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.