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Thrombosis
From Wikipedia, the free encyclopedia
Thrombosis
Contents
1 Causes
1.1 Hypercoagulability
1.2 Endothelial cell injury
1.3 Disturbed blood flow
2 Classification
2.1 Venous thrombosis
2.2 Arterial thrombosis
3 Natural history
4 Embolization
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5 Prevention
6 Treatment
7 See also
8 References
9 External links
Causes
The main causes of thrombosis are given in Virchow's triad which lists hypercoagulability, endothelial cell
injury, and disturbed blood flow.
Hypercoagulability
Hypercoagulability or thrombophilia, is caused by, for example, genetic deficiencies or autoimmune disorders.
Recent studies indicate that neutrophils play a pivotal role in deep vein thrombosis, mediating numerous prothrombotic actions.[3][4][5]
Classification
There are two distinct forms of thrombosis, venous thrombosis and arterial thrombosis, each of which can be
presented by several subtypes.
Venous thrombosis
Venous thrombosis is the formation of a thrombus (blood clot) within a vein. There are several diseases which
can be classified under this category:
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Arterial thrombosis
Arterial thrombosis is the formation of a thrombus within an artery. In most cases, arterial thrombosis follows
rupture of atheroma, and is therefore referred to as atherothrombosis.
Another common cause of arterial occlusion is atrial fibrillation, which causes a blood stasis within the atria
with easy thrombus formation. In addition, it is well known that the direct current cardioversion of atrial
fibrillation carries a great risk of thromboembolism, especially if persisting more than 48 hours.
Thromboembolism strikes approximately 5% of cases not receiving anticoagulant therapy. When cardiac
rhythm is restored clots are pushed out from atria to ventricles and from these to the aorta and its branches.[10]
Arterial thrombosis can embolize and is a major cause of arterial embolism, potentially causing infarction of
almost any organ in the body.
Stroke
A stroke is the rapid decline of brain function due to a disturbance in the supply of blood to the brain. This can
be due to ischemia, thrombus, embolus (a lodged particle) or hemorrhage (a bleed). In thrombotic stroke, a
thrombus (blood clot) usually forms around atherosclerotic plaques. Since blockage of the artery is gradual,
onset of symptomatic thrombotic strokes is slower. Thrombotic stroke can be divided into two categorieslarge
vessel disease and small vessel disease. The former affects vessels such as the internal carotids, vertebral and
the circle of Willis. The latter can affect smaller vessels such as the branches of the circle of Willis.
Myocardial infarction
Myocardial infarction (MI) or heart attack, is caused by ischemia, (restriction in the blood supply), often due to
the obstruction of a coronary artery by a thrombus. This restriction gives an insufficient supply of oxygen to the
heart muscle which then results in tissue death,(infarction). A lesion is then formed which is the infarct. MI can
quickly become fatal if emergency medical treatment is not received promptly. If diagnosed within 12 hours of
the initial episode (attack) then thrombolytic therapy is initiated.
Other sites
Hepatic artery thrombosis usually occurs as a devastating complication after liver transplantation.[11]
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Natural history
If a thrombus forms inside a blood vessel, without medical intervention the thrombosis may proceed to several
possible outcomes:
1. Embolisation: the thrombus detaches from the underlying endothelial wall, leading to distal embolisation
and vessel occlusion. An arterial thromboembolus may lead to a stroke, central retinal artery occlusion,
ischaemic limb, mesenteric ischaemia or some form of localised ischaemia depending on the arterial
circulation of the embolus. A venous thromboembolus may occlude the pulmonary artery leading to
pulmonary embolism.
2. Lysis: the thrombus may be acutely lysed by circulatory plasmin. This is essentially the physiological
equivalent to pharmacological thrombolysis performed in the hospital.
3. Ischaemia/infarction: if an arterial thrombus cannot be lysed by the body and it does not embolise, and if
the thrombus is large enough to impair or occlude blood flow in the involved artery, then local ischaemia
or infarction will result. A venous thrombus may or may not be ischaemic, since veins distribute
deoxygenated blood that is less vital for cellular metabolism. Nevertheless, non-ischaemic venous
thrombosis may still be problematic, due to the swelling caused by blockage to venous drainage. In deep
vein thrombosis this manifests as pain, redness, and swelling; in retinal vein occlusion this may result in
macular oedema and visual acuity impairment, which if severe enough can lead to blindness.
