Venous Thrombosis


Certain pathological situations, usually several, interact to cause the development of a coagulum (thrombus) of clottable protein (fibrin) and cellular blood components within veins, which may cause damage by occluding the venous circulation locally, or by migration (embolization) elsewhere in the vascular tree. Treatment is usually by anticoagulation, which prevents further formation, relying on natural lysis to remove the fibrin.

Keywords: thrombus; pulmonary emboli; coagulation; anticoagulation; fibrinolysis; thrombophilia; thrombophlebitis

Figure 1.

Blood coagulation cascade. HMWK, high‐molecular‐weight kininogen; PL, phospholipid; TF, tissue factor.

Figure 2.

Major coagulation pathways.



Mehta DK (1999) Oral anticoagulants. British National Formulary, Section 2.8.2, pp. 110–111. London: British Medical Association, Royal Pharmaceutical Society of Great Britain.

Khan SR (1998) The clinical diagnosis of deep vein thrombosis. Archives of Internal Medicine 158: 2315–2324.

McCollum C (1998) Avoiding the consequences of deep vein thrombosis. British Medical Journal 317: 696.

Sevitt S and Gallagher NH (1961) Venous thrombosis and pulmonary emboli. A clinicopathological study in injured and burned patients. British Journal of Surgery 48: 475–489.

Further Reading

Cumming AM and Shiach CR (1999) Investigation and management of inherited thrombophilia. Clinical and Laboratory Haematology 21: 77–92.

Greaves M and Taberner DA (1996) Thrombotic disease. In: Weatherall DJ, Ledingham JGG and Warrell DA (eds) Oxford Textbook of Medicine, 3rd edn, pp. 3661–3676. Oxford: Oxford University Press.

Lensing AWA, Prandoni P, Prins MH and Buller HR (1999) Deep‐vein thrombosis. Lancet 353: 479–485.

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How to Cite close
Taberner, David A(Apr 2001) Venous Thrombosis. In: eLS. John Wiley & Sons Ltd, Chichester. [doi: 10.1038/npg.els.0002116]