Venous thrombosis
| Venous thrombosis | |
|---|---|
| Classification and external resources | |
 A deep vein thrombosis in the right leg. Note the swelling and redness. |
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| ICD-10 | I80-I82 |
| ICD-9 | 453 |
| MeSH | D020246 |
A venous thrombosis is a blood clot (thrombus) that forms within a vein. Thrombosis is a medical term for a blood clot occurring inside a blood vessel. A classical venous thrombosis is deep vein thrombosis (DVT), which can break off (embolize), and become a life-threatening pulmonary embolism (PE). The conditions of DVT and PE are referred to collectively with the term venous thromboembolism.[1]
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[edit] Classification
Superficial venous thromboses can cause discomfort but generally do not cause serious consequences, unlike the deep venous thromboses (DVTs) that form in the deep veins of the legs or in the pelvic veins.
Since the veins return blood to the heart, if a piece of a blood clot formed in a vein breaks off it can be transported to the right side of the heart, and from there into the lungs. A piece of thrombus that is transported in this way is an embolism: the process of forming a thrombus that becomes embolic is called a thromboembolism. An embolism that lodges in the lungs is a pulmonary embolism (PE). A pulmonary embolus is a very serious condition that can be fatal if not recognized and treated promptly. Venous thromboembolism refers to both DVTs and PEs.
Systemic embolisms of venous origin can occur in patients with an atrial or ventricular septal defect, through which an embolus may pass into the arterial system. Such an event is termed a paradoxical embolism.
A venous thrombosis which results from vein inflamation is a thrombophlebitis; one that does not is a phlebothrombosis.[2][unreliable medical source?]
[edit] Causes
Venous thrombi are recognized to be caused by a combination of venous stasis and hypercoagulability.[3] Various risk factors increase the likelhood of any one individual developing a throbosis.
[edit] Risk factors
- Acquired
- Major surgery and orthopedic surgery[4]
- Cancers, most particularly pancreatic, but not cancers of the lip, oral cavity, and pharynx[5]
- Immobilization, the sitting position, and travel, particularly by air[3]
- Older age[3]
- Pregnancy and the postpartum period[3]
- Antiphospholipid syndrome[4]
- Obesity[4]
- Trauma[3]
- Oral contraceptives[4]
- Hormonal replacement therapy[4]
- Lupus anticoagulant[6]
- Polycythemia vera[4]
- Chemotherapy[6]
- Heavy smoking[6]
- Central venous catheters[4]
- Orthopedic casts[4]
- Minor injuries[7]
- Mixed
- Hyperhomocysteinemia[3]
- High fibrinogen levels[3]
- High factor VIII levels[3]
- High factor IX levels[3]
- High factor XI levels[3]
- Inherited
- Antithrombin deficiency[3]
- Protein C deficiency/Protein S deficiency[3]
- APC resistance (Factor V Leiden)[3]
- Prothrombin G20210A[3]
- Dysfibrinogenemia[4]
- Non O-blood type[4]
- Factor XIII 34val[4]
- Fibrinogen (G) 10034T[4]
[edit] Pathophysiology
In contrast to the understanding for how arterial thromboses occur, as with heart attacks, venous thrombosis formation is not well understood.[8] With arterial thrombosis, blood vessel wall damage is required for thrombosis formation, as it initiates coagulation,[8] but the majority of venous thrombi form without any injured epithelium.[3]
Red blood cells and fibrin are the main components of venous thrombi,[3] and the thrombi appear to attach to the blood vessel wall endothelium, normally a non-thrombogenic surface, with fibrin.[8] Platelets in venous thorombi attach to downstream fibrin, while in arterial thrombi, they compose the core.[8] As a whole, platelets constitute less of venous thrombi when compared to arterial ones.[3] The beginning of the process is thought to be initated by tissue factor, which leads to fibrin deposition.[6]
[edit] Prevention
Evidence supports the use of heparin in surgical patients whom have a high risk of thrombosis to reduce the risk of DVTs; however, the effect on PEs or overall mortality is not known.[9][10][11] In hospitalized non-surgical patients, heparin results in an almost statistically significant decrease in mortality and may decrease the risk of PE and DVT, but it increases major bleeding events yielding little or no overall clinical benefit.[12][13] It does not appear however to decrease the rate of symptomatic DVTs.[12] In hospitalized non-surgical stroke patients, mechanical measures (compression stockings) resulted in skin damage and no clinical improvement.[12] Data on the effectiveness of compression stockings among hospitalized non-surgical patients without stroke is scarce.[12]
[edit] Treatment
Evidence-based guidelines have been published for the treatment of venous thromboembolism.[14] Medications used to treat this condition include anticoagulants such as heparin, fondaparinux and more recently dabigatran has shown promise.[15] Vitamin K antagonists such as warfarin are also commonly used.
