VIRCHOW TRIAD: COMPONENTS AND FEATURES - MEDICINE - 2025

The Virchow 's triad is the name given to three events or primary alterations which together allow and promote the formation of thrombus which were described by Rudolf Virchow.

It is named after the German pathologist Rudolf Ludwig Karl Virchow, who described and explained for the first time in 1856 this chain of 3 events and conditions that must occur for the production of a thrombosis.

Virchow defined a thrombosis as a blood clot or platelet aggregate that can obstruct a vein or artery.

According to Virchow's description, three primary alterations occur for the formation of thrombi, the initial one can be any, but when the first one occurs, it will almost necessarily determine the onset of the other two in response to the initial event.

The alteration or imbalance of any of the components of the triad places the patient in a state of predisposition to thrombosis or prothrombotic state.

It is important to clarify that the mechanism that forms a clot and the mechanism that forms a thrombus is the same. The difference is that a clot is a homeostatic mechanism that prevents hemorrhage, forming without occluding the vessel and over time it is replaced with connective tissue, that is, it works as a temporary patch in the event of endothelial damage.

On the other hand, the thrombus lacks functionality at the time and place of its appearance, and pathologically obstructs the blood flow of the affected vessel, causing the tissues to suffer ischemia.

Classic features of thrombosis

Hemodynamic factors are responsible for determining the characteristics of thrombi, according to their location or the mechanisms that produce them.

When talking about an artery, because the speed of blood flow in them is greater, thrombi are formed mainly by atheromatous plaques or areas of blood turbulence that can cause endothelial damage.

According to this, the arterial thrombus is formed mainly by platelets that try to repair the endothelial damage, which gives it a whitish appearance.

Regarding the veins, the thrombus is generated mainly in those vessels in which blood pressure and velocity are low. This decrease in speed generates changes in the coagulation system that facilitates platelet aggregation and the fall of natural anticoagulants.

Venous thrombi are usually made up mainly of fibrin and erythrocytes, which give them a reddish hue.

Components of Virchow's Triad

Endothelial injury (damage to the vessel wall)

Endothelial injury is one of the most influential factors in the formation of thrombi in the bloodstream due to primary thrombophilia.

Various aggressions can cause endothelial damage, hypertension, blood turbulence, bacterial toxins, high cholesterol, radiation exposure, pregnancy, exposure to female hormones, among others.

When there is damage to the endothelium, a transient vasoconstriction occurs that decreases the speed of normal blood circulation, giving way to the second component of the triad, since normal blood speed is one of the main anticoagulant mechanisms.

Additionally, platelet aggregation occurs to repair the damage caused, acting as a plug that in turn will decrease the intravascular lumen, also favoring the slowing down of blood circulation.

Tissue factors are then released, prostaglandins I2 are depleted, and tissue plasminogen activators are also depleted. In this way, various prothrombotic phenomena work simultaneously.

Impaired blood flow (slow circulation)

Blood flow is one of the main anticoagulant mechanisms in the body, since the speed of the flow prevents the accumulation of homeostatic factors and activated platelets in a specific place.

Therefore, it is easy to assume that a slowdown in blood flow or stasis, especially if it is venous, is the mechanism that most easily favors the appearance of thrombi.

As mentioned in the first component, this alteration may be the cause or the consequence of an endothelial injury.

The normal flow of blood is laminar, in this way the platelets and other formed elements flow through the center of the lumen and do not touch the endothelium, from which they are separated by a layer of plasma.

When flow slowing occurs, or platelets come into contact with the endothelium, adhesion between leukocytes is promoted and the dilution of clotting factors is prevented.

Various pathologies can produce an alteration of the blood flow acting in different ways. For example, atheromatous plaques produce blood turbulence, arterial dilations produce stagnation of the blood or local stasis, blood hyperviscosity and sickle cell anemia produce stasis in small vessels, and like these, many pathologies.

Hypercoagulability

This term is also known in some cases as thrombophilia, and it refers mainly to an alteration of the coagulation pathways that causes the blood to lose its liquid characteristic.

These alterations in blood viscosity or coagulability can be primary or secondary, with the primary ones referring to hereditary or genetic ones, and the secondary ones, on the other hand, to those acquired thrombophilic factors.

Primary or genetic thrombophilias should be considered in patients under 50 years of age who consult for thrombophilic processes, even in the presence of risk factors.

A series of complex and point mutations of the factor V gene and prothrombin have been demonstrated, which are the most common causes of inherited hypercoagulability.

Similarly, the more common or frequent secondary or acquired thrombophilic factors are predisposing to venous thrombosis rather than arterial thrombosis.

Venous catheterization, family history of varicose veins of any kind, advanced age, cancer, prolonged immobilization, heart failure, among others, are some of the acquired thrombophilic factors that predispose to venous thrombosis.

Hyperestrogenism secondary to taking oral contraceptives or pregnancy has been shown to increase hepatic synthesis of coagulation factors and a reduction in anticoagulant synthesis.

Virchow described these three components as the events prior to thrombus formation, however, he did not relate them as a triad.

It was long after his death that modern scientists grouped these three major events or signs of clotting as a triad for ease of understanding and study.

References

1. Martínez-Murillo C, Quintana-González S, Ambriz-Fernández R, Hernández Paula M. The thrombotic problem. Hematology 2000; 1: 17-20
2. Majluf-Cruz A. Haemostatic mechanisms. In Foundations of Hematology, Ruiz Argüelles GJ, Ed.; Ed. Med. Panamericana 1998: 264-288.
3. David R. Kumar. Virchow's Contribution to the Understanding of Thrombosis and Cellular Biology. Clin Med Res. 2010 Dec; 8 (3-4): 168–172. US National Library of Medicine. National Institutes of Health. Recovered from: ncbi.nlm.nih.gov
4. Bagot CN, Arya R. Virchow and his triad: a question of attribution. Br J Haematol 2008; 143: 180–190. US National Library of Medicine. National Institutes of Health. Recovered from: ncbi.nlm.nih.gov
5. Eric Wong and Sultan Chaudhry. VENOUS THROMBOEMBOLISM (VTE). McMaster Pathophysiology Review. Recovered from: pathophys.org