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__NOTOC__
{{Thrombosis}}
{{Thrombosis}}
 
{{CMG}} {{AE}} {{VE}}
{{Infobox_Disease |
  Name          = {{PAGENAME}} |
  Image          = |
  Caption        = |
  DiseasesDB    = |
  ICD10          = {{ICD10|I|80||i|80}}-{{ICD10|I|82||i|80}} |
  ICD9          = {{ICD9|437.6}}, {{ICD9|453}}, {{ICD9|671.5}}, {{ICD9|671.9}}|
  ICDO          = |
  OMIM          = |
  MedlinePlus    = |
  MeshID        = D013927 |
}}
{{SI}}
{{CMG}}


==Overview==
==Overview==
'''Thrombosis''' is the formation of a [[clot]] or [[thrombus]] inside a [[blood vessel]], obstructing the flow of [[blood]] through the [[circulatory system]]. '''Thromboembolism''' is a general term describing both thrombosis and its main complication which is [[embolism|embolisation]]. The term was coined in 1848 by [[Rudolph Carl Virchow]].<ref>{{cite book|title=The Timetables of Science| first=Alexander| last=Hellemans| coauthors=Bryan Bunch| publisher=Simon and Schuster| location=New York, New York| year=1988| isbn=0671621300 |pages=317}}</ref>
Thrombosis is the formation of a [[clot]] or [[thrombus]] inside a [[blood vessel]], obstructing the flow of [[blood]] through the [[circulatory system]]. Thromboembolism is a general term describing both thrombosis and its main complication which is [[embolism|embolisation]]. The term was coined in 1848 by [[Rudolph Carl Virchow]].<ref>{{cite book|title=The Timetables of Science| first=Alexander| last=Hellemans| coauthors=Bryan Bunch| publisher=Simon and Schuster| location=New York, New York| year=1988| isbn=0671621300 |pages=317}}</ref>


==Classification==
==Classification==
There are two broad forms of thrombosis, [[arterial thrombosis|arterial]] and [[venous thrombosis|venous]]. They are somewhat distinct in their underlying pathophysiology, but there is also a degree of overlap in the underlying pathophysiology.
There are two broad forms of thrombosis, [[arterial]] and [[venous thrombosis|venous]]. They are somewhat distinct in their underlying pathophysiology, but there is also a degree of overlap in the underlying pathophysiology.
 
Among all possible sites of forming arterial thrombosis, cardiac arteries are clinically the most important . Other potential sites of arterial thrombosis formation are relatively rare and the clinical details are yet not fully recognized<ref name="pmid30129979">{{cite journal| author=O'Donnell M, Shatzel JJ, Olson SR, Daughety MM, Nguyen KP, Hum J et al.| title=Arterial Thrombosis in Unusual Sites: A practical review. | journal=Eur J Haematol | year= 2018 | volume=  | issue=  | pages=  | pmid=30129979 | doi=10.1111/ejh.13165 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=30129979  }}</ref>.  


You can read more about [[venous thrombosis]] here:
'''To read more about venous thrombosis, click [[venous thrombosis|here]]'''
{{main|Venous thrombosis}}


==Possible site of thrombosis==
==Possible Site of Thrombosis==
*[[Carotid artery]]
*[[Carotid artery]]
*[[Coronary artery]]
*[[Coronary artery]]
*[[Intracerebral artery]]
*Intracerebral artery
*[[Mesenteric artery]]
*[[Mesenteric artery]]
*[[Peripheral artery]]
*[[Peripheral artery]]
*[[Placental artery]]
*Placental artery
*[[Pulmonary embolization]]
*[[Pulmonary embolization]]
*[[Retinal artery]]
*[[Retinal artery]]
*[[Vertebral artery]]
*[[Vertebral artery]]
*[[Renal artery]]
*[[Adrenal artery]]
*[[Splenic artery]]


