• Virchow’s triad: 3 important factors for thrombus formation
  

1. Venous stasis (blood flow)
   
2. Hypercoagulable state (blood component)
   
3. 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: 

PMCID: PMC3195354
Deep Vein Thrombosis Prophylaxis in Trauma Patients
Serdar Toker,  David J. Hak,  and Steven J. Morgan