4. Organisation: following the thrombotic event, residual vascular thrombus will be re-organised
histologically with several possible outcomes. For an occlusive thrombus (defined as thrombosis within a
small vessel that leads to complete occlusion), wound healing will reorganise the occlusive thrombus into
collagenous scar tissue, where the scar tissue will either permanently obstruct the vessel, or contract down
with myofibroblastic activity to unblock the lumen. For a mural thrombus (defined as a thrombus in a
large vessel that restricts the blood flow but does not occlude completely), histological reorganisation of
the thrombus does not occur via the classic wound healing mechanism. Instead, the platelet-derived
growth factor degranulated by the clotted platelets will attract a layer of smooth muscle cells to cover the
clot, and this layer of mural smooth muscle will be vascularised by the blood inside the vessel lumen
rather than by the vasa vasorum.
Embolization
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 abscesses of a
metastatic nature 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, which unless
treated very quickly will lead to tissue necrosis (an infarction) in the area past the occlusion. If the occlusion is
in the coronary artery, myocardial ischaemia is likely to occur, whereby cardiac myocytes cannot function
properly due to lack of oxygen. This lack of oxygen is then likely to result in a myocardial infarction.
Most thrombi, however, become organized into fibrous tissue, and the thrombosed vessel is gradually
unblocked.
Prevention
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Prophylaxis of venous thromboembolism with heparin in medical patients does not appear to decrease mortality
and while it may decrease the risk of pulmonary embolism and deep vein thrombosis it increases the risk of
bleeding and thus results in little or no overall clinical benefit.[13][14] Mechanical measures also appeared of
little benefit in this group and in those with a stroke resulted in harm.[13] Evidence supports the use of heparin
following surgery which has a high risk of thrombosis to reduce the risk of DVTs; however the effect on PEs or
overall mortality is not known.[15][16][17]
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.[18]
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
thrombosis was 25,000, with at least 50% of these being hospital-acquired.[19] Hence thromboprophylaxis
(prevention of thrombosis) is increasingly emphasized. 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 (LMWH) 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.[20][21] In patients with medical rather than surgical illness, LMWH too is known
to prevent thrombosis,[21][22] 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.[19]
However, thromboprophylaxis can lead to complications such as bleeding. There are new, non-invasive ways to
stratify bleeding risk for patients with VTE and PE, by using tools like the RIETE Registry. The RIETE registry
is an interactive database which uses data from previous and current patients, even groups not typically
recruited like women and elderly as well as those with pre-existing conditions like Cancer or renal failure. The
RIETE Registry offers more personalized options for patients with clotting risk, and it also has created a
predictive calculator based on the registry's findings.[23]
Treatment
Warfarin and Vitamin K antagonists, are anticoagulants that can be taken orally to reduce thromboembolic
occurrence. Where a more effective response is required, heparin can be given (by injection) concomitantly. As
a side effect of any anticoagulant, the risk of bleeding is increased, so the international normalized ratio of
blood is monitored. Self-monitoring and self-management are safe options for competent patients, though their
practice varies. In Germany, about 20% of patients were self-managed while only 1% of U.S. patients did home
self-testing (according to one 2012 study).[24]
See also
National Blood Clot Alliance
Blood clotting tests
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Thromboxane
References
1. Furie B, Furie BC (2008). "Mechanisms of thrombus formation". New England Journal of Medicine 359 (9): 938949.
doi:10.1056/NEJMra0801082 (https://dx.doi.org/10.1056%2FNEJMra0801082). PMID 18753650
(https://www.ncbi.nlm.nih.gov/pubmed/18753650).
2. Handin RI (2005). "Chapter 53: bleeding and thrombosis". In Kasper DL, Braunwald E, Fauci AS et al. Harrison's
Principles of Internal Medicine (16th ed.). New York, NY: McGraw-Hill. ISBN 0-07-139140-1.
3. Fuchs, TA; Brill, A, Duerschmied, D, Schatzberg, D, Monestier, M, Myers DD, Jr, Wrobleski, SK, Wakefield, TW,
Hartwig, JH, Wagner, DD (Sep 7, 2010). "Extracellular DNA traps promote thrombosis."
