| Thrombus | |
|---|---|
| Other names | Blood clot |
 | |
| Diagram of a thrombus (blood clot) that has blocked avein valve | |
| Specialty | Vascular surgery |
| Symptoms | abrupt change inmental status,chest pain, cramp-like feeling,fatigue, passing out (syncope), and swelling in the arm and/or leg |
| Complications | bleeding risks from takinganticoagulants, breathing problems,heart attacks,stroke |
| Duration | c. 3–6 months |
| Types | Superficial thrombophlebitis andthrombophlebitis migrans |
| Causes | injury to the artery, sepsis or viral infection,immobility |
| Risk factors | hospitalization,immobility,obesity,pregnancy,physical trauma |
| Diagnostic method | magnetic resonance angiography,ultrasound, andvenography |
| Prevention | smoking cessation, regular exercise, improved blood flow, management of comorbidities |
| Treatment | Anticoagulants:edoxaban,tinzaparin, unfractionated heparin |
| Medication | apixaban,edoxaban, andrivaroxaban |
| Deaths | 100,000–300,000 each year |
Athrombus (pl.thrombi) is a solid or semisolid aggregate from constituents of the blood (platelets, fibrin, red blood cells, white blood cells) within the circulatory system during life.[1][2] While ablood clot is the final product of theblood coagulation step inhemostasis in or out of the circulatory system. There are two components to a thrombus: aggregatedplatelets andred blood cells that form a plug, and a mesh of cross-linkedfibrin protein. The substance making up a thrombus is sometimes calledcruor. A thrombus is a healthy response toinjury intended to stop and prevent further bleeding, but can be harmful inthrombosis, when a clot obstructs blood flow through a healthyblood vessel in thecirculatory system.
In themicrocirculation consisting of the very small and smallest blood vessels thecapillaries, tiny thrombi known as microclots can obstruct the flow of blood in the capillaries. This can cause a number of problems particularly affecting thealveoli in thelungs of therespiratory system resulting from reduced oxygen supply. Microclots have been found to be a characteristic feature in severe cases ofCOVID-19 and inlong COVID.[3]
Mural thrombi are thrombi that adhere to the wall of a largeblood vessel orheart chamber.[4] They are most commonly found in theaorta, the largestartery in the body, more often in thedescending aorta, and less often in theaortic arch orabdominal aorta.[4] They can restrict blood flow but usually do not block it entirely. They appear grey-red along with alternating light and dark lines (known aslines of Zahn) which represent bands of white blood cells and red blood cells (darker) entrapped in layers of fibrin.[5]
Thrombi are classified into two major groups depending on their location and the relative amount of platelets and red blood cells.[6] The two major groups are:
In themicrocirculation consisting of the very small and smallest blood vessels, thecapillaries, tiny thrombi (microthrombi)[7] known as microclots can obstruct the flow of blood in the capillaries. Microclots are small clumps of blood that form within the circulation, usually as a result of a larger thrombus breaking down into smaller pieces. They can be a cause for concern as they can lead to blockages in small vessels and restrict blood flow, leading to tissue damage and potentially causingischemic events.[citation needed]
Microclots can cause a number of problems particularly affecting thealveoli in thelungs of therespiratory system, resulting from reduced oxygen supply. Microclots have been found to be a characteristic feature in severe cases ofCOVID-19, and inlong COVID.[3][8]
Mural thrombi form and adhere on the inner wall of a largeblood vessel orheart chamber, often as a result of blood stasis.[4] They are most commonly found in theaorta, the largestartery in the body, more often in thedescending aorta, and less often in theaortic arch orabdominal aorta.[4] They can restrict blood flow but usually do not block it entirely. Mural thrombi are usually found in vessels already damaged byatherosclerosis.[5]
A mural thrombus can affect any heart chamber. When found in theleft ventricle it is often a result of a heart attack complication. The thrombus in this case can separate from the chamber, be carried through arteries and block a blood vessel.[4] They appear grey-red with alternating light and dark lines (known aslines of Zahn) which represent bands of white blood cells and red blood cells (darker) entrapped in layers offibrin.[citation needed]
It was suggested over 150 years ago that thrombus formation is a result of abnormalities in blood flow, vessel wall, and blood components. This concept is now known asVirchow's triad. The three factors have been further refined to include circulatory stasis, vascular wall injury, and hypercoagulable state, all of which contribute to increased risk for venous thromboembolism and other cardiovascular diseases.[6]
