WordNet
- the formation or presence of a thrombus (a clot of coagulated blood attached at the site of its formation) in a blood vessel
- within the skull
PrepTutorEJDIC
- 血栓症
Wikipedia preview
出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2013/04/10 00:45:58」(JST)
wiki en
| Thrombosis | |
|---|---|
| Classification and external resources | |
Cyanosis of the lower right extremity, resulting from acute arterial thrombosis of the right leg |
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| ICD-10 | I80-I82 |
| ICD-9 | 437.6, 453, 671.5, 671.9 |
| MeSH | D013927 |
Thrombosis (Greek: θρόμβωσις) is the formation of a blood clot (thrombus; Greek: θρόμβος) inside a blood vessel, obstructing the flow of blood through the circulatory system. When a blood vessel is injured, the body uses platelets (thrombocytes) and fibrin to form a blood clot to prevent blood loss. Even when a blood vessel is not injured, blood clots may form in the body under certain conditions. A clot that breaks free and begins to travel around the body is known as an embolus.[1][2]
When a thrombus occupies more than 75%[citation needed] of cross-sectional area of the lumen of an artery, blood flow to the tissue supplied is reduced enough to cause symptoms because of decreased oxygen (hypoxia) and accumulation of metabolic products like lactic acid. More than 90%[citation needed] obstruction can result in anoxia, the complete deprivation of oxygen, and infarction, a mode of cell death.
Thromboembolism is the combination of thrombosis and its main complication, embolism.
Contents
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Causes
In classical terms, thrombosis is caused by abnormalities in one or more of the following (Virchow's triad):
- The composition of the blood (hypercoagulability or thrombophilia)
- Quality of the vessel wall (endothelial cell injury)
- Nature of the blood flow (stasis, turbulence)
Hypercoagulability
Main article: Thrombophilia
Hypercoagulability is caused by, for example, genetic deficiencies or autoimmune disorders. Recent studies indicate that neutrophils play a pivotal role in deep venous thrombosis, mediating numerous pro-thrombotic actions [3][4][5]
Endothelial cell injury
Causes of injury to the vessel's wall include trauma, surgery, infection or turbulent flow at bifurcations. The main mechanism is exposure of tissue factor to the blood coagulation system.[6]
Disturbed blood flow
Further information: Blood flow
Causes of disturbed blood flow include stagnation of blood flow past the point of injury, or venous stasis which may occur in heart failure[6] or after long periods of sedentary behavior, such as sitting on a long airplane flight. Also, atrial fibrillation, causes stagnant blood in the left atrium (LA) or left atrial appendage (LAA), and can lead to a thromboembolism.[6] Cancers or malignancies such as leukemia may cause increased risk of thrombosis by external compression on a blood vessel for example, or (more rarely) extension into the vasculature (for example, renal cell cancers extending into the renal veins).[6] Also, treatments for cancer (radiation, chemotherapy) often cause additional hypercoagulability.[6]
Classification
There are two distinct forms of thrombosis, venous thrombosis and arterial thrombosis, each of which can be presented by several subtypes.
Venous thrombosis
Main article: 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:
Deep vein thrombosis
Main article: Deep vein thrombosis
Deep vein thrombosis (DVT) is the formation of a blood clot within a deep vein. It most commonly affects leg veins, such as the femoral vein. Three factors are important in the formation of a blood clot within a deep vein—these are the rate of blood flow, the thickness of the blood and qualities of the vessel wall. Classical signs of DVT include swelling, pain and redness of the affected area.
Portal vein thrombosis
Main article: Portal vein thrombosis
Portal vein thrombosis is a form of venous thrombosis affecting the hepatic portal vein, which can lead to portal hypertension and reduction of the blood supply to the liver.[7] It usually has a pathological cause such as pancreatitis, cirrhosis, diverticulitis or cholangiocarcinoma.
Renal vein thrombosis
Main article: Renal vein thrombosis
Renal vein thrombosis is the obstruction of the renal vein by a thrombus. This tends to lead to reduced drainage from the kidney. Anticoagulation therapy is the treatment of choice.
Jugular vein thrombosis
Main article: Jugular vein thrombosis
Jugular vein thrombosis is a condition that may occur due to infection, intravenous drug use or malignancy. Jugular vein thrombosis can have a varying list of complications, including: systemic sepsis, pulmonary embolism, and papilledema. Though characterized by a sharp pain at the site of the vein, it can prove difficult to diagnose, because it can occur at random.[8]
Budd-Chiari syndrome
Main article: Budd-Chiari syndrome
Budd-Chiari syndrome is the blockage of the hepatic vein or the inferior vena cava. This form of thrombosis presents with abdominal pain, ascites and hepatomegaly. Treatment varies between therapy and surgical intervention by the use of shunts.
Paget-Schroetter disease
Main article: Paget-Schroetter disease
Paget-Schroetter disease is the obstruction of an upper extremity vein (such as the axillary vein or subclavian vein) by a thrombus. The condition usually comes to light after vigorous exercise and usually presents in younger, otherwise healthy people. Men are affected more than women.
