Cathcart CJ

Dennis S

Fuster V

Goggs R

Harpster NK

Laste NJ

Schaub RG

Welles EG

Fuentes, V L

RVC Research Online

Arterial thromboembolism: risks, realities and a rational first-line approach

 Practical relevance: Feline arterial thromboembolism (ATE) is a common but devastating complication of myocardial disease, often necessitating euthanasia. A combination of endothelial dysfunction and blood stasis in the left atrium leads to local platelet activation and thrombus formation. Embolisation of the thrombus results in severe ischaemia of the affected vascular bed. With the classic ‘saddle thrombus’ presentation of thrombus in the terminal aorta, the diagnosis can usually be made by physical examination. The prognosis is poor for cats with multiple limbs affected by severe ischaemia, but much better where only one limb is affected or motor function is present.  Patient group: Cats with left atrial enlargement secondary to cardiomyopathy are typically predisposed, although cats with hyperthyroidism, pulmonary neoplasia and supravalvular mitral stenosis may also be at risk.  Management: Analgesia is the main priority, and severe pain should be managed with methadone or a fentanyl constant rate infusion. Congestive heart failure (CHF) requires treatment with furosemide, but tachypnoea due to pain can mimic signs of CHF. Thrombolytic therapy is not recommended, but antithrombotic treatment should be started as soon as possible. Aspirin and clopidogrel are well tolerated.  Evidence base: Several observational studies of ATE have been reported. No randomised, blinded, controlled studies have been reported in cats at risk, for either treatment or prevention of ATE, although such a study comparing aspirin and clopidogrel in cats is currently under way. </jats:p

Virginia Luis Fuentes

Crossref

Journal of Feline Medicine and Surgery

Arterial Thromboembolism

Glaus, Tony M

ZORA

Zurich Open Repository andArchiveUniversity of ZurichMain LibraryStrickhofstrasse 39CH-8057 Zurichwww.zora.uzh.chYear: 2012Arterial thromboembolismGlaus, T MAbstract: UnspecifiedPosted at the Zurich Open Repository and Archive, University of ZurichZORA URL: http://doi.org/10.5167/uzh-71326Originally published at:Glaus, T M (2012). Arterial thromboembolism. In: FECAVA, Milano, Italy, 22 March 2012 - 25 March2012.Thrombosis / Thromboembolism of the descending aorta (A T E) in dogs, diagnosis, pathophysiologic and therapeutic considerations. Tony Glaus, Prof. Dr. med. Vet., Dipl. ACVIM and ECVIM-CA, Head Division of Cardiology, Vetsuisse Faculty University of Zurich, CH-8057 Zurich  Definitions Thrombosis is the local formation of a thrombus inside a vessel leading to vascular occlusion, embolism is the vascular occlusion by various formations like a thrombus, tissue particle, parasite, foreign body, tumor cells or air that have been formed distant to the actual occlusion and that are carried in the vessel to the site of occlusion, and thromboembolism is thus the vascular occlusion specifically by a thrombus that was not produced at the site of occlusion but carried there. Once a thrombus is present in the circulation it may grow. In this text, the abbreviation ATE will be used to describe both aortic thrombosis and / or thromboembolism.   Pathogenesis For ATE to occur an important disturbance in the delicate balance between pro- and antithrombotic body systems has to be present, i.e. there may be excessive abnormal focal vascular triggers of coagulation, or a systemic hypercoagulable state, or a systemic hypofibrinolytic state, or a combination of these. The following notes focus on ATE in dogs.  As opposed to cats, ATE is not a very common problem in dogs. Furthermore, causes of ATE markedly differ in cats and dogs. In cats, around 90% of cases are due to thrombus formation in the left atrium (or ventricle) secondary to stagnant blood flow, mostly due to a severely dilated left atrium secondary to myocardial disease. Around 10% are due to cancer, most commonly carcinomata in the chest. In dogs, ATE is not encountered with atrial dilation, even if severe. As a matter of fact, in many cases no eliciting cause is identified. In some dogs ATE has been reported associated with local vascular pathology, specifically atherosclerosis in the descending aorta, or (adrenal) cancer breaking into the aorta. Furthermore, it has been associated (published and unpublished) with systemic diseases, including Leishmaniosis, nephrotic syndrome (some due to leishmaniasis), protein-losing enteropathy, hypothyroidism, hyperadrenocorticism, endocarditis, ectopic heart worms, cancer, unspecified nephropathy and unspecified cardiac disease.   C linical signs, differential diagnosis and further diagnostics Whereas in some dogs, clinical signs may be peracute with pain, paraplegia, cold extremities, paresthesia and no palpable pulse, like in cats, more commonly the onset of gait abnormalities may be insidious and worsen progressively. A femoral pulse may still be palpable delaying the suspicion of ischemic myopathy as cause of the gait abnormality. Characteristic for narrowing of the aorta and decreased oxygen delivery to the rear legs is exercise induced intermittent claudication. The differential diagnosis for this includes right-to-left PDA, myasthenia gravis, neuropathies and myopathies.  When a pulse is still palpable, it takes a high index of suspicion to consider ATE. In some cases, ATE is found incidentally during abdominal ultrasound. The minimal data base to search for a potential underlying cause includes routine hematology, biochemical profile, urinalysis, urine-proteine-creatinine-ratio, thoracic radiographs and abdominal ultrasound. The latter also is necessary to prove the diagnosis. Further tests may include infectious disease titers (Leishmania), and abdominal CT.   T reatment The treatment aims at 1. symptomatically fight the pain, 2. eliminate the thrombus, 3. eliminate the underlying cause.  To eliminate the thrombus medically, fibrinolytic and antithrombotic therapy are possible. Complications with both include  - breaking off of part of the thrombus, which may cause complete arterial obstruction lower in the arteries, which may lead to paraplegia of a previously ambulatory patient.  - Spontaneous bleeding. In a patient with acute paraplegia and pulselessness of very recent onset, we would consider fibrinolytic treatment using tissue plasminogen activator. In this scenario, an additional risk is severe hyperkalemia secondary to acute reperfusion. In a still ambulatory patient, our approach today is the application of the low-molecular-weight heparin enoxaparine (0.8 mg/kgq6h, ClexaneR) combined with the antiplatelet drug clopidogrel (2-3 mg/kg q24h, PlavixR). To assure that the enoxaparine blood level is in the target range, anti-factorXa-activity is assessed using the human assay. When the thrombus is completely dissolved based on ultrasonographic examination of the descending aorta, the enoxaparine dose is slowly decreased, but never completely stopped. Enoxaparine is expensive.  Prognosis Basically poor, but better than in cats. Depends on underlying cause, onset acute versus chronic, still ambulatory versus paraplegic, and severity of secondary complications like neuropathies, muscle necrosis / fibrosis. Complete recanalisation is possible, however, breaking off of parts of the thrombus may occlude distal arteries with acute paraplegia in a previously walking dog. Relapses are possible.  References Boswood A et al. Aortic and iliac thrombosis in six dogs. J Small Anim Pract 2000;41:109-114. Goncalves R et al. Clinical and neurological characteristics of aortic thromboembolism in dogs. J Small Animl Pract 2008; 49:178-184. Lunsford KV et al. Pharmacokinetics of Subcutaneous Low Molecular Weight Heparin (Enoxaparin) in Dogs. J Am Anim Hosp Assoc 2009; 45: 261-267.   

Arterial thromboembolism

http://www.zora.uzh.ch/71326/1/Glaus_Milano_Arterial_2012.pdf

Arterial thromboembolism

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