==Differential diagnosis of causes of arterial thrombosis==
==Causes==
*[[Abruptio placentae]]
*[[Abruptio placentae]]
*[[Arteritis]]
*[[Arteritis]]
*[[Atherosclerosis]]
*[[Atherosclerosis]]
*Anti-phospholipid syndrome
*[[Cancer]] (particularly [[pancreatic cancer]])
*[[Cancer]] (particularly [[pancreatic cancer]])
*Catheters (indwelling in the venous bloodstream)
*Catheters (indwelling in the venous bloodstream)
Line 47: Line 39:
*[[Embolization]] including [[cholesterol embolization]]
*[[Embolization]] including [[cholesterol embolization]]
*Genetics
*Genetics
*[[Hyperlididemia]]
*[[Heparin-induced thrombocytopenia]]([[Heparin-induced thrombocytopenia|HIT]])
*[[Hyperlipidemia]]
*[[Hypertension]]
*[[Hypertension]]
*[[Nephrotic syndrome]]
*[[Paroxysmal nocturnal hemoglobinuria]]([[Paroxysmal nocturnal hemoglobinuria|PNH]])
*[[Pre-eclampsia]]
*[[Pre-eclampsia]]
*[[Protein S deficiency]]
*[[Polycythemia vera]]
*[[Smoking]]
*[[Smoking]]
*[[Stent]]
*[[Stent]]
Line 55: Line 52:
*[[Vasculitis]]
*[[Vasculitis]]


==Complications of thrombosis including embolization==
==Natural History, Complications and Prognosis==
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 (an [[infarction]]). The effects of an infarction depend on where it occurs.
Arterial thrombosis most commonly occur in association with atherosclerosis<ref name="pmid7804731">{{cite journal| author=Davies MJ| title=Pathology of arterial thrombosis. | journal=Br Med Bull | year= 1994 | volume= 50 | issue= 4 | pages= 789-802 | pmid=7804731 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7804731  }}</ref>. The formation of thrombosis in arteries of any site of the body leads to various consequences resulting from common mechanism. The main effect of thrombus formation in an organ artery is limiting its blood supply which can cause ischemia. The initial signs and symptoms are due to ischemia onset and limitation of O<small>2</small> and nutrient supply to the organ tissue. Acute ischemic pain begins and lasts as long as the tissue pain nerves remain viable. Most thrombi, at this stage, become [[Fibrinolysis|organized into fibrous tissue]], and the thrombosed vessel is gradually recanalized. However, with continuation of insufficient blood supply to the tissue, the tissue function become disturbed and finally with the progressive cellular death, tissue infarction occurs. The effects of an infarction depend on where it occurs. 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 (an [[infarction]]).
 
==Diagnosis==
 
=== Thrombosis formation and Induced ischemia ===
With the occlusion of the tissue artery in each organ, organ specefic symptoms, clinical and para-clinical signs and laboratory findings my be used to confirm the diagnosis. as discussed below(Intracardia thrombosis is also discussed here):
 
Unstable angina and MI: With the thrombus formation and occlusion in coronary arteries, cardiac pain new ECG findings( mainly ST segment changes) occur and with cardiac tissue infarction (MI) specefic cardiac enzymes (Troponin, CK-MB) levels elevate in the plasma.
 
Cerebral stroke and TIA: Beside global or lateralized clinical signs and symptoms of CNS defect, CT scan, MRI and arteriography are used for the diagnosis<ref name="pmid29054448">{{cite journal| author=Vilela P, Rowley HA| title=Brain ischemia: CT and MRI techniques in acute ischemic stroke. | journal=Eur J Radiol | year= 2017 | volume= 96 | issue=  | pages= 162-172 | pmid=29054448 | doi=10.1016/j.ejrad.2017.08.014 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=29054448  }}</ref>.
 
Peripheral arterial occlusions: Clinical signs such as pain, claudication, weakness, paleness and coldness. The diagnosis is confirmed by arteriography<ref name="pmid19626806">{{cite journal| author=Mutirangura P, Ruangsetakit C, Wongwanit C, Sermsathanasawadi N, Chinsakchai K| title=Clinical differentiation between acute arterial embolism and acute arterial thrombosis of the lower extremities. | journal=J Med Assoc Thai | year= 2009 | volume= 92 | issue= 7 | pages= 891-7 | pmid=19626806 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19626806  }}</ref>.
 
Atrial thrombosis: There should be an underlying reason; usually a structural heart defect or arrhythmia.The diagnosis is essentially confirmed by echocardiography.
 
