Thrombosis

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(Redirected from
Arterial thrombosis
)

For the journal, see
Thrombosis (journal)
.
Thrombosis
Cyanosis of the lower right extremity, resulting from acute arterial thrombosis of the right leg (on the left side of the image)
SpecialtyVascular surgery, internal medicine, pulmonology
SymptomsDependent on location

Thrombosis (from

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, or a piece of the clot, that breaks free and begins to travel around the body is known as an embolus.[1][2]

Thrombosis may occur in veins (

arterial thrombosis). Venous thrombosis (sometimes called DVT, deep vein thrombosis) leads to a blood clot in the affected part of the body, while arterial thrombosis (and, rarely, severe venous thrombosis) affects the blood supply and leads to damage of the tissue supplied by that artery (ischemia and necrosis). A piece of either an arterial or a venous thrombus can break off as an embolus, which could then travel through the circulation and lodge somewhere else as an embolism. This type of embolism is known as a thromboembolism. Complications can arise when a venous thromboembolism (commonly called a VTE) lodges in the lung as a pulmonary embolism. An arterial embolus may travel further down the affected blood vessel, where it can lodge as an embolism.[citation needed
]

Signs and symptoms

Thrombosis is generally defined by the type of blood vessel affected (arterial or venous thrombosis) and the precise location of the blood vessel or the organ supplied by it.[citation needed]

Venous thrombosis

Main article: Venous thrombosis

Deep vein thrombosis

Main article: Deep vein thrombosis

Deep vein thrombosis (DVT) is the formation of a blood clot within a

swelling, pain and redness of the affected area.[citation needed
]

Paget-Schroetter disease

Main article:
Paget-Schroetter disease

Paget-Schroetter disease or upper extremity DVT (UEDVT) is the obstruction of an arm 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.[3]

Budd-Chiari syndrome

Main article:
Budd-Chiari syndrome

Budd-Chiari syndrome is the blockage of a

hepatic vein or of the hepatic part of the inferior vena cava. This form of thrombosis presents with abdominal pain, ascites and enlarged liver. Treatment varies between therapy and surgical intervention by the use of shunts.[4]

Portal vein thrombosis

Main article: 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.[5] It usually happens in the setting of another disease such as pancreatitis, cirrhosis, diverticulitis or cholangiocarcinoma.[6]

Renal vein thrombosis

Main article: 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.[7]

Cerebral venous sinus thrombosis

Main article: Cerebral venous sinus thrombosis

Cerebral venous sinus thrombosis (CVST) is a rare form of

MRI scan. The majority of persons affected make a full recovery. The mortality rate is 4.3%.[8]

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.[9]

Cavernous sinus thrombosis

Main article: Cavernous sinus thrombosis

double vision, squint, as well as spread of infection to cause meningitis.[10]

Arterial thrombosis

Arterial thrombosis is the formation of a thrombus within an artery. In most cases, arterial thrombosis follows rupture of atheroma (a fat-rich deposit in the blood vessel wall), and is therefore referred to as atherothrombosis. Arterial embolism occurs when clots then migrate downstream and can affect any organ.[11] Alternatively, arterial occlusion occurs as a consequence of embolism of blood clots originating from the heart ("cardiogenic" emboli). The most common cause is atrial fibrillation, which causes a blood stasis within the atria with easy thrombus formation, but blood clots can develop inside the heart for other reasons too as infective endocarditis.[citation needed]

Stroke

Main article: Stroke
Acute thrombus in the right MCA M1 branch

A stroke is the rapid decline of brain function due to a disturbance in the supply of blood to the brain.

internal carotids, vertebral and the circle of Willis. The latter can affect smaller vessels, such as the branches of the circle of Willis.[citation needed
]

Myocardial infarction

Main article: Myocardial infarction

Myocardial infarction (MI), or heart attack, is caused by ischemia (restriction in the blood supply), which is often due to the obstruction of a

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.[citation needed
]

Limb ischemia

An arterial thrombus or embolus can also form in the limbs, which can lead to

acute limb ischemia.[13]

Other sites

Hepatic artery thrombosis usually occurs as a devastating complication after liver transplantation.[14]

Causes

Thrombosis prevention is initiated with assessing the risk for its development.

hypercoagulability).[16][17] Some risk factors predispose for venous thrombosis while others increase the risk of arterial thrombosis.[citation needed] Newborn babies in the neonatal period are also at risk of a thromboembolism.[18]

