The imaging diagnosis of pulmonary thromboembolism.

A 9-year-old male neutered Boston terrier was presented to the Ontario Veterinary College Teaching Hospital with dyspnea, ascites, limb edema, and lethargy. Physical examination revealed a distended abdomen, subcutaneous edema, dermatitis, and increased upper airway sounds. Diagnostic workup was commenced with laboratory tests and imaging of the thorax and abdomen. Results revealed mild hypoproteinemia, mildly elevated alkaline phosphatase and creatine kinase, normal pro-thrombin time and partial thromboplastin time, urine specific gravity of 1.014 and urine protein of 0.2 g/L. Fecal parasites, Baermann and heartworm tests were negative. The dog had been on heartworm preventative medication. Abdominocentesis revealed a modified transudate. Thoracic radiographs demonstrated right heart enlargement, enlargement of the pulmonary arteries, and blunting of the left caudal lobar artery (Figure 1). Abdominal ultrasound showed mild abdominal free fluid, hepatomegaly and adrenal gland enlargement. Echocardiography demonstrated right ventricular hypertrophy and tricuspid regurgitation. Through measurement of the peak tricuspid regurgitant velocity, the systolic pressure in the pulmonary artery was calculated to be > 77 mmHg (normal: 25 mmHg). There was no evidence of pulmonary stenosis. Figure 1 Left lateral (A) and dorsoventral (B) radiographs of the thorax depicting right heart enlargement, enlargement of the pulmonary arteries, and blunting of the left caudal lobar artery (circled). Our clinical assessment was pulmonary hypertension (PH), which can result from increased blood flow to the lungs, a sustained increase in left atrial pressure, and increased pulmonary vascular resistance. Increased blood flow to the lungs occurs with left to right shunts, such as patent ductus arteriosus (PDA) or ventricular septal defects (VSD). Sustained increases in left atrial pressure can result from mitral regurgitation, cardiomyopathy, or mitral stenosis. Increased pulmonary vascular resistance can occur from pulmonary thromboembolism (PTE), heartworm disease, longstanding pulmonary disease (such as chronic bronchitis and pulmonary fibrosis), and chronic hypoxia (resulting from bronchiectasis, laryngeal paralysis, or tracheal collapse) (1). There are well known risk factors for PTE in dogs: immune-mediated hemolytic anemia, hyperadrenocorticism, renal disease, cardiac disease, neoplasia, heartworm disease, sepsis, intravenous catheterization, exogenous steroid administration, pancreatitis, disseminated intravascular coagulation, blastomycosis, protein losing enteropathy, trauma, major surgery, blood transfusions, and cytotoxic agents (2–4). In cats, PTE is rare and risk factors include neoplasia, pancreatitis, nonhemolytic anemia, dilated cardiomyopathy, hepatic lipidosis, feline infectious peritonitis, glomerulonephritis, pneumonia and encephalitis (5). The clinical signs of PTE include dyspnea, tachypnea and lethargy. Pulmonary thromboembolism should be suspected in a dog which has a well-defined risk factor and is in pulmonary distress without a known cause. Many unsuspected cases are diagnosed on postmortem examination (2). In our patient, Cushing’s disease was suspected and adrenocorticotropic hormone (ACTH) stimulation showed a marked increase in cortisol levels. A high-dose dexamethasone suppression test showed a marked degree of cortisol suppression at 4 and 8 h post dexamethasone administration. These results indicate pituitary-dependent hyperadrenocorticism (PDH). Since our patient had PH and PDH, PTE was strongly suspected, but we wanted to confirm this prior to thrombolytic therapy. Imaging modalities used to diagnose PTE include radiography, nuclear scintigraphy, and pulmonary angiography with or without computed tomography (CT). Radiographic findings in PTE vary with the pathologic effect of the thromboembolic event. Radiographic findings with PTE include normal thoracic radiographs, pulmonary parenchymal changes (hypovascular or alveolar pattern), pulmonary vessel changes, cardiac changes (right heart and main pulmonary artery enlargement), mild to moderate pleural effusion, and pulmonary volume loss. An alveolar pattern indicates infarction, hemorrhage, atelectasis or edema, the latter 2 resulting from loss of surfactant. Alveolar patterns are amorphous with indistinct borders and can be focal or multifocal and peripherally or centrally located. The lobar