The diagnosis of pulmonary thrombo-embolism is difficult. Many animals with minor pulmonary showering by emboli can be completely
asymptomatic, while those with major thromboembolic disease can develop profound respiratory distress and die acutely. The
clinical hallmark of the disease is the development of respiratory difficulty in an animal with a predisposing cause of hypercoagulability.
Auscultation findings are variable, ranging from normal to harsh or even crackles.
Most affected animals have significant hypoxia, which can be determined by clinical parameters, or by arterial blood-gas analysis
or pulse oximetry. Thoracic radiographs are variable and often reveal normal to hyperlucent lung fields. Alternatively some
animals with thromboembolism might have areas of alveolar disease or pleural effusion. Acute pulmonary thromboembolism often
is accompanied by a sudden decrease in platelet count, which presumably is caused by platelet consumption. Definitive diagnosis
of pulmonary thromboembolism is made by selective angiography. The finding of abnormal perfusion on scintigraphic ventilation/perfusion
scanning also is strongly suggestive of thromboembolic disease.
If pulmonary thromboembolism is suspected, several potential therapies can be attempted. Aggressive supportive care, attention
to tissue perfusion, oxygen supplementation and treatment of the underlying disease remain priorities for its management.
If the size of the embolus is not excessive, then the dog's own fibrinolytic system might be able to break it down eventually
and recanalize obstructed vessels. The time required for resolution in critically ill dogs might vary from just a few days
to two or three weeks. "Clot buster" drugs, such as tissue plasminogen activator, streptokinase, or urokinase, actively break
down clots within the circulation. Such drugs are most effective if delivered within two hours of development of the clot
and if delivered directly onto the surface of the clot. This can be difficult to achieve.
If thromboembolic disease is suspected, prophylactic therapy with heparin seems to be helpful to prevent formation of
more thrombi, but it has no effect to break down of thrombi that already are present. Unfractionated heparin doses of 100-300
IU/kg subcutaneously qid or CRI 10-50 IU/kg hourly can be administered. Unfractionated heparin therapy should be monitored
by daily measurement of PTT values. Prolongation of the PTT by 50 percent from the baseline is adequate heparin therapy. Heparin
therapy should be weaned gradually as the clinical state improves because rebound hypercoagulability can occur if it is suddenly
Dr. Hoskins is owner of DocuTech Services. He is a diplomate of the American College of Veterinary Internal Medicine with
specialities in small animal pediatrics. He can be reached at (225) 955-3252, fax: (214) 242-2200, or e-mail: firstname.lastname@example.org