PATHOPHYSIOLOGY OF THROMBOPHLEBITIS

Venous Stasis

Virchow’s
Triad

Hypercoagulability Endothelial Damage

VENOUS STASIS

Spinal injury, Inactivity, Hospitalizati Pregnancy/ Obesity Varicose AMI, HF,

hip fracture, sedentary on/ surgery childbirth veins late shock
joint lifestyle
replacement,
stroke

Paralysis of the Increase pressure on Impaired

extremities lower extremities contractility

Immobilization Prolonged bed rest Dilation of lower

extremity veins

Venous Stasis

HYPERCOAGULABILITY

Family history Prenancy/ Oral Cancer Polycythemia

of blood childbirth contraceptives
clotting
disorder
Release of
procoagulant from
cancerous growth. Increased RBC

Deficiency of antithrombin Increased level of procoagulants Hemoconcentration

III, protein C and protein S

Hypercoagulability
ENDOTHELIAL DAMAGE

Indwelling venous catheter, Hip surgery/ total hip Fx/ dislocation (repetitive
IV meds, pacing wires surgery 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

Prothrombinase

Prothrombin Thrombin

Fibrinogen Fibrin (clot)

Inflammation is triggered, causing

THROMBOPHLEBITIS
tenderness, swelling, and
erythema