Materiały źródłowe

• #1 Thrombophlebitis – wikidoc

  https://www.wikidoc.org/index.php/Thrombophlebitis

  Thrombophlebitis is inflammation of a vein, usually associated with the formation of a thrombus within the superficial venous system. […] The pathogenesis of thrombophlebitis is related to 3 important factors: Venous stasis, Hypercoagulability of blood, Trauma to veins. […] These 3 factors (known as Virchow’s triad) predispose to thrombus formation within the veins and subsequently to thrombophlebitis.

• #2 Thrombophlebitis: Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/1086399-overview

  Thrombophlebitis involves the formation of a blood clot in the presence of venous inflammation or injury. Many innate conditions may predispose patients to thrombophlebitis by means of a variety of hypercoagulopathy syndromes. […] Risk factors for thrombophlebitis include obesity, older age, oral contraceptive use and estrogen replacement therapy, autoimmune or infectious diseases, recent trauma or surgery, active malignancy, history of venous thromboembolic disease, respiratory or cardiac failure, and a history of varicose veins. […] Traumatic events can also initiate a thrombophlebitic reaction. […] Superficial thrombophlebitis is a common inflammatory-thrombotic disorder in which a thrombus develops in a vein located near the surface of the skin. […] Septic thrombophlebitis is a condition characterized by venous thrombosis, inflammation, and bacteremia or fungemia.

• #2 Superficial Thrombophlebitis: Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/463256-overview

  Microscopic thrombosis is a normal part of the dynamic balance of hemostasis. In 1846, the German pathologist Virchow recognized that if this dynamic balance were altered by venous stasis or turbulence, abnormal coagulability, or vessel wall injuries, then microthrombi could propagate to form macroscopic thrombi. […] In the absence of a triggering event, neither venous stasis nor abnormal coagulability alone causes clinically important thrombosis, but vascular endothelial injury does reliably result in thrombus formation. The initiating injury triggers an inflammatory response that results in immediate platelet adhesion at the injury site. Further platelet aggregation is mediated by thromboxane A2 (TxA2) and by thrombin. […] This is why aspirin and other NSAIDs are somewhat effective in preventing arterial thrombosis, where platelet aggregation is mediated via TxA2, as seen in patients with stroke and myocardial infarction (MI), but are not very effective in preventing venous thrombophlebitis, where it is believed that clot formation is more of a result of thrombin activation.

• #3 Deep Vein Thrombosis and Pulmonary Embolism | Yellow Book | CDC

  https://www.cdc.gov/yellow-book/hcp/travel-air-sea/deep-vein-thrombosis-and-pulmonary-embolism.html

  Virchow’s classic triad for thrombus formation is venous stasis, vessel wall damage, and a hypercoagulable state. […] Prolonged, cramped sitting during long-distance travel interferes with venous flow in the legs, creating venous stasis. […] Coagulation activation can result from an interaction between air cabin conditions (e.g., hypobaric hypoxia) and individual risk factors for VTE. […] Studies of the pathophysiologic mechanisms for the increased risk of VTE after long-distance travel have not produced consistent results, but venous stasis appears to play a major role. […] Other factors specific to air travel might increase coagulation activation, particularly in travelers with preexisting risk factors for VTE.

• #4 Deep vein thrombosis: pathogenesis, diagnosis, and medical management – Stone – Cardiovascular Diagnosis and Therapy

  https://cdt.amegroups.org/article/view/16872/html

  Virchows Triad, first described in 1856, implicates three contributing factors in the formation of thrombosis: venous stasis, vascular injury, and hypercoagulability. Venous stasis is the most consequential of the three factors, but stasis alone appears to be insufficient to cause thrombus formation. […] However, the concurrent presence of venous stasis and vascular injury or hypercoagulability greatly increases the risk for clot formation. The clinical conditions most closely associated with DVT are fundamentally related to the elements of Virchows Triad; these include surgery or trauma, malignancy, prolonged immobility, pregnancy, congestive heart failure, varicose veins, obesity, advancing age, and a history of DVT. […] Venous thrombosis tends to occur in areas with decreased or mechanically altered blood flow such as the pockets adjacent to valves in the deep veins of the leg.

• #5 The Basic Principles of Pathophysiology of Venous Thrombosis

  https://www.mdpi.com/1422-0067/25/21/11447

  The past few decades have brought tremendous insight into the molecular and pathophysiological mechanisms responsible for thrombus generation. […] The pathophysiology of venous thrombosis has historically been explained with Virchow’s triad, which consists of hypercoagulability, venous stasis, and injury to the endothelium of the blood vessels. […] Studies in animal models have improved our understanding of the pathophysiology of thrombosis. […] The events on a molecular level during venous stasis have been investigated. […] Thromboinflammation has become a major player in the field. […] Situations when venous stasis is implicated in the generation of thrombosis include deep vein thrombosis (DVT) in the lower extremity during immobilization, left atrial appendage thrombus formation in atrial fibrillation, left ventricle thrombosis due to akinetic myocardium and infarction or due to actual obstruction of the blood flow such as external compression from an expansive process (typically a tumor), or from restricted venous lumen in catheter-related arm vein thrombosis or possibly also in recurrent DVT where there is residual thrombus or fibrotic scar from a prior event.

• #6

  https://www.jci.org/articles/view/60229

  In the 19th century, the noted physician Virchow proposed a triad of physiological alterations that increase the risk of VTE: changes in blood flow, in the blood itself, and in the endothelial cells lining the blood vessel. […] Reduced blood flow and stasis allow the accumulation of procoagulant proteases, such as thrombin, that may overcome the local anticoagulant pathways and induce thrombosis. […] Thrombophilia describes a disorder in which the blood has a tendency to clot. Thrombophilia can be caused by increases in procoagulant proteins, the presence of variant clotting proteins that are more procoagulant, decreases in anticoagulant proteins, and/or decreased fibrinolysis. […] The endothelial lining of blood vessels plays a critical role in preventing thrombosis by providing a surface that prevents attachment of cells and proteins required for clotting.

• #7 Superficial Thrombophlebitis: Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/463256-overview

  Microscopic thrombosis is a normal part of the dynamic balance of hemostasis. In 1846, the German pathologist Virchow recognized that if this dynamic balance were altered by venous stasis or turbulence, abnormal coagulability, or vessel wall injuries, then microthrombi could propagate to form macroscopic thrombi. […] In the absence of a triggering event, neither venous stasis nor abnormal coagulability alone causes clinically important thrombosis, but vascular endothelial injury does reliably result in thrombus formation. The initiating injury triggers an inflammatory response that results in immediate platelet adhesion at the injury site. Further platelet aggregation is mediated by thromboxane A2 (TxA2) and by thrombin. […] This is why aspirin and other NSAIDs are somewhat effective in preventing arterial thrombosis, where platelet aggregation is mediated via TxA2, as seen in patients with stroke and myocardial infarction (MI), but are not very effective in preventing venous thrombophlebitis, where it is believed that clot formation is more of a result of thrombin activation.

• #8 Superficial Thrombophlebitis: Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/463256-overview

  Microscopic thrombosis is a normal part of the dynamic balance of hemostasis. In 1846, the German pathologist Virchow recognized that if this dynamic balance were altered by venous stasis or turbulence, abnormal coagulability, or vessel wall injuries, then microthrombi could propagate to form macroscopic thrombi. […] In the absence of a triggering event, neither venous stasis nor abnormal coagulability alone causes clinically important thrombosis, but vascular endothelial injury does reliably result in thrombus formation. The initiating injury triggers an inflammatory response that results in immediate platelet adhesion at the injury site. Further platelet aggregation is mediated by thromboxane A2 (TxA2) and by thrombin. […] This is why aspirin and other NSAIDs are somewhat effective in preventing arterial thrombosis, where platelet aggregation is mediated via TxA2, as seen in patients with stroke and myocardial infarction (MI), but are not very effective in preventing venous thrombophlebitis, where it is believed that clot formation is more of a result of thrombin activation.

• #9 Superficial Thrombophlebitis – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK556017/

  Superficial thrombophlebitis is an inflammatory disorder of superficial veins with coexistent venous thrombosis. […] More recently, superficial thrombophlebitis, also called superficial venous thrombosis (SVT), has been associated with other venous thromboembolic disorders, primarily deep venous thrombosis (DVT) and pulmonary embolism (PE). […] Superficial thrombophlebitis starts with microscopic thrombosis. When venous turbulence or stasis, vessel wall injuries, abnormal coagulability, or vessel wall injuries, microthrombi could propagate and subsequently form macroscopic thrombi. Vascular endothelial injury reliably results in thrombus formation by triggering an inflammatory response that results in immediate platelet adhesion. Platelet aggregation is mediated by thrombin and thromboxane A2.

