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Excerpt from Deep Venous Thrombosis and Thrombophlebitis


Synonyms, Key Words, and Related Terms: deep venous thrombosis, DVT, deep vein thrombosis, deep-vein thrombosis, deep vein thrombi, venous thrombosis, venous thrombosis in the legs, leg swelling, lower extremity DVT, deep vein blood clots, deep-vein blood clots, pulmonary embolism, PE, deep venous thrombophlebitis, deep vein thrombophlebitis, deep-vein thrombophlebitis, superficial vein thrombophlebitis, superficial-vein thrombophlebitis, superficial thrombophlebitis, heparin, low-molecular-weight-heparin, LMWH, Virchow triad, venous stasis, vessel wall injury, hypercoagulable state, calf vein DVT, isolated calf vein DVT, peripheral venous disease, varicose veins, catheter-induced DVT, calf vein thrombi, chronic venous insufficiency, venous ulceration, phlegmasia cerulea dolens, leg pain, Homans sign, phlegmasia alba dolens, long plane trips, long car trips, acute myocardial infarction, immobilization longer than 3 days, stroke, systemic lupus erythematosus, SLE, Behçet syndrome, homocystinuria, polycythemia rubra vera, thrombocytosis, inherited disorders of coagulation, inherited disorders of fibrinolysis, antithrombin III deficiency, protein C deficiency, protein S deficiency, factor V Leyden, dysfibrinogenemias, disorders of plasminogen activation, IV drug abuse, oral contraceptives, estrogens, heparin-induced thrombocytopenia, Wells Clinical Score for DVT

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Background

Deep venous thrombosis (DVT) and its sequela, pulmonary embolism (PE), are the leading causes of preventable in-hospital mortality in the United States. Although PE is discussed in other articles, it must be emphasized that it is primarily a complication of DVT.

The first reference to peripheral venous disease was recorded on the Ebers papyrus in 1550 BC and documented the potential fatal hemorrhage that may ensue from surgery on varicose veins. In 1644, Schenk first observed venous thrombosis when he described an occlusion in the inferior vena cava. In 1846, Virchow recognized the association between venous thrombosis in the legs and PE. Heparin was only introduced to clinical practice in 1937. Over the last 25 years, considerable progress has been made in the pathophysiology, diagnosis, and treatment of DVT.

Pathophysiology

The Virchow triad, as first formulated (ie, venous stasis, vessel wall injury, hypercoagulable state), is still the primary mechanism for the development of venous thrombosis. The relative importance of each factor is still debated. The formation, propagation, and dissolution of venous thrombi represent a balance between thrombogenesis and the body's protective mechanisms, specifically the circulating inhibitors of coagulation and the fibrinolytic system.

In practical terms, the development of venous thrombosis is best understood as the activation of coagulation in areas of reduced blood flow. This explains why the most successful prophylactic regimens are anticoagulation and minimizing venous stasis. DVT of the lower extremity usually begins in the deep veins of the calf around the valve cusps or within the soleal plexus. A minority of cases arise primarily in the ileofemoral system as a result of direct vessel wall injury, as seen with hip surgery or catheter-induced DVT. The vast majority of calf vein thrombi dissolve completely without therapy. Approximately 20% propagate proximally. Propagation usually occurs before embolization. The process of adherence and organization of the venous thrombus does not begin until 5-10 days after thrombus formation. Until this process has been established fully, the nonadherent disorganized thrombus may propagate and/or embolize.

Not all venous thrombi pose equal embolic risk. Studies have shown that isolated calf vein thrombi carry a limited risk of PE. Furthermore, studies have suggested that isolated calf vein thrombi are smaller and do not cause significant morbidity or mortality if they embolize. Contradictory evidence from several other studies has indicated that isolated calf vein thrombi do embolize, suggesting that propagation proximally may occur rapidly and that fatal PE arising from isolated calf vein DVT is a significant risk.

The current diagnostic and therapeutic management of DVT is strongly influenced by the different risks assigned to proximal and calf vein thrombi. The propagation and organization of the venous thrombus usually result in destruction of venous valves and produce varying degrees of venous outflow obstruction. Spontaneous lysis and complete recanalization of established proximal DVT occurs in fewer than 10% of patients, even with anticoagulation. These factors are the most important pathogenic mechanisms in the development of chronic venous insufficiency.

Frequency

United States

The exact incidence of DVT is unknown because most studies are limited by the inherent inaccuracy of clinical diagnosis. More importantly, most DVT is occult and usually resolves spontaneously without complication. Existing data that underestimate the true incidence of DVT suggest that about 80 cases per 100,000 persons occur annually. Approximately 1 person in 20 will develop a DVT in the course of his or her lifetime. About 600,000 hospitalizations per year occur for DVT in the United States.

In hospitalized patients, the incidence of venous thrombosis is considerably higher and varies from 20-70%. Venous ulceration and venous insufficiency of the lower leg, which are long-term complications of DVT, affect 0.5% of the entire population. Extrapolation of this data reveals that as many as 5 million people have venous stasis and varying degrees of venous insufficiency.

Mortality/Morbidity

Death from DVT is attributed to massive PE, which causes 200,000 deaths annually in the United States. PE is the leading cause of preventable in-hospital mortality.

Sex

The male-to-female ratio is 1.2:1.

Age

DVT usually affects individuals older than 40 years.

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