Ventricular thrombosis: The underlying cause is usually myocardial infarction, and some case reports have pointed to the role of hypereosinophilia<ref name="pmid25189313">{{cite journal| author=Lee KG, Chuah MB, Tang HC, Chua TS| title=Hypereosinophilic syndrome with large intracardiac thrombus. | journal=Singapore Med J | year= 2014 | volume= 55 | issue= 8 | pages= e129-31 | pmid=25189313 | doi= | pmc=4294101 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25189313  }}</ref>.The diagnosis is essentially confirmed by echocardiography<ref name="pmid26476503">{{cite journal| author=Weinsaft JW, Kim J, Medicherla CB, Ma CL, Codella NC, Kukar N et al.| title=Echocardiographic Algorithm for Post-Myocardial Infarction LV Thrombus: A Gatekeeper for Thrombus Evaluation by Delayed Enhancement CMR. | journal=JACC Cardiovasc Imaging | year= 2016 | volume= 9 | issue= 5 | pages= 505-15 | pmid=26476503 | doi=10.1016/j.jcmg.2015.06.017 | pmc=5104336 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26476503  }}</ref>.
 
Aortic mural thrombosis: Mostly occurs in association of aortic wall defects and aneurysms but can also occur as a primary lesion; Trans esophageal echocardiograph(TEE) is the imaging modality of choice but the presence of thrombus can also be confirmed by CT angiography<ref name="pmid301299792">{{cite journal| author=O'Donnell M, Shatzel JJ, Olson SR, Daughety MM, Nguyen KP, Hum J et al.| title=Arterial Thrombosis in Unusual Sites: A practical review. | journal=Eur J Haematol | year= 2018 | volume=  | issue=  | pages=  | pmid=30129979 | doi=10.1111/ejh.13165 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=30129979  }}</ref>.  


Most thrombi, however, become [[Fibrinolysis|organized into fibrous tissue]], and the thrombosed vessel is gradually recanalized.
Visceral arteries thrombosis: Mainly consists renal, adrenal, mesenteric and splenic arteries. beside visceral pain and organ specific signs and symptoms, the diagnosis is confirmed by CT angiography, color -doppler sonography and/or MRI as proposed by majority of studies.


==Diagnostic evaluation of underlying cause==
=== Underlying etiology ===
'''cDNA-PCR assays for gene mutations and polymorphisms:'''
:*4G/5G [[polymorphism]] of the [[plasminogen activator inhibitor]]-1 gene (PAI-1)
:*[[Cystathionine beta synthetase]] (CBS) CBS T833C & G919A
:*[[Factor V Leiden]]
:*[[Glycoprotein IIIa]] A1/A2 (platelet glycoprotein)
:*[[Methylenetetrahydrofolate reductase]] (MTHFR) MTHFR C677T
:*[[Prothrombin]] G20210A


'''Serologic (blood) tests:'''
===Laboratory Findings===
:*[[Anticardiolipin antibodies]] (ACLA) IgG and IgM ACLA
====cDNA-PCR Assays for Gene Mutations and Polymorphisms====
:*[[Antithrombin III]]
*4G/5G [[polymorphism]] of the [[plasminogen activator inhibitor]]-1 gene (PAI-1)
:*[[Factor VIII]]
*Cystathionine beta synthetase (CBS) CBS T833C & G919A
:*[[Homocysteine]]
*[[Factor V Leiden]]
:*[[Lupus anticoagulant]] (LA)
*Glycoprotein IIIa A1/A2 (platelet glycoprotein)
:*[[Proteins C]]
*[[Methylenetetrahydrofolate reductase]] (MTHFR) MTHFR C677T
:*[[Protein S]]
*[[Prothrombin]] G20210A


'''Evaluation of hypofibrinolysis'''
====Serologic (blood) Tests====
:*4G/5G [[polymorphism]] of the [[plasminogen activator inhibitor]]-1 gene ([[PAI-1]])(requires cDNA-PCR assay for gene mutation)
*[[Anticardiolipin antibodies]] (ACLA) IgG and IgM ACLA
:*[[Lipoprotein a]] [[Lp(a)]]
*[[Antithrombin III]]
*[[Factor VIII]]
*[[Homocysteine]]
*[[Lupus anticoagulant]] (LA)
*[[Protein C]]
*[[Protein S]]
 
====Evaluation of Hypofibrinolysis====
*4G/5G [[polymorphism]] of the [[plasminogen activator inhibitor]]-1 gene ([[PAI-1]]) (requires cDNA-PCR assay for gene mutation)
*Lipoprotein a (Lp a)


==Prevention==
==Prevention==
Thrombosis and embolism can be partially prevented with anticoagulants in those deemed at risk. 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 [[hypertension|high blood pressure]]) needs to outweigh the small but known risk of major bleeding associated with the use of [[warfarin]].<ref>{{NICE|36|Atrial fibrillation|June 2006}}</ref>
Thrombosis and embolism can be partially prevented with anticoagulants in those deemed at risk. Generally, a risk-benefit analysis is required, as all anticoagulants increase the risk of bleeding. In [[atrial fibrillation]], for instance, the risk of [[stroke]] (calculated on the basis of additional risk factors, such as advanced age and [[hypertension|high blood pressure]]) outweigh the risk of bleeding associated with [[warfarin]] use.<ref>{{NICE|36|Atrial fibrillation|June 2006}}</ref>
 
