Venous diseases (overview) I87.

Disease patterns of the body's venous vascular system are widespread in the Central European population. Risk factors for venous diseases include genetic disposition, advanced age and the number of pregnancies.

Acute venous diseases

• phlebitis/acute thrombotic events
  • Superficial veins
    • Phlebitis: This is usually understood to be an inflammatory disease of the superficial veins (term is not used uniformly). Phlebitis of the superficial and deep veins usually occurs reactively as a result of a thrombotic process (of different genesis) of a vein segment.
    • Phlebitis saltans
    • Coronary lymphangitis non venereal
    • String-shaped phlebitis(Mondor disease)
    • Thrombophlebitis
    • Varicophlebitis
    • Coumarin necrosis
  • Deep veins
    • Deep vein thrombosis (DVT)
    • Phlegmasia coerulea dolens (maximum form of deep pelvic and leg vein thrombosis)

Chronic venous diseases

• Varicosis (varices)
  • Superficial veins
    • Spider veins varices
    • Reticular varices (see below varices)
  • Deep veins
    • truncal varicosis of the vena saphena magna or the vena saphena parva
    • Side branch or perforating varices (see below transfascial veins)
  • Dermatologically relevant varicoses in special localization
    • Pelvic vein syndrome
    • s.a. iliac vein spur
    • Varicocele
    • Tongue varices
    • Finger varicosis
    • Angioma seniles of the lips
    • Varicosis after arterio-venous shunt (e.g. in dialysis patients)
    • Varicosis in the wake of an arm vein thrombosis Paget-von-Schroetter
    • Varicoses of superficial and/or deep vein systems in the context of vascular malformations
• Chronic venous insufficiency
  • Postthrombotic syndrome
  • Stasis dermatitis with CVI
  • Dermatoliposclerosis
  • Purpura jaune d'ocre
  • Angiodermite purple et pigmentée
  • Atrophie blanche
  • venous leg ulcer

Varicose veins are found in about 20% of the general population, although this statement varies with age.

The frequency of more serious signs of chronic venous insufficiency such as eczema, pigmentation, dermatoliposclerosis and ulcer formation are found in 5% of the general population.

The more differentiated CEAP classifications(C0 = no appearance, C1 = spider veins and reticular varices, C2 = varices, C3 = oedema, C4a = pigmentation, purpura, eczema, C4b = hypodermitis, lipodermatosclerosis, atrophie blanche, C5 = healed ulcer, C6 = open ulcer) were based on international clinical studies in recent years and thus comparable to those of other countries:

For stages C0 and C1 (no symptoms / spider veins + reticular varices): 50-70%.

For stadiums C2-C6: <10%.

For stage C5 (healed venous leg ulcer): 0.6% (Bonn vein study)

For stage C6 (open venous leg ulcer): 0-0.5%.

The venous system takes over the important task of transporting the blood out of the tissue and back to the heart. Veins belong to the low pressure system of the blood circulation. The venous blood pressure is 10-15 mm Hg, which is significantly lower than the arterial blood pressure.

The blood flows much more slowly in the veins than in the arteries. The venous wall is constructed like the arterial wall but is thinner in comparison. Veins are many times more elastic than arteries. Arteries and veins are enclosed by a common connective tissue sheath. This arterio-venous coupling leads to an arterial pulse wave that accelerates the blood flow in the corresponding vein in the direction of the heart. This return transport of the blood to the heart is further ensured by the contractions of the skeletal muscles (muscle pump) and by venous valves. The "caliber stronger" leg veins are equipped with numerous venous valves. Their frequency decreases from the periphery towards the central veins.

The venous system of the legs consists functionally of two different parts:

• the superficial low pressure vein system(extrafascial veins: blood pressure is 10-15 mm Hg) which runs under the skin and drains the blood from the subcutaneous fatty tissue
• the deep venous system(intrafascial veins), which is connected to the large arteries of the extremities and transports blood back from muscles and bones
• the system of perforating veins also transfascial veins, connecting scenes between the superficial and deep venous system. These penetrate the muscular fasciae, which act as the anatomical and functional boundary between the two venous systems.

The biological aging of the venous system led to a degeneration of the venous valves. If the number of venous valves is set at 100% at birth, 17% of the valves recede by the age of 25, 40% by the age of 24 and 80% by the age of 70.

The following risk factors are proven for varicose veins (V) and chronic venous insufficiency (varies according to Rabe):

_______________V _____________CVI__________

Higher age + +

Positive FA + +

Women + +

pregnancy + +

Overweight + +

Women are more frequently affected than men

Disturbances in venous hemodynamics lead to decompensation of the venous low pressure system with pressure increase, extravasation of fibrosis of the affected tissue.

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2. Carruthers TN et al.(2014) Interventions on the Superficial Venous System for Chronic Venous Insufficiency by Surgeons in the Modern Era: An Analysis of ACS-NSQIP. Vasc Endovascular Surg PubMed PMID: 25487248.

3. Evans CJ et al (1999) Prevalence of varicose veins and chronic venous insufficiency in men and women inthe
   general population: Edinburgh Vein Study. J Epidemiol Community Health 53:149-153.

4. Gallenkemper G et al (1998) Guideline for the diagnosis and treatment of chronic venous insufficiency (CVI) . Phlebol 27:32-35
5. Younger (2013) Venous diseases. Certified CME further training. Available through the Bauernfeind company. www.bauerfeind.com/de/service/servicekonzept/kontakt/servicenummern.html

6. Kovač M et al (2014) Clinical characteristics of first venous thrombosis among women under and over 45 years of age. Med Pregl 67:328-333

7. Rabe E et al (2010) Epidemiology of chronic venous diseases. In: T Noppeney, H Nüllen Diagnosis and therapy of varicosis. Springer Medizin Verlag Heidelberg p 38 -41