Thrombosis
| Thrombosis | |
| ICD-10 | I80-I82 |
|---|---|
| ICD-9 | 437.6, 453, 671.5, 671.9 |
| MeSH | D013927 |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
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Overview
Thrombosis is the formation of a clot or thrombus inside a blood vessel, obstructing the flow of blood through the circulatory system. Thromboembolism is a general term describing both thrombosis and its main complication which is embolisation. The term was coined in 1848 by Rudolph Carl Virchow.[1]
Causes
Classically, thrombosis is caused by abnormalities in one or more of the following (Virchow's triad):
- The composition of the blood (hypercoagulability)
- Quality of the vessel wall (endothelial cell injury)
- Nature of the blood flow (hemostasis)
The formation of a thrombus is usually caused by the top three causes, known as Virchow's triad. To elaborate, the pathogenesis includes: an injury to the vessel's wall (such as by trauma, infection, or turbulent flow at bifurcations); by the slowing or stagnation of blood flow past the point of injury (which may occur after long periods of sendentary behavior - for example, sitting on a long airplane flight; by a blood state of hypercoagulability (caused for example, by genetic deficiencies or autoimmune disorders).
High altitude has also been known to induce thrombosis [3][4]. Occasionally, abnormalities in coagulation are to blame.
Intravascular coagulation follows, forming a structureless mass of red blood cells, leukocytes, and fibrin.
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 (upper extremity vein)
- Cerebral venous sinus thrombosis
- Thoracic outlet syndrome (the cause of most Subclavian Vein Thrombosis unrelated to trauma)
Arterial thrombosis
- Stroke (either thrombotic or embolic)
- Myocardial infarction (usually coronary thrombosis due to rupture of an atherosclerotic plaque)
- Thoracic outlet syndrome (may precipitate arterial thrombosis as well as venous)
Embolisation
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.
Most thrombi, however, become organized into fibrous tissue, and the thrombosed vessel is gradually recanalized.
Prevention
Thrombosis and embolism can be partially prevented with anticoagulants in those deemed at risk. Generally, a risk-benefit analysis is required, as all anticoagulants lead to a small increase in the risk of major bleeding. In atrial fibrillation, for instance, the risk of stroke (calculated on the basis of additional risk factors, such as advanced age and high blood pressure) needs to outweigh the small but known risk of major bleeding associated with the use of warfarin.[2]
In people admitted to hospital, thrombosis is a major cause for complications and occasionally death. In the UK, for instance, the Parliamentary Health Select Committee heard in 2005 that the annual rate of death due to hospital-acquired thrombosis was 25,000.[3] In patients admitted for surgery, graded compression stockings are widely used, and in severe illness, prolonged immobility and in all orthopedic surgery, professional guidelines recommend low molecular weight heparin administration, mechanical calf compression or (if all else is contraindicated and the patient has recently suffered deep vein thrombosis) the insertion of a vena cava filter.[4][5] In patients with medical rather than surgical illness, LMWH too is known to prevent thrombosis,[5][6] and in the United Kingdom the Chief Medical Officer has issued guidance to the effect that preventative measures should be used in medical patients, in anticipation of formal guidelines.[3]
See also
References
- ↑ Hellemans, Alexander (1988). The Timetables of Science. New York, New York: Simon and Schuster. p. 317. ISBN 0671621300. Unknown parameter
|coauthors=ignored (help) - ↑ National Institute for Health and Clinical Excellence. Clinical guideline 36: Atrial fibrillation. London, June 2006.
- ↑ 3.0 3.1 Hunt BJ (2008). "Awareness and politics of venous thromboembolism in the United kingdom". Arterioscler. Thromb. Vasc. Biol. 28 (3): 398–9. doi:10.1161/ATVBAHA.108.162586. PMID 18296598. Unknown parameter
|month=ignored (help) - ↑ National Institute for Health and Clinical Excellence. Clinical guideline 46: Venous thromboembolism (surgical). London, April 2007.
- ↑ 5.0 5.1 Geerts WH, Pineo GF, Heit JA; et al. (2004). "Prevention of venous thromboembolism: the Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy". Chest. 126 (3 Suppl): 338S–400S. doi:10.1378/chest.126.3_suppl.338S. PMID 15383478. Unknown parameter
|month=ignored (help) - ↑ Dentali F, Douketis JD, Gianni M, Lim W, Crowther MA (2007). "Meta-analysis: anticoagulant prophylaxis to prevent symptomatic venous thromboembolism in hospitalized medical patients" (PDF). Ann. Intern. Med. 146 (4): 278–88. PMID 17310052. Unknown parameter
|month=ignored (help)
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