A young man with a history of
deep vein thrombosis and
pulmonary embolism 11 years ago presented again with acute
pulmonary embolism and was treated initially with intravenous
heparin at our institution. Five days later he had another massive bout of
pulmonary embolism causing
hypotension. Pulmonary angiography confirmed the presence of thrombi in both pulmonary arteries, with complete obstruction of the left pulmonary artery. He was treated successfully by emergency pulmonary
embolectomy. Blood investigations later confirmed the diagnosis of
protein S deficiency and he was started on
warfarin therapy for life. Massive
pulmonary embolism should be treated aggressively.
Thrombolytic therapy accelerates clot lysis, reduces pulmonary pressures, restores pulmonary capillary volume and reverses right
heart failure faster than
heparin alone. There is also a trend towards decreased mortality with thrombolysis. In the presence of
shock, the patient should be resuscitated and if facilities for emergency
embolectomy are available, surgery is a viable alternative to thrombolysis, especially if the clot burden is massive. In young patients with recurrent
venous thromboembolism in the absence of obvious predisposing factors, it is important to exclude inherited
plasma protein deficiencies of
protein S,
protein C,
antithrombin III,
plasminogen and
fibrinogen.