| Venous thrombosis |
| Classification and external resources |
A deep vein thrombosis in the right leg. Note the swelling and redness. |
| 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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Contents
- 1 Classification
- 2 Causes
- 3 Pathophysiology
- 4 Prevention
- 5 Treatment
- 6 See also
- 7 References
- 8 External links
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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 (VTE) 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 inflammation is a thrombophlebitis; one that does not is a phlebothrombosis.[2][unreliable medical source?]
Causes
Venous thrombi are recognized to be caused mainly by a combination of venous stasis and hypercoagulability—but to a lesser extent endothelial damage and activation.[3] The three factors of stasis, hypercoaguability, and alterations in the blood vessel wall represent Virchow's triad, and changes to the vessel wall are the least understood.[4] Various risk factors increase the likelhood of any one individual developing a thrombosis.
Risk factors
- Acquired
- Older age (the strongest risk factor)[4]
- Major surgery and orthopedic surgery[5]
- Cancers, most particularly pancreatic, but not cancers of the lip, oral cavity, and pharynx[6]
- Immobilization, the sitting position, and travel, particularly by air[3]
- Pregnancy and the postpartum period[3]
- Antiphospholipid syndrome[5]
- Obesity[5]
- Trauma[3]
- Oral contraceptives[5]
- Hormonal replacement therapy[5]
- Lupus anticoagulant[4]
- Polycythemia vera[5]
- Chemotherapy[4]
- Heavy smoking[4]
- Central venous catheters[5]
- Orthopedic casts[5]
- 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[5]
- Non O-blood type[5]
- Factor XIII 34val[5]
- Fibrinogen (G) 10034T[5]
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 thrombi 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 initiated by tissue factor effected thrombin production, which leads to fibrin deposition.[4]
The valves of veins are a recognized site of VT initiation. Due to the blood flow pattern, the base of the valve sinus is particularly deprived of oxygen (hypoxic). Stasis excacerbates hypoxia, and this state is linked to the activation of white blood cells (leukocytes) and the endothelium. Specifically, the two pathways of hypoxia-inducible factor-1 (HIF-1) and early growth response 1 (EGR-1) are activated by hypoxia, and they contribute to monocyte and endothelial activation. Hypoxia also causes reactive oxygen species (ROS) production that can activate HIF-1, EGR-1, and nuclear factor-κB (NF-κB), which regulates HIF-1 transcription.[4]
HIF-1 and EGR-1 pathways lead to monocyte association with endothelial proteins, such as P-selectin, prompting monocytes to release tissue factor filled microvesicles, which presumably initiate fibrin deposition (via thrombin) after binding the endothelial surface.[4]
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]
A 2011 clinical guideline from the American College of Physicians (ACP) gave three strong recommendations with moderate quality evidence on VTE prevention in non-surgical patients: that hospitalized patients be assessed for their risk of thromboembolism and bleeding before prophylaxis (prevention); that heparin or a related drug is used if potential benefits are thought to outweigh potential harms; and that graduated compression stockings not be used.[1] As an ACP policy implication, the guideline stated a lack of support for any performance measures that incentivize physicians to apply universal prophylaxis without regard to the risks.[1]
Treatment
Evidence-based clinical guidelines from the American College of Chest Physicians were published in February 2012 for the treatment of VTE.[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.
See also
References
- ^ a b c 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 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 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.
- ^ 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.
- ^ 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. doi:10.1002/14651858.CD003679. PMID 14583989.
- ^ Handoll, HH; Farrar, MJ, McBirnie, J, Tytherleigh-Strong, G, Milne, AA, Gillespie, WJ (2002). Handoll, Helen HG. ed. "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 (2011-11-01). "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. http://www.annals.org/content/155/9/602.long.
- ^ Alikhan, R; Cohen, AT (2009-07-08). Alikhan, Raza. ed. "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.
- ^ Guyatt GH, Akl EA, Crowther M, Gutterman DD, Schuünemann HJ, and for the American College of Chest Physicians Antithrombotic Therapy and Prevention of Thrombosis Panel (February 2012). "Executive Summary: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines". Chest 141 (2 suppl): 7S–47S. doi:10.1378/chest.1412S3. PMID 22315257. http://chestjournal.chestpubs.org/content/141/2_suppl.
- ^ 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.
External links
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Cardiovascular disease: vascular disease · Circulatory system pathology (I70–I99, 440–456)
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Arteries, arterioles
and capillaries |
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Inflammation
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Arteritis (Aortitis) · Buerger's disease
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Arterial occlusive disease/
peripheral vascular disease
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Arteriosclerosis
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Atherosclerosis (Foam cell, Fatty streak, Atheroma, Intermittent claudication) · Monckeberg's arteriosclerosis · Arteriolosclerosis (Hyaline, Hyperplastic, oxycholesterol, cholesterol, LDL, trans fat)
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Stenosis
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Renal artery stenosis · Carotid artery stenosis
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Other
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Fibromuscular dysplasia · Degos disease · Aortoiliac occlusive disease · Raynaud's phenomenon/Raynaud's disease · Erythromelalgia
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Aneurysm/dissection/
pseudoaneurysm
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torso: Aortic aneurysm (Thoracic aortic aneurysm, Abdominal aortic aneurysm) · Aortic dissection · Coronary artery aneurysm
head/neck: Cerebral aneurysm · Intracranial berry aneurysm · Carotid artery dissection · Vertebral artery dissection · Familial aortic dissection
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Vascular malformation
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Arteriovenous malformation · Arteriovenous fistula · Telangiectasia (Hereditary hemorrhagic telangiectasia)
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Vascular nevus
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Spider angioma · Halo nevus · Cherry hemangioma
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| Veins |
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Inflammation
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Phlebitis
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Venous thrombosis/
Thrombophlebitis
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primarily lower limb (Deep vein thrombosis)
abdomen (Hepatic veno-occlusive disease, Budd–Chiari syndrome, May-Thurner syndrome, Portal vein thrombosis, Renal vein thrombosis)
upper limb/torso (Paget-Schroetter disease, Mondor's disease)
head (Cerebral venous sinus thrombosis)
Post-thrombotic syndrome
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Varicose veins
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Varicocele · Gastric varices · Portacaval anastomosis (Hemorrhoid, Esophageal varices, Caput medusae)
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Other
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Superior vena cava syndrome · Inferior vena cava syndrome · Venous ulcer · Chronic venous insufficiency · Chronic cerebrospinal venous insufficiency
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| Arteries or veins |
Vasculitis · Thrombosis · Embolism (Pulmonary embolism, Cholesterol embolism, Paradoxical embolism) · Angiopathy (Macroangiopathy, Microangiopathy)
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| Blood pressure |
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Hypertension
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Hypertensive heart disease · Hypertensive nephropathy · Essential hypertension · Secondary hypertension (Renovascular hypertension) · Pulmonary hypertension · Malignant hypertension · Benign hypertension · Systolic hypertension · White coat hypertension
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Hypotension
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Orthostatic hypotension
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anat(a:h/u/t/a/l,v:h/u/t/a/l)/phys/devp/cell/prot
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noco/syva/cong/lyvd/tumr, sysi/epon, injr
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proc, drug(C2s+n/3/4/5/7/8/9)
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- Postgraduate Medicine Journal: A Clinical Review of Venous Thromboembolism
