Distal aortic thromboembolism (ATE) is most commonly recognized as a devastating sequel to underlying cardiac disease in the cat. The purpose of the following pages is to present the reader with a review of the veterinary literature as it pertains to pathophysiology, diagnosis, treatment, and prognosis for cats with ATE as well as to provide some comparisons between different treatment and prophylactic measures.

Incidence and Pathophysiology:

ATE most commonly affects middle-aged (5-7year) male domestic variety cats. (male:female ratio 2:1 – 3:1). Most affected cats are spayed or neutered, however, analysis has not identified sterilization or lack thereof as a significant risk factor. The vast majority of cats with ATE have clinical evidence of underlying cardiac disease, however, neoplasia, aortic surgery, infectious disease, sepsis, and foreign body have all been associated with this condition. On rare occasion, a predisposing condition is not identified. ATE is seen in approximately 10-20% of cats with underlying cardiac diseases and is associated with concurrent evidence of congestive heart failure (CHF) in greater than 50% of cases.

ATE is an embolic event. It is believed that the thrombus forms within the enlarged left atrium and is then ejected into the systemic circulation, most commonly lodging in the terminal aorta. Mere obstruction of the lumen of the aorta is not the only factor contributing to decreased perfusion to the hind-limbs as it has been well documented that even after ligation of the terminal aorta, collateral circulation will maintain oxygen delivery to the hind-limbs. It is strongly believed that the interplay of the activated platelets within the ATE results in the elaboration of numerous vasoactive mediators including but not limited to Thromboxane A₂ (TXA₂₎ and serotonin. These mediators cause vasoconstriction and limit flow through the collateral circulation. A well-established model of ATE in cats is characterized by ligation of the terminal aorta, 6^th lumbar, and deep circumflex iliac arteries and aortic injection of bovine thromboplastin.

Diagnosis:

Distal ATE is most often a clinical / physical examination diagnosis that is later confirmed through ancillary diagnostic testing such as angiography, aortic ultrasound, differential blood flow as detected by Doppler between the fore and hind-limbs, or differential hind-limb: central glucose (significantly decreased in hind-limbs) and lactate concentrations (significantly increased in hind-limbs).

Physical examination findings consistent with distal ATE include absent or weak hind-limb pulses, hind-limb pain, hyporeflexia / areflexia, cool extremities, cyanotic nail beds, firm gastrocnemius muscles, and paresis or paralysis. In cases where distal ATE extends more proximally, additional clinical signs referable to acute renal failure or ischemic gastrointestinal disease may be present.

When ultrasonographically imaging the distal aorta, the clinician must recognize that immature emboli tend to be relatively hypoechoic and difficult to identify when compared to more mature emboli. Color doppler ultrasound techniques may aid in better imaging the area in question. Alternatives including angiography or non-selective CT aided angiography can help identify the extent of the ATE.