Virchow's triad describes thepathogenesis of thrombus formation:[9][10]
Disseminated intravascular coagulation (DIC) involves widespread microthrombi formation throughout the majority of the blood vessels. This is due to excessive consumption of coagulation factors and subsequent activation offibrinolysis using all of the body's availableplatelets and clotting factors. The result is hemorrhaging and ischemic necrosis of tissue/organs. Causes aresepticaemia, acuteleukaemia,shock, snake bites,fat emboli from broken bones, or other severe traumas. DIC may also be seen inpregnant females. Treatment involves the use offresh frozen plasma to restore the level of clotting factors in the blood, as well as platelets and heparin to prevent further thrombi formation.[citation needed]
A thrombus occurs when the hemostatic process, which normally occurs in response to injury, becomes activated in an uninjured or slightly injured vessel. A thrombus in a large blood vessel will decrease blood flow through that vessel (termed a mural thrombus). In a small blood vessel, blood flow may be completely cut off (termed an occlusive thrombus), resulting in death of tissue supplied by that vessel. If a thrombus dislodges and becomes free-floating, it is considered anembolus.[citation needed] If an embolus becomes trapped within a blood vessel, it blocks blood flow and is termed as an embolism. Embolisms, depending on their specific location, can cause more significant effects like strokes, heart attacks, or even death.[13]
Some of the conditions which increase the risk of blood clots developing includeatrial fibrillation (a form ofcardiac arrhythmia), heart valve replacement, a recentheart attack (also known as amyocardial infarction), extended periods of inactivity (seedeep venous thrombosis), and genetic or disease-related deficiencies in the blood's clotting abilities.[citation needed]
Platelet activation occurs through injuries that damage theendothelium of the blood vessels, exposing the enzyme calledfactor VII, a protein normally circulating within the vessels, to thetissue factor, which is a protein encoded by the F3 gene.The platelet activation can potentially cause a cascade, eventually leading to the formation of the thrombus.[14] This process is regulated throughthromboregulation.
Anticoagulants are drugs used to prevent the formation of blood clots, reducing the risk ofstroke,heart attack andpulmonary embolism.Heparin andwarfarin are used to inhibit the formation and growth of existing thrombi, with the former used for acute anticoagulation while the latter is used for long-term anticoagulation.[10] The mechanism of action of heparin and warfarin are different as they work on different pathways of thecoagulation cascade.[15]
Heparin works by binding to and activating the enzyme inhibitorantithrombin III, an enzyme that acts by inactivating thrombin and factor Xa.[15] In contrast, warfarin works by inhibitingvitamin K epoxide reductase, an enzyme needed to synthesize vitamin K dependent clotting factors II, VII, IX, and X.[15][16] Bleeding time with heparin and warfarin therapy can be measured with the partial thromboplastin time (PTT) andprothrombin time (PT), respectively.[16]
Once clots have formed, other drugs can be used to promotethrombolysis or clot breakdown.Streptokinase, an enzyme produced bystreptococcal bacteria, is one of the oldest thrombolytic drugs.[16] This drug can be administeredintravenously to dissolve blood clots incoronary vessels. However, streptokinase causes systemic fibrinolytic state and can lead to bleeding problems.Tissue plasminogen activator (tPA) is a different enzyme that promotes the degradation of fibrin in clots but not free fibrinogen.[16] This drug is made by transgenic bacteria and converts plasminogen into the clot-dissolving enzyme,plasmin.[17] Recent research indicates that tPA could have toxic effects in the central nervous system. In cases of severe stroke, tPA can cross theblood–brain barrier and enter interstitial fluid, where it then increases excitotoxicity, potentially affecting permeability of the blood–brain barrier,[18] and causing cerebral hemorrhage.[19]
There are also some anticoagulants that come from animals that work by dissolvingfibrin. For example,Haementeria ghilianii, anAmazonleech, produces an enzyme calledhementin from itssalivary glands.[20]
Thrombus formation can have one of four outcomes: propagation, embolization, dissolution, and organization and recanalization.[21]
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