Virchow's Triad and Deep Vein Thrombosis (DVT)

Suspected Deep Vein Thrombosis (DVT):
Authors: Dean Percy Yan Yu Reviewers: Tristan Jones Ryan Brenneis Man-Chiu Poon* Maitreyi Raman* * MD at time of publication
Pregnancy, Oral Contraceptives (OCP)
Pathogenesis and Complications
Platelet Activation
Increased clot formation
Hypercoagulable State
↑ ability for the blood to coagulate upon stimulation
Inherited Disorders
Congenital defect in coagulation (ie. Factor V Leiden, Factor II
mutation, Protein S/C deficiency) ↑ blood clotting ability
Estrogen promotes
hypercoagulability, especially in presence of other risk factors
• Venous thrombus causes pulmonary embolism, arterial thrombus causes stroke
• Previous DVT is risk factor for current DVT
Abnormal release of coagulation-promoting cytokines
Systemic injuryà activation of coagulation cascade
Bacteria Artificial Valve
Physically damages blood vessel walls
Adhere/invade vessel wall
Abnormal surface
Vessel Injury
Exposes tissue factor on damaged cells and subendothelium for vWF binding
Virchow’s Triad
Venous Stasis
Low blood flow rate over site of vessel injury, concentrating blood clotting factors at that site
Fat contains more aromatase, converts more androgens to estrogen
Sedentary lifestyle, poor venous return
Clot formation typically occurs in leg veins
Deep, large veins allow for blood pooling (stasis, hypercoagulability) Venous return from legs often against gravity (stasis)
Valves in leg veins prone to backflow (stasis)
↓ muscle motion = ↓ venous blood flow
Fracture, immobilization, bedrest, long vehicle/airplane ride
Destruction of vein valve by clot
Venous Insufficiency
Clot prevents blood from returning to heart. Blood accumulating in the leg results in unilateral leg edema and venous inflammation (redness, warmth, tenderness)
1. 2. 3.
Clot embolizes to the lungs
-*Pulmonary embolism (acute life threatening complication)
-Chronic thromboembolic pulmonary hypertension
Sign/Symptom/Lab Finding
Re-Published September 1, 2019 on