Thrombosis: Difference between revisions
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To view main article on venous thrombosis, click '''[[Venous thromboembolism|here]]''' | |||
To view main article on arterial thrombosis, click '''[[ST elevation myocardial infarction|here for myocardial thrombosis]]''' or '''[[Ischemic stroke|here for ischemic stroke]]''' | |||
==Overview== | ==Overview== | ||
Revision as of 16:19, 29 August 2018
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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]
To view main article on venous thrombosis, click here To view main article on arterial thrombosis, click here for myocardial thrombosis or here for ischemic stroke
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:
{{#ev:youtube|X_POCRsy7i4}}
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
There are two distinct forms of thrombosis:
Venous Thrombosis
- Deep venous thrombosis (with or without pulmonary embolism; together classified as venous thromboembolism/VTE)
- Portal vein thrombosis
- Renal vein thrombosis
- hepatic vein thrombosis (Budd-Chiari syndrome)
- Paget-Schroetter disease
- Cerebral venous sinus thrombosis
- Thoracic outlet syndrome (the cause of most Subclavian vein thrombosis unrelated to trauma)
Arterial Thrombosis
Classification of Embolism Based on Direction of Blood Flow
If a bacterial infection is present at the site of thrombosis, the thrombus may break down, spreading particles of infected material throughout the circulatory system (pyemia, septic embolus) and setting up metastatic abscesses wherever they come to rest.
Without an infection, the thrombus may become detached and enter circulation as an embolus, finally lodging in and completely obstructing a blood vessel (an infarction). The effects of an infarction depend on where it occurs.
The pathway of the embolism can be one of three types:
- Anterograde
- Retrograde
- Paradoxical
In anterograde embolism, the movement of emboli is in the direction of blood flow. In retrograde embolism, however, the emboli move in opposition to the blood flow direction; this is usually significant only in blood vessels with low pressure (veins) or with emboli of high weight. In paradoxical embolism, also known as crossed embolism, an embolus from the veins crosses to the arterial blood system. This is generally found only with heart problems such as septal defects between the atria or ventricles.
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