Risk factors for thrombosis
Factor Notes References
Previous episodes of thrombosis [16]
Vasoconstriction [19]
Slow or turbulent blood flow slow flow is modifiable with exercise [19]
Stroke [20]
Heart failure [20]
Sedentary life style modifiable [19]
Plaster cast transient [20]
Dehydration modifiable [19]
Acute respiratory failure [20]
Dysrhythmias
 [19]
Shock [19]
Obesity modifiable [15][20][21][22][23]
Pregnancy and the post-partum period [15][22][23]
Varicose veins [20][22]
Surgery [15][22]
Trauma [15][20][22]
Estrogen-based
oral contraceptive
 discontinuation reduces risk [15][19][22]
Hormone replacement therapy discontinuation reduces risk [15]
Ovarian hyper-stimulation therapy to treat infertility [15]
Compression of a vein or artery by abnormality, tumor, hematoma [15]
Long surgeries [21]
Pacing wires [22][24]
Local vein damage, incompetent valves [19][22][23]
Central venous catheters [22]
Dialysis catheters [22]
Repetitive motion injury
 [22]
Immobility modifiable risk [20][22]
Spinal cord injury [22]
Age [15][19][20][22]
Cancers [22]
Sepsis [22]
Polycythemia [22]
Protein C and/or S deficiency congenital; associated with Warfarin necrosis [22]
Antiphospholipid antibody syndrome altered coagulation [22]
Factor V Leiden defect altered coagulation [22]
Prothrombin G20210A defect altered coagulation [22]
Elevated
PAI-1
 inhibits physiological breakdown of blood clots [25]
Hyperhomocysteinemia altered coagulation [22]
Elevated factors II, VIII, IX, XI altered coagulation [22]
Antithrombin III deficiency altered coagulation [22]
Falls and hip fracture related to immobility [26]
Selective estrogen-receptor modulators [15]
Erythropoiesis-stimulating agents [15]
Acute medical illness [15]
Inflammatory bowel disease [15]
Nephrotic syndrome [15]
Myeloproliferative disorders [15]
Paroxysmal nocturnal hemoglobinnuria [15]
Thrombophilias [15]
Post-menopausal hormone replacement therapy discontinuation reduces risk [15]
Right heart failure [23]
Venous inflammation/phlebitis when a thrombus forms, it is thrombophlebitis [19]
Ambient air pollution thought to be related to inflammation [27][28][29]

Mechanism

Pathogenesis

Main article:
blood flow. Generally speaking the risk for thrombosis increases over the life course of individuals, depending on life style factors like smoking, diet, and physical activity, the presence of other diseases like cancer or autoimmune disease, while also platelet properties change in aging individuals which is an important consideration as well.[30]

Hypercoagulability

Main article: Thrombophilia

Hypercoagulability or thrombophilia, is caused by, for example, genetic deficiencies or autoimmune disorders. Recent studies indicate that white blood cells play a pivotal role in deep vein thrombosis, mediating numerous pro-thrombotic actions.[31]

Endothelial cell injury

Any inflammatory process, such as trauma, surgery or infection, can cause damage to the endothelial lining of the vessel's wall. The main mechanism is exposure of tissue factor to the blood coagulation system.[32] Inflammatory and other stimuli (such as hypercholesterolemia) can lead to changes in gene expression in endothelium producing to a pro-thrombotic state.[33] When this occurs, endothelial cells downregulate substances such as thrombomodulin, which is a key modulator of thrombin activity.[34] The result is a sustained activation of thrombin and reduced production of protein C and tissue factor inhibitor, which furthers the pro-thrombotic state.[33]

Endothelial injury is almost invariably involved in the formation of thrombi in arteries, as high rates of blood flow normally hinder clot formation. In addition, arterial and cardiac clots are normally rich in platelets–which are required for clot formation in areas under high stress due to blood flow.[33]

Disturbed blood flow

Further information:
Blood flow
Cancer-associated thrombosis can result from: (1) stasis, i.e., direct pressure on blood vessels by the tumor mass, poor performance status, and bed rest following surgical procedures; (2) iatrogenic, due to treatment with antineoplastic medications; and (3) secretion of heparanase from malignant tumors that results in degradation of endogenous heparin. Source: Potential Mechanisms of Cancer-Related Hypercoagulability. Nasser NJ, Fox J, Agbarya A. Cancers (Basel). 2020 Feb 29;12(3):566. https://doi.org/10.3390/cancers12030566[35]

Causes of disturbed blood flow include stagnation of blood flow past the point of injury, 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).[32] Also, treatments for cancer (radiation, chemotherapy) often cause additional hypercoagulability.[32] There are scores that correlate different aspects of patient data (comorbidities, vital signs, and others) to risk of thrombosis, such as the POMPE-C, which stratifies risk of mortality due to pulmonary embolism in patients with cancer, who typically have higher rates of thrombosis.[36] Also, there are several predictive scores for thromboembolic events, such as Padua,[37] Khorana,[38][39] and ThroLy score.[40]

Pathophysiology

Natural history

Fibrinolysis is the physiological breakdown of blood clots by enzymes such as plasmin.

