Aetiology

Virchow's triad is still the preferred aetiological model for VTE.[8]

  • Vessel wall damage: endothelial cell damage promotes thrombus formation, usually at the venous valves. Trauma, previous deep vein thrombosis, surgery, venous harvest, and central venous catheterisation can cause damage to the vessel wall.[9]

  • Venous stasis: the formation of thrombi is promoted by poor blood flow and stasis. Venous stasis and congestion result in valvular damage, further promoting thrombus formation. The following factors increase the risk for venous stasis: age >40 years, immobility, general anaesthesia, paralysis, spinal cord injury, myocardial infarction, prior cerebrovascular accident, varicose veins, advanced congestive heart failure, and advanced COPD.

  • Hypercoagulability: a number of other conditions (both inherited and acquired) increase the risk of VTE. These include cancer, high-oestrogen states (obesity, pregnancy, and hormone replacement), inflammatory bowel disease, nephrotic syndrome, sepsis, and inherited thrombophilias (factor V Leiden mutation, prothrombin gene mutation, protein C and S deficiency, anti-thrombin III deficiency, and anti-phospholipid antibody syndrome).

Pathophysiology

The most common initial site for thrombi forming in the deep venous system of the leg is just above and behind a venous valve.[10][11]​​ Less commonly, deep vein thrombosis (DVTs) can occur in the upper extremities. Usually, they resolve spontaneously. However, when a thrombus does propagate, it expands and grows in a proximal direction and across the lumen of the vein. In most cases, a small amount of flow continues on the extreme periphery of the thrombus, although complete obstruction can occur. Thrombi start in the calf veins and propagate in a proximal direction. However, in some instances, such as during pregnancy or following total hip arthroplasty, thrombus formation might initially be in the groin or iliac vein region. Endothelial damage appears to be less important in DVT than in arterial thrombosis.[12] Thrombi do not develop de novo in the pulmonary vasculature. Thus, a pulmonary embolism (PE) occurs when a thrombus dislodges from elsewhere and becomes trapped in the pulmonary vasculature.[13] The pathophysiology of PE is therefore directly related to that of DVT.

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