Pathophysiology of Thrombophlebitis [PDF]

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PATHOPHYSIOLOGY OF THROMBOPHLEBITIS Venous Stasis



Vircho w’s Triad Hypercoagulability



Endothelial Damage



VENOUS STASIS Spinal injury, hip fracture, joint replacemen t, stroke



Inactivity, sedentary lifestyle



Hospitaliza tion/ surgery



Pregnancy / childbirth



Paralysis of the extremities



Obesity



Varico se veins



Increase pressure on lower



Immobilizatio n



Prolonged bed rest



AMI, HF, late shock



Impaired contractility



Dilation of lower extremity



Venous Stasis HYPERCOAGULABILITY Family history of blood clotting disorder



Prenancy/ childbirth



Deficiency of antithrombin III, protein C and protein ENDOTHELIAL DAMAGE



Oral contraceptiv es



Cancer



Release of procoagulant from cancerous growth. Increased level of procoagulants



Hypercoagulabilit y



Polycythemi a



Increased RBC Hemoconcentrati on



Indwelling venous catheter, IV meds, pacing wires



Hip surgery/ total hip surgery



Fx/ dislocation (repetitive motion injury)



Direct trauma to the veins (especially femoral an iliac) infection/ inflammatory/ inflammation of the vein



Endothelial Damage



Injury to vessel



Connective tissue exposed, chemicals released Active clotting factors



Inactive clotting factor



Calcium and platelet chemicals Prothrombina se



Prothromb in



Thrombi n Fibrinogen



THROMBOPHLEBITIS



Fibrin (clot)



Inflammation is triggered, causing tenderness, swelling, and erythema