URGO MEDICAL

Ref.: Consensus Statement, Phlebology, 1995.

It should be noted that, today, this classification makes it possible to differentiate between :

• chronic venous disease (CVD), which has a chronic course and encompasses all the clinical signs consecutive to a venous disease in the lower limbs
• chronic venous insufficiency (CVI), which primarily corresponds to decompensation of venous disease (severe stages of the CEAP classification)

However, the term CVI is still very widely used to designate the disease itself.

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C0

At this stage, no structural or functional abnormality is found in the venous system in the lower limbs. The patient may complain of symptoms caused by the presence of certain mediators released following a slowdown in blood flow, triggered by prolonged standing: feeling of heavy legs, pains in the legs, pruritus, but no clinical or palpable signs of venous disease.

C1

Stage at which the first clinical signs of venous disease appear: presence of telangiectasia or reticular veins. These form due to increased venous pressure in certain segments of the leg veins or due to other factors, such as: a hormonal influence during pregnancy, the use of oral contraception, significant weight variation, etc.

C2 : Development of varicose veins.

An increased venous pressure in all or a major proportion of the venous system in the lower limbs causes visible and palpable varicose veins to form, which reflect marked dilation of the vein diameter. This condition can develop either following the presence of an obstacle to venous blood circulation or because of congenital weakness of the venous walls.

   

C3 : Presence of venous oedema.

The increase in venous pressure causes leakage of intravascular fluid and makes it difficult for the venous network to reabsorb fluids.
The visible result of this venous hypertension is venous oedema (without trophic changes).

 

C4 : Trophic changes of venous origin.

Progression of the disorders cited in C3 leads to extravasation of blood cell elements and, in particular, macromolecules (proteins, different pro-inflammatory mediators, etc.), which exacerbate stasis.
All these phenomena trigger areas of tissue damage, which, once repaired, leave behind traces, such as atrophie blanche, which simply consists of small scars.
Extravasation of red cells and their disintegration leads to pigmented purpuric dermatitis.
Other trophic changes, such as varicose eczema, can also develop.

 

Atrophie blanche

Varicose eczema

 

Pigmented purpuric dermatitis

C5 : Healed ulcer with trophic changes.

Once healed, a leg ulcer is always a weak point in terms of skin trophicity and the risk of recurrence of a healed ulcer is greater than the risk of developing a venous leg ulcer on skin that has never previously had one, particularly if the trophic changes persist after healing of the wound.

C6 : Presence of one or more active venous ulcers, often accompanied by trophic changes.

A venous leg ulcer, which is the last stage in chronic venous insufficiency, is full-thickness loss of skin substance. It results from an accumulation of cell metabolism waste products that has not been properly eliminated and the capillary ischaemia that accompanies the development of venous oedema. The ulcer may form following a minor injury or develop spontaneously.
A leg ulcer is a sign that venous hypertension has reached a critical level.

Characteristics of venous ulcers (read more...)

A venous ulcer is a chronic loss of skin substance, with no tendency to heal spontaneously, caused by tissue damage.
This condition affects 1 to 2% of the population over the age of 60 and is a major expense in terms of public health spending. The majority of leg ulcers are vascular in origin and are a complication of venous, arterial or microcirculatory disease.

It is characterised by the following clinical signs:

• location: usually on the lower third of the inside surface of the leg
  
  
• clinical appearance:
  • In its initial phase, with oedema of venous origin, the ulcer is usually highly exudative and covered in fibrin and it is not exceptional for the skin around the ulcer to show signs of maceration. The margins are often irregular and slope down gradually towards the centre of the wound. Multiple ulcers are sometimes seen, but do not occur in the majority of cases.
    
    
  • The colour of the ulcer depends on its phase:
    • In the moist necrosis phase, the base of the ulcer is yellowish-grey
    • A fibrinous ulcer is yellow
    • During the healing process, when the ulcer is granulating, it is red
    • At the end of the healing process, the pink colour shows that re-epithelialisation is underway
      
      
  • If venous return is properly managed with, in particular, etiological treatment of the ulcer using venous compression, exudates should decrease from the first few weeks of treatment. Elimination of necrotic tissue is then observed, followed by granulation. Once granulation is well established, the wound no longer weeps.

Active ulcer            and…            after healing

 

 

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