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.[citation needed]

Ischemia/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

macular oedema and visual acuity
impairment, which if severe enough can lead to blindness.

Embolization

Further information: Embolus

A 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. Venous thrombosis can lead to pulmonary embolism when the migrated embolus becomes lodged in the lung. In people with a "shunt" (a connection between the pulmonary and systemic circulation), either in the heart or in the lung, a venous clot can also end up in the arteries and cause arterial embolism.[citation needed]

Arterial embolism can lead to obstruction of blood flow through the blood vessel that is obstructed by it, and a lack of oxygen and nutrients (ischemia) of the downstream tissue. The tissue can become irreversibly damaged, a process known as necrosis. This can affect any organ; for instance, arterial embolism of the brain is one of the causes of stroke.[citation needed]

Prevention

Main article: Thrombosis prevention

The use of

Chief Medical Officer has issued guidance to the effect that preventative measures should be used in medical patients, in anticipation of formal guidelines.[42]

Treatment

The treatment for thrombosis depends on whether it is in a vein or an artery, the impact on the person, and the risk of complications from treatment.

Anticoagulation

Main article: Anticoagulant

direct Xa inhibitors are increasingly being used instead of warfarin.[citation needed
]

Thrombolysis

recombinant tissue plasminogen activator, which enhances the normal destruction of blood clots by the body's enzymes. This carries an increased risk of bleeding so is generally only used for specific situations (such as severe stroke or a massive pulmonary embolism).[47]

Surgery

Arterial thrombosis may require surgery if it causes

acute limb ischemia.[citation needed
]

Endovascular treatment

Mechanical clot retrieval and catheter-guided thrombolysis are used in certain situations.[48]

Antiplatelet agents

Arterial thrombosis is platelet-rich, and inhibition of platelet aggregation with antiplatelet drugs such as aspirin may reduce the risk of recurrence or progression.[49]

Targeting ischemia/reperfusion injury

Main article: Reperfusion injury

With reperfusion comes ischemia/reperfusion (IR) injury (IRI), which paradoxically causes cell death in reperfused tissue[50] and contributes significantly to post-reperfusion mortality and morbidity.[51][52] For example, in a feline model of intestinal ischemia, four hours of ischemia resulted in less injury than three hours of ischemia followed by one hour of reperfusion.[50] In ST-elevation myocardial infarction (STEMI), IRI contributes up to 50% of final infarct size despite timely primary percutaneous coronary intervention. This is a key reason for the continued high mortality and morbidity in these conditions, despite endovascular reperfusion treatments and continuous efforts to improve timeliness and access to these treatments. Hence, protective therapies are required to attenuate IRI alongside reperfusion in acute ischemic conditions to improve clinical outcomes.[53] Therapeutic strategies that have potential to improve clinical outcomes in reperfused STEMI patients include remote ischemic conditioning (RIC), exenatide, and metoprolol. These have emerged amongst a multitude of cardioprotective interventions investigated with largely neutral clinical data.[54] Of these, RIC has the most robust clinical evidence, especially in the context of STEMI, but also emerging for other indications such as acute ischemic stroke and aneurysmal subarachnoid hemorrhage.[53]

Neonatal thrombosis

Treatment options for full-term and preterm babies who develop thromboembolism include expectant management (with careful observation), nitroglycerin ointment,

pharmacological therapy (thrombolytics and/or anticoagulants), and surgery.[18] The evidence supporting these treatment approaches is weak. For anticoagulant treatment, it is not clear if unfractionated and/or low molecular weight heparin treatment is effective at decreasing mortality and serious adverse events in this population.[18] There is also insufficient evidence to understand the risk of adverse effects associated with these treatment approaches in term or preterm infants.[18]

See also

References

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  9. ^ "eMedicine Article on Internal Jugular Vein Thrombosis by Dale K. Mueller". Archived from the original on April 14, 2021. Retrieved December 8, 2015.
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  17. ^ Brunner, p. 874.
  18. ^
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  19. ^ a b c d e f g h i j Copstead, p. 320.
  20. ^ a b c d e f g h i Moliterno, p. 307.
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  22. ^ a b c d e f g h i j k l m n o p q r s t u v w x Brunner, p. 875.
  23. ^ a b c d Copstead, p. 329.
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Bibliography

External links
Retrieved from "https://en.wikipedia.org/w/index.php?title=Thrombosis&oldid=1217097091#Arterial_thrombosis"