Also see Thrombosis, Embolism, and Aneurysm.
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 patients with certain disease states it is considerable and 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 may be mild to profound, reflecting the severity of cardiorespiratory compromise. Dyspnea, tachypnea, and depression are commonly observed. 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. Thoracic radiographs can be normal in 9–27% of dogs and 9% of cats with PTE. 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 rule out 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 rule out 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 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. Thrombolytic therapy can rapidly cause clot lysis, improved cardiovascular function, and improved hemodynamic stability, thereby reducing mortality in patients with massive PTE and shock. Veterinary experience with thrombolytic agents such as streptokinase and tissue plasminogen activator is limited.
Last full review/revision March 2012 by Ned F. Kuehn, DVM, MS, DACVIM; Steven L. Marks, BVSc, MS, MRCVS, DACVIM