Pulmonary thromboembolism describes the occlusion of pulmonary vessels by a clot. It has usually arisen from the systemic venous circulation, embolises to the pulmonary circulation and causes obstruction of the arterial supply to an area of the lung. This results in ventilation perfusion mismatch occurring where there are areas of the lung which continue to be ventilated but do not receive adequate blood supply. This can result in severe hypoxia and marked signs of respiratory distress if the area of underperfused but ventilated lung is large.
Causes of pulmonary thromboembolism include:
- Cardiac disease: Dirofilaria immitis, dilated cardiomyopathy, chronic mitral valve insufficiency, endocarditis
- Neoplasia: lymphosarcoma, bronchoalveolar carcinoma, pancreatic carcinoma
- Disseminated Intravascular Coagulation
- Protein-losing nephropathy: amyloidosis, glomerulonephritis
- Protein-losing enteropathy
- Eosinophilic lung disease
- Air emboli
- Autoimmune haemolytic anaemia
- Iatrogenic: indwelling vascular catheters, transfusions
Clinical signs are usually non-specific. There may be an acute onset of respiratory distress, with increased depth, rate and effort of breathing. Patients may also present with an acute onset of signs of right sided heart failure due to the sudden increase in pulmonary vascular resistance.
There may be signs of an underlying disease such as Cushing's or intestinal disease.
Diagnosis is difficult ante-mortem.
History and clinical signs are usually vague and non-specific.
Radiography may demonstrate a diminution or loss of peripheral vessels and an increase in size of the central pulmonary artery, but are often normal.
Blood gas analysis will reveal the ventilation perfusion mismatch and there will be hypoxemia, hypocapnia and respiratory alkalosis.
Nuclear perfusion scintigraphy is a safe and sensitive test and will detect if there is a lack of perfusion of part of the lung.
Lung Ultrasound may reveal wedge shaped defects on the air-chest wall interface. Found to be 43% sensitive and 98% specific in a multi-center human trial compared to CT. 
This primarily involves treating the underlying cause.
Supportive care includes oxygen supplementation, strict cage confinement and careful parenteral fluid therapy.
Anticoagulant therapy should be considered in severe cases to prevent extension of the clot within the pulmonary circulation. Heparin has a rapid onset and short-term effects.
Fibrinolytic therapy is very expensive and lacks selectivity, but includes drugs such as streptokinase, urokinase and tissue plasminogen activator.
Prognosis is poor to guarded in cats and dogs. Recurrence is possible, especially if the cause has not been resolved.
|Pulmonary Thromboembolism Learning Resources|
Test your knowledge using flashcard type questions
|Small Animal Abdominal and Metabolic Disorders Q&A 01|
- Thoracic ultrasound for diagnosing pulmonary embolism slide share (accessed June 2016)
Pasquini, C. (1999) Tschauner's Guide to Small Animal Clinics Sudz Publishing
Boswood, A. (2010) Pulmonary parenchymal disease RVC Student Notes
|This article has been peer reviewed but is awaiting expert review. If you would like to help with this, please see more information about expert reviewing.|
|WikiVet® Introduction - Help WikiVet - Report a Problem|