Thrombosis
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Thrombosis Microchapters |
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Site of Thrombosis |
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Differentiating Thrombosis from other Diseases |
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Diagnosis |
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Treatment |
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Thrombosis On the Web |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Thrombosis is the formation of a thrombus (medical term for a clot) inside a blood vessel. This can dislodge from the site it was formed and can move along the flow of blood to distant places in the body. A piece of thrombus that is transported in this way is called an embolus (plural emboli). This process of formation an emboli, from a thrombus is called thromboembolism. The term was coined in 1848 by Rudolph Carl Virchow.
The most important sites of thrombosis formation, based on their frequency and clinical effect are coronary arteries and deep veins of the legs. Former, the most important site of arterial thrombosis and latter the most important site of venous thrombosis.
Pathophysiology
Rudolf Virchow noted several factors affecting the clot formation, which are as follows:
1) Alterations in blood flow (stasis): Blood flows throughout the circulatory system, without significantly stopping or slowing any where. In certain pathological conditions where the blood flow slows down or stops, it causes:
- Increase in platelet to endothelium contact
- 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: Intrinsic or secondary to external trauma (eg, catheterization) can cause intimal damage and stimulates clot formation. See Coagulation.
3) Alterations in the constitution of blood (hypercoagulability): It is the propensity to develop thrombosis due to an abnormality in the system of coagulation.
These three conditions are collectively known as Virchow's triad and lead to intravascular coagulation, forming a mass of red blood cells, leukocytes, and fibrin.
Shown below is a table depicting the elements of Virchow's triad and their modern counterparts.
| Virchow's | Modern | Notes |
|---|---|---|
| Phenomena of interrupted blood-flow | "Stasis" or "venous stasis" | The first category, alterations in normal blood flow, refers to several situations. These include turbulence, stasis, mitral stenosis, and varicose veins. The equivalence of Virchow's version and the modern version has been disputed. |
| Phenomena associated with irritation of the vessel and its vicinity | "Endothelial injury" or "vessel wall injury" | The second category, injuries and/or trauma to endothelium includes damage to the veins arising from shear stress or hypertension. |
| Phenomena of blood-coagulation | "Hypercoagulability" | The last category, alterations in the constitution of blood, has numerous possible risk factors such as hyperviscosity, deficiency of antithrombin III, nephrotic syndrome, changes after severe trauma or burn, disseminated cancer, late pregnancy and delivery, race, age, whether the patient is a smoker, and obesity. All of these risk factors lead to hypercoagulability. |
Thrombus Formation
- Usually there is a balance between the coagulation and fibrinolysis systems in order to not having abnormal thrombosis in the body.
- Factors that increase the risk for a homeostatic imbalance include:
Immobilization
- An insult to homeostatic balance can expose the sub-endothelium 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 is characteristically found to first develop in the calf veins and progressively grow in the direction of blood flow (leading to the heart).
- An exceedingly extensive thrombosis in deep veins can extend well into the iliac veins or the inferior vena cava.
- Atherosclerosis is a miss balance between lipids and the hemostasis system which caused clot in arteries. By occluding the artery myocardial infarction, stroke could happen .
- Thrombosis can happen in both Bare Metal Stent (BMS) and Drug Eluting Stent (DES).
Factors that serve as nidus for development stent thrombosis are:
Delayed endothelialization.
Inflammatory response to the stent material.
Hypersensitivity reaction around the stent material in DES serving as nidus for ST.
- Pregnancy increases risk of having thrombosis in both veins and arteries because of hypercoagulate state .
- Acquired risk factors for thrombosis are:
Oral contraceptive use,
Advanced age
Surgery
Prolonged immobilization like hospitalization .
This video explains the process of thrombosis:
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Genetics
Genetic factors that play roles in causing thrombosis :
- Non-O blood groups
- Factor V Leiden mutation
- Prothrombin G20210A gene variants
- Polymorphisms in factors IX17 or XI
Gross Pathology
- Dull appearance.
- Zahn line from platelets and fibrin with layers of RBCs in pulmonary venous thromboembolism.
- Gross picture of thrombosis is different in live and dead person.
In live person it is gray and firm.
In dead person it is dark purple or yellow elastic called "chicken fat".
Microscopic Pathology
- lamination
- Zahn line
Classification
Arterial | Venous | Arterial and Venous Thrombosis: Differences and Similarities
Causes
Site of Thrombosis
Arterial | Venous
Differentiating Thrombosis from other Diseases
Arterial | Venous
Risk Factors
The following are the risk factors for thrombosis:
- Medical
- Familial
- Antithrombin III deficiency
- Protein C deficiency/Protein S deficiency
- APC resistance (Factor V Leiden)
- Dysfibrogenemia
- Hypoplasminogenemia
- Familial homocysteinemia
Natural History, Complications and Prognosis
Diagnosis
Diagnostic Evaluation
Treatment
Risk Factor Modifications | Prevention