In-hospital patients, thrombosis is a major cause for complications and is occasionally fatal. In 2005, a Parliamentary [[Health Select Committee]] in UK, stated that the annual rate of death due to hospital-acquired thrombosis was 25,000.<ref name="Hunt">{{cite journal |author=Hunt BJ |title=Awareness and politics of venous thromboembolism in the United kingdom |journal=Arterioscler. Thromb. Vasc. Biol. |volume=28 |issue=3 |pages=398–9 |year=2008 |month=March |pmid=18296598 |doi=10.1161/ATVBAHA.108.162586 |url=http://atvb.ahajournals.org/cgi/content/full/28/3/398}}</ref>
 
In patients admitted for surgery, [[compression stockings]] are widely used. In severe illness, prolonged immobility and in all [[orthopedic surgery]], [[clinical practice guideline|professional guidelines]] recommend:
*[[Low molecular weight heparin]] administration
*Mechanical calf compression
*[[Inferior vena cava filter|Vena cava filter]] (if LMWH or mechanical compression is contraindicated and the patient has recently suffered [[deep vein thrombosis]]).<ref>{{NICE|46|Venous thromboembolism (surgical)|April 2007}}</ref><ref name="ACCP">{{cite journal |author=Geerts WH, Pineo GF, Heit JA, ''et al'' |title=Prevention of venous thromboembolism: the Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy |journal=Chest |volume=126 |issue=3 Suppl |pages=338S–400S |year=2004 |month=September |pmid=15383478 |doi=10.1378/chest.126.3_suppl.338S |url=http://www.chestjournal.org/cgi/content/full/126/3_suppl/338S}}</ref>
 
In patients with medical rather than surgical illness, LMWH is known to prevent thrombosis.<ref name="ACCP" /><ref>{{cite journal |author=Dentali F, Douketis JD, Gianni M, Lim W, Crowther MA |title=Meta-analysis: anticoagulant prophylaxis to prevent symptomatic venous thromboembolism in hospitalized medical patients |journal=Ann. Intern. Med. |volume=146 |issue=4 |pages=278–88 |year=2007 |month=February |pmid=17310052 |url=http://www.annals.org/cgi/reprint/146/4/278.pdf |format=PDF}}</ref>
 
In the United Kingdom, the [[Chief Medical Officer (United Kingdom)|Chief Medical Officer]] has issued guidelines that preventative measures should be used in patients, in anticipation of formal guidelines.<ref name="Hunt" />
 
 
====Contraindicated medications====


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.<ref name=Hunt>{{cite journal |author=Hunt BJ |title=Awareness and politics of venous thromboembolism in the United kingdom |journal=Arterioscler. Thromb. Vasc. Biol. |volume=28 |issue=3 |pages=398–9 |year=2008 |month=March |pmid=18296598 |doi=10.1161/ATVBAHA.108.162586 |url=http://atvb.ahajournals.org/cgi/content/full/28/3/398}}</ref> In patients admitted for surgery, graded [[compression stockings]] are widely used, and in severe illness, prolonged immobility and in all [[orthopedic surgery]], [[clinical practice guideline|professional guidelines]] recommend [[low molecular weight heparin]] administration, mechanical calf compression or (if all else is contraindicated and the patient has recently suffered deep vein thrombosis) the insertion of a [[Inferior vena cava filter|vena cava filter]].<ref>{{NICE|46|Venous thromboembolism (surgical)|April 2007}}</ref><ref name=ACCP>{{cite journal |author=Geerts WH, Pineo GF, Heit JA, ''et al'' |title=Prevention of venous thromboembolism: the Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy |journal=Chest |volume=126 |issue=3 Suppl |pages=338S–400S |year=2004 |month=September |pmid=15383478 |doi=10.1378/chest.126.3_suppl.338S |url=http://www.chestjournal.org/cgi/content/full/126/3_suppl/338S}}</ref> In patients with medical rather than surgical illness, LMWH too is known to prevent thrombosis,<ref name=ACCP/><ref>{{cite journal |author=Dentali F, Douketis JD, Gianni M, Lim W, Crowther MA |title=Meta-analysis: anticoagulant prophylaxis to prevent symptomatic venous thromboembolism in hospitalized medical patients |journal=Ann. Intern. Med. |volume=146 |issue=4 |pages=278–88 |year=2007 |month=February |pmid=17310052 |url=http://www.annals.org/cgi/reprint/146/4/278.pdf |format=PDF}}</ref> and in the United Kingdom the [[Chief Medical Officer (United Kingdom)|Chief Medical Officer]] has issued guidance to the effect that preventative measures should be used in medical patients, in anticipation of formal guidelines.<ref name=Hunt/>
{{MedCondContrAbs