• #10 Venous Thrombosis: Pathogenesis and Potential for Embolism

  https://www.uspharmacist.com/article/venous-thrombosis-pathogenesis-and-potential-for-embolism

  Inappropriate thrombus formation is a disruption of homeostasis and may result from an alteration in any of the factors listed below. The dominant influence, and the one factor that by itself can lead to thrombosis, is endothelial injury.2,5,6 […] Endothelial injury causes subendothelial collagen exposure and platelet adherence, among other changes; many factors can contribute to the injury, including hypertension, vasculitis, scarred valves, bacterial endotoxins, cholesterolemia, and chemicals from cigarette smoke.2,5,7 […] Stasis and turbulence are alterations in normal blood flow, which can cause endothelial injury.2 Aneurisms (aortic and arterial dilations) cause local turbulence; a dilated atrium in the presence of atrial fibrillation is a site of significant stasis that may provoke thrombus development.2 Additional conditions are associated with stasis, such as sickle cell anemia and polycythemia, both of which may predispose a patient to thrombosis.2

• #11 Superficial Thrombophlebitis: Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/463256-overview

  Microscopic thrombosis is a normal part of the dynamic balance of hemostasis. In 1846, the German pathologist Virchow recognized that if this dynamic balance were altered by venous stasis or turbulence, abnormal coagulability, or vessel wall injuries, then microthrombi could propagate to form macroscopic thrombi. […] In the absence of a triggering event, neither venous stasis nor abnormal coagulability alone causes clinically important thrombosis, but vascular endothelial injury does reliably result in thrombus formation. The initiating injury triggers an inflammatory response that results in immediate platelet adhesion at the injury site. Further platelet aggregation is mediated by thromboxane A2 (TxA2) and by thrombin. […] This is why aspirin and other NSAIDs are somewhat effective in preventing arterial thrombosis, where platelet aggregation is mediated via TxA2, as seen in patients with stroke and myocardial infarction (MI), but are not very effective in preventing venous thrombophlebitis, where it is believed that clot formation is more of a result of thrombin activation.

• #12

  https://step2.medbullets.com/cardiovascular/120036/superficial-thrombophlebitis

  a thrombotic disorder characterized by thrombi and inflammation (phlebitis) in the superficial veins […] endothelial injury can trigger thrombus formation and an inflammatory response

• #13 Superficial Thrombophlebitis: Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/463256-overview

  Microscopic thrombosis is a normal part of the dynamic balance of hemostasis. In 1846, the German pathologist Virchow recognized that if this dynamic balance were altered by venous stasis or turbulence, abnormal coagulability, or vessel wall injuries, then microthrombi could propagate to form macroscopic thrombi. […] In the absence of a triggering event, neither venous stasis nor abnormal coagulability alone causes clinically important thrombosis, but vascular endothelial injury does reliably result in thrombus formation. The initiating injury triggers an inflammatory response that results in immediate platelet adhesion at the injury site. Further platelet aggregation is mediated by thromboxane A2 (TxA2) and by thrombin. […] This is why aspirin and other NSAIDs are somewhat effective in preventing arterial thrombosis, where platelet aggregation is mediated via TxA2, as seen in patients with stroke and myocardial infarction (MI), but are not very effective in preventing venous thrombophlebitis, where it is believed that clot formation is more of a result of thrombin activation.

• #14

  https://www.jci.org/articles/view/60229

  In the 19th century, the noted physician Virchow proposed a triad of physiological alterations that increase the risk of VTE: changes in blood flow, in the blood itself, and in the endothelial cells lining the blood vessel. […] Reduced blood flow and stasis allow the accumulation of procoagulant proteases, such as thrombin, that may overcome the local anticoagulant pathways and induce thrombosis. […] Thrombophilia describes a disorder in which the blood has a tendency to clot. Thrombophilia can be caused by increases in procoagulant proteins, the presence of variant clotting proteins that are more procoagulant, decreases in anticoagulant proteins, and/or decreased fibrinolysis. […] The endothelial lining of blood vessels plays a critical role in preventing thrombosis by providing a surface that prevents attachment of cells and proteins required for clotting.

• #15

  https://www.jci.org/articles/view/60229

  However, activated endothelial cells downregulate expression of the anticoagulant protein thrombomodulin and upregulate expression of the procoagulant protein TF. […] Blood is returned from the venous system of the lower limbs to the heart by the calf muscles in the legs acting as pumps. […] However, the valve sinus is prone to thrombosis because of the irregular patterns of blood flow and the potential for a low oxygen tension, especially during immobilization or long-haul travel. […] At present, the triggers for venous thrombosis are unknown. However, it is tempting to speculate that the potent procoagulant TF plays a key role in some forms of VTE because under pathological conditions it is present on circulating monocytes, MVs, and possibly activated endothelium. […] Importantly, major surgery is associated with an induction of TF expression by circulating monocytes. […] These studies suggest that blocking the binding of leukocytes and MVs to the activated endothelium may represent a novel strategy to reduce VTE.

• #16 The Basic Principles of Pathophysiology of Venous Thrombosis

  https://www.mdpi.com/1422-0067/25/21/11447

  It can then be hypothesized that, during venous stasis, there is a change in the balance towards hypercoagulability. […] The blood flow in veins is characterized by a low shear rate, which is typically about 100/s. […] The initiation of thrombus formation happens when factor VIIa, together with TF, expressed on monocytes, activates factor X to Xa, which, in turn, with factor Va as cofactor on a phospholipid bilayer (monocyte or endothelium), activates factor II (prothrombin) to IIa (thrombin). […] This is the more recent addition to Virchow’s triad and an area of intensive research. […] Neutrophils that become activated by damaged endothelium or by activated platelets will then release tissue factor as well as neutrophil extracellular traps (NETs). […] These prothrombotic responses are collectively termed thromboinflammation (sometimes interchangeably with immunothrombosis), which implies a pathophysiologic condition with injured vascular endothelium, impaired anti-inflammatory and antithrombotic functions.

• #17 Migratory Thrombophlebitis – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK547702/

  Reports exist of tissue factor (TF) as a cause of Trousseau syndrome. Cancer cells express abnormally high TF and release TF-positive microparticles that are highly procoagulant. […] Inflammatory cytokines produced by cancer cells induce TF expression in vascular cells, where it does not usually get expressed. Cancer cells also induce monocytes and macrophages to release TF. TF promotes the conversion of factor VII to factor VIIa, activating the coagulation cascade’s extrinsic pathway. […] Cancer procoagulant, also described as cysteine proteinase, expressed by malignant cells and normal cells (except fetal tissue), directly induces the conversion of factor X to factor Xa. […] There are reports that hypoxia increases the expression of TF and plasminogen activator inhibitor type1 that facilitates coagulation.

• #18 Deep vein thrombosis: pathogenesis, diagnosis, and medical management – Stone – Cardiovascular Diagnosis and Therapy

  https://cdt.amegroups.org/article/view/16872/html

  The hypercoagulable micro-environment that ensues may downregulate certain antithrombotic proteins that are preferentially expressed on venous valves including thrombomodulin and endothelial protein C receptor (EPCR). […] Debate remains regarding the precise location of tissue factor in this process, whether expressed on the endothelium or by cells within the extravascular tissue, but there is general agreement that tissue factor serves as the primary nidus for thrombus formation. […] Thrombus formation appears to require both tissue factor and P-selectin. […] A venous thrombus has essentially two components, an inner platelet rich white thrombus forming the so-called lines of Zahn surrounded by an outer red cell dense fibrin clot. […] As the ratio of procoagulants to anticoagulants increases, so does the risk of thrombus formation.

• #19 Molecular mechanisms of venous thrombosis | JIR

  https://www.dovepress.com/recent-advances-on-the-molecular-mechanism-and-clinical-trials-of-veno-peer-reviewed-fulltext-article-JIR

  Venous thromboembolism is a condition that includes deep vein thrombosis and pulmonary embolism. […] Over the past few years, growing research suggests that venous thrombosis is also related to the immune system and inflammatory factors have been confirmed to be involved in venous thrombosis. […] P-selectin leads to platelet-monocyte aggregation and stimulates vascular inflammation and thrombosis. […] The dysregulation of miRNAs has also been reported in venous thrombosis, suggesting the involvement of miRNAs in the progression of venous thrombosis. […] Plasminogen activator inhibitor-1 (PAI-1) is a crucial component of the plasminogen-plasmin system, and elevated levels of PAI-1 in conjunction with advanced age are significant risk factors for thrombosis. […] In addition, it has been showed that one of the ways that neutrophils promote venous thrombosis is the formation of neutrophil extracellular traps (NETs).

• #20 Molecular mechanisms of venous thrombosis | JIR

  https://www.dovepress.com/recent-advances-on-the-molecular-mechanism-and-clinical-trials-of-veno-peer-reviewed-fulltext-article-JIR

  Venous thromboembolism is a condition that includes deep vein thrombosis and pulmonary embolism. […] Over the past few years, growing research suggests that venous thrombosis is also related to the immune system and inflammatory factors have been confirmed to be involved in venous thrombosis. […] P-selectin leads to platelet-monocyte aggregation and stimulates vascular inflammation and thrombosis. […] The dysregulation of miRNAs has also been reported in venous thrombosis, suggesting the involvement of miRNAs in the progression of venous thrombosis. […] Plasminogen activator inhibitor-1 (PAI-1) is a crucial component of the plasminogen-plasmin system, and elevated levels of PAI-1 in conjunction with advanced age are significant risk factors for thrombosis. […] In addition, it has been showed that one of the ways that neutrophils promote venous thrombosis is the formation of neutrophil extracellular traps (NETs).

• #21 Molecular mechanisms of venous thrombosis | JIR

  https://www.dovepress.com/recent-advances-on-the-molecular-mechanism-and-clinical-trials-of-veno-peer-reviewed-fulltext-article-JIR

  Inflammation stimulates endothelial cells to release tPA and PAI-1 locally. […] Besides, since platelets are the major circulating pool of PAI-1, activated platelets release a great number of PAI-1, leading to locally high levels of PAI-1 at growing fibrin clot sites, thus increased PAI-1 is a risk factor for thrombosis. […] There is growing evidence showed that inflammatory factors linked to venous thrombosis. […] The role of inflammation and inflammation-related biomarkers in cerebrovascular thrombotic disease is a subject of ongoing debate. […] Elevated levels of inflammatory factors interleukin-1 (IL-1), tissue factor (TF), xanthine oxidase (XOD) and nuclear factor kappa B (NF-B) may accelerate thrombosis. […] The NLRP3/IL-1/NF-B signaling mechanisms regulate IL-1 and tumor necrosis factor alpha (TNF-), which may be essential signs of the prethrombotic condition due to slowed blood flow, impaired vascular endothelium, and elevated tissue factor expression.

