Arterial thromboembolism in the cat

By | 2013-08-05

Cats with any form of cardiomyopathy have a predilection to form intracardiac thrombi in the left atrium; the incidence is highest in cats with hypertrophic cardiomyopathy. These thrombi often become lodged at the bifurcation of the iliac arteries; less frequently they may occlude the brachia!, coeliac or renal arteries.


Altered blood flow and vascular stasis predispose to thrombus formation. Localized release of vasoactive substances such as serotonin and thromboxane at the site of vascular occlusion result in vasoconstriction of the collateral blood supply adjacent to the occluded vessel. Moreover, the release of serotonin induces platelets to aggregate which further potentiates clot formation. Occlusion at the iliac bifurcation (a so called *saddle* thrombus) results in ischaemic damage to the muscles and nerves of both hind limbs (ischaemic neuromyopathy).

Clinical signs

Iliac thrombosis is characterized by the sudden onset of crying and hindlimb paresis which results in dragging of one or both hind limbs (occlusion of a brachial artery may cause similar signs in a fore limb). The cat may present with acute dyspnoea and mouth breathing and the mucous membranes may appear cyanotic (particularly if a pulmonary artery is thrombosed). The affected muscles become firm and painful to touch after 24 hours. One or both femoral pulses may be absent and the paws and distal limbs are hypothermic (pink pads may appear pale).


Diagnosis is usually based on the history and clinical signs. Since most cases of iliac thrombosis are associated with cardiomyopathy echocardiography should be performed as soon as the cat is stabilized. Non-selective angiocardiography may be helpful to determine the extent of the thrombosis and also the integrity of the collateral blood supply. Acute muscle damage results in increased plasma concentrations of aspartate aminotransferase (AST) and creatine kinase (CK). Urea and creatinine concentrations may increase after embolization of a renal artery.

Since the clinical signs of iliac thrombosis resemble those of lower motor neurone paralysis, spinal cord lesions, for example, acute spinal cord trauma, intervertebral discprotrusion (rarein the cat) or haemorrhage, and intravertebral tumours (lymphosarcoma) should be considered as differential diagnoses.

Arterial thromboembolism: Treatment

Treatment should he directed at alleviating signs associated with the thrombus as well as the underlying cardiac disorder responsible for its formation. Aspirin (25 mg kg-1 body weight per os every 72 h) should be given to inhibit platelet function. One study showed that the administration of aspirin resulted in significant preservation of collateral blood supply in eats after experimental induction of iliac thrombosis and a shortening of the recovery period. However, there is evidence to suggest that aspirin is not effective in preventing further embolic episodes. The use of acepromazine (0,2-0.4 mg kg-1 bodyweight subcutaneously three times daily) has been advocated for its vasodilator properties. Heparin may be given to prevent further activation of the coagulation process (an initial intravenous dose of 1000 USP followed 3 h later by 50 USP units kg-1 body weight subcutancously and thereafter 50 USP units kg-1 bodyweight every 6-8 b). Regular daily monitoring of activated partial thromboplastin lime (APTT) is advised so that the APTT is not prolonged by more than 1.5-2,0 times the preheparin baseline values. Morphine (0.1 mg kg-1 bodyweight) can be given as an analgesic for the first 24-48 h.

The use of the serotonin antagonist, cyproheptadine, and thrombolvtic agents such as streptokinase, urokinase and tissue plasminogen activator (t-PA) have yet to be fully evaluated and to date the results have been equivocal.


The prognosis is at best guarded. Many animals fail to respond to medical management or succumb to the underlying cardiomyopathy. Recurrence is common. Spontaneous recanalization of the clot may occur with or without drug therapy after 2-4 days. Many cats are left with signs of residual peripheral nerve damage. Full recovery may take up to 4-6 weeks.