Daniel F. Hogan,     West Lafayette, Indiana

Background

Arterial thromboembolism (ATE) is a sudden interruption of arterial blood flow caused by thrombotic material that is derived from a distant site. This obstruction leads to infarction of tissues served by that arterial bed. Localized arterial thrombosis is associated with abnormalities of the vascular endothelium or vascular wall and may stem from high-shear flow within a narrowed blood vessel. This condition seems relatively rare in dogs and cats. Conversely, ATE occurs commonly in small animals.

In some cases of ATE, the site of the originating thrombus is either known or reliably suspected. For example, cardiogenic embolism (CE) typically results from thrombi located within a dilated left atrium or auricle, whereas septic cardioemboli develop with valvular or mural endocarditis. However, in other cases, such as neoplasia, protein-losing nephropathy, hyperadrenocorticism, and immune-mediated hemolytic anemia, the thrombus source cannot be determined. It has been suggested that in some cases of ATE where a source of the arterial thrombus cannot be identified, systemic venous thrombi may be the source of the embolic material, causing paradoxical (right-to-left) ATE. In human patients paradoxical ATE often is associated with deep venous thrombosis in which thrombotic material crosses a congenital cardiac defect from the right to the left side of the circulation, often across a patent foramen ovale (PFO). Cryptogenic stroke (a stroke of uncertain origin) is three times more likely in human patients with a PFO, and human patients with a PFO are 34 times more likely to experience silent brain infarction. Paradoxic embolism has been reported in veterinary medicine and in one recent study (Hogan and Meltzer, 2011) evidence of right-to-left shunting at the atrial level was identified in approximately 50% of dogs with congenital heart disease using agitated saline contrast echocardiography. Such findings could explain the relatively high frequency of silent renal infarcts on abdominal ultrasonography in cats and dogs and the development of systemic ATE in veterinary patients with hypercoagulable disorders.

Pathogenesis

In the normal healthy state, there is an equilibrium between thrombus formation and thrombus dissolution, which prevents unregulated thrombus formation. Primary hemostasis occurs when platelets are exposed to subendothelial collagen. This leads to platelet adhesion and activation, with subsequent aggregation and release of proaggregating and vasoconstrictive substances. Platelet release products, in conjunction with circulating factors within the plasma, initiate the coagulation cascade. Fibrinolytic and antithrombotic mechanisms are activated simultaneously to break down the developing hemostatic plug, which prevents excessive thrombus formation. Pathologic thrombosis can result from any combination of impaired or overwhelmed antithrombotic mechanisms, increased function of prothrombotic mechanisms, or impaired fibrinolysis.

The development of pathologic thrombosis classically has been linked to Virchow’s triad, which includes endothelial injury, blood stasis, and the presence of a hypercoagulable state, with each arm adding to the risk of thrombosis (cumulative thrombotic risk). Examples of endothelial injury are a dilated left atrium in a cat with hypertrophic cardiomyopathy, a damaged aortic valve in a dog with subaortic stenosis, and tumor invasion of the arterial tree. Blood stasis is associated with dilated or poorly contracting cardiac chambers, restricted blood flow from tumor growth, or sluggish venous flow. The hypercoagulability arm of the triad has been poorly defined in domestic animal species, although there are known clinical conditions associated with thrombosis in animals (see Chapter 166).

Known hypercoagulable states in humans include inherited abnormalities in the procoagulant factors IIa (thrombin), Va, and VIIIa as well as the antithrombotic proteins antithrombin (AT), protein C, and protein S. Additional hypercoagulable states include platelet hypersensitivity and increases in homocysteine, lipoprotein (a), plasminogen activator inhibitor, and thrombin-activatable fibrinolysis inhibitor. Suspected hypercoagulable states in dogs and cats include platelet hypersensitivity, decreased AT and protein C activity, and increased levels of in factors II, V, VII, VIII, IX, X, XII, and fibrinogen.

Early pathologic thrombus composition is classified as platelet rich but progressively becomes more fibrin rich as the thrombus continues to grow. As the thrombus ages, superficial portions can break off forming emboli that cause infarction in distant arterial beds. The clinical signs that result from the arterial infarction depend on the site and completeness of the arterial obstruction, the availability of arterial anastomoses and collateral circulation, and the metabolic demands of the tissues. Platelet-released vasoactive substances reduce the collateral flow around the site of obstruction and contribute to the clinical signs of ischemic neuromyopathy. This is similar to what is observed in humans with thrombotic stroke, cardiogenic embolism, and pulmonary embolism. In experimental feline models of aortic ATE, pretreatment with the antiserotonergic drug cyproheptadine and clopidogrel (which inhibits platelet activation and has a vasomodulating effect) maintains the collateral network and reduces the signs of ischemic neuromyopathy.

Clinical Signs

The type and severity of clinical signs relates to the location and completeness of the arterial obstruction. Organs often have a collateral network that can be recruited to provide blood flow around a site of arterial obstruction, but flow through these networks appears to be impaired with acute thrombotic infarction.

Renal infarction can present with renal pain and acute renal failure, whereas infarction of the cranial mesenteric artery can result in severe abdominal pain, vomiting, and diarrhea. Nonspecific signs of lethargy, anorexia, vomiting, and diarrhea have been reported with splenic infarction. The clinical signs of cerebrovascular accidents or stroke can be profound, depending on the neural location of the infarction and the territory served by the affected artery. Signs can include paresis, vestibular dysfunction, cranial nerve deficits, and seizures.

Infarction caused by obstruction of the distal aortic trifurcation (a saddle thromboembolus) accounts for the majority of ATE cases in dogs and cats and results in a loss of blood flow to the pelvic limbs, causing ischemic neuromyopathy. Paresis or paralysis of the pelvic limbs with absence of segmental reflexes, firm and painful pelvic limb musculature, and cold and pulseless limbs with cyanotic nail beds are typical features. These findings can be bilateral and symmetric, or unilateral and asymmetric, depending on the degree of infarction and blood flow through collateral vessels. The tail often is involved. Cats appear to be more severely affected with ischemic neuromyopathy than are dogs, which may be indicative of species differences in platelet function or preservation of the collateral circulation. The clinical signs of ischemic neuromyopathy are peracute in onset and can worsen, but usually remain stagnant or improve over the following several days to 3 weeks.

Infarction of the subclavian artery, typically the right subclavian, is the second most common site for ATE in cats and occasionally is seen in dogs. The clinical signs associated with infarction at this site are essentially identical to those for infarction of the aortic trifurcation, although the signs are confined to the affected forelimb.

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