- Virchow’s triad: 3 important factors for thrombus formation
- Venous stasis (blood flow)
- Hypercoagulable state (blood component)
Endothelial injury (blood vessels)
–Major trauma often precipitates one or all of the above risk factors; trauma pts. often have all three of these factors leading to a high risk of thromboembolism.
-Major trauma leads to significantly increased & persistent thrombin with disruption of its regulation.
- Direct injury to blood vessels→ intimal damage→ thrombosis.
- Prolonged bed rest, Immobilization, Hypoperfusion, & Paralysis, all promote venous stasis.
- ↓ed levels of antithrombin III & suppression of fibrinolysis may lead the trauma patient to become hypercoagulable.
- Thromboplastin (Tissue factor; TF) & markers of thrombin generation increase after trauma & that levels of natural anticoagulants such as Antithrombin, Protein C & Potein S are reduced.
- ↑ed severity of hypoperfusion → an increase in plasma thrombomodulin & a reduction in Protein C levels. This suggests that acute coagulopathy is due to systemic anticoagulation through activation of the protein C pathway.
- Besides consumption of clotting factors, Acidosis & hypothermia →reduced activity; & dilution from IV fluids & packed cell administration are also accepted causes of traumatic coagulopathy.
- In Acute traumatic coagulopathy– shock itself is associated with a coagulopathy: due to the systemic activation of anticoagulant & fibrinolytic pathways (not due to coagulation factor consumption or dysfunction because of acidosis, moderate hypothermia, or dilution)
- Immobility – a recognized cause of VTE; Immobility due to paralysis- a major contributing factor for the development of DVT in patients with trauma to the spinal cord. The lack of pumping action of the contracting muscles→ reduced blood flow & pooling of blood in the intramuscular sinuses of the calf→DVT.
- Increased hematocrits, elevated fibrinogen, & von Willebrand factor macromolecular complex levels increase blood viscosity, further influencing blood flow. Decreased blood flow could lead to endothelial damage, local accumulation of activation products of coagulation, & local decrease in inhibitor levels, all increasing coagulability of the blood.
- Associations with immobilization and obesity suggest that VTE after injury is a systemic hypercoagulable disorder with local manifestations of thrombosis related to lower extremity stasis.
Please see the article: