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Thrombosis
Formation of blood clots inside the blood vessels

Thrombosis is the formation of a blood clot inside a blood vessel, which can be a vein or an artery, obstructing blood flow through the circulatory system. Blood clots form naturally to prevent blood loss using platelets and fibrin, but clots can also form abnormally. These clots may break free as an embolus and travel through the bloodstream, potentially causing an embolism. Thrombosis occurs as venous thrombosis (e.g., DVT) or arterial thrombosis, with complications like tissue damage (ischemia, necrosis) or life-threatening events such as pulmonary embolism. This process is collectively termed thromboembolism.

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Signs and symptoms

Thrombosis is generally defined by

  • the type of blood vessel affected (artery or vein) and
  • the precise location of the blood vessel or the organ supplied:

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.5 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.

Stroke

Main article: Stroke

A stroke is the rapid decline of brain function due to a disturbance in the supply of blood to the brain.6 This can be due to ischemia, thrombus, embolus (a lodged particle) or hemorrhage (a bleed).7

In thrombotic stroke, a thrombus (blood clot) usually forms around atherosclerotic plaques. Since blockage of the artery is gradual, the onset of symptomatic thrombotic strokes is slower. Thrombotic stroke can be divided into two categories — large vessel disease or 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

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 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.

Limb ischemia

An arterial thrombus or embolus can also form in the limbs, which can lead to acute limb ischemia.8

Other sites

Hepatic artery thrombosis usually occurs as a devastating complication after liver transplantation.9

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 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.10

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.11

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.12

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.13 It usually happens in the setting of another disease such as pancreatitis, cirrhosis, diverticulitis or cholangiocarcinoma.14

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.15

Cerebral venous sinus thrombosis

Main article: 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 4.3%.16

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.17

Cavernous sinus thrombosis

Main article: 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.18

Causes

Thrombosis prevention is initiated with assessing the risk for its development. Some people have a higher risk of developing thrombosis and its possible development into thromboembolism.19 Some of these risk factors are related to inflammation.

"Virchow's triad" has been suggested to describe the three factors necessary for the formation of thrombosis:

Some risk factors predispose for venous thrombosis while others increase the risk of arterial thrombosis. Newborn babies in the neonatal period are also at risk of a thromboembolism.22

Risk factors for thrombosis
FactorNotesReferences
Previous episodes of thrombosis23
Vasoconstriction24
Slow or turbulent blood flowslow flow is modifiable with exercise25
Stroke26
Heart failure27
Sedentary life stylemodifiable28
Plaster casttransient29
Dehydrationmodifiable30
Acute respiratory failure31
Dysrhythmias32
Shock33
Obesitymodifiable3435363738
Pregnancy and the post-partum period394041
Varicose veins4243
Surgery4445
Trauma464748
Estrogen-based oral contraceptivediscontinuation reduces risk495051
Hormone replacement therapydiscontinuation reduces risk52
Ovarian hyper-stimulation therapy to treat infertility53
Compression of a vein or artery by abnormality, tumor, hematoma54
Long surgeries55
Pacing wires5657
Local vein damage, incompetent valves585960
Central venous catheters61
Dialysis catheters62
Repetitive motion injury63
Immobilitymodifiable risk6465
Spinal cord injury66
Age67686970
Cancers71
Sepsis72
Polycythemia73
Protein C and/or S deficiencycongenital; associated with Warfarin necrosis74
Antiphospholipid antibody syndromealtered coagulation75
Factor V Leiden defectaltered coagulation76
Prothrombin G20210A defectaltered coagulation77
Elevated PAI-1inhibits physiological breakdown of blood clots78
Hyperhomocysteinemiaaltered coagulation79
Elevated factors II, VIII, IX, XIaltered coagulation80
Antithrombin III deficiencyaltered coagulation81
Falls and hip fracturerelated to immobility82
Selective estrogen-receptor modulators83
Erythropoiesis-stimulating agents84
Acute medical illness85
Inflammatory bowel disease86
Nephrotic syndrome87
Myeloproliferative disorders88
Paroxysmal nocturnal hemoglobinnuria89
Thrombophilias90
Post-menopausal hormone replacement therapydiscontinuation reduces risk91
Right heart failure92
Venous inflammation/phlebitiswhen a thrombus forms, it is thrombophlebitis93
Ambient air pollutionthought to be related to inflammation949596

Mechanism

Pathogenesis

Main article: Virchow's triad

The main causes of thrombosis are given in Virchow's triad which lists thrombophilia, endothelial cell injury, and disturbed 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.97

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.98

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.99 Inflammatory and other stimuli (such as hypercholesterolemia) can lead to changes in gene expression in endothelium producing to a pro-thrombotic state.100 When this occurs, endothelial cells downregulate substances such as thrombomodulin, which is a key modulator of thrombin activity.101 The result is a sustained activation of thrombin and reduced production of protein C and tissue factor inhibitor, which furthers the pro-thrombotic state.102

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.103

Disturbed blood flow

Further information: 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,104 or after long periods of sedentary behaviour, 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.105 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).106 Also, treatments for cancer (radiation, chemotherapy) often cause additional hypercoagulability.107 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.108 Also, there are several predictive scores for thromboembolic events, such as Padua,109 Khorana,110111 and ThroLy score.112

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.

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 ischemia or infarction will result. A venous thrombus may or may not be ischemic, since veins distribute deoxygenated blood that is less vital for cellular metabolism. Nevertheless, non-ischemic 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.

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.

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.

Prevention

Main article: Thrombosis prevention

The use of heparin following surgery is common if there are no issues with bleeding. Generally, a risk-benefit analysis is required, as all anticoagulants lead to an increased risk of bleeding.113 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.114 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 developed deep vein thrombosis) the insertion of a vena cava filter.115116 In patients with medical rather than surgical illness, LMWH too is known to prevent thrombosis,117118 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.119

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

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).120 Other medications such as direct thrombin inhibitors and direct Xa inhibitors are increasingly being used instead of warfarin.

Thrombolysis

Thrombolysis is the pharmacological destruction of blood clots by administering thrombolytic drugs including 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).121

Surgery

Arterial thrombosis may require surgery if it causes acute limb ischemia.

Endovascular treatment

Mechanical clot retrieval and catheter-guided thrombolysis are used in certain situations.122

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.123

Targeting ischemia/reperfusion injury

Main article: Reperfusion injury

With reperfusion comes ischemia/reperfusion (IR) injury (IRI), which paradoxically causes cell death in reperfused tissue124 and contributes significantly to post-reperfusion mortality and morbidity.125126 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.127 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.128 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.129 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.130

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.131 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.132 There is also insufficient evidence to understand the risk of adverse effects associated with these treatment approaches in term or preterm infants.133

See also

Bibliography

  • Brunner L (2010). Brunner & Suddarth's textbook of medical-surgical nursing. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins. ISBN 978-0-7817-8590-7.
  • Copstead L (2013). Pathophysiology. St. Louis, Mo: Elsevier. ISBN 978-1-4557-2650-9.
  • Hoffman B (2012). Williams gynecology. New York: McGraw-Hill Medical. ISBN 978-0-07-171672-7.
  • Moliterno D (2013). Therapeutic advances in thrombosis. Chichester, West Sussex: Wiley-Blackwell. ISBN 978-1-4051-9625-3.
  • Abele H (2014). Atlas of gynecologic surgery. Stuttgart: Thieme. ISBN 978-3-13-650704-9.
  • Media related to Thrombosis at Wikimedia Commons

References

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  29. Moliterno 2013, p. 307. - Moliterno D (2013). Therapeutic advances in thrombosis. Chichester, West Sussex: Wiley-Blackwell. ISBN 978-1-4051-9625-3. ↩

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  33. Copstead 2013, p. 320. - Copstead L (2013). Pathophysiology. St. Louis, Mo: Elsevier. ISBN 978-1-4557-2650-9. ↩

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  35. Moliterno 2013, p. 307. - Moliterno D (2013). Therapeutic advances in thrombosis. Chichester, West Sussex: Wiley-Blackwell. ISBN 978-1-4051-9625-3. ↩

  36. Abele 2014. - Abele H (2014). Atlas of gynecologic surgery. Stuttgart: Thieme. ISBN 978-3-13-650704-9. ↩

  37. Brunner 2010, p. 875. - Brunner L (2010). Brunner & Suddarth's textbook of medical-surgical nursing. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins. ISBN 978-0-7817-8590-7. ↩

  38. Copstead 2013, p. 329. - Copstead L (2013). Pathophysiology. St. Louis, Mo: Elsevier. ISBN 978-1-4557-2650-9. ↩

  39. Hoffman 2012, p. 960. - Hoffman B (2012). Williams gynecology. New York: McGraw-Hill Medical. ISBN 978-0-07-171672-7. ↩

  40. Brunner 2010, p. 875. - Brunner L (2010). Brunner & Suddarth's textbook of medical-surgical nursing. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins. ISBN 978-0-7817-8590-7. ↩

  41. Copstead 2013, p. 329. - Copstead L (2013). Pathophysiology. St. Louis, Mo: Elsevier. ISBN 978-1-4557-2650-9. ↩

  42. Moliterno 2013, p. 307. - Moliterno D (2013). Therapeutic advances in thrombosis. Chichester, West Sussex: Wiley-Blackwell. ISBN 978-1-4051-9625-3. ↩

  43. Brunner 2010, p. 875. - Brunner L (2010). Brunner & Suddarth's textbook of medical-surgical nursing. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins. ISBN 978-0-7817-8590-7. ↩

  44. Hoffman 2012, p. 960. - Hoffman B (2012). Williams gynecology. New York: McGraw-Hill Medical. ISBN 978-0-07-171672-7. ↩

  45. Brunner 2010, p. 875. - Brunner L (2010). Brunner & Suddarth's textbook of medical-surgical nursing. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins. ISBN 978-0-7817-8590-7. ↩

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  47. Moliterno 2013, p. 307. - Moliterno D (2013). Therapeutic advances in thrombosis. Chichester, West Sussex: Wiley-Blackwell. ISBN 978-1-4051-9625-3. ↩

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