The Virchow’s Triad is defined as an organizational structure that presents risk factors and causes of thrombosis and pulmonary embolism. Understanding the three corners of its triangle will help broaden our knowledge on blood clot formation, stroke, and deep vein thrombosis.
Rudolf Virchow, also known as “The Father of Pathology,” who formulated the Virchow’s Triad, introduced the concept of embolism, defining it as the separation of the large and smaller fragments that flow with the blood current and lodging into distant or remote vessels. This created the widespread method known as Embolia.
The clinical significance of Virchow’s triad demonstrates the basic physiology that causes the formation of thrombus in the blood vessels. When clots are formed in the vasculature areas of the body, the patient will have a higher risk of thromboembolic events such as Cerebrovascular accidents, myocardial infarction, pulmonary embolism, and ischemia. Understanding the triad could help health care providers and clinicians perceive the risk factors of developing deep vein thrombosis.
To easily recall the three corners of the triad, let us remember the acronym “SHE,” which stands for:
Stasis of Venous Circulation
Stasis of Venous Circulation
Venous stasis only happens when there is an obstruction that slows down the blood flow in the veins. This causes the thickening and accumulation of microthrombi that slows down fluid movement. Venous stasis is more likely to happen in people with prolonged immobility, hip or knee surgery, prolonged traveling, and patients with valvular heart disease and atrial fibrillation.
It is also known as thrombophilia. It describes the exaggerated tendency of blood to coagulate. The blood flow is normalized by the balance between the anti-thrombotic and procoagulant factors. Hypercoagulability happens when there are not enough anticoagulants or too many procoagulant factors. This only means that the patient has a higher risk of forming blood clots. Having thrombophilic disorders may either be inherited genetically or acquired.
Hypercoagulability can occur due to clinical conditions such as usage of oral contraceptives, Heparin-Induced Thrombocytopenia, chemotherapy drugs, postpartum period, Protein S and C deficiency, and sepsis caused by a severe illness.
Endothelial Damage to the Vein
The endothelium is described as a “cellophane” wrapped around the vascular tree and making it selectively penetrable to water and electrolytes. It holds an important role in maintaining homeostatic balance. The endothelial cells prevent blood clots through various antiplatelet agents such as prostacyclin and anticoagulant agents by forming a luminal vascular layer regulating coagulation. It also regulates the binding sites for coagulant factors on the surface of the cell and maintains the fluidity of the blood. Damage to the endothelium heightens the risk of blood clot formation through a number of mechanisms.
When the endothelium is punctured or ripped, the tissue factor that commences the coagulation cascade is exposed and increases the risk for sepsis and atherosclerosis. Endothelial dysfunction characterized by the imbalance between the procoagulant and anticoagulant agents plays a role in the pathogenesis of the development of thromboembolic diseases.