Potential mechanisms by which various clinical conditions may facilitate deep-vein thrombosis. Risk factors or clinical conditions that increase the risk of DVT can be classified as either increasing the baseline propensity for thrombosis, or precipitating the thrombotic event acutely. According to Virchow’s triad, these conditions promote thrombosis through one (or more) of three major mechanisms: (1) inducing hypercoagulability, (2) directly injuring the vein wall, and (3) causing blood stasis.
. | Increased Baseline Propensity for Thrombosis . | Acute Insult . |
---|---|---|
Abbreviations: AT, antithrombin; HRT, hormone replacement therapy; OCT, oral contraceptives | ||
Hypercoagulability | Genetic | Increased Coagulants |
Increased coagulants | Blood-borne tissue factor | |
Prothrombin mutation G20210A | Malignancy (Trousseau’s syndrome) | |
Decreased anticoagulants | Congestive heart failure (?) | |
AT deficiency | Systemic infection (?) | |
Protein C deficiency | Exogenous administration of clotting factors | |
Protein S deficiency | rVIIa | |
Factor V Leiden | rVIII | |
Acquired | Acute Loss of Anticoagulants | |
Malignancy | Nephrotic syndrome (loss of AT) | |
Hyperhomocysteinemia | Initial warfarin therapy without heparin | |
HRT/OCT (?) | ||
Pregnancy (hormone-related) | ||
Nephrotic syndrome (loss of AT) | ||
Antiphospholipid syndrome | ||
Increased levels of clotting factors | ||
Direct Vessel Injury | Direct vessel injury would most often represent an acute insult | Intravascular catheters |
Trauma | ||
Examples of low-grade, chronic vessel injury that increase the baseline propensity for thrombosis may include: | Surgery | |
Endothelial injury secondary to chemotherapy | ||
Hyperhomocysteinemia | ||
Vasculitis | ||
Antiphospholipid syndrome | ||
Blood Stasis | More commonly functioning as an acute insult precipitating thrombosis, rather than increasing the baseline propensity for thrombosis: | Hospitalization/bed ridden |
Pregnancy (stasis) | ||
Limb paralysis (e.g., stroke, plaster casts) | ||
Age | Right heart failure | |
Obesity | Long-haul flights | |
Pregnancy (gradual immobility/stasis) | Vein compression (e.g., enlarged lymph node) | |
Sedentarism |
. | Increased Baseline Propensity for Thrombosis . | Acute Insult . |
---|---|---|
Abbreviations: AT, antithrombin; HRT, hormone replacement therapy; OCT, oral contraceptives | ||
Hypercoagulability | Genetic | Increased Coagulants |
Increased coagulants | Blood-borne tissue factor | |
Prothrombin mutation G20210A | Malignancy (Trousseau’s syndrome) | |
Decreased anticoagulants | Congestive heart failure (?) | |
AT deficiency | Systemic infection (?) | |
Protein C deficiency | Exogenous administration of clotting factors | |
Protein S deficiency | rVIIa | |
Factor V Leiden | rVIII | |
Acquired | Acute Loss of Anticoagulants | |
Malignancy | Nephrotic syndrome (loss of AT) | |
Hyperhomocysteinemia | Initial warfarin therapy without heparin | |
HRT/OCT (?) | ||
Pregnancy (hormone-related) | ||
Nephrotic syndrome (loss of AT) | ||
Antiphospholipid syndrome | ||
Increased levels of clotting factors | ||
Direct Vessel Injury | Direct vessel injury would most often represent an acute insult | Intravascular catheters |
Trauma | ||
Examples of low-grade, chronic vessel injury that increase the baseline propensity for thrombosis may include: | Surgery | |
Endothelial injury secondary to chemotherapy | ||
Hyperhomocysteinemia | ||
Vasculitis | ||
Antiphospholipid syndrome | ||
Blood Stasis | More commonly functioning as an acute insult precipitating thrombosis, rather than increasing the baseline propensity for thrombosis: | Hospitalization/bed ridden |
Pregnancy (stasis) | ||
Limb paralysis (e.g., stroke, plaster casts) | ||
Age | Right heart failure | |
Obesity | Long-haul flights | |
Pregnancy (gradual immobility/stasis) | Vein compression (e.g., enlarged lymph node) | |
Sedentarism |