Cerebral venous sinus thrombosis
Main article: Cerebral venous sinus thrombosis
Cerebral venous sinus thrombosis (CVST) is a rare form of stroke which results from the blockage of the dural venous sinuses by a thrombus. Symptoms may include headache, abnormal vision, any of the symptoms of stroke such as weakness of the face and limbs on one side of the body and seizures. The diagnosis is usually made with a CT or MRI scan. The majority of persons affected make a full recovery. The mortality rate is 4.3%.[9]
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
Main article: 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 categories—large 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
Main article: Myocardial infarction
Myocardial infarction (MI) is caused by an infarct (death of tissue due to ischemia), often due to the obstruction of a coronary artery by a thrombus. 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]
An arterial embolus can also form in the limbs.[12]
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 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, 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 recanalized.
Prevention
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 hospital-acquired thrombosis was 25,000.[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]
Treatment
Vitamin K antagonist-oral anticoagulants reduce thromboembolic occurrence. As side effect, 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.[23]
See also
- National Blood Clot Alliance
- Blood clotting tests
References
- ^ Furie B, Furie BC (2008). "Mechanisms of thrombus formation". New England Journal of Medicine 359 (9): 938–949. doi:10.1056/NEJMra0801082. PMID 18753650.
- ^ 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.
- ^ Fuchs, TA; Brill, A, Duerschmied, D, Schatzberg, D, Monestier, M, Myers DD, Jr, Wrobleski, SK, Wakefield, TW, Hartwig, JH, Wagner, DD (2010 Sep 7). "Extracellular DNA traps promote thrombosis.". Proceedings of the National Academy of Sciences of the United States of America 107 (36): 15880–5. doi:10.1073/pnas.1005743107. PMC 2936604. PMID 20798043.
- ^ Brill, A; Fuchs, TA, Savchenko, A, Thomas, GM, Martinod, K, De Meyer, SF, Bhandari, AA, Wagner, DD (2011 Nov 1). "Neutrophil Extracellular Traps Promote Deep Vein Thrombosis in Mice.". Journal of thrombosis and haemostasis : JTH. doi:10.1111/j.1538-7836.2011.04544.x. PMID 22044575.
- ^ Borissoff, JI; ten Cate, H (2011 Sep). "From neutrophil extracellular traps release to thrombosis: an overshooting host-defense mechanism?". Journal of thrombosis and haemostasis : JTH 9 (9): 1791–4. doi:10.1111/j.1538-7836.2011.04425.x. PMID 21718435.
- ^ a b c d e labtestsonline > Hypercoagulable Disorders This article was last reviewed on May 23, 2007 and was last modified on March 6, 2010.
- ^ Webster, GJ; Burroughs AK, Riordan SM (January 2005). "Review article: portal vein thrombosis – new insights into aetiology and management". Alimentary Pharmacology & Therapeutics 21 (1): 1–9. doi:10.1111/j.1365-2036.2004.02301.x. PMID 15644039.
- ^ eMedicine Article on Internal Jugular Vein Thrombosis by Dr. Dale K. Mueller|http://www.emedicine.com/med/topic2762.htm
- ^ Canhão, P; Ferro JM, Lindgren AG et al. (August 2005). "Causes and predictors of death in cerebral venous thrombosis". Stroke 36 (8): 1720–1725. doi:10.1161/01.STR.0000173152.84438.1c. PMID 16002765.
- ^ 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". Thromb J 3 (1): 2. doi:10.1186/1477-9560-3-2. PMC 555849. PMID 15748296.
- ^ 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.
- ^ MedlinePlus > Arterial embolism Update Date: 5/8/2008. Updated by: Sean O. Stitham, MD and David C. Dugdale III, MD. Also reviewed by David Zieve, MD
- ^ a b 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): 602–15. doi:10.1059/0003-4819-155-9-201111010-00008. PMID 22041949.
- ^ Alikhan, R; Cohen, AT (2009-07-08). "Heparin for the prevention of venous thromboembolism in general medical patients (excluding stroke and myocardial infarction).". Cochrane database of systematic reviews (Online) (3): CD003747. doi:10.1002/14651858.CD003747.pub2. PMID 19588346.
- ^ Oates-Whitehead, RM; D'Angelo, A, Mol, B (2003). "Anticoagulant and aspirin prophylaxis for preventing thromboembolism after major gynaecological surgery.". Cochrane database of systematic reviews (Online) (4): CD003679. doi:10.1002/14651858.CD003679. PMID 14583989.
- ^ Handoll, HH; Farrar, MJ, McBirnie, J, Tytherleigh-Strong, G, Milne, AA, Gillespie, WJ (2002). "Heparin, low molecular weight heparin and physical methods for preventing deep vein thrombosis and pulmonary embolism following surgery for hip fractures.". Cochrane database of systematic reviews (Online) (4): CD000305. doi:10.1002/14651858.CD000305. PMID 12519540.
