Pathophysiology of Venous Thromboembolism Formation
Hemostasis refers to a tightly regulated mechanism that maintains the integrity of the circulatory system in the setting of vascular damage. The pathophysiology of venous thromboembolism is centered around the pillars of Virchow's triad of venous stasis, endothelial damage, and hypercoagulability. Disruption of the endothelial lining results in activation and deposition of circulating platelets. Simultaneously, exposure to tissue factor activates the coagulation cascade, culminating in thrombin generation and fibrin deposition to stabilize the platelet plug. Under normal conditions, thrombus formation is contained by regulatory mechanisms, such as the antithrombotic and fibrinolytic pathways. When pathological processes overwhelm these regulatory mechanisms, excessive thrombin generation may occur and cause thrombosis.[9,11] Surgery increases the risk via trauma, endothelial damage, and immobilization. A prospective study demonstrated that the risk of venous thromboembolism is highest during the first 6 weeks after inpatient surgery but remains elevated for up to 12 weeks.
Deep vein thrombosis typically starts in the calf veins near venous valves, likely due to hypoxia and stasis. While most thrombi in the calf veins remain asymptomatic and spontaneously resolve, about 25 percent progress to involve proximal veins. Proximal deep vein thrombosis is typically symptomatic, and if left untreated, symptomatic proximal deep vein thrombosis progresses to symptomatic pulmonary embolism in one-third to one-half of patients. Once treated, risk of recurrence of venous thromboembolism is about 10 percent per year.[14–16]
Plast Reconstr Surg. 2022;149(1):121e-129e. © 2022 Lippincott Williams & Wilkins