Deep vein thrombosis pathophysiology

Editors-in-Chief: C. Michael Gibson, M.S., M.D. Associate Editor-In-Chief: Ujjwal Rastogi, MBBS [1]; Kashish Goel, M.D.

Deep Vein Thrombosis Microchapters
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Patient Information
Overview
Classification
Pathophysiology
Causes
Differentiating Deep vein thrombosis from other Diseases
Epidemiology and Demographics
Risk Factors
Triggers
Screening
Natural History, Complications and Prognosis
Diagnosis
Diagnostic Approach
Assessment of Clinical Probability and Risk Scores
Assessment of Probability of Subsequent VTE and Risk Scores
History and Symptoms
Physical Examination
Laboratory Findings
Ultrasound
Venography
CT
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Treatment
Treatment Approach
Medical Therapy
IVC Filter
Invasive Therapy
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Prevention
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Future or Investigational Therapies
Special Scenario
Upper extremity DVT
Recurrence
Pregnancy
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Overview

Venous thrombosis is a conglomerate of three mechanisms, described as the Virchow's triad:

1. Alterations in blood flow (stasis): Venous stasis is a major risk factor for development of thrombosis and occurs in certain pathological conditions (as in heart failure) wherein it causes an increase in platelet to endothelium contact and decrease the dilution of clotting factors. This increases the risk of clot formation and form microthrombi, which further grow and propagate.

2. Injury to the vascular endothelium or Endothelial dysfunction: Intrinsic or secondary to external trauma (Eg. catheterization) can cause intimal damage and stimulate clot formation. For details, please see Coagulation.

3. Alterations in the constitution of blood or hypercoagulability: Increased propensity to develop thrombosis due to an abnormality in the coagulation system.

Thrombus formation

A balance between the coagulation and fibrinolysis systems of the body maintains normal homeostasis. Anything that causes an imbalance in this leads to formation of a thrombus or hemorrhage. These factors include thrombopilias and other risk factors like immobilization, trauma, etc. An insult may expose the sub-endothelium and lead to collection of various coagulation factors leading to the formation of a thrombus of red blood cells,leukocytes, and fibrin. Thrombi usually develop first in the calf veins, and grow the direction of blood flow towards the heart. Sometimes, very extensive DVTs can extend to the iliac veins or the inferior vena cava.

Venous insuffiency

Chronic venous insufficiency may develop in patients who have DVT. Prospective studies have shown the incidence of venous insufficiency, also known as post-phlebitic syndrome is around 30% after 10 years of follow-up. The basic mechanism for development of venous insufficiency involves valvular incompetence. Valves of the deep veins can get involved early during the formation of DVT and ultimately get damaged, leading to back flow of blood into the veins. With the contraction of calf muscles, the blood moves into superficial veins leading to superficial venous insufficiency.

Special conditions

• May-Thurner syndrome: More DVT's occur in the left leg than in the right, because the right common iliac artery compresses the left common iliac vein.
• Phlegmasia alba dolens: Leg turns milky white after an acute DVT. The cause is not clear, however may include edema-induced compartment syndrome leading to tissue ischemia and gangrene.
• Phlegmasia cerulea dolens: Complete occlusion of the venous flow secondary to massive ilio-femoral thrombus and excessive edema.

This video explains the process of thrombosis: {{#ev:youtube|X_POCRsy7i4}}

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