A complete necropsy was performed. With the exception of hepatic lipidosis, mild membranoproliferative glomerulonephritis,
and focal jejunal hemorrhage, the principal abnormalities were confined to the heart and lungs. The primary cardiac finding
was an enlarged right ventricle. The pulmonary valve leaflets were normal, as was the right ventricular outflow tract. The
lungs had sharply delineated areas of severe congestion, hemorrhage, and edema. These changes affected all of the right cranial
and middle lung lobes as well as portions of the left cranial lobe. Thrombi were present in the arteries entering the infarcted
lobes, and there was a firm and tightly adhered 1-x-0.75-cm thrombus at the junction of the main pulmonary artery and left
pulmonary artery (Figure 3A). Close inspection of the main pulmonary artery surface revealed a diffuse thickening and irregularity of the intima (Figure 3A). The bulk of the thrombotic material appeared to originate at the distal limit of the abnormal intimal tissue. Histologic
evaluation of the main pulmonary artery revealed extensive thickening of the intima and media due to mucin (glycosaminoglycan)
deposition in these layers (Figure 3B).
Figure 3A. This necropsy specimen shows the main pulmonary artery (MPA) and a pulmonary artery (PA) branch feeding the left
caudal lung lobe. The arrows define a tightly adhered pulmonary thrombus (T) at the distal limit of the main pulmonary artery.
This thrombus was obstructing the artery supplying the left caudal lobe and right middle lobe. Other thrombi were noted in
this region but were removed as part of the necropsy procedure. The intimal lining of the main pulmonary artery is covered
with extensive deposition of irregular, raised, whitish tissue that commences just above the pulmonary valve and extends to
the level of the thrombus. The pulmonary artery’s lining appears to be grossly normal.
Pulmonary thromboembolism is a well-recognized problem in dogs,2,3 but this case is unusual because it highlights diffuse and fatal thrombosis probably due to extensive main pulmonary artery
disease. The only known similar description of this condition was reported by investigators in Sweden4 and included seven cases in Cavalier King Charles spaniels (8 to 9 years old) that died or were euthanized because of chronic
valvular disease. One of the dogs had pulmonary thromboembolism, but all of the dogs had wrinkling and irregularity of the
main pulmonary artery. The pulmonary valve was normal in all the dogs. The authors speculated that the abnormal main pulmonary
artery tissue led to thromboembolism in the one dog and postulated that the disease in the main pulmonary artery of all seven
dogs may have been related to thrombocytopenia and macrothrombocytosis. These platelet abnormalities are common in this breed.4 Furthermore, the authors pointed out that the histologic changes in the pulmonary artery wall were similar to what is seen
in the cardiac valves in chronic valvular disease. They concluded that chronic valvular disease and the pulmonary artery changes
might be manifestations of generalized connective tissue disease.
The subject of our report did not have any evidence of primary heart disease, including chronic valvular disease, on the basis
of the history and the echocardiographic examination and necropsy findings. The platelets were not evaluated because of the
nature of the presentation and the rapid demise of the animal; however, there was no evidence that this dog had clinically
relevant platelet pathology.
Figure 3B. This photomicrograph shows the histologic features of the abnormal tissue in the main pulmonary artery. Mucin fills
the intima (above the internal elastic membrane [IEM]) and media (below the IEM) (alcian blue-periodic acid-Schiff stain;
bar = 50 µm).
This dog had pathologic evidence of glomerulonephritis, which can be associated with pulmonary thromboembolism.5 However, the histopathologic findings were mild and no hypoproteinemia was noted, so it is unlikely that glomerular disease
played a role in the vascular changes or development of the thrombus in this case.
The enlargement of the right ventricle was most likely due to high right ventricular afterload. There was no evidence that
this dog had turbulent blood flow that might explain the lesions in the main pulmonary artery. In addition, there was no echocardiographic
or necropsy evidence of heartworms. Indeed, the owner reported that the dog had received a monthly heartworm preventive since
6 months of age. Furthermore, the normal gross appearance of the distal pulmonary arteries supports the view that heartworm
disease was not involved in this animal's pulmonary problem.
This case may represent a generally unrecognized but important cause of pulmonary thrombosis in dogs. Based on the gross and
histologic features, it is likely that the pulmonary vascular changes would escape clinical and echocardiographic detection
until a thrombus develops. However, with improved echocardiographic capabilities, including transesophageal techniques, it
may be possible in the future to identify pulmonary vascular lesions before a thrombus develops. If this were to occur, long-term
antithrombotic therapy with heparin, warfarin, or aspirin might be indicated and could greatly benefit dogs with pulmonary
vascular disease similar to the subject in this report.