Virchow Triad


Article Author:
Abigail Kushner
William West, DO


Article Editor:
Leela Sharath Pillarisetty


Editors In Chief:
Myron Bodman
Donald Kushner


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Sandeep Sekhon


Updated:
3/27/2019 10:18:03 AM

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. 


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Virchow Triad - Questions

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Which of the following is not part of the Virchow triad for deep venous thrombosis development?



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A 75-year-old female with a past medical history of obesity, breast cancer with metastasis to the lungs, and hypertension presents with five days of swelling and pain in her right lower extremity. She denies injury or trauma to the area, but is very active and states that the pain is limiting her ability to walk. She denies fevers, chills, nausea, shortness of breath, chest pain, sensory deficits or motor deficits. From the given history, what is most likely to be contributing to the patient's formation of a deep venous thrombosis?



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Which of the following is Virchow triad?



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Which of the following are the components of Virchow's triad?



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A 17-year-old female with no past medical history presents to the emergency department with the onset of left calf pain. She describes the pain as achy, non-radiating, and inhibiting her ability to walk comfortably. The patient denies medial history but has a family history of lung cancer. The patient is currently on birth control pills and occasionally takes ibuprofen for headaches. She is typically physically active, but recently fractured her right ankle while traveling in Brazil, so has been predominately sedentary for the past week. She returned from Brazil to the United States yesterday. Which of the following factors did not increase the patient's risk for deep venous thrombosis?



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Virchow Triad - References

References

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

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