Table 1.

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 BaselinePropensity for ThrombosisAcute 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 BaselinePropensity for ThrombosisAcute 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  

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