• #22 The Basic Principles of Pathophysiology of Venous Thrombosis

  https://www.mdpi.com/1422-0067/25/21/11447

  It can then be hypothesized that, during venous stasis, there is a change in the balance towards hypercoagulability. […] The blood flow in veins is characterized by a low shear rate, which is typically about 100/s. […] The initiation of thrombus formation happens when factor VIIa, together with TF, expressed on monocytes, activates factor X to Xa, which, in turn, with factor Va as cofactor on a phospholipid bilayer (monocyte or endothelium), activates factor II (prothrombin) to IIa (thrombin). […] This is the more recent addition to Virchow’s triad and an area of intensive research. […] Neutrophils that become activated by damaged endothelium or by activated platelets will then release tissue factor as well as neutrophil extracellular traps (NETs). […] These prothrombotic responses are collectively termed thromboinflammation (sometimes interchangeably with immunothrombosis), which implies a pathophysiologic condition with injured vascular endothelium, impaired anti-inflammatory and antithrombotic functions.

• #23 The Basic Principles of Pathophysiology of Venous Thrombosis

  https://www.mdpi.com/1422-0067/25/21/11447

  It can then be hypothesized that, during venous stasis, there is a change in the balance towards hypercoagulability. […] The blood flow in veins is characterized by a low shear rate, which is typically about 100/s. […] The initiation of thrombus formation happens when factor VIIa, together with TF, expressed on monocytes, activates factor X to Xa, which, in turn, with factor Va as cofactor on a phospholipid bilayer (monocyte or endothelium), activates factor II (prothrombin) to IIa (thrombin). […] This is the more recent addition to Virchow’s triad and an area of intensive research. […] Neutrophils that become activated by damaged endothelium or by activated platelets will then release tissue factor as well as neutrophil extracellular traps (NETs). […] These prothrombotic responses are collectively termed thromboinflammation (sometimes interchangeably with immunothrombosis), which implies a pathophysiologic condition with injured vascular endothelium, impaired anti-inflammatory and antithrombotic functions.

• #24 Deep vein thrombosis – Wikipedia

  https://en.wikipedia.org/wiki/Deep_vein_thrombosis

  The mechanism behind DVT formation typically involves some combination of decreased blood flow, increased tendency to clot, changes to the blood vessel wall, and inflammation. […] The beginning of venous thrombosis is thought to arise from „activation of endothelial cells, platelets, and leukocytes, with initiation of inflammation and formation of microparticles that trigger the coagulation system” via tissue factor. […] Importantly, the activated endothelium of veins interacts with circulating white blood cells (leukocytes). […] While leukocytes normally help prevent blood from clotting (as does normal endothelium), upon stimulation, leukocytes facilitate clotting. […] Neutrophils are recruited early in the process of venous thrombi formation. […] They release pro-coagulant granules and neutrophil extracellular traps (NETs) or their components, which play a role in venous thrombi formation.

• #25 Hemolysis and Venous Thrombosis: Which Link?

  https://clinmedjournals.org/articles/cmrcr/clinical-medical-reviews-and-case-reports-cmrcr-7-329.php?jid=cmrcr

  Thus, haemolysis results in NO scavenging, systemic vasoconstriction and increased blood stasis, there by affecting one of the principle components of Virchow’s Triad. […] Furthermore, Reactive oxygen species (ROS) induction by haem directly, oxidize cell membrane constituents to induce cytotoxicity and promote inflammation and thrombosis. […] Haem affects neutrophils in multiple ways. DNA component of neutrophil extracellular traps (NETs) also enhances thrombin generation via the intrinsic coagulation pathway. Thus, NETs recruit RBCs, activate platelets and promote fibrin deposition, appear to contribute to the pathogenesis of deep venous thrombosis. […] The link between hemolysis and venous thrombosis is multifactorial, and involves prothrombotic specific mechanisms related to hemolysis and classic Thrombotic risk factors. Pathological haemolysis overwhelms the physiological defences against the toxicity of iron from the haem group of haemoglobin. The pro-oxidant, pro-inflammatory and NO scavenging capacity of free haem affects the three elements of Virchow’s triad by causing vasoconstriction, activating coagulation and damaging endothelial cells.

• #26 Molecular mechanisms of venous thrombosis | JIR

  https://www.dovepress.com/recent-advances-on-the-molecular-mechanism-and-clinical-trials-of-veno-peer-reviewed-fulltext-article-JIR

  Inflammation stimulates endothelial cells to release tPA and PAI-1 locally. […] Besides, since platelets are the major circulating pool of PAI-1, activated platelets release a great number of PAI-1, leading to locally high levels of PAI-1 at growing fibrin clot sites, thus increased PAI-1 is a risk factor for thrombosis. […] There is growing evidence showed that inflammatory factors linked to venous thrombosis. […] The role of inflammation and inflammation-related biomarkers in cerebrovascular thrombotic disease is a subject of ongoing debate. […] Elevated levels of inflammatory factors interleukin-1 (IL-1), tissue factor (TF), xanthine oxidase (XOD) and nuclear factor kappa B (NF-B) may accelerate thrombosis. […] The NLRP3/IL-1/NF-B signaling mechanisms regulate IL-1 and tumor necrosis factor alpha (TNF-), which may be essential signs of the prethrombotic condition due to slowed blood flow, impaired vascular endothelium, and elevated tissue factor expression.

• #27 Deep vein thrombosis – Wikipedia

  https://en.wikipedia.org/wiki/Deep_vein_thrombosis

  The mechanism behind DVT formation typically involves some combination of decreased blood flow, increased tendency to clot, changes to the blood vessel wall, and inflammation. […] The beginning of venous thrombosis is thought to arise from „activation of endothelial cells, platelets, and leukocytes, with initiation of inflammation and formation of microparticles that trigger the coagulation system” via tissue factor. […] Importantly, the activated endothelium of veins interacts with circulating white blood cells (leukocytes). […] While leukocytes normally help prevent blood from clotting (as does normal endothelium), upon stimulation, leukocytes facilitate clotting. […] Neutrophils are recruited early in the process of venous thrombi formation. […] They release pro-coagulant granules and neutrophil extracellular traps (NETs) or their components, which play a role in venous thrombi formation.

• #28 Deep vein thrombosis – Wikipedia

  https://en.wikipedia.org/wiki/Deep_vein_thrombosis

  The mechanism behind DVT formation typically involves some combination of decreased blood flow, increased tendency to clot, changes to the blood vessel wall, and inflammation. […] The beginning of venous thrombosis is thought to arise from „activation of endothelial cells, platelets, and leukocytes, with initiation of inflammation and formation of microparticles that trigger the coagulation system” via tissue factor. […] Importantly, the activated endothelium of veins interacts with circulating white blood cells (leukocytes). […] While leukocytes normally help prevent blood from clotting (as does normal endothelium), upon stimulation, leukocytes facilitate clotting. […] Neutrophils are recruited early in the process of venous thrombi formation. […] They release pro-coagulant granules and neutrophil extracellular traps (NETs) or their components, which play a role in venous thrombi formation.

• #29

  https://link.springer.com/article/10.1007/s12185-024-03735-x

  Patients with cancer have a higher risk of venous thromboembolism (VTE), including deep vein thrombosis (DVT) and pulmonary embolism (PE), compared to the general population. […] Cancer-associated thrombosis (CAT) is a thrombotic event that occurs as a complication of cancer or cancer therapy. […] This implies that the mechanism of VTE differs between cancer types and that specific VTE pathways may exist for different cancer types. […] This review summarizes the specific pathways that contribute to VTE in cancer patients, with a particular focus on leukocytosis, neutrophil extracellular traps (NETs), tissue factor (TF), thrombocytosis, podoplanin (PDPN), plasminogen activator inhibitor-1 (PAI-1), the intrinsic coagulation pathway, and von Willebrand factor (VWF). […] Hisada Y, Mackman N. Mechanisms of cancer-associated thrombosis. Res Pract Thromb Haemost. 2023;7: 100123.

• #30 Acute and chronic venous thrombosis: Pathogenesis and new insights | 8

  https://www.taylorfrancis.com/chapters/edit/10.1201/9781315382449-8/acute-chronic-venous-thrombosis-pathogenesis-new-insights-jose-diaz-thomas-wakefield-peter-henke

  The acute phase or thrombogenesis is led by neutrophils and the chronic phase or thrombus resolution is led by monocytes, progressively increasing fibrin deposition. […] Pro-inflammatory and anti-inflammatory mediators are involved in the ultimate vein wall and thrombus response. […] Tissue factor expression on monocyte surfaces promotes monocyte interactions with activated platelets and endothelial cells, leading to fibrin formation and deposition into the developing thrombus. […] Although polymorphonuclear neutrophils may cause vein wall injury, they are essential for early thrombus resolution by promoting both fibrinolysis and collagenolysis.

• #31 Thrombophlebitis: Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/1086399-overview

  A number of primary and secondary hypercoagulable states can be assessed by obtaining an appropriate patient history and review of systems. […] Inherited hypercoagulable states are divided by experts into five main categories, as follows: Qualitative or quantitative defects of coagulation factor inhibitors, Increased level or function of coagulation factors, Hyperhomocysteinemia, Defects of the fibrinolytic system, Altered platelet function. […] The specific inherited thrombophilias are listed below. […] Resistance to APC is the most common genetic risk factor associated with venous thrombosis. […] Although endothelial damage is speculated to be necessary for symptomatic thrombosis to occur, venous thrombosis may be associated with a deficiency in one of several anticoagulant factors.

