|Classification and external resources|
A deep vein thrombosis in the right leg. Note the swelling and redness.
A venous thrombosis or phlebothrombosis is a blood clot (thrombus) that forms within a vein. Thrombosis is a term for a blood clot occurring inside a blood vessel. A classical venous thrombosis is deep vein thrombosis (DVT), which can break off (embolize), and become a life-threatening pulmonary embolism (PE). The disease process venous thromboembolism (abbreviated as VTE or DVT/PE) can refer to DVT and/or PE. An inflammatory reaction is usually present, mainly in the superficial veins and, for this reason this pathology is called most of the time thrombophlebitis. In fact, the inflammatory reaction and the white blood cells play a role in the resolution of venous clots.
Superficial venous thromboses causes discomfort but generally do not cause serious consequences, as the deep venous thromboses (DVTs) that form in the deep veins of the legs or in the pelvic veins. Nevertheless they can progress to the deep veins through the perforator veins or, they can be responsible for a lung embolism mainly if the head of the clot is poorly attached to the vein wall and is situated near the sapheno-femoral junction.
Since the veins return blood to the heart, if a piece of a blood clot formed in a vein breaks off it can be transported to the right side of the heart, and from there into the lungs. A piece of thrombus that is transported in this way is an embolus: the process of forming a thrombus that becomes embolic is called a thromboembolism. An embolism that lodges in the lungs is a pulmonary embolism (PE). A pulmonary embolism is a very serious condition that can be fatal dependeing of the embolus dimensions. Venous thromboembolism (VTE) refers to both DVTs and PEs.
Systemic embolisms of venous origin can occur in patients with an atrial or ventricular septal defect, through which an embolus may pass into the arterial system. Such an event is termed a paradoxical embolism.
Venous thrombi are caused mainly by a combination of venous stasis and hypercoagulability—but to a lesser extent endothelial damage and activation. The three factors of stasis, hypercoaguability, and alterations in the blood vessel wall represent Virchow's triad, and changes to the vessel wall are the least understood. Various risk factors increase the likelhood of any one individual developing a thrombosis.
Risk factors for DVT/PE 
In contrast to the understanding for how arterial thromboses occur, as with heart attacks, venous thrombosis formation is not well understood. With arterial thrombosis, blood vessel wall damage is required for thrombosis formation, as it initiates coagulation, but the majority of venous thrombi form without any injured epithelium.
Red blood cells and fibrin are the main components of venous thrombi, and the thrombi appear to attach to the blood vessel wall endothelium, normally a non-thrombogenic surface, with fibrin. Platelets in venous thrombi attach to downstream fibrin, while in arterial thrombi, they compose the core. As a whole, platelets constitute less of venous thrombi when compared to arterial ones. The beginning of the process is thought to be initiated by tissue factor effected thrombin production, which leads to fibrin deposition.
The valves of veins are a recognized site of VT initiation. Due to the blood flow pattern, the base of the valve sinus is particularly deprived of oxygen (hypoxic). Stasis excacerbates hypoxia, and this state is linked to the activation of white blood cells (leukocytes) and the endothelium. Specifically, the two pathways of hypoxia-inducible factor-1 (HIF-1) and early growth response 1 (EGR-1) are activated by hypoxia, and they contribute to monocyte and endothelial activation. Hypoxia also causes reactive oxygen species (ROS) production that can activate HIF-1, EGR-1, and nuclear factor-κB (NF-κB), which regulates HIF-1 transcription.
HIF-1 and EGR-1 pathways lead to monocyte association with endothelial proteins, such as P-selectin, prompting monocytes to release tissue factor filled microvesicles, which presumably initiate fibrin deposition (via thrombin) after binding the endothelial surface.
Evidence supports the use of heparin in surgical patients who have a high risk of thrombosis to reduce the risk of DVTs; however, the effect on PEs or overall mortality is not known. In hospitalized non-surgical patients, heparin results in an almost statistically significant decrease in mortality and may decrease the risk of PE and DVT, but it increases major bleeding events yielding little or no overall clinical benefit. It does not appear however to decrease the rate of symptomatic DVTs. In hospitalized non-surgical stroke patients, mechanical measures (compression stockings) resulted in skin damage and no clinical improvement. Data on the effectiveness of compression stockings among hospitalized non-surgical patients without stroke is scarce.
A 2011 clinical guideline from the American College of Physicians (ACP) gave three strong recommendations with moderate quality evidence on VTE prevention in non-surgical patients: that hospitalized patients be assessed for their risk of thromboembolism and bleeding before prophylaxis (prevention); that heparin or a related drug is used if potential benefits are thought to outweigh potential harms; and that graduated compression stockings not be used. As an ACP policy implication, the guideline stated a lack of support for any performance measures that incentivize physicians to apply universal prophylaxis without regard to the risks.
Despite development of various practice guidelines for prevention of VTE, they remain underused in most countries.[medical citation needed]
Evidence-based clinical guidelines from the American College of Chest Physicians were published in February 2012 for the treatment of VTE. Medications used to treat this condition include anticoagulants such as heparin, fondaparinux and more recently dabigatran has shown promise. Vitamin K antagonists such as warfarin are also commonly used.
See also 
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