Acquired Causes of Thromboembolism
Condition | Comments |
|---|---|
Autoimmune disorder with increased risk of venous or arterial thrombi and pregnancy complications due to the presence of antiphospholipid antibodies | |
Increases risk of arterial thrombi Higher risk in patients with preexisting stenosis When atherosclerotic plaques rupture, they expose or release tissue factor, activate coagulation, initiate local platelet adhesion and aggregation, and cause thrombosis | |
Cancer (pancreas, stomach, lung, breast, prostate, colon, promyelocytic leukemia) | May activate coagulation by expressing and exposing tissue factor on membrane surfaces, by secreting a factor X–activating protease, or both |
Associated with the development of antibodies directed against heparin-platelet factor 4 complexes that activate platelets, leading to consumptive thrombocytopenia and venous or arterial thrombosis | |
Possible cause Due to deficiency of folate, vitamin B12, or vitamin B6 or mutations in the genes coding for cystathionine-beta synthase (homocystinuria) or methylene-tetrahydrofolate reductase | |
Infection, if severe (eg, sepsis) | Increases risk of venous thromboembolism Increases expression and exposure of tissue factor by monocytes and macrophages Decreases formation of activated protein C Increases factor VIII levels |
Oral contraceptives that contain estrogen | Low absolute risk (3–9/10,000) of venous thrombosis but higher than in nonpregnant nonusers (1–5/10,000) More frequent in patients who have a genetic abnormality that predisposes to venous thromboembolism, and in patients who smoke or are ≥ 35 years of age |
Tissue injury | Due to trauma or surgery |
Venous stasis | Due to surgery, orthopedic or paralytic immobilization, heart failure, pregnancy, bed rest, travel, or obesity |