==See also==
|MedCond = High risk of arterial thrombosis|Drospirenone and Ethinyl estradiol}}
 
==Related Chapters==
* [[Anticoagulant]]s
* [[Anticoagulant]]s


==References==
==References==
{{reflist}}
{{Reflist|2}}


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Latest revision as of 09:01, 29 January 2019

Thrombosis Microchapters

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Arterial
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Arterial and Venous Thrombosis: Differences and Similarities

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Arterial
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Differentiating Thrombosis from other Diseases

Arterial
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Natural History, Complications and Prognosis

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Arterial thrombosis On the Web

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Vahid Eidkhani, M.D.

Overview

Thrombosis is the formation of a clot or thrombus inside a blood vessel, obstructing the flow of blood through the circulatory system. Thromboembolism is a general term describing both thrombosis and its main complication which is embolisation. The term was coined in 1848 by Rudolph Carl Virchow.[1]

Classification

There are two broad forms of thrombosis, arterial and venous. They are somewhat distinct in their underlying pathophysiology, but there is also a degree of overlap in the underlying pathophysiology.

Among all possible sites of forming arterial thrombosis, cardiac arteries are clinically the most important . Other potential sites of arterial thrombosis formation are relatively rare and the clinical details are yet not fully recognized[2].

To read more about venous thrombosis, click here

Possible Site of Thrombosis

Causes

Natural History, Complications and Prognosis

Arterial thrombosis most commonly occur in association with atherosclerosis[3]. The formation of thrombosis in arteries of any site of the body leads to various consequences resulting from common mechanism. The main effect of thrombus formation in an organ artery is limiting its blood supply which can cause ischemia. The initial signs and symptoms are due to ischemia onset and limitation of O2 and nutrient supply to the organ tissue. Acute ischemic pain begins and lasts as long as the tissue pain nerves remain viable. Most thrombi, at this stage, become organized into fibrous tissue, and the thrombosed vessel is gradually recanalized. However, with continuation of insufficient blood supply to the tissue, the tissue function become disturbed and finally with the progressive cellular death, tissue infarction occurs. The effects of an infarction depend on where it occurs. 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 (an infarction).

Diagnosis

Thrombosis formation and Induced ischemia

With the occlusion of the tissue artery in each organ, organ specefic symptoms, clinical and para-clinical signs and laboratory findings my be used to confirm the diagnosis. as discussed below(Intracardia thrombosis is also discussed here):

Unstable angina and MI: With the thrombus formation and occlusion in coronary arteries, cardiac pain new ECG findings( mainly ST segment changes) occur and with cardiac tissue infarction (MI) specefic cardiac enzymes (Troponin, CK-MB) levels elevate in the plasma.

Cerebral stroke and TIA: Beside global or lateralized clinical signs and symptoms of CNS defect, CT scan, MRI and arteriography are used for the diagnosis[4].

Peripheral arterial occlusions: Clinical signs such as pain, claudication, weakness, paleness and coldness. The diagnosis is confirmed by arteriography[5].

Atrial thrombosis: There should be an underlying reason; usually a structural heart defect or arrhythmia.The diagnosis is essentially confirmed by echocardiography.

Ventricular thrombosis: The underlying cause is usually myocardial infarction, and some case reports have pointed to the role of hypereosinophilia[6].The diagnosis is essentially confirmed by echocardiography[7].

Aortic mural thrombosis: Mostly occurs in association of aortic wall defects and aneurysms but can also occur as a primary lesion; Trans esophageal echocardiograph(TEE) is the imaging modality of choice but the presence of thrombus can also be confirmed by CT angiography[8].

Visceral arteries thrombosis: Mainly consists renal, adrenal, mesenteric and splenic arteries. beside visceral pain and organ specific signs and symptoms, the diagnosis is confirmed by CT angiography, color -doppler sonography and/or MRI as proposed by majority of studies.

