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

Abstract

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.

Figure 1

Thrombus (arrow) present in the terminal aorta in a cat presented with ATE

Figure 2

Echocardiographic image showing a thrombus (arrow) in the left auricular appendage in a cat with HCM and left atrial enlargement. This is a right parasternal short axis view. Ao = aortic valve, LA = left atrium

Figure 3

Typical stance of a cat with a ‘saddle thrombus’, showing bilateral pelvic limb paresis

Figure 4

Lateral thoracic radiograph from a cat with ATE, showing a mass lesion in the caudodorsal thorax. Tumour emboli are probably responsible for the thromboembolic signs in cats with pulmonary neoplasia

Figure 5

ATE affecting the left pelvic limb of a Sphynx cat. A well demarcated region of ischaemia is evident as darker skin (a). Two days later, progression of ischaemic skin damage is evident over the lateral aspect of the tarsometatarsal area (b)

Figure 6

The left panel of the diagram shows the normal state, where a healthy endothelium contributes to a microenvironment that inhibits thrombosis within a blood vessel (‘thromboresistant’). Endothelial production of nitric oxide (NO), antithrombin (AT) and prostacyclin (PGI₂), and endothelial expression of thrombomodulin inhibit attachment and activation of platelets. The right panel represents an environment that promotes thrombogenesis, where the endothelium is damaged or missing, and collagen is exposed. Platelets attach to collagen-bound von Willebrand factor (vWF), resulting in platelet activation. Activated platelets release adenosine diphosphate (ADP) and thromboxane A₂ (TXA₂), which activate additional platelets. Tissue factor results in thrombin generation, which amplifies the effects of platelet activation and leads to further thrombin production, as coagulation factors such as Xa become involved. Platelet–platelet affinity is enhanced as attachments form with fibrinogen and vWF, leading to a more stable thrombus. The sites of action of aspirin, clopidogrel and heparin are shown

Sparky at presentation