Summary
A saddle thrombus is a blood clot (called a "thrombus") that lodges at the base of the aorta just as it branches into two distinct arteries, thereby obstructing blood flow to the hind limbs. It is so named because of the saddle-like shape it roughly resembles once it takes up residence in this location.
The clot itself forms in the heart, eventually dislodging and embolizing (moving through the circulatory system) just prior to getting stuck at the circulatory system's next point of constriction.
Because this narrow point may not necessarily coincide with the actual point of trifurcation of the aorta (what's typically considered its base), "aortic thromboembolism" (ATE) is the more accurate term for this disease process in general. It's important to note, however, that 90% of cats with ATE have clots that do lodge at this highly sensitive location.The effects of ATE are typically devastating, as these blood clots typically cause hind limb paralysis due to a lack of blood flow to these tissues. Severe pain is always a component of this process.
ATE is an altogether too-common occurrence in cats, especially in those suffering from cardiac diseases. In one study, ninety percent of ATE cats suffered from underlying cardiac diseases, including:
Hypertrophic cardiomyopathy (HCM) (12% to 28%)
Unclassified cardiomyopathy (27%)
Right ventricular cardiomyopathy (much less often)
Cancer and hyperthyroidism are considered other risk factors.
As certain breeds of cats are predisposed to certain heart diseases, a genetic predisposition for ATE is assumed, albeit obliquely.
Sadly, cats who suffer from ATE typically succumb to this disease process, either through a) the pain, shock, and/or other effects of tissue death, b) euthanasia, or c) if successfully treated, eventually as a result of the underlying heart disease.
Symptoms and Identification
Cats afflicted by ATE will display symptoms consistent with the sudden onset of pain and paralysis. Vocalization (crying), hiding, panting or breathing rapidly, and an inability to use the hind limbs are most typically observed. Cool hind limbs, firm and painful muscles, and weak or absent pulses are also evident, though these signs tend to be appreciated best by veterinary professionals.
These cats may or may not have a history of heart disease. A heart murmur and/or arrhythmia may not be part of the clinical picture, but often is.
Though, technically, a definitive diagnosis is only possible by visualizing the affected area through angiography, surgery, or necropsy (post-mortem examination), the signs of this disease are generally regarded as unmistakable. Helpful tests, however, include the following:
Complete blood count
Serum biochemistry analysis
Urinalysis
Blood flow analysis (via Doppler ultrasound imaging or blood glucose testing)
Coagulation profile
Thyroid testing
X-rays of the chest (to evaluate the heart and lungs)
Ultrasound of the heart (to definitively diagnose any underlying cardiac disease and identify the presence of more clots in the heart)
Affected Breeds
Since ATE affects cats with HCM, breeds predisposed to this disease are therefore at higher risk of ATE.
Perhaps the most notoriously affected breed is the Maine Coon. Genetic mutations in the Maine Coon and the Ragdoll associated with HCM have been identified. Search for presumed mutations in other breeds who appear predisposed is ongoing. These breeds include the Norwegian Forest Cat and Sphynx.
However, it's important to note that any breed of cat be affected.
Treatment
Unfortunately, at this time there's no approach to the treatment of this condition the veterinary community considers adequately effective due to the severity of this condition and the advanced nature of the underlying cardiac disease most of these cats suffer from.
Some cats, however, can recover fairly well, especially if they receive immediate treatment, if their cardiac disease is not so severe, the blood clot doesn't completely occlude blood flow, and additional thrombi are not noted in the heart. These approaches are most often undertaken in these cases:
Pain management
Treatment of any concurrent heart failure
Treatment of any electrolyte imbalances
Supportive therapy (fluids, feeding, etc.)
Treatment of the thromboembolism
Unfortunately, studies have thus far shown that treatment designed to "dissolve" or remove the clot is no more effective than supportive care alone. Nonetheless, aggressive treatment through these methods continues as veterinary medicine attempts to find a satisfactory solution to ATE. These following methods are considered most commonly employed in these cases:
Heparin and/or aspirin ("blood thinning" drugs to help prevent further clot formation)
Thrombolytic drugs (to help "dissolve" the clot itself, sometimes applied to the clot itself)
Surgery (to remove the clot)
Veterinary Cost
Because it's such a devastating disease process that a) involves the presence of a severe underlying disease, and b) requires many days (or even weeks!) of intensive care, ATE is considered a very expensive problem -- more so if pricey thrombolytic drugs and/or surgery are elected:
Initial intensive care efforts alone can reach into the thousands in some complicated cases.
Surgery requires a board certified surgeon's skills and, as such, fees of $1,500 to $3,000 are fairly typical for the surgery itself.
Daily supportive care can range anywhere from the low hundreds to a thousand dollars or more, depending on geographical location, whether a specialty facility is sought, and the aggressiveness with which treatment is pursued.
Prevention
There is no known mode of prevention for most of the cardiac diseases that predispose cats to saddle thrombus formation. The actual prevention of thrombus formation, however, has been the subject of considerable investigation and even dispute within the feline veterinary community over the past decade.
Though not yet proven too satisfactorily effective, anti-coagulation treatment is often initiated in an effort to prevent further thrombosis for cats with cardiac disease. This is typically accomplished with medications such as aspirin, warfarin, heparin, clopidogrel, or coumarin.
References
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Kittleson MD, Kienle RD. Thromboembolic disease. In: Small animal cardiovascular medicine. St. Louis, Mo: Mosby, 1998;540-547.
Laste NJ, Harpster NK. A retrospective study of 100 cases of feline distal aortic thromboembolism: 1977-1993. J Am Anim Hosp Assoc 1995;31(6):492-500.
Paige CF, Abbott JA, Elvinger F, Pyle RL. Prevalence of cardiomyopathy in apparently healthy cats. J Am Vet Med Assoc. 2009 Jun 1;234(11):1398-403.
Peterson EN, Moise NS, Brown CA, et al. Heterogeneity of hypertrophy in feline hypertrophic heart disease. J Vet Intern Med 1993;7(3):183-189.
Rush JE, Freeman LM, Fenollosa NK, et al. Population and survival characteristics of cats with hypertrophic cardiomyopathy: 260 cases (1990-1999). J Am Vet Med Assoc 2002;220(2):202-207.
Smith SA, Tobias AH, Jacob KA, et al. Arterial thromboembolism in cats: acute crisis in 127 cases (1992-2001) and long-term management with low-dose aspirin in 24 cases. J Vet Intern Med 2003;17(1):73-83.
Smith SA, Tobias AH. Feline arterial thromboembolism: an update. Vet Clin North Am Small Anim Pract 2004;34(5):1245-1271.