Arterial 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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Arterial thrombosis On the Web |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
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]
Classification
There are two broad forms of thrombosis, arterial and venous. They are somewhat distinct in their underlying pathophysiology, but there is also a degree of overlap in the underlying pathophysiology.
You can read more about venous thrombosis here:
Possible site of thrombosis
- Carotid artery
- Coronary artery
- Intracerebral artery
- Mesenteric artery
- Peripheral artery
- Placental artery
- Pulmonary embolization
- Retinal artery
- Vertebral artery
Causes
- Abruptio placentae
- Arteritis
- Atherosclerosis
- Cancer (particularly pancreatic cancer)
- Catheters (indwelling in the venous bloodstream)
- Cholesterol embolization
- Diabetes mellitus
- Eclampsia
- Embolization including cholesterol embolization
- Genetics
- Hyperlididemia
- Hypertension
- Pre-eclampsia
- Smoking
- Stent
- Thoracic outlet syndrome
- Vasculitis
Natural History, Complications and Prognosis
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.
Diagnosis
Laboratory Findings
cDNA-PCR assays for gene mutations and polymorphisms:
- 4G/5G polymorphism of the plasminogen activator inhibitor-1 gene (PAI-1)
- Cystathionine beta synthetase (CBS) CBS T833C & G919A
- Factor V Leiden
- Glycoprotein IIIa A1/A2 (platelet glycoprotein)
- Methylenetetrahydrofolate reductase (MTHFR) MTHFR C677T
- Prothrombin G20210A
Serologic (blood) tests:
- Anticardiolipin antibodies (ACLA) IgG and IgM ACLA
- Antithrombin III
- Factor VIII
- Homocysteine
- Lupus anticoagulant (LA)
- Proteins C
- Protein S
Evaluation of hypofibrinolysis
- 4G/5G polymorphism of the plasminogen activator inhibitor-1 gene (PAI-1)(requires cDNA-PCR assay for gene mutation)
- Lipoprotein a Lp(a)
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 increase the risk of 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) outweigh the risk of bleeding associated with warfarin use.[2]
In-hospital patients, thrombosis is a major cause for complications and is occasionally fatal. In 2005,a Parliamentary Health Select Committee in UK, stated that the annual rate of death due to hospital-acquired thrombosis was 25,000.[3]
In patients admitted for surgery, compression stockings are widely used. In severe illness, prolonged immobility and in all orthopedic surgery, professional guidelines recommend
- low molecular weight heparin administration
- mechanical calf compression
- vena cava filter (if LMWH or mechanical compression is contraindicated and the patient has recently suffered deep vein thrombosis).[4][5]
In patients with medical rather than surgical illness, LMWH is known to prevent thrombosis,[5][6]
In United Kingdom, the Chief Medical Officer has issued guidelines that preventative measures should be used in patients, in anticipation of formal guidelines.[3]
Related Chapters
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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