Underlying etiology

Laboratory Findings

cDNA-PCR Assays for Gene Mutations and Polymorphisms

Serologic (blood) Tests

Evaluation of Hypofibrinolysis

Prevention

Thrombosis and embolism can be partially prevented with anticoagulants in those deemed at risk. Generally, a risk-benefit analysis is required, as all anticoagulants increase the risk of 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) outweigh the risk of bleeding associated with warfarin use.[9]

In-hospital patients, thrombosis is a major cause for complications and is occasionally fatal. In 2005, a Parliamentary Health Select Committee in UK, stated that the annual rate of death due to hospital-acquired thrombosis was 25,000.[10]

In patients admitted for surgery, compression stockings are widely used. In severe illness, prolonged immobility and in all orthopedic surgery, professional guidelines recommend:

In patients with medical rather than surgical illness, LMWH is known to prevent thrombosis.[12][13]

In the United Kingdom, the Chief Medical Officer has issued guidelines that preventative measures should be used in patients, in anticipation of formal guidelines.[10]


Contraindicated medications

High risk of arterial thrombosis is considered an absolute contraindication to the use of the following medications:

Related Chapters

References

  1. ↑ Hellemans, Alexander (1988). The Timetables of Science. New York, New York: Simon and Schuster. p. 317. ISBN 0671621300. Unknown parameter |coauthors= ignored (help)
  2. ↑ O'Donnell M, Shatzel JJ, Olson SR, Daughety MM, Nguyen KP, Hum J; et al. (2018). "Arterial Thrombosis in Unusual Sites: A practical review". Eur J Haematol. doi:10.1111/ejh.13165. PMID 30129979.
  3. ↑ Davies MJ (1994). "Pathology of arterial thrombosis". Br Med Bull. 50 (4): 789–802. PMID 7804731.
  4. ↑ Vilela P, Rowley HA (2017). "Brain ischemia: CT and MRI techniques in acute ischemic stroke". Eur J Radiol. 96: 162–172. doi:10.1016/j.ejrad.2017.08.014. PMID 29054448.
  5. ↑ Mutirangura P, Ruangsetakit C, Wongwanit C, Sermsathanasawadi N, Chinsakchai K (2009). "Clinical differentiation between acute arterial embolism and acute arterial thrombosis of the lower extremities". J Med Assoc Thai. 92 (7): 891–7. PMID 19626806.
  6. ↑ Lee KG, Chuah MB, Tang HC, Chua TS (2014). "Hypereosinophilic syndrome with large intracardiac thrombus". Singapore Med J. 55 (8): e129–31. PMC 4294101. PMID 25189313.
  7. ↑ Weinsaft JW, Kim J, Medicherla CB, Ma CL, Codella NC, Kukar N; et al. (2016). "Echocardiographic Algorithm for Post-Myocardial Infarction LV Thrombus: A Gatekeeper for Thrombus Evaluation by Delayed Enhancement CMR". JACC Cardiovasc Imaging. 9 (5): 505–15. doi:10.1016/j.jcmg.2015.06.017. PMC 5104336. PMID 26476503.
  8. ↑ O'Donnell M, Shatzel JJ, Olson SR, Daughety MM, Nguyen KP, Hum J; et al. (2018). "Arterial Thrombosis in Unusual Sites: A practical review". Eur J Haematol. doi:10.1111/ejh.13165. PMID 30129979.
  9. ↑ National Institute for Health and Clinical Excellence. Clinical guideline 36: Atrial fibrillation. London, June 2006.
  10. ↑ 10.0 10.1 Hunt BJ (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. Unknown parameter |month= ignored (help)
  11. ↑ National Institute for Health and Clinical Excellence. Clinical guideline 46: Venous thromboembolism (surgical). London, April 2007.
  12. ↑ 12.0 12.1 Geerts WH, Pineo GF, Heit JA; et al. (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. Unknown parameter |month= ignored (help)
  13. ↑ Dentali F, Douketis JD, Gianni M, Lim W, Crowther MA (2007). "Meta-analysis: anticoagulant prophylaxis to prevent symptomatic venous thromboembolism in hospitalized medical patients" (PDF). Ann. Intern. Med. 146 (4): 278–88. PMID 17310052. Unknown parameter |month= ignored (help)

cs:Trombóza de:Thrombose eo:Trombozo it:Trombosi he:תרומבוס ms:Trombotik nl:Trombose fi:Verihiutale

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