• #32 Venous Thrombosis: Pathogenesis and Potential for Embolism

  https://www.uspharmacist.com/article/venous-thrombosis-pathogenesis-and-potential-for-embolism

  Hypercoagulability can be described as any alteration of the coagulation pathway that places the patient at risk for thrombosis.2 There are two types of hypercoagulability states; primary disorders are genetically inherited (e.g., mutations in factor V, allelic variations in prothrombin levels) and secondary disorders are acquired (e.g., tissue damage such as surgery, fractures, burns; myocardial infarction; cancer; heparin-induced thrombocytopenia [HIT]).2 Hypercoagulability associated with advancing age is thought to be due to an increase in platelet aggregation and a reduction in prostacyclin, a potent vasodilator and inhibitor of platelet aggregation that is released by the endothelium.2

• #33 Thrombophlebitis: Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/1086399-overview

  A number of primary and secondary hypercoagulable states can be assessed by obtaining an appropriate patient history and review of systems. […] Inherited hypercoagulable states are divided by experts into five main categories, as follows: Qualitative or quantitative defects of coagulation factor inhibitors, Increased level or function of coagulation factors, Hyperhomocysteinemia, Defects of the fibrinolytic system, Altered platelet function. […] The specific inherited thrombophilias are listed below. […] Resistance to APC is the most common genetic risk factor associated with venous thrombosis. […] Although endothelial damage is speculated to be necessary for symptomatic thrombosis to occur, venous thrombosis may be associated with a deficiency in one of several anticoagulant factors.

• #34 Thrombophlebitis: Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/1086399-overview

  A number of primary and secondary hypercoagulable states can be assessed by obtaining an appropriate patient history and review of systems. […] Inherited hypercoagulable states are divided by experts into five main categories, as follows: Qualitative or quantitative defects of coagulation factor inhibitors, Increased level or function of coagulation factors, Hyperhomocysteinemia, Defects of the fibrinolytic system, Altered platelet function. […] The specific inherited thrombophilias are listed below. […] Resistance to APC is the most common genetic risk factor associated with venous thrombosis. […] Although endothelial damage is speculated to be necessary for symptomatic thrombosis to occur, venous thrombosis may be associated with a deficiency in one of several anticoagulant factors.

• #35 Thrombophlebitis: Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/1086399-overview

  A number of primary and secondary hypercoagulable states can be assessed by obtaining an appropriate patient history and review of systems. […] Inherited hypercoagulable states are divided by experts into five main categories, as follows: Qualitative or quantitative defects of coagulation factor inhibitors, Increased level or function of coagulation factors, Hyperhomocysteinemia, Defects of the fibrinolytic system, Altered platelet function. […] The specific inherited thrombophilias are listed below. […] Resistance to APC is the most common genetic risk factor associated with venous thrombosis. […] Although endothelial damage is speculated to be necessary for symptomatic thrombosis to occur, venous thrombosis may be associated with a deficiency in one of several anticoagulant factors.

• #36 Superficial thrombophlebitis

  https://dermnetnz.org/topics/superficial-thrombophlebitis

  The cause of superficial thrombophlebitis is not completely clear but it is believed to be associated with a change in the dynamic balance of haemostasis. […] In 1846, the German pathologist Virchow showed that damage to a blood vessel wall, abnormal blood flow, or a change in blood constituents causing abnormal blood clotting, could lead to inflammation or formation of blood clots in the veins. […] Thrombophlebitis is especially of concern in pregnant women who carry prothrombin G20210A gene mutation or factor V Leiden, as they have a predisposition to clotting. […] High dose oestrogen treatments may increase the risk of thrombosis by 312 times. […] Superficial thrombophlebitis is not usually a serious condition and often settles down and goes away on its own within 26 weeks. However, it can be recurrent and persistent and cause significant pain and immobility. In addition, complications may occur if the affected veins become infected or the blood clot moves further up the vein to where the superficial and deep veins join; leading to a more serious condition called deep vein thrombosis (DVT).

• #37 Venous Thrombosis: Pathogenesis and Potential for Embolism

  https://www.uspharmacist.com/article/venous-thrombosis-pathogenesis-and-potential-for-embolism

  Hypercoagulability can be described as any alteration of the coagulation pathway that places the patient at risk for thrombosis.2 There are two types of hypercoagulability states; primary disorders are genetically inherited (e.g., mutations in factor V, allelic variations in prothrombin levels) and secondary disorders are acquired (e.g., tissue damage such as surgery, fractures, burns; myocardial infarction; cancer; heparin-induced thrombocytopenia [HIT]).2 Hypercoagulability associated with advancing age is thought to be due to an increase in platelet aggregation and a reduction in prostacyclin, a potent vasodilator and inhibitor of platelet aggregation that is released by the endothelium.2

• #38 Venous Thrombosis: Pathogenesis and Potential for Embolism

  https://www.uspharmacist.com/article/venous-thrombosis-pathogenesis-and-potential-for-embolism

  Hypercoagulability can be described as any alteration of the coagulation pathway that places the patient at risk for thrombosis.2 There are two types of hypercoagulability states; primary disorders are genetically inherited (e.g., mutations in factor V, allelic variations in prothrombin levels) and secondary disorders are acquired (e.g., tissue damage such as surgery, fractures, burns; myocardial infarction; cancer; heparin-induced thrombocytopenia [HIT]).2 Hypercoagulability associated with advancing age is thought to be due to an increase in platelet aggregation and a reduction in prostacyclin, a potent vasodilator and inhibitor of platelet aggregation that is released by the endothelium.2

• #39 Thrombosis – Wikipedia

  https://en.wikipedia.org/wiki/Thrombosis

  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. […] 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. […] 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.

• #40 Thrombophlebitis: Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/1086399-overview

  Antiphospholipid antibodies are a cause of both venous and arterial thrombosis, as well as recurrent spontaneous abortion. […] The mechanism for thromboembolic disease in women who use oral contraceptives is multifactorial. […] The highest rate of thromboembolism occurs with the use of large doses of estrogen, with some studies showing an 11-fold increase in thromboembolism. […] The hypercoagulable condition of the immediate antepartum period is responsible, in large part, for the development of superficial thrombophlebitis and DVT in 0.15% and 0.04% of this patient population, respectively. […] Hypercoagulability occurs in association with a number of malignancies, with the classic example being Trousseau syndromea thrombotic event occurring prior to an occult malignancy, usually a mucin-producing visceral carcinoma. […] Thrombophlebitis in this patient population is promoted by a combination of hypercoagulability and venous stasis. […] Thrombophlebitis may also be a complication of medications that interfere with the coagulation pathway, anticoagulant treatment, or infections.

• #41 Pathogenic Mechanisms of Thrombosis in Antiphospholipid Syndrome (APS) | IntechOpen

  https://www.intechopen.com/chapters/23222

  Significant in vitro and in vivo studies confirm that aPL are pathogenic. The exact mechanism by which these antibodies participate in the prothrombotic tendency of APS, remain to be clearly defined. However, it has been illustrated that the heterogeneity of antibodies is associated with multiple mechanisms of action. These include briefly: the activation of cellular components (endothelial cells, platelets and monocytes), activation of the coagulation cascade, inhibition of the fibrinolytic system, inhibition of natural anticoagulant pathways and activation of the complement system. […] The interaction of aPL with endothelial cells has until now been in frequent disputes and misunderstandings. Regarding the study of endothelium in the pathogenesis of APS, major questions have arisen: a) Under what conditions the aPL bind to the surface of endothelial cells in vitro and in vivo; b) What molecular structures on the surface of endothelial cells are responsible for the binding d) What signaling pathways are activated.

• #42 Superficial Thrombophlebitis – Venous Diseases – Vascular Diseases, Peripheral – Cardiovascular Diseases – Diseases – McMaster Textbook of Internal Medicine

  https://empendium.com/mcmtextbook/chapter/B31.II.2.30.

  Superficial thrombophlebitis refers to inflammation of the veins located above the fascial layer that is usually accompanied by thrombosis of varying severity. […] The mechanism of thrombophlebitis includes stasis in the varicose veins and abnormalities of the venous wall, which lead to thrombosis and subsequent inflammation of the venous wall. […] Factors contributing to the development of thrombophlebitis include large-bore catheters, central venous catheters inserted via a peripheral vein (eg, antecubital vein), infection, hypercoagulability, hormone treatment, and irritants (eg, drugs or potassium chloride administered via the catheter). […] In patients with thrombophlebitis of previously normal (nonvaricose) veins, consider underlying causes such as oral contraceptive use, vasculitis (eg, Behet disease), or thrombophilia.

• #43 Superficial Thrombophlebitis – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK556017/

  Superficial thrombophlebitis is an inflammatory disorder of superficial veins with coexistent venous thrombosis. […] More recently, superficial thrombophlebitis, also called superficial venous thrombosis (SVT), has been associated with other venous thromboembolic disorders, primarily deep venous thrombosis (DVT) and pulmonary embolism (PE). […] Superficial thrombophlebitis starts with microscopic thrombosis. When venous turbulence or stasis, vessel wall injuries, abnormal coagulability, or vessel wall injuries, microthrombi could propagate and subsequently form macroscopic thrombi. Vascular endothelial injury reliably results in thrombus formation by triggering an inflammatory response that results in immediate platelet adhesion. Platelet aggregation is mediated by thrombin and thromboxane A2.

• #44 Superficial Thrombophlebitis – Venous Diseases – Vascular Diseases, Peripheral – Cardiovascular Diseases – Diseases – McMaster Textbook of Internal Medicine

  https://empendium.com/mcmtextbook/chapter/B31.II.2.30.

