli are larger than any artery exiting off the aorta. Consequently, blood flow pushes them the length of the aorta. They lodge at the aortic trifurcation, where the aorta divides into the two external iliac arteries and the common origin of the internal iliac arteries. Here they obstruct blood flow to the hind limbs.

Constriction of Collateral Vessels

Physical obstruction is only a part of the pathophysiology. Experimentally, the terminal aorta has been ligated in an attempt to reproduce the disease. Surprisingly, cats with aortic ligation exhibit no pain and walk following surgery, although the femoral pulses are absent and caudal limb blood flow is only 30% of the baseline. Slight weakness and hyporeflexia are present but even these resolve within 72 hours, when caudal limb blood flow is 90% of the baseline. Aortograms in these cats confirm the presence of collateral blood flow through the lumbar vertebral arteries and the cranial and caudal epigastric arteries. The disease can be reproduced, however, if a thrombus is created within the terminal aorta. Aortograms from these experimental cats are identical to those from spontaneous clinical cases. Both demonstrate very poor collateral flow beyond the region of the thromboembolus. Pretreatment with an antiserotoninergic agent or with indomethacin prevents the loss of collateral circulation and serotonin or thromboxane A2 injection reproduces the clinical situation when injected into a caudal aortic segment. It is hypothesized that thromboemboli release serotonin and thromboxane A2, agents present in platelets and known to produce intense vasoconstriction, and disrupt collateral flow. Antiserotonin agents (e.g., cyproheptadine) and indomethacin prevent vasoconstriction distal to the thromboembolus when administered prior to producing an experimental thrombus. Administering such agents after a thromboembolus is present apparently has no effect.

Mark D. Kittleson, D.V.M., Ph.D. All rights reserved.