- A combination of venous stasis, hypercoagulability (or activated coagulation in response to trauma) and endothelial damage (which constitute Virchow’s triad) may be observed in the majority of orthopaedic patients. One or more of these factors will lead to the formation of platelet aggregates at any sites of altered or turbulent blood flow (including valves or sites of compression) with consequent local release of thrombogenic substances, stimulating the formation and further expansion of a fibrin thrombus.
- The deep veins in the calf are the most common site, leading to the formation of deep vein thrombosis (DVT). Venous return relies on local muscle contraction (or muscle pump) and valves to prevent back-flow.
Risk factors for thrombogenesis
- Systemic:
- Malignancy
- Surgery or trauma
- Infection
- Obesity
- ? Smoking
- Patient specific:
- Immobility
- Previous DVT/PE
- Family history
- Known clotting abnormality/thrombophilia
- Pregnancy or hormone therapy
- Lower limb surgery (particularly hip fracture)
- Major surgery
- Varicose veins
Consequences of thrombogenesis
- Many patients will remain asymptomatic while others may develop symptomatic pulmonary embolism without evidence of DVT. Potential outcomes following a deep vein thrombosis include:
- Eventual dissolution of the clot or re-canalisation if total occlusion was present.
- Embolisation to distant locations, often lodging in, and potentially occluding, the pulmonary arteries (pulmonary embolism, PE). PE may lead to VQ (ventilation/perfusion) mismatch, which results in hypoxia and right heart failure, which can be fatal.
- Organisation within the deep veins possibly causing incompetence of local valves. Long-term this can result in venous stasis leading to oedema, ulceration, pain and the possibility of recurrent emboli (termed post-thrombotic syndrome).