DIAGNOSIS
The main differential diagnosis for aortic thromboembolism is spinal cord disease (acute spinal injury, intervertebral disk
disease, spinal neoplasia, and fibrocartilaginous emboli). Definitive diagnosis involves documenting arterial occlusion and
determining the underlying cause.
Blood flow evaluation
Various methods exist to evaluate blood flow (or lack thereof) to the limb. Palpation of pulses may not be a reliable indicator
since pulses may be difficult to palpate in any situation of poor perfusion (such as hypovolemic shock). Blood flow in the
artery can be assessed by applying a Doppler transducer over the dorsal pedal artery or palmar artery. Absence of a Doppler
signal may indicate lack of blood flow. The accuracy may be affected by poor perfusion and hypotension due to other conditions.
Other means of assessing blood flow include measuring glucose or lactate concentrations in the affected limb by obtaining
a blood sample from the medial saphenous vein and comparing it with the systemic values. The glucose should be lower and the
lactate should be higher in the ischemic limb. Angiography provides the best information regarding blood flow, but this procedure
is not practical and is rarely needed in most cases of thromboembolism.
Laboratory testing
A minimum database consisting of a complete blood count (CBC), serum chemistry profile, and urinalysis should be performed
in all cases. The CBC and urinalysis findings are typically normal.
The serum chemistry profile may reveal nonspecific changes such as hyperglycemia and increased alanine transaminase and aspartate
transaminase activities. The cats may be azotemic from decreased renal perfusion or occlusion of the renal artery by the thrombus.
Hyperkalemia may be present on admission or may develop as treatment progresses related to concurrent renal infarction or
reperfusion syndrome (released from ischemic skeletal muscle cells). The hyperkalemia can be severe and may require treatment.
Other abnormalities include hypocalcemia, hyperphosphatemia, hypokalemia, and hyponatremia.2 Serum creatine kinase activity is also markedly increased.28
Prothrombin time (PT) and activated partial thromboplastin time (aPTT) are usually normal on presentation.9 D-dimer concentrations (products of the breakdown of cross-linked fibrin) can be measured and have been found to be elevated
in only up to 50% of cats with ATE.17 D-dimers are fairly nonspecific as they can be elevated with other causes of thrombosis (e.g. disseminated intravascular coagulation, neoplasia, hepatopathy, hemorrhage).
Thyroid testing may also be indicated since ATE has been reported in cats with hyperthyroidism.2
Radiography
A thoracic radiographic examination is beneficial even if pulmonary auscultation is normal. Cardiomegaly was documented in
88% of cats with ATE in one study.1 Cardiomegaly in a previously asymptomatic cat provides evidence of underlying cardiac disease. Pulmonary edema or pleural
effusion may also be evident on thoracic radiographs, as well as support for pulmonary neoplasia.
Echocardiography
An echocardiographic examination is extremely valuable for determining whether cardiac disease is a cause of ATE. Echocardiography
can also be used to look for evidence of additional thrombus formation. Occasionally, a thrombus may be seen in the left auricle
or atrium. As previously discussed, SEC may be present, indicating increased risk for thrombus formation.
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