Arterial thrombosis
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Thrombosis Microchapters |
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Site of Thrombosis |
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Differentiating Thrombosis from other Diseases |
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Diagnosis |
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Treatment |
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Arterial thrombosis On the Web |
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
- Carotid artery
- Coronary artery
- Intracerebral artery
- Mesenteric artery
- Peripheral artery
- Placental artery
- Pulmonary embolization
- Retinal artery
- Vertebral artery
- Renal artery
- Adrenal artery
- Splenic artery
Causes
- Abruptio placentae
- Arteritis
- Atherosclerosis
- Anti-phospholipid syndrome
- Cancer (particularly pancreatic cancer)
- Catheters (indwelling in the venous bloodstream)
- Cholesterol embolization
- Diabetes mellitus
- Eclampsia
- Embolization including cholesterol embolization
- Genetics
- Heparin-induced thrombocytopenia(HIT)
- Hyperlipidemia
- Hypertension
- Nephrotic syndrome
- Paroxysmal nocturnal hemoglobinuria(PNH)
- Pre-eclampsia
- Protein S deficiency
- Polycythemia vera
- Smoking
- Stent
- Thoracic outlet syndrome
- Vasculitis
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
- 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
- Anticardiolipin antibodies (ACLA) IgG and IgM ACLA
- 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
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:
- Low molecular weight heparin administration
- Mechanical calf compression
- Vena cava filter (if LMWH or mechanical compression is contraindicated and the patient has recently suffered deep vein thrombosis).[11][12]
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
- ↑ Hellemans, Alexander (1988). The Timetables of Science. New York, New York: Simon and Schuster. p. 317. ISBN 0671621300. Unknown parameter
|coauthors=ignored (help) - ↑ 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.
- ↑ Davies MJ (1994). "Pathology of arterial thrombosis". Br Med Bull. 50 (4): 789–802. PMID 7804731.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ National Institute for Health and Clinical Excellence. Clinical guideline 36: Atrial fibrillation. London, June 2006.
- ↑ 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) - ↑ National Institute for Health and Clinical Excellence. Clinical guideline 46: Venous thromboembolism (surgical). London, April 2007.
- ↑ 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) - ↑ 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)
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