Chronic venous insufficiency

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Classification according to ICD-10
I87.2 Venous insufficiency (chronic, peripheral)
ICD-10 online (WHO version 2019)

The Chronic venous insufficiency (CVI), and chronic venous stasis syndrome , chronic venous insufficiency called, based on a microcirculation disturbance of the vessels due to a venous obstruction. The consequences are sometimes severe changes in veins and skin.

Epidemiology

In the USA, 6 to 7 million patients are believed to be affected by chronic venous insufficiency. The most difficult complication is venous ulceration , the prevalence of which is up to 5%.

Risk factors

The risk of suffering from chronic venous insufficiency, increases with age , obesity , a history of phlebitis , deep vein thrombosis and severe leg trauma. CVI is twice as common in women as it is in men.

etiology

Basic diseases that can cause chronic venous insufficiency are varicose veins (varicose veins, both trunk varicose veins and perforated varicose veins), phlebothrombosis (CVI as late post-thrombotic syndrome), arterio-venous fistulas and venous angiodysplasias (congenital defects of the venous valves ).

Pathophysiology

The decisive factor for the development of chronic venous insufficiency is the presence of pathological high blood pressure in the superficial veins. This is normal at 20 to 30  mmHg , but increases to 60 to 90 mmHg due to venous thrombosis, primary or secondary pathological venous valves or a weakened muscle pump . This high pressure causes the anatomical, physiological and histological changes in the vessels that are responsible for the later complications.

The most important changes caused by venous high pressure affect the venous valves . Thromboses cause a venous high pressure and destroy the venous valves at the same time, so the high pressure persists even with z. B. recanalization. This creates a vicious circle . The changes in the vessel wall due to high pressure cause further valve damage and thus the high pressure is self-sustaining.

Under physiological conditions, the capillary bed is protected from strong changes in pressure, since precapillary arterioles can contract reflexively. However, patients with chronically increased venous pressure seem to have lost this reflex; This means that when the body position changes, changes in pressure are passed on directly to the capillary bed.

With permanently increased venous pressure, changes occur that affect the capillary walls. These include widening and lengthening the capillary bed, increased endothelial surface , increased storage of collagen IV in the basement membrane and pericapillary storage of fibrin . The interaction of increased venous pressure and abnormal capillaries with increased permeability lead to a leaching of water, large proteins and red blood cells into the extracellular space . The accumulating fibrin also appears to be less easy to resolve. At the same time, there is a reduced gas exchange, i.e. cutaneous hypoxia . Among other things, this leads to leukocyte activation . The interaction of these pathological conditions leads to local tissue proliferation, inflammatory processes and capillary thrombosis.

Graduation

Clinically, chronic venous insufficiency according to Widmer and the modification according to Marshall and Wüstenberg (among others) is divided into three grades. This classification refers to the visible and tactile changes in the skin:

Chronic venous insufficiency (stage III)
  • Grade I: Reversible edema, corona phlebectatica (dark blue skin vein changes on the med. And Latin edge of the foot), perimalleolar cortex veins
  • Grade II: persistent edema of various origins, hemosiderosis and purpura jaune d'ocre - ocher-colored discoloration of the skin as a result of the storage of water-insoluble iron-protein compounds in the lower leg area, dermatosclerosis and lipodermatosclerosis, atrophy blanche , stasis eczema , cyanotic skin color.
  • Grade IIIa: Healed leg ulcer (ulcer scar)
  • Grade IIIb: strongly developed (florid) leg ulcer

Diagnosis

Most of the time, the skin changes described are sufficient for diagnosis. Nevertheless, in some cases it is important to carry out a more extensive diagnosis in order to determine the etiology and possibly the further course of action. Ascending press phlebography was the gold standard here , but it was invasive and expensive. So one usually uses duplex sonography . Changes in the vein wall and surrounding structures can be detected using B-image sonography, and flow conditions can be detected using Doppler. In order to be able to rule out arterial vascular disease, since compression treatment would then be excluded, the ABI (ankle-brachial index) should also be determined. In order to make a diagnosis, it is also important to know the signs of CVI. On the one hand, there would be Corona phlebectatica (blue discoloration on the affected area) and Atrophie Blanche (white discolouration on the affected area). In addition, there is a pigment shift, that is, the affected limb has spots that resemble pigment spots.

therapy

Symptomatic

  • Elevating the legs for 30 minutes 4 to 5 times a day already significantly reduces the tendency to edema and improves microcirculation. Of course, this is only enough on its own in very easy stages, and it is likely difficult for busy people to put their legs up several times a day.
  • Manual lymph drainage
  • Compression therapy : The compression therapy z. B. with compression stockings is an important part of the therapy. Compression reduces the venous cross-section and increases the return flow of the blood. In addition, this form of therapy restores the functionality of venous valves that have not yet been completely destroyed . Compression therapy is designed to improve cutaneous hemodynamics , decrease the speed of blood flow in the deep veins, lymphatic flow, and venous pressure. It is even said to increase fibrinolysis and thus counteract vascular sclerosis. It reduces the occurrence of edema and ulceration. Class II is usually sufficient (~ 30 mmHg ankle pressure). Compression stockings can be ineffective in patients with severe obesity and edema. Here you use z. B. pneumatic compression pumps. Contraindications are: AVK with ankle pressure <80 mmHg, decompensated heart failure and unstable angina pectoris .
  • Antiseptics for wound healing
  • Medicinal therapy : Coumarin (α-Benzopyrone), flavonoids (γ-Benzopyrone), horse chestnut extracts (Saponoside) as well as acetylsalicylic acid and pentoxifylline are used for therapy.

Invasive

Under certain circumstances, underlying diseases such as varicosis must be treated appropriately interventionally or surgically.

See also

Individual evidence

  1. ↑ Kerstin Protz: Modern wound care. 7th edition Elsevier Urban & Fischer, Munich 2014, ISBN 978-3-437-27884-6 , p. 91.
  2. ↑ Stefanie Reich-Schupke: Mode of action of compression therapy . In: S. Reich-Schupke, M. Stücker: Modern compression therapy a practical guide. ViavitalVerlag, Cologne 2013, ISBN 978-3-934371-50-7 , pp. 36–39.

literature