You are on page 1of 9

Thrombosis - Wikipedia, the free encyclopedia

6/15/15, 22:23

From Wikipedia, the free encyclopedia

Thrombosis (Greek: ) is the

formation of a blood clot (thrombus;
Greek: ) 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 is significantly large
enough to reduce the blood flow to a
tissue, hypoxia (oxygen deprivation) can
occur and metabolic products such as
lactic acid can accumulate. A larger
thrombus causing a much greater
obstruction to the blood flow may result
in anoxia, the complete deprivation of
oxygen and infarction, tissue death.
There are also a number of other
conditions that can arise according to the
location of the thrombus and the organs


Cyanosis of the lower right extremity, resulting from acute arterial

thrombosis of the right leg (on the left side of the image)
Classification and external resources
ICD-10 I80
ICD-9 437.6 (,
453 (,
671.5 (,
671.9 (
MeSH D013927 (

Thromboembolism is the combination of thrombosis and its main complication, embolism.

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

Page 1 of 9

Thrombosis - Wikipedia, the free encyclopedia

6/15/15, 22:23

5 Prevention
6 Treatment
7 See also
8 References
9 External links

The main causes of thrombosis are given in Virchow's triad which lists hypercoagulability, endothelial cell
injury, and disturbed blood flow.

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]

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

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] in 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 possible activation of the coagulation system by cancer cells or secretion of procoagulant
substances (paraneoplastic syndrome), by external compression on a blood vessel when a solid tumor is present,
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]

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:

Page 2 of 9

Thrombosis - Wikipedia, the free encyclopedia

6/15/15, 22:23

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
Portal vein thrombosis affects 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
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
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
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
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
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

Page 3 of 9

Thrombosis - Wikipedia, the free encyclopedia

6/15/15, 22:23

Cavernous sinus thrombosis

Cavernous sinus thrombosis is a specialised form of cerebral venous sinus thrombosis, where there is
thrombosis of the cavernous sinus of the basal skull dura, due to the retrograde spread of infection and
endothelial damage from the danger triangle of the face. The facial veins in this area anastomose with the
superior and inferior ophthalmic veins of the orbit, which drain directly posteriorly into the cavernous sinus
through the superior orbital fissure. Staphyloccoal or Streptococcal infections of the face, for example nasal or
upper lip pustules may thus spread directly into the cavernous sinus, causing stroke-like symptoms of double
vision, squint, as well as spread of infection to cause meningitis.

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.
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]

Page 4 of 9

Thrombosis - Wikipedia, the free encyclopedia

6/15/15, 22:23

An arterial embolus can also form in the limbs.[12]

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.

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


Page 5 of 9

Thrombosis - Wikipedia, the free encyclopedia

6/15/15, 22:23

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]

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

Page 6 of 9

Thrombosis - Wikipedia, the free encyclopedia

6/15/15, 22:23


1. Furie B, Furie BC (2008). "Mechanisms of thrombus formation". New England Journal of Medicine 359 (9): 938949.
doi:10.1056/NEJMra0801082 ( PMID 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."
( Proceedings of the National Academy of Sciences of the
United States of America 107 (36): 158805. doi:10.1073/pnas.1005743107
( PMC 2936604
( PMID 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"
( Journal of thrombosis and haemostasis : JTH 10 (1): 136
44. doi:10.1111/j.1538-7836.2011.04544.x ( PMC 3319651
( PMID 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 ( PMID 21718435
6. labtestsonline > Hypercoagulable Disorders
( 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" (
Alimentary Pharmacology & Therapeutics 21 (1): 19. doi:10.1111/j.1365-2036.2004.02301.x
( PMID 15644039
8. eMedicine Article on Internal Jugular Vein Thrombosis by Dale K.
9. Canho, P; Ferro JM, Lindgren AG et al. (August 2005). "Causes and predictors of death in cerebral venous thrombosis"
( Stroke 36 (8): 17201725.
doi:10.1161/01.STR.0000173152.84438.1c (
PMID 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"
( Thromb J 3 (1): 2. doi:10.1186/1477-9560-3-2
( PMC 555849 (
PMID 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 ( 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

Page 7 of 9

Thrombosis - Wikipedia, the free encyclopedia









6/15/15, 22:23

guideline". Annals of internal medicine 155 (9): 60215. doi:10.1059/0003-4819-155-9-201111010-00008

( PMID 22041949
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
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 (December 2005). "Towards evidencebased 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): iiiiv, ixx, 178. PMID 16336844 (
National Institute for Health and Clinical Excellence. Clinical guideline 36: Atrial fibrillation
( London, June 2006.
Hunt BJ (March 2008). "Awareness and politics of venous thromboembolism in the United kingdom"
( Arterioscler. Thromb. Vasc. Biol. 28 (3): 3989.
doi:10.1161/ATVBAHA.108.162586 ( PMID 18296598
National Institute for Health and Clinical Excellence. Clinical guideline 46: Venous thromboembolism (surgical)
( London, April 2007.
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): 338S400S.
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): 27888. doi:10.7326/0003-4819146-4-200702200-00007 ( PMID 17310052
"Information about the Registry" ( S&H Medical Science Service.
Retrieved 2014-08-15.
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): 322334. doi:10.1016/S0140-6736(11)61294-4

External links
Media related to Thrombosis at Wikimedia Commons
Retrieved from ""

Page 8 of 9

Thrombosis - Wikipedia, the free encyclopedia

6/15/15, 22:23

Categories: Hematology
This page was last modified on 29 May 2015, at 18:02.
Text is available under the Creative Commons Attribution-ShareAlike License; additional terms may
apply. By using this site, you agree to the Terms of Use and Privacy Policy. Wikipedia is a registered
trademark of the Wikimedia Foundation, Inc., a non-profit organization.

Page 9 of 9