(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2936604). Proceedings of the National Academy of Sciences of the
United States of America 107 (36): 158805. doi:10.1073/pnas.1005743107
(https://dx.doi.org/10.1073%2Fpnas.1005743107). PMC 2936604
(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2936604). PMID 20798043
(https://www.ncbi.nlm.nih.gov/pubmed/20798043).
4. Brill, A; Fuchs, TA, Savchenko, A, Thomas, GM, Martinod, K, De Meyer, SF, Bhandari, AA, Wagner, DD (Nov 1,
2011). "Neutrophil Extracellular Traps Promote Deep Vein Thrombosis in Mice"
(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3319651). Journal of thrombosis and haemostasis : JTH 10 (1): 136
44. doi:10.1111/j.1538-7836.2011.04544.x (https://dx.doi.org/10.1111%2Fj.1538-7836.2011.04544.x). PMC 3319651
(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3319651). PMID 22044575
(https://www.ncbi.nlm.nih.gov/pubmed/22044575).
5. Borissoff, JI; ten Cate, H (September 2011). "From neutrophil extracellular traps release to thrombosis: an overshooting
host-defense mechanism?". Journal of thrombosis and haemostasis : JTH 9 (9): 17914. doi:10.1111/j.15387836.2011.04425.x (https://dx.doi.org/10.1111%2Fj.1538-7836.2011.04425.x). PMID 21718435
(https://www.ncbi.nlm.nih.gov/pubmed/21718435).
6. labtestsonline > Hypercoagulable Disorders
(http://www.labtestsonline.org/understanding/conditions/hypercoagulable_disorders-3.html) This article was last
reviewed on May 23, 2007 and was last modified on March 6, 2010.
7. Webster, GJ; Burroughs AK, Riordan SM (January 2005). "Review article: portal vein thrombosis new insights into
aetiology and management" (http://www3.interscience.wiley.com/cgi-bin/fulltext/118696389/HTMLSTART).
Alimentary Pharmacology & Therapeutics 21 (1): 19. doi:10.1111/j.1365-2036.2004.02301.x
(https://dx.doi.org/10.1111%2Fj.1365-2036.2004.02301.x). PMID 15644039
(https://www.ncbi.nlm.nih.gov/pubmed/15644039).
8. eMedicine Article on Internal Jugular Vein Thrombosis by Dale K.
Mueller|http://www.emedicine.com/med/topic2762.htm
9. Canho, P; Ferro JM, Lindgren AG et al. (August 2005). "Causes and predictors of death in cerebral venous thrombosis"
(http://stroke.ahajournals.org/cgi/content/full/36/8/1720). Stroke 36 (8): 17201725.
doi:10.1161/01.STR.0000173152.84438.1c (https://dx.doi.org/10.1161%2F01.STR.0000173152.84438.1c).
PMID 16002765 (https://www.ncbi.nlm.nih.gov/pubmed/16002765).
10. Hatzinikolaou-Kotsakou E, Kartasis Z, Tziakas D et al. (March 2005). "Clotting state after cardioversion of atrial
fibrillation: a haemostasis index could detect the relationship with the arrhythmia duration"
(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC555849). Thromb J 3 (1): 2. doi:10.1186/1477-9560-3-2
(https://dx.doi.org/10.1186%2F1477-9560-3-2). PMC 555849 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC555849).
PMID 15748296 (https://www.ncbi.nlm.nih.gov/pubmed/15748296).
11. Bekker J, Ploem S, de Jong KP. Early hepatic artery thrombosis after liver transplantation: a systematic review of the
incidence, outcome and risk factors. Am J Transplant 2009; 9(4):746-57.
12. MedlinePlus > Arterial embolism (http://www.nlm.nih.gov/medlineplus/ency/article/001102.htm) Update Date:
5/8/2008. Updated by: Sean O. Stitham, MD and David C. Dugdale III, MD. Also reviewed by David Zieve, MD
13. Lederle, FA; Zylla, D, Macdonald, R, Wilt, TJ (2011-11-01). "Venous thromboembolism prophylaxis in hospitalized
medical patients and those with stroke: a background review for an american college of physicians clinical practice
guideline". Annals of internal medicine 155 (9): 60215. doi:10.1059/0003-4819-155-9-201111010-00008
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External links
Media related to Thrombosis at Wikimedia Commons
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Categories: Hematology
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