Pulmonary thromboembolism (PTE) is an obstruction of one or more pulmonary vessels by a blood clot. The actual incidence of PTE is uncertain, although in critically ill animals or in those with certain disease states (eg, immune-mediated hemolytic anemia, corticosteroid administration, bacterial infections, protein-losing enteropathy or nephropathy, neoplasia, trauma, feline infectious peritonitis, diabetes mellitus, hyperadrenocorticism, hypothyroidism, disseminated intravascular coagulation, dirofilariasis) the incidence is considerable, and PTE is underdiagnosed. Mortality rates of PTE in animals are uncertain but probably significant. Survival depends on early diagnosis and early appropriate therapy.
Thromboemboli in the venous circulation become trapped in the pulmonary vasculature and, if occlusion is substantial, pulmonary and hemodynamic sequelae result. Animals with preexisting cardiac or respiratory compromise may be affected earlier or more severely. The acute pulmonary consequences of PTE include ventilation-perfusion mismatch, hypoxemia, hyperventilation, and bronchoconstriction. Hemodynamic consequences of PTE are related to the magnitude of the obstruction and presence of coexisting cardiopulmonary disease. Myocardial ischemia, arrhythmias, or right ventricular failure may result. Decreased cardiac output may ensue with severe obstruction to pulmonary arterial blood flow as a result of decreased venous cardiac return.
In dogs, PTE is associated with protein-losing nephropathy, heartworm disease, endocarditis, cardiomyopathy, necrotizing pancreatitis, hypercortisolism, immune-mediated hemolytic anemia, sepsis, diabetes mellitus, neoplasia, atherosclerosis, trauma, and major surgical procedures. Cardiomyopathy and neoplasia are most commonly associated with PTE in cats.
Clinical signs are nonspecific and most often subclinical or may be mild to profound, reflecting the severity of cardiorespiratory compromise. Dyspnea, tachypnea, and depression are commonly seen. Coughing, cyanosis, hemoptysis, collapse, shock, and sudden death can occur.
Diagnosis is often difficult because PTE can resemble many other conditions, including pneumonia, pulmonary edema or hemorrhage, neoplasia, or pleural effusion. Routine diagnostic tests such as thoracic radiography or arterial blood gas analysis are nonspecific and rarely confirm diagnosis. Arterial blood gas analysis will identify hypoxemia present in 80% of dogs, although response to oxygen is variable. Thoracic radiographs can be normal in 9%–27% of dogs and in 9% of cats with PTE. Abnormal radiographic findings with PTE include alveolar or interstitial pulmonary infiltrates or regional hypovascular lung areas. However, thoracic radiographs that underestimate the degree of clinical respiratory compromise should raise suspicion of PTE. Blood gas analysis may reveal hypoxemia and hypocapnia, indicating inefficient gas exchange, but the presence of normal blood gas values does not exclude PTE. Echocardiography can aid in assessment, demonstrating changes suggestive of PTE and pulmonary hypertension (dilation of the right ventricle, pulmonary artery, inferior vena cava; right ventricular hypokinesis; tricuspid regurgitation; abnormal septal wall motion). A normal echocardiogram does not exclude diagnosis of PTE. Spiral CT angiography or selective pulmonary angiography remain gold standards for diagnosis of PTE in people, but these advanced imaging studies are available at few veterinary institutions.
Therapy should begin as soon as possible and include support of respiratory and cardiovascular systems, prevention of thrombus development and recurrence, and possibly thrombolysis. Oxygen supplementation and bronchodilators are indicated when dyspnea is evident or when arterial oxygen saturation is <92%. Although anticoagulants such as warfarin or unfractionated or low-molecular-weight heparin do not lyse existing thrombi, their use is indicated to inhibit thrombus propagation and prevent recurrent venous thrombosis. Antiplatelet drugs such as aspirin or clopidogrel can be given together with, but not in lieu of, anticoagulant therapy. Sildenafil may benefit animals with documented pulmonary hypertension. Thrombolytic therapy can rapidly cause clot lysis and improve cardiovascular function and hemodynamic stability, thereby reducing mortality in animals with massive PTE and shock. Veterinary experience with thrombolytic agents such as streptokinase and tissue plasminogen activator is limited.