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Deep Vein Thrombosis: Pathogenesis, Diagnosis, and Medical Management

Deep vein thrombosis (DVT) occurs when a blood clot forms in a deep vein, usually in the legs. It affects about 1 in 1,000 people annually. DVT can lead to pulmonary embolism in about 1/3 of cases and post-thrombotic syndrome in up to 50% of patients within 2 years. DVT pathogenesis is explained by Virchow's Triad of venous stasis, vascular injury, and hypercoagulability. Risk factors include surgery, trauma, malignancy, prolonged immobility, and genetic or acquired defects in natural anticoagulant pathways.

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53 views

Deep Vein Thrombosis: Pathogenesis, Diagnosis, and Medical Management

Deep vein thrombosis (DVT) occurs when a blood clot forms in a deep vein, usually in the legs. It affects about 1 in 1,000 people annually. DVT can lead to pulmonary embolism in about 1/3 of cases and post-thrombotic syndrome in up to 50% of patients within 2 years. DVT pathogenesis is explained by Virchow's Triad of venous stasis, vascular injury, and hypercoagulability. Risk factors include surgery, trauma, malignancy, prolonged immobility, and genetic or acquired defects in natural anticoagulant pathways.

Uploaded by

nerdoo3
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as PPTX, PDF, TXT or read online on Scribd
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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

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