  Superficial thrombophlebitis refers to inflammation of the veins located above the fascial layer that is usually accompanied by thrombosis of varying severity. […] The mechanism of thrombophlebitis includes stasis in the varicose veins and abnormalities of the venous wall, which lead to thrombosis and subsequent inflammation of the venous wall. […] Factors contributing to the development of thrombophlebitis include large-bore catheters, central venous catheters inserted via a peripheral vein (eg, antecubital vein), infection, hypercoagulability, hormone treatment, and irritants (eg, drugs or potassium chloride administered via the catheter). […] In patients with thrombophlebitis of previously normal (nonvaricose) veins, consider underlying causes such as oral contraceptive use, vasculitis (eg, Behet disease), or thrombophilia.

• #45

  https://www.jci.org/articles/view/60229

  Venous thrombosis is a leading cause of morbidity and mortality in industrialized countries, especially in the elderly. Many risk factors have been identified for venous thrombosis that alter blood flow, activate the endothelium, and increase blood coagulation. However, the precise mechanisms that trigger clotting in large veins have not been fully elucidated. […] The most common site for initiation of the thrombus appears to be the valve pocket sinus, due to its tendency to become hypoxic. Activation of endothelial cells by hypoxia or possibly inflammatory stimuli would lead to surface expression of adhesion receptors that facilitate the binding of circulating leukocytes and microvesicles. Subsequent activation of the leukocytes induces expression of the potent procoagulant protein tissue factor that triggers thrombosis. Understanding the mechanisms of venous thrombosis may lead to the development of new treatments.

• #46 Thrombophlebitis: Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/1086399-overview

  Thrombophlebitis involves the formation of a blood clot in the presence of venous inflammation or injury. Many innate conditions may predispose patients to thrombophlebitis by means of a variety of hypercoagulopathy syndromes. […] Risk factors for thrombophlebitis include obesity, older age, oral contraceptive use and estrogen replacement therapy, autoimmune or infectious diseases, recent trauma or surgery, active malignancy, history of venous thromboembolic disease, respiratory or cardiac failure, and a history of varicose veins. […] Traumatic events can also initiate a thrombophlebitic reaction. […] Superficial thrombophlebitis is a common inflammatory-thrombotic disorder in which a thrombus develops in a vein located near the surface of the skin. […] Septic thrombophlebitis is a condition characterized by venous thrombosis, inflammation, and bacteremia or fungemia.

• #47 Catheter-related septic thrombophlebitis – UpToDate

  https://www.uptodate.com/contents/catheter-related-septic-thrombophlebitis

  Catheter-related septic thrombophlebitis is a complication of catheter-related bloodstream infection (CRBSI). This usually involves inflammation and suppuration within the wall of the vein, infected thrombus within the lumen, surrounding soft tissue inflammation, and persistent bacteremia. […] The epidemiology, microbiology, clinical manifestations, diagnosis, and treatment of catheter-related septic thrombophlebitis will be reviewed here. […] Risk factors for catheter-related septic thrombophlebitis include burns, cut-downs in burn patients for vein access, glucocorticoid use, and injection drug use. Burn patients may be at particular risk due to a variety of factors (eg, altered skin flora, impairment of local defense due to loss of skin integrity).

• #48 Catheter-related septic thrombophlebitis – UpToDate

  https://www.uptodate.com/contents/catheter-related-septic-thrombophlebitis

  Catheter-related septic thrombophlebitis is a complication of catheter-related bloodstream infection (CRBSI). This usually involves inflammation and suppuration within the wall of the vein, infected thrombus within the lumen, surrounding soft tissue inflammation, and persistent bacteremia. […] The epidemiology, microbiology, clinical manifestations, diagnosis, and treatment of catheter-related septic thrombophlebitis will be reviewed here. […] Risk factors for catheter-related septic thrombophlebitis include burns, cut-downs in burn patients for vein access, glucocorticoid use, and injection drug use. Burn patients may be at particular risk due to a variety of factors (eg, altered skin flora, impairment of local defense due to loss of skin integrity).

• #49 Thrombophlebitis: Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/1086399-overview

  Antiphospholipid antibodies are a cause of both venous and arterial thrombosis, as well as recurrent spontaneous abortion. […] The mechanism for thromboembolic disease in women who use oral contraceptives is multifactorial. […] The highest rate of thromboembolism occurs with the use of large doses of estrogen, with some studies showing an 11-fold increase in thromboembolism. […] The hypercoagulable condition of the immediate antepartum period is responsible, in large part, for the development of superficial thrombophlebitis and DVT in 0.15% and 0.04% of this patient population, respectively. […] Hypercoagulability occurs in association with a number of malignancies, with the classic example being Trousseau syndromea thrombotic event occurring prior to an occult malignancy, usually a mucin-producing visceral carcinoma. […] Thrombophlebitis in this patient population is promoted by a combination of hypercoagulability and venous stasis. […] Thrombophlebitis may also be a complication of medications that interfere with the coagulation pathway, anticoagulant treatment, or infections.

• #50 Migratory Thrombophlebitis – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK547702/

  Migratory thrombophlebitis or thrombophlebitis migrans is an inflammatory reaction of the vein accompanied by a thrombus. […] Thrombophlebitis is an inflammatory reaction of the vein accompanied by a thrombus. […] Phlebitic syndrome in association with cancer is distinctive, and its pathogenesis is not well understood. Research has reported the spectrum of overlapping mechanisms in Trousseau syndrome. […] Early reports noted that Trousseau syndrome commonly occurs in mucin-producing adenocarcinomas; however, not all cases correlate with mucin-producing carcinomas. […] Mucins are highly glycosylated glycoproteins secreted by epithelial cells. In patients with carcinomas, mucins are aberrantly glycosylated and get inappropriately secreted into the blood; the liver clears the bulk of these mucins, and a small fraction is resistant. These mucins interact with L-selectin adhesion molecules expressed on leukocytes and P-selection adhesion molecules expressed on platelet and endothelial cells, producing platelet-rich microthrombi.

• #51

  https://journals.lww.com/hemasphere/fulltext/2019/06002/mechanisms_of_cancer_associated_thrombosis.9.aspx

  In 1865, Armand Trousseau was the first to establish a relationship between cancer and thrombosis. He reported that superficial thrombophlebitis is a sign of an occult visceral malignancy. Currently, it is known that VTE, including DVT and PE, is a frequent clinical complication in patients suffering from cancer. The incidence of VTE depends on the type of cancer, with a more pronounced risk in pancreatic (20%), bladder (8%) or lung (5%) cancers. Different mechanisms leading to activation of the blood coagulation cascade and/or platelets have been currently identified and play a crucial role in thrombosis associated with cancer. Cancer cells themselves can activate platelets and the coagulation system by direct interaction (in the bloodstream) or indirectly via the production of microparticles and/or secreted factors and cytokines. In turn, activated platelets participate in tumor development and formation of metastasis.

• #52 Migratory Thrombophlebitis – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK547702/

  Migratory thrombophlebitis or thrombophlebitis migrans is an inflammatory reaction of the vein accompanied by a thrombus. […] Thrombophlebitis is an inflammatory reaction of the vein accompanied by a thrombus. […] Phlebitic syndrome in association with cancer is distinctive, and its pathogenesis is not well understood. Research has reported the spectrum of overlapping mechanisms in Trousseau syndrome. […] Early reports noted that Trousseau syndrome commonly occurs in mucin-producing adenocarcinomas; however, not all cases correlate with mucin-producing carcinomas. […] Mucins are highly glycosylated glycoproteins secreted by epithelial cells. In patients with carcinomas, mucins are aberrantly glycosylated and get inappropriately secreted into the blood; the liver clears the bulk of these mucins, and a small fraction is resistant. These mucins interact with L-selectin adhesion molecules expressed on leukocytes and P-selection adhesion molecules expressed on platelet and endothelial cells, producing platelet-rich microthrombi.

• #53 Migratory Thrombophlebitis – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK547702/

  Migratory thrombophlebitis or thrombophlebitis migrans is an inflammatory reaction of the vein accompanied by a thrombus. […] Thrombophlebitis is an inflammatory reaction of the vein accompanied by a thrombus. […] Phlebitic syndrome in association with cancer is distinctive, and its pathogenesis is not well understood. Research has reported the spectrum of overlapping mechanisms in Trousseau syndrome. […] Early reports noted that Trousseau syndrome commonly occurs in mucin-producing adenocarcinomas; however, not all cases correlate with mucin-producing carcinomas. […] Mucins are highly glycosylated glycoproteins secreted by epithelial cells. In patients with carcinomas, mucins are aberrantly glycosylated and get inappropriately secreted into the blood; the liver clears the bulk of these mucins, and a small fraction is resistant. These mucins interact with L-selectin adhesion molecules expressed on leukocytes and P-selection adhesion molecules expressed on platelet and endothelial cells, producing platelet-rich microthrombi.

• #54 Migratory Thrombophlebitis – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK547702/

  Reports exist of tissue factor (TF) as a cause of Trousseau syndrome. Cancer cells express abnormally high TF and release TF-positive microparticles that are highly procoagulant. […] Inflammatory cytokines produced by cancer cells induce TF expression in vascular cells, where it does not usually get expressed. Cancer cells also induce monocytes and macrophages to release TF. TF promotes the conversion of factor VII to factor VIIa, activating the coagulation cascade’s extrinsic pathway. […] Cancer procoagulant, also described as cysteine proteinase, expressed by malignant cells and normal cells (except fetal tissue), directly induces the conversion of factor X to factor Xa. […] There are reports that hypoxia increases the expression of TF and plasminogen activator inhibitor type1 that facilitates coagulation.

