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__Chronic venous insufficiency__

Varixes on the right lower limb

This is the most common complication of varicose veins. The term is used for signs and symptoms associated with chronic venous hypertension.

Pathogenesis[edit | edit source]

Dk diagram of varicose veins

It is caused by an increase in pressure, which arose as a result of valvular incompetence, reflux, obstruction. The most serious forms are found in postthrombotic syndrome, milder ones arise as a result of varices. In 80% it is the result of deep vein thrombosis (such as the so-called postphlebitic syndrome), in the remaining 20% primary varices, valvular agenesis and congenital AV shunts apply. There are two main factors of its occurrence - muscle pump failure'' and valvular insufficiency with reflux. It can be in the form of compensated - the muscle pump is able to cope with volume overload, or decompensated - skin changes - the muscle pump can no longer cope, venous hypertension occurs.

Clinical picture[edit | edit source]

The classic manifestation is permanent swelling that does not respond to the supine position. It is often accompanied by skin hyperpigmentation, eczema, subcutaneous fibrosis (lipodermatosclerosis), white' atrophy and ulceration, then pressure and heaviness in the limbs' and night cramps. Another manifestation can be the so-called corona phlebectatica - dilated red to blue veins' near the inner ankle. At the most severe stage of insufficiency, 'ulcus cruris occurs.

The CEAP classification is used for the clinical characteristics:
C - clinical classification:
C0 No visible or palpable  signs of venous disease

Telangiectasia, reticular varices


Varicose veins

C3 Swelling
C4a Pigmentation, eczema
C4b Lipodermatosclerosis, white atrophy
C5 Healed ulcer
C6 Active ulcer
S Symptomatic
A Asymptomatic
E - etiological classification:
Ec congenital
Ep primary
Es secondary
En no venous etiology
A - anatomical classification:
As superficial veins
App perforators
Ad deep veins
no localization of veins found
P - pathophysiological classification:
Ex reflux
Mon obstruction
Pr,o reflux and obstruction
Pn not detected

Therapy[edit | edit source]

Conservative[edit | edit source]

  • in postthrombotic syndromewarfarin to prevent recurrence of thrombosis
  • lifestyle change (exercise, weight reduction, regular bowel movements...)
  • 'compression, venotonics

Sclerotherapy[edit | edit source]

Surgical[edit | edit source]

  • removal of varicose veins, interruption of perforators, ...
  • Palme's reconstruction - when closing the external or common pelvic vein, the v. femoralis on the affected side is sewn crosswise v. saphena magna from the other side

Skin changes[edit | edit source]

Skin changes are divided into 3 degrees:

  • 1. grade – corona phlebectatica paraplantaris, perimalleolar edema;
  • 2. grade – DK swelling, skin changes (hyperpigmentation, varicose dermatitis, hypodermatitis, dermatosclerosis);
  • '3. degree - ulcus cruris venosum.

Ulcus cruris venosum[edit | edit source]

It is a chronic leg ulcer, the predilection site is the area above the ankles. It arises as a result of chronic venous insufficiency. The provoking factor is usually a completely banal trauma.

Leg Ulcer Treatment[edit | edit source]

Treatment must be comprehensive.

  • compression walking (intermittent pneumatic compression in immobile patients)
  • external treatment
    • poultices with chloramine, covering around ulcers, poultices with zinc paste, gentian violet, enzymatic preparations (collagenase)
    • we apply granulation (AgNO3) and then epithelising agents (pine vaseline) to the cleaned ulcers
  • surgical treatment
    • ligature of insufficient perforator, extirpation of massive varices
    • excision of callous edges of ulcers
    • transplantation of skin grafts
  • pharmacotherapy - pentoxyphylline

Links[edit | edit source]

Related Articles[edit | edit source]

Source[edit | edit source]

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