artery and vein may not be identifiable or the lobar artery may attenuate rapidly. Pleural effusion is associated with pulmonary infarction. Radiography does not confirm PTE, but it excludes other diseases and provides correlation with other imaging techniques. Pulmonary thromboembolism should be considered in dyspneic animals with associated risk factors and normal thoracic radiographs without upper airway obstruction (6). Nuclear scintigraphy is the administration of radioactive atoms (radionuclides) bound to a biological marker. Gamma rays are emitted as the radionuclides decay and are detected with the use of a scintillation camera. The most commonly used radionuclide is technetium-99m (99mTc). Pulmonary perfusion studies are done by intravenous injection of 99mTc tagged with macroaggregates of albumin (99mTc-MAA). 99mTc-MAA travels to the lungs via pulmonary arteries and as it is trapped in capillary beds, it is distributed throughout the lungs proportional to the blood flow. Normal lung fields have uniform radioactivity except for areas over the heart. Areas of vascular occlusion show photopenic defects. Pulmonary perfusion scans have the advantage of being safe, quick, noninvasive, and not requiring anesthesia. Pulmonary perfusion scintigraphy is highly sensitive and normal perfusion excludes a diagnosis of PTE. The main disadvantage is the limited availability as nuclear scintigraphy is largely restricted to academic institutions. Pulmonary perfusion scans are not specific for PTE if pulmonary parenchymal disease (such as pneumonia) is present, since reduction in blood flow to a poorly ventilated area of the lung is a normal reflex response. Therefore current radiographs are necessary to evaluate perfusion scans. Pulmonary ventilation studies, in which the patient inhales a radioaerosol, can be used with perfusion studies to increase specificity but are usually only done in research settings because of the need for general anesthesia and specialized scavenge equipment (7). Selective angiography is the gold standard for the diagnosis of PTE, but it is invasive, requires expertise, and has risks and limitations. Contrast medium is injected directly into the main pulmonary artery and a positive diagnosis of PTE is made by direct observation of a filling defect. If more liberal criteria, such as vessel pruning and regional hypovascularity, are used to diagnose PTE, there are significantly higher false positives. In humans, selective angiography has resulted in death and major complications (renal failure, respiratory failure, hemorrhage, arrhythmias, perforation, bronchospasm, pulmonary edema, and anaphylaxis) in 1.3% of the cases (8). Computed tomographic angiography (CTA) has replaced selective angiography because it is quick, has a low risk of complications due to its noninvasiveness, and requires a lower dose of contrast medium. In people, CTA has been shown to be more sensitive and specific in the diagnosis of PTE than pulmonary perfusion/ventilation scintigraphy and selective angiography. Computed tomographic angiography identifies the emboli within the pulmonary arteries, pulmonary parenchymal changes, and other thoracic disease (8,9). In animals, general anesthesia is required. A pulmonary perfusion study was performed on our patient and demonstrated a photopenic defect in the left caudal pulmonary field confirming PTE (Figure 2). He was hospitalized for 9 d, during which he had intermittent syncope and dyspnea. He was treated with abdominocentesis; oxygen; low molecular weight heparin, 1 mg/kg body weight (BW), q12h, for the thromboembolus; pimobendan, 0.25 mg/kg BW q12h, for the pulmonary hypertension; and mitotane, 250 mg q12h, for the PDH. Two weeks after initial presentation, he was rechecked and an ACTH stimulation test demonstrated a good response to mitotane. An echocardiogram used to calculate the pulmonary arterial pressure indicated that it was 60 mmHg. The mitotane was reduced to 250 mg twice weekly for maintenance and the pimobendan was increased by 50% and abdominocentesis was repeated as required. He was euthanized 5 wk after initial presentation due to continued right heart failure. Figure 2 Pulmonary perfusion scans showing dorsal views of the patient (left) and a normal dog (right). The black areas indicate radioactivity. The scan shows a large photopenic area (within rectangle) in the left caudal pulmonary field.

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