• #55

  https://journals.lww.com/hemasphere/fulltext/2019/06002/mechanisms_of_cancer_associated_thrombosis.9.aspx

  Here we will describe the different mechanisms involved in cancer-associated thrombosis with a special focus on the role of Tissue factor (TF), microparticles and podoplanin. […] In retrospective studies, Khorana et al showed that there is a direct correlation between the increased incidence of VTE and Tissue Factor (TF) expression in pancreatic cancer patients. In addition, cancer patients with the Trousseau syndrome present an augmentation of microparticles that express activated TF. Under physiological conditions, TF is the primary activator of the coagulation cascade; it also plays a critical role during the development of the vasculature, leading to embryonic lethality when it is inactivated in mice. Tissue factor, which is aberrantly expressed in many tumor cell types, is clearly involved in tumor-associated hypercoagulability and in promoting tumor angiogenesis.

• #56 Migratory Thrombophlebitis – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK547702/

  Reports exist of tissue factor (TF) as a cause of Trousseau syndrome. Cancer cells express abnormally high TF and release TF-positive microparticles that are highly procoagulant. […] Inflammatory cytokines produced by cancer cells induce TF expression in vascular cells, where it does not usually get expressed. Cancer cells also induce monocytes and macrophages to release TF. TF promotes the conversion of factor VII to factor VIIa, activating the coagulation cascade’s extrinsic pathway. […] Cancer procoagulant, also described as cysteine proteinase, expressed by malignant cells and normal cells (except fetal tissue), directly induces the conversion of factor X to factor Xa. […] There are reports that hypoxia increases the expression of TF and plasminogen activator inhibitor type1 that facilitates coagulation.

• #57 The Mechanism of Oral Contraceptive (Birth Control Pill) Induced Clot or Thrombus Formation (DVT, VTE, PE)

  https://www.ebmconsult.com/articles/oral-contraceptive-clotting-factors-thrombosis-dvt-pe

  The estimated incidence of venous thromboembolism (VTE) in women of child bearing age who are not taking oral contraceptives is 1 in 10,000 per year. This is increased 3-5 fold when women of child bearing age use estrogen containing oral contraceptives. […] Estrogen containing oral contraceptives increase the plasma concentration of clotting factors II, VII, X, XII, factor VIII, and fibrinogen. […] Estrogen, like many lipophilic hormones, affects the gene transcription of various proteins. Thus, estrogen increases plasma concentrations of these clotting factors by increasing gene transcription. […] Higher doses of estrogen appear to confer a greater risk of venous thrombus formation. This can be explained by a greater degree of nuclear receptor binding and overall activation of gene transcription for these clotting factors.

• #58 Thrombophlebitis: Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/1086399-overview

  Antiphospholipid antibodies are a cause of both venous and arterial thrombosis, as well as recurrent spontaneous abortion. […] The mechanism for thromboembolic disease in women who use oral contraceptives is multifactorial. […] The highest rate of thromboembolism occurs with the use of large doses of estrogen, with some studies showing an 11-fold increase in thromboembolism. […] The hypercoagulable condition of the immediate antepartum period is responsible, in large part, for the development of superficial thrombophlebitis and DVT in 0.15% and 0.04% of this patient population, respectively. […] Hypercoagulability occurs in association with a number of malignancies, with the classic example being Trousseau syndromea thrombotic event occurring prior to an occult malignancy, usually a mucin-producing visceral carcinoma. […] Thrombophlebitis in this patient population is promoted by a combination of hypercoagulability and venous stasis. […] Thrombophlebitis may also be a complication of medications that interfere with the coagulation pathway, anticoagulant treatment, or infections.

• #59 The Mechanism of Oral Contraceptive (Birth Control Pill) Induced Clot or Thrombus Formation (DVT, VTE, PE)

  https://www.ebmconsult.com/articles/oral-contraceptive-clotting-factors-thrombosis-dvt-pe

  The estimated incidence of venous thromboembolism (VTE) in women of child bearing age who are not taking oral contraceptives is 1 in 10,000 per year. This is increased 3-5 fold when women of child bearing age use estrogen containing oral contraceptives. […] Estrogen containing oral contraceptives increase the plasma concentration of clotting factors II, VII, X, XII, factor VIII, and fibrinogen. […] Estrogen, like many lipophilic hormones, affects the gene transcription of various proteins. Thus, estrogen increases plasma concentrations of these clotting factors by increasing gene transcription. […] Higher doses of estrogen appear to confer a greater risk of venous thrombus formation. This can be explained by a greater degree of nuclear receptor binding and overall activation of gene transcription for these clotting factors.

• #60 The Mechanism of Oral Contraceptive (Birth Control Pill) Induced Clot or Thrombus Formation (DVT, VTE, PE)

  https://www.ebmconsult.com/articles/oral-contraceptive-clotting-factors-thrombosis-dvt-pe

  Estrogen, like many lipophilic hormones, affects the gene transcription of various proteins. Thus, estrogen increases plasma concentrations of these clotting factors by increasing gene transcription. […] The degree of influence that estrogen has on gene transcription is unfortunately more complex and not limited to nuclear receptor binding to DNA. Estrogen bound to nuclear receptors (estrogen receptors) also regulates gene expression through protein-protein interaction with other transcription factors. […] Therefore, it is likely that a combination of all of these intracellular reactions brought about by estrogen and the type of progesterone used influence gene expression and excess production of clotting factors.

• #61 The Mechanism of Oral Contraceptive (Birth Control Pill) Induced Clot or Thrombus Formation (DVT, VTE, PE)

  https://www.ebmconsult.com/articles/oral-contraceptive-clotting-factors-thrombosis-dvt-pe

  The estimated incidence of venous thromboembolism (VTE) in women of child bearing age who are not taking oral contraceptives is 1 in 10,000 per year. This is increased 3-5 fold when women of child bearing age use estrogen containing oral contraceptives. […] Estrogen containing oral contraceptives increase the plasma concentration of clotting factors II, VII, X, XII, factor VIII, and fibrinogen. […] Estrogen, like many lipophilic hormones, affects the gene transcription of various proteins. Thus, estrogen increases plasma concentrations of these clotting factors by increasing gene transcription. […] Higher doses of estrogen appear to confer a greater risk of venous thrombus formation. This can be explained by a greater degree of nuclear receptor binding and overall activation of gene transcription for these clotting factors.

• #62 Thrombophlebitis: Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/1086399-overview

  Antiphospholipid antibodies are a cause of both venous and arterial thrombosis, as well as recurrent spontaneous abortion. […] The mechanism for thromboembolic disease in women who use oral contraceptives is multifactorial. […] The highest rate of thromboembolism occurs with the use of large doses of estrogen, with some studies showing an 11-fold increase in thromboembolism. […] The hypercoagulable condition of the immediate antepartum period is responsible, in large part, for the development of superficial thrombophlebitis and DVT in 0.15% and 0.04% of this patient population, respectively. […] Hypercoagulability occurs in association with a number of malignancies, with the classic example being Trousseau syndromea thrombotic event occurring prior to an occult malignancy, usually a mucin-producing visceral carcinoma. […] Thrombophlebitis in this patient population is promoted by a combination of hypercoagulability and venous stasis. […] Thrombophlebitis may also be a complication of medications that interfere with the coagulation pathway, anticoagulant treatment, or infections.

• #63 Deep vein thrombosis: pathogenesis, diagnosis, and medical management – Stone – Cardiovascular Diagnosis and Therapy

  https://cdt.amegroups.org/article/view/16872/html

  The hypercoagulable micro-environment that ensues may downregulate certain antithrombotic proteins that are preferentially expressed on venous valves including thrombomodulin and endothelial protein C receptor (EPCR). […] Debate remains regarding the precise location of tissue factor in this process, whether expressed on the endothelium or by cells within the extravascular tissue, but there is general agreement that tissue factor serves as the primary nidus for thrombus formation. […] Thrombus formation appears to require both tissue factor and P-selectin. […] A venous thrombus has essentially two components, an inner platelet rich white thrombus forming the so-called lines of Zahn surrounded by an outer red cell dense fibrin clot. […] As the ratio of procoagulants to anticoagulants increases, so does the risk of thrombus formation.

• #64 Deep vein thrombosis – Wikipedia

  https://en.wikipedia.org/wiki/Deep_vein_thrombosis

  Tissue factor, via the tissue factor-factor VIIa complex, activates the extrinsic pathway of coagulation and leads to conversion of prothrombin to thrombin, followed by fibrin deposition. […] Fresh venous clots are red blood cell and fibrin rich. […] The process of fibrinolysis, where DVT clots can be dissolved back into the blood, acts to temper the process of thrombus growth. […] Aside from the potentially deadly process of embolization, a clot can resolve through organization, which can damage the valves of veins, cause vein fibrosis, and result in non-compliant veins. […] Organization of a thrombus into the vein can occur at the third stage of its pathological development, in which collagen becomes the characteristic component.

• #65

  https://journals.lww.com/hemasphere/fulltext/2019/06002/mechanisms_of_cancer_associated_thrombosis.9.aspx

  The specific loss of endogenous TF expression by cancer cells leads to an important decrease of the tumor growth, a finding that correlates with those of previous studies. TF is also involved in several steps of malignancy, including tumor progression, angiogenesis and the development of metastasis. […] Depending on the tumor, other mechanisms, TF and/or microparticles independents, may also activate platelets leading to the formation of a thrombus. These mechanisms include the production by the tumor of the platelet agonists ADP and Thromboxane A2 (TXA2), the secretion of Matrix metalloproteinases (MMPs) participating in the Tumor Cell Induced Platelet Aggregation (TCIPA) and of Cathepsin cysteine proteases, such as cathepsin B and K, which cleave the Tissue Factor Pathway Inhibitor (TFPI) and favor the activation of the TF pathway.

