Page 259 - Small Animal Internal Medicine, 6th Edition

CHAPTER 12 Thromboembolic Disease 231

(claudication) and have weak femoral pulses on the affected cardiac abnormalities. Evidence for CHF or pulmonary
side. In contrast to cats, most dogs have more chronic clinical abnormalities associated with TE disease (e.g., neopla-
VetBooks.ir signs (>2 weeks before presentation). Less than a quarter of sia, HWD, other infections) may also be found. Echocar-
diography is indicated to identify and characterize heart
dogs have peracute paralysis without prior signs of lameness.
These species differences support the notion that aortic
cardiac neoplasia. Thrombi within the left or right heart
thrombi in dogs form in situ in the caudal aorta, rather than disease (if present), particularly vegetative endocarditis or
embolizing from a distant location as in cats. Clinical signs chambers and proximal great vessels can be readily seen
in dogs include unilateral or bilateral hindlimb lameness or with two-dimensional echocardiography. In dogs with coro-
paresis (which may be progressive or intermittent), exercise nary TE disease, the echocardiographic examination might
intolerance, pain, and self-trauma or hypersensitivity of the indicate reduced myocardial contractility with or without
affected limb(s) or lumbar area. Most dogs are ambulatory regional dysfunction. Spontaneous echo-contrast (“swirling
on presentation. Intermittent claudication, common in smoke”) could be seen in one or both ventricles; similar to
people with peripheral occlusive vascular disease, can be a cats, this finding is thought to indicate increased risk for
manifestation of distal aortic TE disease. This involves pain, TE disease.
weakness, and lameness that develop during exercise. Inad- Routine laboratory test results depend largely on the
equate perfusion during exercise leads to lactic acid accumu- disease process underlying the TE event(s). Azotemia and
lation and cramping. These signs intensify until walking proteinuria are common, because protein-losing nephropa-
becomes impossible and they then disappear with rest. thy is the most common disease causing aortic thrombosis.
Key physical examination findings in dogs with aortic Systemic arterial TE disease also produces elevated muscle
thrombosis include absent or weak femoral pulses and enzyme activities from skeletal muscle ischemia and necro-
hindlimb neuromuscular dysfunction. Cool extremities, sis, including CK, AST, and ALT.
hindlimb pain, loss of sensation in the digits, hyperesthesia, Coagulation test results in dogs with thrombotic disease
and cyanotic nailbeds are variably present. Occasionally, a are variable. The concentration of FDPs or D-dimers may be
brachial or other artery is embolized. TE disease involving increased, but this can occur in patients with inflammatory
an abdominal organ causes abdominal pain, with clinical disease and is not specific for a TE event or DIC. Modestly
and laboratory evidence of damage to the affected organ. increased D-dimer concentrations also can occur in diseases
Coronary artery thromboembolism usually results in associated with procoagulant states, such as neoplasia, liver
arrhythmias, as well as ST segment and T-wave changes on disease, and IMHA, as well as in body cavity hemorrhage
ECG. Ventricular (or other) tachyarrhythmias are common, (due to increased fibrin formation). Elevation of D-dimers is
although if the atrioventricular (AV) nodal area is injured, therefore a sensitive but nonspecific test for pathologic
conduction block may result. Clinical signs of acute myocar- thromboembolism. It is important to interpret D-dimer
dial infarction/necrosis can mimic those of pulmonary TE results in the context of other clinical and test findings.
disease; these include weakness, dyspnea, and collapse. Assays for circulating AT and proteins C and S are available
Patients might have a heart murmur, tachycardia, and weak for dogs and cats also. Deficiencies of these proteins are
pulses. Respiratory difficulty can develop as a result of left- associated with increased risk of thrombosis.
sided CHF (depending on degree of myocardial dysfunc- TEG provides an easy point-of-care method of assessing
tion) or concurrent pulmonary abnormalities, including global hemostasis and can be used to demonstrate hyperco-
pulmonary thromboembolism. Coronary artery thrombo- agulability in patients with TE disease. However, in most
embolism also can cause sudden death; the associated acute Greyhounds and other sighthounds with aortic thrombosis,
ischemic myocardial injury might not be detectable on results of TEG are within normal limits for the breed.
routine histopathology.
Treatment and Prognosis
Diagnosis Although the clinical presentation often is more subtle and
Definitive diagnosis requires direct visualization of the chronic in canine aortic thrombosis compared with feline
thrombus. Typically, abdominal ultrasonography is used to ATE, the goals of therapy are the same: stabilize the patient
identify an intraluminal or mural mass in the distal aorta (or by supportive treatment as indicated, prevent extension of
other vessels). Doppler studies can demonstrate partial or the existing thrombus and additional TE events, and restore
complete obstruction to blood flow in some cases. Com- perfusion. Supportive care is given to improve and maintain
puted tomography (CT) with contrast or angiography can adequate tissue perfusion, minimize further endothelial
also demonstrate presence of the thrombus and vascular damage and blood stasis, and optimize organ function, as
occlusion. Contrast imaging can be valuable in cases where well as to allow time for collateral circulation development.
ultrasound is inconclusive, to demonstrate collateral circula- Correcting or managing underlying disease(s), to the extent
tion, or if concurrent CT imaging of other body areas is possible, is important. Antiplatelet and anticoagulant thera-
desired. pies are used to reduce platelet aggregation and growth of
Once the diagnosis of aortic thrombosis is confirmed, existing thrombi (see p. 232 and Box 12.3). Coagulation
additional testing is indicated to look for an underlying testing, including TEG if available, should be used to monitor
cause. Thoracic radiography provides an initial screen for response to anticoagulants in patients with TE disease.