Deep vein thrombosis pathophysiology: Difference between revisions
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==Overview== | ==Overview== | ||
Venous thrombosis is | Venous thrombosis is composed of three mechanisms, collectively 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 [[Congestive heart failure|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. | '''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 [[Congestive heart failure|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 | '''2. Injury to the vascular endothelium ([[Endothelial dysfunction]])''': Intrinsic or secondary to external trauma, such as [[catheterization]], can cause [[Tunica intima|intimal]] damage and [[coagulation|stimulate clot formation]]. | ||
'''3. Alterations in the constitution of blood | '''3. Alterations in the constitution of blood ([[Hypercoagulability]])''': Abnormal changes in coagulation can increase the propensity to develop thrombosis. | ||
==Thrombus formation== | ==Thrombus formation== | ||
* Normal [[homeostasis]] is maintained by the balance between the [[coagulation]] and [[fibrinolysis]] systems of the body. | |||
* A homeostatic imbalance leads to formation of a [[thrombus]] or [[hemorrhage]]. | |||
:* Factors that increase the risk for a homeostatic imbalance include: | |||
::*[[Thrombopilias]] | |||
::*Immobilization | |||
::*Trauma | |||
* An insult to homeostatic balance can expose the subendothelium and lead to the collection of various coagulation factors. Accumulation of coagulation factors can lead to the formation of a thrombus of [[red blood cell|red blood cells]], [[leukocyte|leukocytes]], and [[fibrin]]. | |||
* A thrombus are characteristically found to develop first in the calf veins and progressively grow in the direction of blood flow (leading to the heart). | |||
* An exceedingly extensive DVT can extend well into the [[iliac vein|iliac veins]] or [[inferior vena cava|the inferior vena cava]]. | |||
==Venous insuffiency== | ==Venous insuffiency== | ||
[[ | * In patients with DVT, there is a potential to develop [[chronic venous insufficiency]], also known as [[post-phlebitic syndrome]]. | ||
* At 10 years of follow-up, the incidence of venous insufficiency is around 30%. | |||
* Valvular incompetence is the mechanism responsible for [[venous insufficiency]] development. Valves within the deep veins may be involved early in the formation of a deep vein thrombus and subsequently become damaged. This damage causes lack of blood flow back into the involved veins. When the calf muscle is contracted, the blood moves to superficial veins and can ultimately lead to superficial venous insufficiency. | |||
==Special conditions== | ==Special conditions== | ||
* [[May-Thurner syndrome]]: | * [[May-Thurner syndrome]]: As a result of the right common iliac artery compressing the left common iliac vein, DVTs occur more commonly in left leg vasculature than the right. | ||
* [[Phlegmasia alba dolens]]: | * [[Phlegmasia alba dolens]]: Following an acute episode of DVT, the leg may turn a milky white color. Causation is not clear but may be linked to edema-induced compartment syndrome resulting to tissue ischemia and gangrene. | ||
* [[Phlegmasia cerulea dolens]]: Complete occlusion of the venous flow secondary to massive ilio-femoral thrombus and excessive edema. | * [[Phlegmasia cerulea dolens]]: Complete occlusion of the venous flow secondary to massive ilio-femoral thrombus and excessive edema. | ||
===Video: The Process of Thrombosis=== | |||
{{#ev:youtube|X_POCRsy7i4}} | {{#ev:youtube|X_POCRsy7i4}} | ||
Revision as of 18:58, 14 June 2012
Editor(s)-In-Chief: The APEX Trial Investigators, C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Cafer Zorkun, M.D., Ph.D. [2] Ujjwal Rastogi, MBBS [3]; Kashish Goel, M.D.; Assistant Editor(s)-In-Chief: Justine Cadet
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Deep vein thrombosis pathophysiology On the Web |
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Risk calculators and risk factors for Deep vein thrombosis pathophysiology |
Overview
Venous thrombosis is composed of three mechanisms, collectively 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 (Endothelial dysfunction): Intrinsic or secondary to external trauma, such as catheterization, can cause intimal damage and stimulate clot formation.
3. Alterations in the constitution of blood (Hypercoagulability): Abnormal changes in coagulation can increase the propensity to develop thrombosis.
Thrombus formation
- Normal homeostasis is maintained by the balance between the coagulation and fibrinolysis systems of the body.
- A homeostatic imbalance leads to formation of a thrombus or hemorrhage.
- Factors that increase the risk for a homeostatic imbalance include:
- Thrombopilias
- Immobilization
- Trauma
- An insult to homeostatic balance can expose the subendothelium and lead to the collection of various coagulation factors. Accumulation of coagulation factors can lead to the formation of a thrombus of red blood cells, leukocytes, and fibrin.
- A thrombus are characteristically found to develop first in the calf veins and progressively grow in the direction of blood flow (leading to the heart).
- An exceedingly extensive DVT can extend well into the iliac veins or the inferior vena cava.
Venous insuffiency
- In patients with DVT, there is a potential to develop chronic venous insufficiency, also known as post-phlebitic syndrome.
- At 10 years of follow-up, the incidence of venous insufficiency is around 30%.
- Valvular incompetence is the mechanism responsible for venous insufficiency development. Valves within the deep veins may be involved early in the formation of a deep vein thrombus and subsequently become damaged. This damage causes lack of blood flow back into the involved veins. When the calf muscle is contracted, the blood moves to superficial veins and can ultimately lead to superficial venous insufficiency.
Special conditions
- May-Thurner syndrome: As a result of the right common iliac artery compressing the left common iliac vein, DVTs occur more commonly in left leg vasculature than the right.
- Phlegmasia alba dolens: Following an acute episode of DVT, the leg may turn a milky white color. Causation is not clear but may be linked to edema-induced compartment syndrome resulting to tissue ischemia and gangrene.
- Phlegmasia cerulea dolens: Complete occlusion of the venous flow secondary to massive ilio-femoral thrombus and excessive edema.
Video: The Process of Thrombosis
{{#ev:youtube|X_POCRsy7i4}}