Clinical signs of chronic venous disease

Clinical signs are used to assess the progression of this disease since they are the direct consequence of the processes described earlier.
A new international classification is now an essential tool: the CEAP classification (standing for Clinical signs, Etiological classification, Anatomical distribution and Pathophysiological dysfunction) which is used to evaluate the progression of the disease on the basis of the clinical signs present.


C for clinical signs (grade 0-6)
supplemented by (A) for asymptomatic and (S) for symptomatic.

0 No visible or palpable signs of venous disease
1 Presence of telangiectasia or reticular veins
2 Varicose veins
3 Oedema
4 Skin changes (trophic changes): pigmentation, eczema, lipodermatosclerosis
5 Trophic changes indicated in 4 with healed ulcer
6 Trophic changes indicated in 4 with active ulcer

E for the etiological classification, the following categories are used :

C for congenital
P for primary
S for secondary (post-thrombotic, post-traumatic, other)

A for the anatomical distribution, depending on the sector involved :

S for superficial
D for deep
P for perforating
(these lesions can involve one or more sectors)

P for the pathophysiological dysfunction responsible :

R for reflux
O for obstruction
(these two mechanisms can be isolated or combined)

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 related to 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 define the disease itself.

 

 

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 slowing of blood flow, triggered by prolonged standing: feeling of heavy legs, pains in the legs and pruritus. At this stage, however, there are 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 areas 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 from following an obstruction 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 into the tissues 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 from 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 the wound has healed.


 

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 metabolic waste products that have 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.


venous ulcer with varicose eczema
Characteristics of venous ulcers

A venous ulcer is a chronic loss of skin substance, caused by tissue damage, with no ability to heal spontaneously.
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 exuding and covered in fibrin. It is not unusual 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, exudate 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 should no longer weep.

Active ulcer            and…            after healing