Deep venous thrombosis and pulmonary emboli: etiology, medical treatment, and prophylaxis

Risk factors for venous thrombosis include conditions leading to venous stasis, hypercoagulable states, and trauma to veins. The most important factor is venous stasis. Both extrinsic and intrinsic coagulation pathways are intimately involved in the thrombotic process. In recent years, the importance in thrombus formation of the endothelium, platelet products, the fibrinolytic system, and inhibitors of clotting mechanisms has been discovered. Deficiencies of proteins that normally protect against venous thrombosis have been found. Heparin therapy with subsequent warfarin therapy is still the primary treatment for deep venous thrombosis or pulmonary emboli. Fibrinolytic agents lyse pulmonary emboli but are not as effective in deep venous thrombosis. The incidence of serious bleeding complications has hampered the use of fibrinolytic agents except in emergency situations. Even the newer agents, which act more specifically on thrombi instead of on plasma factors, are associated with a similar incidence of hemorrhagic events. Dextrans are a suitable alternative for treatment of deep venous thrombosis when heparin cannot be used. In the prophylaxis of deep venous thrombosis, minidose heparin (5,000 U every 8 hours subcutaneously) is effective, safe, and convenient in most situations. Heparin-dihydroergotamine, dextran, or warfarin can also be used. Aspirin has been disappointing. In orthopaedic surgery, minidose heparin is not protective; large pulmonary emboli may be prevented by starting warfarin therapy at the time of surgery or by daily dextran infusions. Finally, recent studies have shown that lower doses of warfarin than previously recommended are protective against recurrent venous thrombosis and have a reduced risk of hemorrhagic complications.