Venous Thrombosis

 

 

Pathophysiology

Superficial veins: thick walled muscular structures that lie just under the skin

Deep veins: thin walled and have less muscle in their media than superficial

  • veins sun parallel to arteries
  • deep and superficial both have valves that permit unidirectional flow back tot he heart
  • valves lie at the base of a segment of the vein that is expanded into a sinus
  • sinus allows valves to open without coming in contact with the vein wall

 

Perforating veins:

  • vessels with valves that allow one-way blood flow from the superficial system tot he deep system

 

Virchow’s triad

  • 3 factors key to venous thrombosis development:
  1. blood stasis
  2. vessel wall injury
  3. altered blood coagulation

 

Venous Stasis:

  • reduced blood flow
  • eg heart failure or shock
  • dilated veins
  • due to skeletal muscle contraction reduced
  • bed rest reduces blood flow by at least 50%
  • damage to vessel creates site for clot formation
  • chemical irritation to vein
  • vessel disease
  • coagulation occurs most commonly when pt is abruptly withdrawn from anticoagulants

 

Thrombus formation frequently accompanies thrombophlebitis

 

Upper thrombosis may occur from:

  1. IV catheters
  2. internal vasculature trauma
  3. pacemaker leads
  4. chemotherapy ports
  5. dialysis catheters
  6. TPN lines
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