[edit] See also
[edit] References
- ^ Qaseem A, Chou R, Humphrey LL, Starkey M, Shekelle P, Clinical Guidelines Committee of the American College of Physicians (2011). "Venous thromboembolism prophylaxis in hospitalized patients: a clinical practice guideline from the American College of Physicians". Ann Intern Med 155 (9): 625–32. doi:10.1059/0003-4819-155-9-201111010-00011. PMID 22041951. http://www.annals.org/content/155/9/625.long.
- ^ Jahangir Moini (22 October 2008). Fundamental pharmacology for pharmacy technicians. Cengage Learning. p. 218. ISBN 978-1-4180-5357-4. http://books.google.com/books?id=EOWu8A9pmWYC&pg=PA218. Retrieved 12 January 2012.
- ^ a b c d e f g h i j k l m n o p q Martinelli I, Bucciarelli P, Mannucci PM (2010). "Thrombotic risk factors: basic pathophysiology". Crit Care Med 38 (2 Suppl): S3-9. doi:10.1097/CCM.0b013e3181c9cbd9. PMID 20083911.
- ^ a b c d e f g h i j k l Rosendaal FR, Reitsma PH (July 2009). "Genetics of venous thrombosis". J. Thromb. Haemost. 7 Suppl 1: 301–4. doi:10.1111/j.1538-7836.2009.03394.x. PMID 19630821. http://onlinelibrary.wiley.com/doi/10.1111/j.1538-7836.2009.03394.x/full.
- ^ Stein PD, Beemath A, Meyers FA, Skaf E, Sanchez J, Olson RE (2006). "Incidence of venous thromboembolism in patients hospitalized with cancer". Am J Med 119 (1): 60–8. doi:10.1016/j.amjmed.2005.06.058. PMID 16431186.
- ^ a b c d Bovill EG, van der Vliet A (2011). "Venous valvular stasis-associated hypoxia and thrombosis: what is the link?". Annu Rev Physiol 73: 527-45. doi:10.1146/annurev-physiol-012110-142305. PMID 21034220.
- ^ van Stralen KJ, Rosendaal FR, Doggen CJ (2008). "Minor injuries as a risk factor for venous thrombosis". Arch Intern Med 168 (1): 21–6. doi:10.1001/archinternmed.2007.5. PMID 18195191. http://archinte.ama-assn.org/cgi/content/short/168/1/21.
- ^ a b c d López JA, Chen J (2009). "Pathophysiology of venous thrombosis". Thromb Res 123 (Suppl 4): S30-4. doi:10.1016/S0049-3848(09)70140-9. PMID 19303501.
- ^ 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. 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.
- ^ a b c d Lederle, FA; Zylla, D, Macdonald, R, Wilt, TJ (2011 Nov 1). "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. http://www.annals.org/content/155/9/602.long.
- ^ Alikhan, R; Cohen, AT (2009 Jul 8). "Heparin for the prevention of venous thromboembolism in general medical patients (excluding stroke and myocardial infarction).". Cochrane database of systematic reviews (Online) (3): CD003747. PMID 19588346.
- ^ Geerts WH, Bergqvist D, Pineo GF, Heit JA, Samama CM, Lassen MR, Colwell CW; American College of Chest Physicians (2008). "Prevention of venous thromboembolism: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition)". Chest 133 (6): 381S–453S. doi:10.1378/chest.08-0656. PMID 18574271. http://hinari-gw.who.int/whalecomchestjournal.chestpubs.org/whalecom0/content/133/6_suppl/381S.long.
- ^ Schulman S, Kearon C, Kakkar AK, et al (2009). "Dabigatran versus warfarin in the treatment of acute venous thromboembolism". N Engl J Med 361 (24): 2342–52. doi:10.1056/NEJMoa0906598. PMID 19966341. http://content.nejm.org/cgi/content/abstract/NEJMoa0906598v1.
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