• #66 Molecular mechanism of cerebral venous thrombosis discovered – Rudolf Virchow Center for Integrative and Translational Bioimaging

  https://www.uni-wuerzburg.de/en/rvz/rvz-news/single/news/molekulare-ursache-von-hirnvenenthrombosen-entdeckt/

  Cerebral venous thrombosis is a rare form of cerebral circulatory disorder that, unlike classic stroke, more often affects younger people. For unknown reasons, blood clots (thrombi) form in cerebral veins, obstructing blood flow and causing damage to brain tissue. […] Scientists from the Rudolf Virchow Center for Integrative and Translational Bioimaging at the University of Wrzburg (RVZ) and the University Hospital Wrzburg, who are collaborating with colleagues from Tbingen and Greifswald in the Collaborative Research Center Transregio (SFB TR) 240, have now been able to show for the first time that the activation of two specific receptors on the surface of blood platelets leads to cerebral venous thrombosis. […] We hypothesize that the binding of the antibody alters the properties of the CLEC-2 receptor so that it transmits signals into the cell. This activates platelets and they clump together in the cerebral venous circulation, triggering cerebral venous thrombosis.

• #67 Molecular mechanism of cerebral venous thrombosis discovered – Rudolf Virchow Center for Integrative and Translational Bioimaging

  https://www.uni-wuerzburg.de/en/rvz/rvz-news/single/news/molekulare-ursache-von-hirnvenenthrombosen-entdeckt/

  The research group found that in addition to CLEC-2, a second platelet receptor, GPIIb/IIIa, is involved in the development of cerebral venous thrombosis and that only the interaction of both receptors leads to thrombus formation in the brain. […] When these were blocked in advance, cerebral venous thrombosis did not develop. „The most interesting finding, however, was that inhibition of platelets by blocking the GPIIb/IIIa receptor, was extremely effective even after the onset of neurological symptoms, i.e. in the acute course of the disease,” says Vanessa Gb, also first author of the study. […] Prof. Guido Stoll of the Department of Neurology adds, „These results were surprising and may pave the way for the use of GPIIb/IIIa blockers in those patients in whom cerebral venous thrombosis progresses despite heparin treatment, often leading to death.”

• #68

  https://journals.lww.com/hemasphere/fulltext/2019/06002/mechanisms_of_cancer_associated_thrombosis.9.aspx

  Here we will describe the different mechanisms involved in cancer-associated thrombosis with a special focus on the role of Tissue factor (TF), microparticles and podoplanin. […] In retrospective studies, Khorana et al showed that there is a direct correlation between the increased incidence of VTE and Tissue Factor (TF) expression in pancreatic cancer patients. In addition, cancer patients with the Trousseau syndrome present an augmentation of microparticles that express activated TF. Under physiological conditions, TF is the primary activator of the coagulation cascade; it also plays a critical role during the development of the vasculature, leading to embryonic lethality when it is inactivated in mice. Tissue factor, which is aberrantly expressed in many tumor cell types, is clearly involved in tumor-associated hypercoagulability and in promoting tumor angiogenesis.

• #69 Cancer-Associated Stroke: Thrombosis Mechanism, Diagnosis, Outcome, and Therapeutic Strategies

  https://www.j-stroke.org/journal/view.php?viewtype=pubreader&number=523

  Cancer can induce hypercoagulability, which may lead to stroke. […] Tumor cells activate platelets by generating thrombin and expressing tissue factor, resulting in tumor cell-induced platelet aggregation. […] Histopathological studies of thrombi obtained during endovascular thrombectomy in patients with acute stroke and active cancer have shown a high proportion of platelets and thrombin. […] Thrombosis mechanism in cancer is well understood, and distinct therapeutic targets involving thrombin and platelets have been identified. […] Tumor cells activate platelets through thrombin generation and tissue factor expression. […] Thrombin plays a crucial role in platelet activation induced by tumor cells, as these cells directly generate thrombin. […] Thrombin generation is further enhanced by tissue factor expressed on tumor cells.

• #70 Cancer-Associated Stroke: Thrombosis Mechanism, Diagnosis, Outcome, and Therapeutic Strategies

  https://www.j-stroke.org/journal/view.php?viewtype=pubreader&number=523

  Cancer can induce hypercoagulability, which may lead to stroke. […] Tumor cells activate platelets by generating thrombin and expressing tissue factor, resulting in tumor cell-induced platelet aggregation. […] Histopathological studies of thrombi obtained during endovascular thrombectomy in patients with acute stroke and active cancer have shown a high proportion of platelets and thrombin. […] Thrombosis mechanism in cancer is well understood, and distinct therapeutic targets involving thrombin and platelets have been identified. […] Tumor cells activate platelets through thrombin generation and tissue factor expression. […] Thrombin plays a crucial role in platelet activation induced by tumor cells, as these cells directly generate thrombin. […] Thrombin generation is further enhanced by tissue factor expressed on tumor cells.

• #71 Cancer-Associated Stroke: Thrombosis Mechanism, Diagnosis, Outcome, and Therapeutic Strategies

  https://www.j-stroke.org/journal/view.php?viewtype=pubreader&number=523

  Thus, thrombin-related platelet activation is maximized in cancer. […] The inhibition of thrombin using hirudin, a specific thrombin inhibitor, has been shown to inhibit tumor growth and metastasis in mice. […] Histopathological studies of cerebral thrombi revealed distinct features of cancer-associated stroke, characterized by compositions rich in platelets and thrombin and low in erythrocytes.

• #72 Cancer-Associated Stroke: Thrombosis Mechanism, Diagnosis, Outcome, and Therapeutic Strategies

  https://www.j-stroke.org/journal/view.php?viewtype=pubreader&number=523

  Thus, thrombin-related platelet activation is maximized in cancer. […] The inhibition of thrombin using hirudin, a specific thrombin inhibitor, has been shown to inhibit tumor growth and metastasis in mice. […] Histopathological studies of cerebral thrombi revealed distinct features of cancer-associated stroke, characterized by compositions rich in platelets and thrombin and low in erythrocytes.

• #73 Deep vein thrombosis – Wikipedia

  https://en.wikipedia.org/wiki/Deep_vein_thrombosis

  Tissue factor, via the tissue factor-factor VIIa complex, activates the extrinsic pathway of coagulation and leads to conversion of prothrombin to thrombin, followed by fibrin deposition. […] Fresh venous clots are red blood cell and fibrin rich. […] The process of fibrinolysis, where DVT clots can be dissolved back into the blood, acts to temper the process of thrombus growth. […] Aside from the potentially deadly process of embolization, a clot can resolve through organization, which can damage the valves of veins, cause vein fibrosis, and result in non-compliant veins. […] Organization of a thrombus into the vein can occur at the third stage of its pathological development, in which collagen becomes the characteristic component.

• #74 Thrombophlebitis: Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/1086399-overview

  Thrombophlebitis involves the formation of a blood clot in the presence of venous inflammation or injury. Many innate conditions may predispose patients to thrombophlebitis by means of a variety of hypercoagulopathy syndromes. […] Risk factors for thrombophlebitis include obesity, older age, oral contraceptive use and estrogen replacement therapy, autoimmune or infectious diseases, recent trauma or surgery, active malignancy, history of venous thromboembolic disease, respiratory or cardiac failure, and a history of varicose veins. […] Traumatic events can also initiate a thrombophlebitic reaction. […] Superficial thrombophlebitis is a common inflammatory-thrombotic disorder in which a thrombus develops in a vein located near the surface of the skin. […] Septic thrombophlebitis is a condition characterized by venous thrombosis, inflammation, and bacteremia or fungemia.

• #75 Deep Vein Thrombosis and Pulmonary Embolism | Yellow Book | CDC

  https://www.cdc.gov/yellow-book/hcp/travel-air-sea/deep-vein-thrombosis-and-pulmonary-embolism.html

  Virchow’s classic triad for thrombus formation is venous stasis, vessel wall damage, and a hypercoagulable state. […] Prolonged, cramped sitting during long-distance travel interferes with venous flow in the legs, creating venous stasis. […] Coagulation activation can result from an interaction between air cabin conditions (e.g., hypobaric hypoxia) and individual risk factors for VTE. […] Studies of the pathophysiologic mechanisms for the increased risk of VTE after long-distance travel have not produced consistent results, but venous stasis appears to play a major role. […] Other factors specific to air travel might increase coagulation activation, particularly in travelers with preexisting risk factors for VTE.

• #76 Thrombophlebitis: Causes, Symptoms and Treatment

  https://my.clevelandclinic.org/health/diseases/23311-thrombophlebitis

  Genetic (inherited) conditions. Mutations in your DNA can cause your blood to clot too easily. Some people inherit these mutations from their parents. Genetic conditions like this are often treatable but will be life-long and aren’t curable. […] Trauma. Injuries to or close to veins can cause inflammation that leads to clot formation. […] Medical procedures and medications. Intravenous (IV) lines and catheters, which are tubes that deliver medications and fluids directly into your veins, can cause clots that lead to thrombophlebitis. […] Conditions or circumstances that otherwise affect clotting. Various potential risk factors include cancer, obesity, lupus and certain blood disorders. […] Thrombophlebitis tends to be a short-lived condition, especially with quick diagnosis and treatment. Its rare for it to last more than a few hours because the longer you have it, the greater the risk of it becoming a more dangerous problem. […] On its own, thrombophlebitis is usually not dangerous. However, having it does mean you have a much higher risk of developing other conditions like DVT or pulmonary embolism, both of which are medical emergencies. The longer you wait to get treatment, the more dangerous this condition becomes.

