Editing Thrombus (section)

==Cause==
[[File:Blausen 0053 Artery NormalvsDiseasedVessel.png|thumb|Illustration comparing normal artery with diseased artery with a blood clot.]]
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 as [[Virchow'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.<ref name=":3" />

[[Virchow's triad]] describes the [[pathogenesis]] of thrombus formation:<ref name=":0">{{Cite book|title=Robbins & Cotran Pathologic Basis of Disease|last1=Kumar |first1=Vinay |last2=Abbas |first2=Abul |last3=Aster |first3=Jon |isbn=9781455726134|edition= 9th |publisher=Elsevier |location=Philadelphia|oclc=879416939|year = 2014}}</ref><ref name=":1">{{Cite web|url=http://www.pathophys.org/vte/|title=Venous thromboembolism (VTE) {{!}} McMaster Pathophysiology Review|website=www.pathophys.org|date=26 September 2012 |language=en-US|access-date=2018-11-03}}</ref>

# Endothelial injury: Injury to the [[endothelium]] (interior surface of blood vessel), causing platelet activation and aggregation;
#* Common causes include: [[Injury|trauma]], [[Health effects of tobacco|smoking]], [[hypertension]], [[atheroma]].
# [[Hemodynamics|Hemodynamic]] changes (stasis, turbulence): Blood stasis promotes greater contact between platelets/coagulative factors with vascular endothelium. If rapid blood circulation (e.g., because of [[tachycardia]]) occurs within vessels that have endothelial injuries, that creates disordered flow (turbulence) that can lead to the formation of thrombosis;<ref>{{Citation|last1=Kushner|first1=Abigail|title=Virchow Triad|date=2020|url=http://www.ncbi.nlm.nih.gov/books/NBK539697/|work=StatPearls|place=Treasure Island (FL)|publisher=StatPearls Publishing|pmid=30969519|access-date=2020-06-18|last2=West|first2=William P.|last3=Pillarisetty|first3=Leela Sharath}}</ref>
#* Common causes of stasis include anything that leads to prolonged immobility and reduced blood flow such as: [[Injury|trauma]]/[[Bone fracture|broken bones]] and extended [[air travel]].
# Hypercoagulability (also called [[thrombophilia]]; any disorder of the blood that predisposes to thrombosis);<ref>{{cite journal |vauthors=Ataga KI |date=10 May 2020 |title=Hypercoagulability and thrombotic complications in hemolytic anemias |journal=Haematologica |volume=94 |issue=11 |pages=1481–1484 |doi=10.3324/haematol.2009.013672 |pmc=2770956 |pmid=19880774 |doi-access=free}}</ref>
#* Common causes include: cancer ([[leukaemia]]), [[factor V]] mutation ([[Factor V Leiden|Leiden]]) – prevents Factor V inactivation leading to increased coagulability.

[[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 of [[fibrinolysis]] using all of the body's available [[platelets]] and clotting factors. The result is hemorrhaging and ischemic necrosis of tissue/organs. Causes are [[septicaemia]], acute [[leukaemia]], [[shock (circulatory)|shock]], snake bites, [[Fat embolism|fat emboli]] from broken bones, or other severe traumas. DIC may also be seen in [[Pregnancy|pregnant females]]. Treatment involves the use of [[fresh 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|date=February 2021}}. Both [[Disseminated intravascular coagulation]] and [[sepsis]] are closely correlated<ref>{{cite journal |last1=Schofield |first1=J |last2=Absrams |first2=ST |last3=Jenkins |first3=R |last4=Lane |first4=S |last5=Wang |first5=G |last6=Toh |first6=CH |title=Microclots, as defined by amyloid-fibrinogen aggregates, predict risks of disseminated intravascular coagulation and mortality |journal=Blood Adv |date=2024 |volume=8 |pages=2499-2508 |pmid=38507683 |url=https://ashpublications.org/bloodadvances/article/8/10/2499/515373/Microclots-as-defined-by-amyloid-fibrinogen}}</ref> with the presence of fibrinaloid microclots in the circulation.