Anatomy and Pathophysiology

DVT typically presents in the lower limb, although it can also rarely occur in the upper limb.


The venous anatomy of the leg predisposes itself to the formation of thrombosis: low flow areas such as soleal sinuses, valve pockets and at venous confluences are common sites of clot formation. Clearly the lower limbs are also more prone to the dependent effects of gravity than the upper limbs.

Detectable clot is most commonly found in the distal venous circulation:

  • Anterior tibial vein
  • Posterior tibial vein
  • Peroneal vein

This clot can then propagate proximally into the popliteal, femoral and iliac veins.


What are the three components of Virchow’s triad?

(i) Venous stasis, (ii) hypercoagulable state and (iii) endothelial vessel wall damage.

DVT was first described in the Ebers Papyrus in 1550BC but it wasn’t until the 19th century that Rudolf Virchow2 reported the relationship between venous stasis, a hypercoaguable state and endothelial vessel wall damage and risk of thrombosis – the so called “Virchow Triad”.

Fig 1: Virchow’s Triad

There exists an equilibrium between clotting and clot breakdown; a combination of risk factors may tip this equilibrium in favour of clot formation (thrombosis).

Virchow’s Triad forms the basis for the pathophysiology of DVT.  A combination of the triad of factors is required for thrombosis to form – one factor in isolation is not usually sufficient. The presence of each constituent of Virchow’s triad is, in turn, determined by various factors which collectively determine risk of DVT in any individual patient.

Fig 2: Risk factors underpinning Virchow’s triad

The presence and combination of these factors may trigger the pathophysiological process that results in local cytokine production and facilitation of leukocyte adhesion to the endothelium.  Whilst the relative contribution of each factor has been long debated, the process reflects the dynamic equilibrium between the pro- and anti-thrombotic tendencies in the deep venous system. The standard treatment strategies for DVT are determined by these factors and are centred on anticoagulation and the prevention of venous stasis.

If the condition goes unrecognised over time, the thrombus subsequently organises and inflammatory cells infiltrate into the clot resulting in intimal thickening.  The wall thickens further over time, the likelihood of venous contractility increases, as does the tendency to chronic venous insufficiency causing long term morbidity and increased risk of recurrence.

Regardless of the many described risk factors, only a few have been selected for formal risk stratification in proven clinical studies (see later section).

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