The Triad of Virchow is the name given to three events or primary alterations that together allow and favor the formation of a thrombus and which were described by Rudolf Virchow.
It receives its name from 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 a platelet aggregate that can clog a vein or artery.
According to Virchow's description, three primary alterations occur for the formation of the thrombi, which may be the initial one, but when the first occurs, it will almost necessarily determine the start 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 lies in the fact 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 functions as a temporary patch before an 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.
Index
- 1 Classical characteristics of thrombosis
- 2 Components of the Virchow Triad
- 2.1 Endothelial injury (damage to the vessel wall)
- 2.2 Altered blood flow (slowness of circulation)
- 2.3 Hypercoagulability
- 3 References
Classical characteristics of thrombosis
The hemodynamic factors are responsible for determining the characteristics of the thrombi, according to the location or the mechanisms that produce them.
When speaking of 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.
As for the veins, the thrombus is generated mainly in those vessels in which the velocity and blood pressure are low. This decrease in speed generates changes in the coagulation system that facilitates platelet aggregation and the fall of natural anticoagulants.
The venous thrombi are usually formed mainly by fibrin and erythrocytes, which give it a reddish tone.
Components of the Virchow 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 by primary thrombophilia.
Various aggressions can produce endothelial damage, hypertension, blood turbulence, bacterial toxins, high cholesterol, exposure to radiation, pregnancy, exposure to female hormones, among others.
When there is injury of the endothelium, a transient vasoconstriction occurs that decreases the speed of the normal blood circulation, giving way to the second component of the triad, because the normal blood velocity 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 intravascular light, also favoring the slowing down of blood circulation.
Tissue factors are then released, prostaglandins I2 are depleted and tissue plasminogen activators are depleted. In this way, various prothrombotic phenomena work simultaneously.
Altered blood flow (slowness of circulation)
Blood flow is one of the main anticoagulant mechanisms of the organism, since the speed of the flow prevents accumulation of homeostatic factors and activated platelets at a specific site.
Therefore, it is easy to assume that a slowing of blood flow or stasis, especially if it is venous, is the mechanism that favors the appearance of thrombi more easily.
As mentioned in the first component, this alteration may be the cause or consequence of an endothelium lesion.
The normal flow of the blood is laminar, in this way the platelets and other formed elements flow through the center of the light and do not touch the endothelium, from which they are separated by a layer of plasma.
When the slowing of the flow occurs, or the platelets come into contact with the endothelium, the adherence between the leukocytes is favored and prevents the dilution of the coagulation factors.
Various pathologies can produce an alteration of blood flow acting in different ways. For example, atheromatous plaques produce blood turbulence, arterial dilatations cause 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 refers mainly to an alteration of the coagulation pathways that causes the blood to lose its liquid characteristic.
These alterations in the blood viscosity or coagulability can be primary or secondary, being that the primary ones refer to the hereditary or genetic ones, and the secondary ones, on the other hand, to those thrombophilic factors acquired.
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 specific mutations of the factor V gene and prothrombin have been demonstrated, which are the most frequent causes of hereditary hypercoagulability.
Similarly, the most common or common thrombophilic 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 venous thrombosis.
It has been shown that hyperestrogenism secondary to taking oral contraceptives or pregnancy increases hepatic synthesis of coagulation factors and a reduction in the synthesis of anticoagulants.
Virchow described these three components as the events prior to the formation of a thrombus, however, he did not relate them as a triad.
It was long after his death, when modern scientists grouped these three events or main signs of coagulation as a triad to facilitate their understanding and study.
References
- Martínez-Murillo C, Quintana-González S, Ambriz-Fernández R, Hernández Paula M. The thrombotic problem. Hematology 2000; 1: 17-20
- Majluf-Cruz A. Hemostatic mechanisms. In Fundamentals of Hematology, Ruiz Argüelles GJ, Ed.; Ed. Med. Panamericana 1998: 264-288.
- 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. Retrieved from: ncbi.nlm.nih.gov
- 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. Retrieved from: ncbi.nlm.nih.gov
- Eric Wong and Sultan Chaudhry. VENOUS THROMBOEMBOLISM (VTE). McMaster Pathophysiology Review. Retrieved from: pathophys.org