Deep vein thrombosis:

pathogenesis, diagnosis, and

medical management
• Deep vein thrombosis (DVT), a subset of venous thromboembolism
(VTE)
• Incidence of VTE : 1 per 1,000 people annually; 2/3 is DVT
• Complication :
• 1/3 case leads to pulmonary embolism
• Post-thrombotic syndrome (in up to 50% of patients within 2 years of DVT)
including leg pain, swelling, and in severe cases, venous ulcers
 Pathogenesis
Virchow’s Triad
The clinical conditions related to the elements of Virchow’s Triad;
Venous statsis include surgery or trauma, malignancy, prolonged immobility,
pregnancy, congestive heart failure, varicose veins, obesity,
Vascular injury advancing age, and a history of DVT
Hypercoagulability

tends to occur in areas with altered blood

flow (e.g. pockets adjacent to valves in the
deep veins of the leg)

blood flow ↓, oxygen tension declines

with a coincident increase in hematocrit
reducing important anticoagulant proteins (thrombomodulin
and endothelial protein C receptor) & drives the expression of
certain procoagulants (P-selectin )
Venous thrombus components : lines of Zahn (an inner platelet rich white thrombus forming
the so-called) surrounded by an outer red cell dense fibrin clot

Fibrin and extracellular DNA complexed with histone proteins forms the outer scaffold ,
used to determining thrombus susceptibility to tissue plasminogen activator (TPA) and
thrombolysis

ratio of procoagulants to anticoagulants ↑, risk of thrombus formation↑

DEFECT in
• the protein C anticoagulant pathway (protein C, protein S,
risk of thrombus formation↑
thrombomodulin, and perhaps EPCR)
• heparin-antithrombin pathway
• tissue factor inhibitor pathway

Risk factors for clot formation include :

5% of Caucasians and increases the risk of thrombosis 7-fold, , (factor Va resistant to the inhibitory
influence of protein C); cancer, oral contraceptives, obesity, and advancing age