Virchow Triad: Origin, Vial Irritation, Blood Disruption and Coagulation

It was enunciated for the first time by the German pathologist Rudolf Virchow in the year 1856.

He postulated that the anomalies in the blood flow, the hypercoagulability of the blood, and the lesions in the endothelium, which are cells that line the internal area of ​​all the blood vessels, are related to the origin of the formation of thrombi.

However, it should be noted that Virchow never identified a Triad of thrombosis as such but did identify the aspects related to the formation of thrombi.

But it was not until long after the death of Rudolf Virchow that modern scientists began to group these three main signs of coagulation and thrombus formation into a triad.

Then it was defined as the Virchow Triad (in recognition of the unpublished work of Rudolf Virchow linked to these issues).

Rudolf Virchow is considered by many as “the father of pathology.”

The postulation of his famous theory Omnis cellula e cellula or “each cell originates from another similar cell,” published in 1858, rejected the belief that hitherto prevailed, that organisms could arise spontaneously from a non-living matter.


Since it was previously believed that the worms appeared spontaneously due to the decomposition of the meat.

Another achievement attributed to Rudolf Virchow was clarifying the mechanisms of pulmonary thromboembolism.

He also developed the concept of thrombosis and embolism.

When Rudolf Virchow defined the conditions or risk factors that could lead to the abnormal formation of thrombi, he grouped them into three categories:

Factors that are due to the irritation of the vessel and its environment (Endothelial damage):

When the physiology of the endothelium is altered by structural or functional damage, the risk of thrombus formation increases.

The loss of the endothelial cells when tissue damage occurs causes the subendothelium to contact the blood, releasing the tissue factor in contact with the coagulation factor VII.

This is activated, triggering the formation of thrombi; these thrombi can also be formed by the adhesion of platelets, the local depletion of type two prostaglandin, and the absence of tissue plasminogen activator found in the endothelium.

This damage to the endothelial cells initiates coagulation. The conditions that fall into this category of risk include atherosclerosis, bacterial sepsis, and damage to the veins due to hypertension.

Factors that are due to the interruption of the bloodstream (abnormal blood flow):

In this category, abnormal blood flow is applied to those patients who reduce their mobility a long way or those who have varicose veins, cardiac arrhythmias, turbulence, stasis, and mitral stenosis.

When this happens, the blood accumulates or stagnates, thus increasing the chances of thrombus formation.

Turbulence or abnormal blood flow can:

  1.  Interrupting the laminar flow of the bloodstream and putting the platelets in contact with the endothelium.
  2. To cause the dilution of the coagulation factors activated by the presence of fresh blood.
  3. To delay the entrance of the coagulation factor inhibitors and allow the accumulation of thrombi.
  4. Favor the activation of endothelial cells, which causes thrombosis, and the adherence of leukocytes, among others.

Factors that are due to blood clotting (Hypercoagulability):

The final category of the triad is hypercoagulability; this can be caused mainly due to genetic disorders and can also be caused by some acquired problems.

Generally, these causes include many different factors, such as oral contraceptives, antithrombin III deficiency, hyperviscosity, nephrotic syndrome, obesity, and prolonged immobilization.

As well as the presentation of thrombi after trauma, disseminated intravascular coagulation, myocardial infarction, burns, disseminated cancer, and hereditary thrombotic disorders (such as factor V Leiden).

Cases were also reported in the prothrombin gene mutation, antithrombin III deficiency, protein C deficiency, protein S deficiency, pregnancy, and late delivery, atrial fibrillation, and heparin-induced thrombocytopenia.

In addition to race, prosthetic heart valves, sickle cell anemia, age, and smoking.

In most cases, thrombi are caused by various risk factors, but there is also the possibility of a hereditary thrombotic disorder.

These concepts to describe the factors that can cause thrombosis have been guiding principles for many researchers.

Although there is not much clarity on the origin of the Virchow triad, it has undeniably contributed to modern clinical practices, becoming a basis for more advanced valuations.

The advances in molecular biology and the new knowledge of physiopathology have facilitated more sophisticated instruments and have expanded this Virchow triad.