• #77 Management of superficial venous thrombophlebitis associated with peripheral venous catheters: A review. | Published in Global Journal of Surgery and Case Reports

  https://www.gjscr.com/article/118529-management-of-superficial-venous-thrombophlebitis-associated-with-peripheral-venous-catheters-a-review

  Local inflammation of the wall of the vein at the catheter site is considered to be the initiating event in a cascade that ultimately leads to thrombophlebitis. […] The venous endothelium can be injured by the chemical irritation caused by the infusate, physical trauma by the catheter, or microorganisms colonizing the cannula. […] Injury to the venous endothelium causes a prostaglandin-mediated activation of the inflammatory cascade and the coagulation pathway leading to thrombosis. […] Furthermore, inflammation of the endothelium causes venoconstriction at the catheter leading to local stasis of the blood which in turn promotes thrombosis and increased irritation of the endothelium by the infusate. […] Histopathologic studies confirm this cascade by showing that peripheral vein infusion thrombophlebitis is associated with swelling of the endothelial cells, leukocytic infiltration of the vein wall, and fibrin deposition and thrombus formation.

• #78 Management of superficial venous thrombophlebitis associated with peripheral venous catheters: A review. | Published in Global Journal of Surgery and Case Reports

  https://www.gjscr.com/article/118529-management-of-superficial-venous-thrombophlebitis-associated-with-peripheral-venous-catheters-a-review

  Local inflammation of the wall of the vein at the catheter site is considered to be the initiating event in a cascade that ultimately leads to thrombophlebitis. […] The venous endothelium can be injured by the chemical irritation caused by the infusate, physical trauma by the catheter, or microorganisms colonizing the cannula. […] Injury to the venous endothelium causes a prostaglandin-mediated activation of the inflammatory cascade and the coagulation pathway leading to thrombosis. […] Furthermore, inflammation of the endothelium causes venoconstriction at the catheter leading to local stasis of the blood which in turn promotes thrombosis and increased irritation of the endothelium by the infusate. […] Histopathologic studies confirm this cascade by showing that peripheral vein infusion thrombophlebitis is associated with swelling of the endothelial cells, leukocytic infiltration of the vein wall, and fibrin deposition and thrombus formation.

• #79 Thrombophlebitis: Causes, Symptoms and Treatment

  https://my.clevelandclinic.org/health/diseases/23311-thrombophlebitis

  Genetic (inherited) conditions. Mutations in your DNA can cause your blood to clot too easily. Some people inherit these mutations from their parents. Genetic conditions like this are often treatable but will be life-long and aren’t curable. […] Trauma. Injuries to or close to veins can cause inflammation that leads to clot formation. […] Medical procedures and medications. Intravenous (IV) lines and catheters, which are tubes that deliver medications and fluids directly into your veins, can cause clots that lead to thrombophlebitis. […] Conditions or circumstances that otherwise affect clotting. Various potential risk factors include cancer, obesity, lupus and certain blood disorders. […] Thrombophlebitis tends to be a short-lived condition, especially with quick diagnosis and treatment. Its rare for it to last more than a few hours because the longer you have it, the greater the risk of it becoming a more dangerous problem. […] On its own, thrombophlebitis is usually not dangerous. However, having it does mean you have a much higher risk of developing other conditions like DVT or pulmonary embolism, both of which are medical emergencies. The longer you wait to get treatment, the more dangerous this condition becomes.

• #80 Superficial thrombophlebitis

  https://dermnetnz.org/topics/superficial-thrombophlebitis

  The cause of superficial thrombophlebitis is not completely clear but it is believed to be associated with a change in the dynamic balance of haemostasis. […] In 1846, the German pathologist Virchow showed that damage to a blood vessel wall, abnormal blood flow, or a change in blood constituents causing abnormal blood clotting, could lead to inflammation or formation of blood clots in the veins. […] Thrombophlebitis is especially of concern in pregnant women who carry prothrombin G20210A gene mutation or factor V Leiden, as they have a predisposition to clotting. […] High dose oestrogen treatments may increase the risk of thrombosis by 312 times. […] Superficial thrombophlebitis is not usually a serious condition and often settles down and goes away on its own within 26 weeks. However, it can be recurrent and persistent and cause significant pain and immobility. In addition, complications may occur if the affected veins become infected or the blood clot moves further up the vein to where the superficial and deep veins join; leading to a more serious condition called deep vein thrombosis (DVT).

• #81 Thrombosis – Wikipedia

  https://en.wikipedia.org/wiki/Thrombosis

  Also, atrial fibrillation, causes stagnant blood in the left atrium (LA), or left atrial appendage (LAA), and can lead to a thromboembolism. […] 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).

• #82 Thrombophlebitis: Causes, Symptoms and Treatment

  https://my.clevelandclinic.org/health/diseases/23311-thrombophlebitis

  Genetic (inherited) conditions. Mutations in your DNA can cause your blood to clot too easily. Some people inherit these mutations from their parents. Genetic conditions like this are often treatable but will be life-long and aren’t curable. […] Trauma. Injuries to or close to veins can cause inflammation that leads to clot formation. […] Medical procedures and medications. Intravenous (IV) lines and catheters, which are tubes that deliver medications and fluids directly into your veins, can cause clots that lead to thrombophlebitis. […] Conditions or circumstances that otherwise affect clotting. Various potential risk factors include cancer, obesity, lupus and certain blood disorders. […] Thrombophlebitis tends to be a short-lived condition, especially with quick diagnosis and treatment. Its rare for it to last more than a few hours because the longer you have it, the greater the risk of it becoming a more dangerous problem. […] On its own, thrombophlebitis is usually not dangerous. However, having it does mean you have a much higher risk of developing other conditions like DVT or pulmonary embolism, both of which are medical emergencies. The longer you wait to get treatment, the more dangerous this condition becomes.

• #83 Hemolysis and Venous Thrombosis: Which Link?

  https://clinmedjournals.org/articles/cmrcr/clinical-medical-reviews-and-case-reports-cmrcr-7-329.php?jid=cmrcr

  The association hemolysis and venous thrombosis remains unknown to clinicians, despite our advances in comrehension of pathophysiological bases. […] Haemolysis, which is observed in multiple diseases, can affect all three components of Virchow’s triad. It is not surprising that there is a link between haemolytic disorders and thrombosis. […] The link between venous thrombosis and hemolysis seems multifactorial, involving mechanisms related to hemolysis and classic risk factors for Venous Thromboembolic Diseases. […] The mechanism through which haemolysis leads to thrombosis is multifaceted. Circulating free haemoglobin and haem can have many deleterious effects. In fusion of haem into humans is associated with disturbances in coagulation and thrombophlebitis. […] The main mediator of these adverse effects is thought to be free haem via its effects on NO scavenging, pro-inflammatory cytokine responses, and reactive oxygen species (ROS) generation.

• #84 Superficial thrombophlebitis

  https://dermnetnz.org/topics/superficial-thrombophlebitis

  The cause of superficial thrombophlebitis is not completely clear but it is believed to be associated with a change in the dynamic balance of haemostasis. […] In 1846, the German pathologist Virchow showed that damage to a blood vessel wall, abnormal blood flow, or a change in blood constituents causing abnormal blood clotting, could lead to inflammation or formation of blood clots in the veins. […] Thrombophlebitis is especially of concern in pregnant women who carry prothrombin G20210A gene mutation or factor V Leiden, as they have a predisposition to clotting. […] High dose oestrogen treatments may increase the risk of thrombosis by 312 times. […] Superficial thrombophlebitis is not usually a serious condition and often settles down and goes away on its own within 26 weeks. However, it can be recurrent and persistent and cause significant pain and immobility. In addition, complications may occur if the affected veins become infected or the blood clot moves further up the vein to where the superficial and deep veins join; leading to a more serious condition called deep vein thrombosis (DVT).

• #85 Thrombophlebitis – Symptoms & causes – Mayo Clinic

  https://www.mayoclinic.org/diseases-conditions/thrombophlebitis/symptoms-causes/syc-20354607

  Complications from superficial thrombophlebitis are rare. However, if you develop deep vein thrombosis (DVT), the risk of serious complications increases. […] A pulmonary embolism (PE) occurs when a blood clot gets stuck in an artery in the lung, blocking blood flow to part of the lung. Blood clots most often start in the legs and travel up through the right side of the heart and into the lungs.

• #86 Thrombophlebitis – Symptoms & causes – Mayo Clinic

  https://www.mayoclinic.org/diseases-conditions/thrombophlebitis/symptoms-causes/syc-20354607

  Complications from superficial thrombophlebitis are rare. However, if you develop deep vein thrombosis (DVT), the risk of serious complications increases. […] A pulmonary embolism (PE) occurs when a blood clot gets stuck in an artery in the lung, blocking blood flow to part of the lung. Blood clots most often start in the legs and travel up through the right side of the heart and into the lungs.

• #87 Thrombophlebitis: Causes, Symptoms and Treatment

  https://my.clevelandclinic.org/health/diseases/23311-thrombophlebitis

  Genetic (inherited) conditions. Mutations in your DNA can cause your blood to clot too easily. Some people inherit these mutations from their parents. Genetic conditions like this are often treatable but will be life-long and aren’t curable. […] Trauma. Injuries to or close to veins can cause inflammation that leads to clot formation. […] Medical procedures and medications. Intravenous (IV) lines and catheters, which are tubes that deliver medications and fluids directly into your veins, can cause clots that lead to thrombophlebitis. […] Conditions or circumstances that otherwise affect clotting. Various potential risk factors include cancer, obesity, lupus and certain blood disorders. […] Thrombophlebitis tends to be a short-lived condition, especially with quick diagnosis and treatment. Its rare for it to last more than a few hours because the longer you have it, the greater the risk of it becoming a more dangerous problem. […] On its own, thrombophlebitis is usually not dangerous. However, having it does mean you have a much higher risk of developing other conditions like DVT or pulmonary embolism, both of which are medical emergencies. The longer you wait to get treatment, the more dangerous this condition becomes.

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