- ^ Roderick, P; Ferris, G, Wilson, K, Halls, H, Jackson, D, Collins, R, Baigent, C (2005 Dec). "Towards evidence-based guidelines for the prevention of venous thromboembolism: systematic reviews of mechanical methods, oral anticoagulation, dextran and regional anaesthesia as thromboprophylaxis.". Health technology assessment (Winchester, England) 9 (49): iii–iv, ix–x, 1–78. PMID 16336844.
- ^ National Institute for Health and Clinical Excellence. Clinical guideline 36: Atrial fibrillation. London, June 2006.
- ^ a b Hunt BJ (March 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.
- ^ National Institute for Health and Clinical Excellence. Clinical guideline 46: Venous thromboembolism (surgical). London, April 2007.
- ^ a b Geerts WH, Pineo GF, Heit JA, et al. (September 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.
- ^ Dentali F, Douketis JD, Gianni M, Lim W, Crowther MA (February 2007). "Meta-analysis: anticoagulant prophylaxis to prevent symptomatic venous thromboembolism in hospitalized medical patients" (PDF). Ann. Intern. Med. 146 (4): 278–88. PMID 17310052.
- ^ Heneghan C, Ward A, Perera R (2012). "Self-monitoring of oral anti-coagulation: systematic review and meta-analysis of individual patient data". The Lancet 379 (9813): 322–334. doi:10.1016/S0140-6736(11)61294-4.
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UpToDate Contents
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- 1. 脳静脈血栓症の病因、臨床的特徴、および診断 etiology clinical features and diagnosis of cerebral venous thrombosis
- 2. 脳静脈血栓症の治療および予後 treatment and prognosis of cerebral venous thrombosis
- 3. 成人における頭蓋内圧亢進の評価および管理 evaluation and management of elevated intracranial pressure in adults
- 4. 脳血管障害を合併した妊娠 cerebrovascular disorders complicating pregnancy
- 5. 急性重度外傷性脳損傷の管理 management of acute severe traumatic brain injury
English Journal
- Neonatal Cerebral Sinovenous Thrombosis: Neuroimaging and Long-term Follow-up.
- Kersbergen KJ, Groenendaal F, Benders MJ, de Vries LS.Source1Department of Neonatology, Wilhelmina Children's Hospital, University Medical Center, Utrecht, the Netherlands.
- Journal of child neurology.J Child Neurol.2011 Sep;26(9):1111-20. Epub 2011 Jun 21.
- Neonates are known to have a higher risk of cerebral sinovenous thrombosis than children of other age groups. The exact incidence in neonates remains unknown and is likely to be underestimated, as clinical presentation is nonspecific and diagnosis can only be made when dedicated neuroimaging techniq
- PMID 21693652
- Intracranial haemorrhage associated with cerebral infections: A review.
- Radwan W, Sawaya R.SourceDepartment of Internal Medicine, Division of Neurology, American University Medical Center , Beirut , Lebanon.
- Scandinavian journal of infectious diseases.Scand J Infect Dis.2011 Sep;43(9):675-82. Epub 2011 May 23.
- Abstract We present a review of the different viral, bacterial, parasitic and fungal infections that are associated with intracranial haemorrhages. We summarize the clinical presentation of the infection and its cerebral complication. We elucidate the pathology and pathophysiology of the haemorrhage
- PMID 21599547
Japanese Journal
- S状静脈洞血栓症を伴った乳様突起炎例
- 水越 彬文,平海 晴一,山本 典生,坂本 達則,伊藤 壽一
- 耳鼻咽喉科臨床 104(6), 415-418, 2011
- … Mastoiditis is one of common suppurative complications of acute otitis media, which sometimes induces severe intracranial complications. … We report on a case of mastoiditis accompanied with sigmoid sinus thrombosis. … CT examination is a decisive diagnostic tool to classify the mastoiditis as incipient or coalescent, to detect intracranial complications, and to determine the type of therapy. …
- NAID 130000804890
- 感染性脳動脈瘤を伴った海綿静脈洞血栓症の1例
- 大川 聡,華園 晃,菅原 正伯,高橋 聡,柳澤 俊晴,溝井 和夫,大西 洋英,豊島 至
- 脳卒中 32(3), 307-313, 2010-05-25
- NAID 10027054307
Related Links
- thrombosis /throm・bo・sis/ (throm-bo´sis) the formation or presence of a thrombus .thrombot´ic. cerebral thrombosis thrombosis of a cerebral vessel, which may result in cerebral infarction. coronary thrombosis thrombosis of a coronary ...
Related Pictures
★リンクテーブル★
| リンク元 | 「頭蓋内血栓症」 |
| 関連記事 | 「intracranial」 |
「頭蓋内血栓症」
「intracranial」
- adj.
- 頭蓋内の