Virchow Triad

Article Author:
Abigail Kushner
Article Author (Archived):
William West, DO
Article Editor:
Leela Sharath Pillarisetty
Updated:
3/27/2019 10:18:03 AM
PubMed Link:
Virchow Triad

Definition/Introduction

Virchow’s triad consists of three factors which may predispose a person to the development of venous thrombosis. These factors include:

  • Hypercoagulability
  • Stasis
  • Endothelial injury

Historically, Rudolf Virchow, a nineteenth-century Berlin scientist, and physician is credited with recognition of these factors due to his extensive work on venous thrombosis.[1]  These concepts are also relevant to the development of arterial thrombosis.[2]

Rudolf Virchow was one of the first physicians to examine disease at the cellular level, believing that most diseases, including pathological thrombosis, were caused by cellular pathology. Known as the "father of modern pathology," Virchow was a physician, scientist, anthropologist, prehistorian, and biologist in addition to his endeavors in pathology.  He is credited with work in cell biology, early cancer research and for recognizing that the left supraclavicular lymph node (now called Virchow’s node), when enlarged and hard to palpation, is associated with gastric cancer. Charles Emile Troisier later recognized the further association of other abdominal cancers as well as testicular cancer with the presence of Virchow’s node. Virchow sought to explain the causation of pulmonary thromboembolism and theorized that pulmonary arterial embolus arises from peripheral/distant thrombosis.  He attempted to explain the mechanism or define what specific conditions were necessary to initiate peripheral clotting and how a thrombus may dislodge from a peripheral vein, travel to the right heart and then enter the pulmonary arterial system. The three factors of Virchow's Triad include intravascular vessel wall damage, stasis of flow and the presence hypercoagulable state. Understanding the factors involved in the thrombus formation and subsequent thromboembolic events enables the clinician to stratify risk, direct clinical decision making regarding treatment and establish preventative measures.

Issues of Concern

Thrombosis, by definition, is the formation of a clot within a blood vessel. As described, Virchow’s Triad represents three qualities in physiology that can result in thrombosis which can lead to pathologies such as pulmonary embolism and deep venous thrombosis. These include:

Endothelial damage:

  • Damage to the endothelial wall of a vessel alters the dynamics of blood flow. Endothelial disturbance can result from insults such as smoking, chronically elevated blood pressure, and atherosclerotic disease secondary to hyperlipidemia. When an insult to the wall occurs, flow disruption or “turbulence” occurs. Turbulent flow within a vessel occurs when the rate of blood flow becomes too rapid, or blood flow passes over an affected surface; this creates disordered flow and eddy currents, increasing the friction of flow within a vessel. The tendency for turbulence to occur can be represented by Reynold’s number.[2][3]
  • Re = (v x d x p) / n
    • Where v = mean velocity, d = diameter (in centimeters), n = viscosity (in poise) and p = density.
  • Turbulence within the vessel may occur due to a variety of factors such as irregular atheromas from plaque formation, bifurcations in the vessel, and areas of stenosis, most prominent in patients with vascular disease.[2][3]

Venous stasis

  • Venous stasis is more likely to occur in patients with atrial fibrillation, valvular heart disease: prolonged immobility such as bedridden patients or prolonged travel, surgery, and trauma.[2][4] 
  • Exposure to cell proteins triggers anticoagulant pathways on the surface of endothelial cells.
  • The thinking is that as blood flow slows through vascular beds, flow reduces, and the natural anticoagulant properties from interaction with surface proteins are affected, resulting in thrombi production.[5]

Hypercoagulability

  • Hypercoagulability can occur due to a variety of clinical statuses such as pregnancy, use of oral contraceptive medications, cancer, chemotherapy drugs, and inherited thrombophilias.[6] 
  • Thrombophilias can include disease states such as protein C deficiency, protein S deficiency, antithrombin deficiency, hyperhomocysteinemia and homocystinuria, and antiphospholipid syndrome.[6]

Clinical Significance

The function of Virchow's triad is to demonstrate the underlying physiology that drives the formation of venous thrombus.  Formation of clots within the vasculature places the patient at risk for thromboembolic events such as CVA, pulmonary arterial embolus or organ infarction, ischemia, and cell death.  Understanding the physiology enables clinicians to better understand risk factors for the development of deep vein thrombosis. 


References

[1] Bagot CN,Arya R, Virchow and his triad: a question of attribution. British journal of haematology. 2008 Oct;     [PubMed PMID: 18783400]
[2] Chung I,Lip GY, Virchow's triad revisited: blood constituents. Pathophysiology of haemostasis and thrombosis. 2003 Sep-2004 Dec;     [PubMed PMID: 15692259]
[3] Hosseinzadegan H,Tafti DK, Prediction of Thrombus Growth: Effect of Stenosis and Reynolds Number. Cardiovascular engineering and technology. 2017 Jun;     [PubMed PMID: 28470538]
[4] Watson T,Shantsila E,Lip GY, Mechanisms of thrombogenesis in atrial fibrillation: Virchow's triad revisited. Lancet (London, England). 2009 Jan 10;     [PubMed PMID: 19135613]
[5] Esmon CT, Basic mechanisms and pathogenesis of venous thrombosis. Blood reviews. 2009 Sep;     [PubMed PMID: 19683659]
[6] Monie DD,DeLoughery EP, Pathogenesis of thrombosis: cellular and pharmacogenetic contributions. Cardiovascular diagnosis and therapy. 2017 Dec;     [PubMed PMID: 29399533]