Chronic venous insufficiency

The Chronic venous insufficiency ( CVI), venous stasis syndrome and chronic, called Chronic venous insufficiency is based on a microcirculatory disturbance of the vessels as a result of venous outflow obstruction. Result is partly heavy veins and skin changes.

Epidemiology

In the U.S., should be affected by the chronic venous insufficiency 6-7 million patients. The most difficult complication are venous ulcers, 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 occurs in women twice as often as in men.

Etiology

Underlying conditions which may cause chronic venous insufficiency, varicose veins are ( varicose veins, both Stammvarikosen and Perforansvarikosen ) phlebothrombosis (CVI as post-thrombotic syndrome late ), arteriovenous fistulas and venous angiodysplasia ( congenital defects of the venous valves ).

Pathophysiology

Important for the development of chronic venous insufficiency is the presence of a pathological high blood pressure of the superficial veins. Normal this is at 20-30 mmHg, but increased by venous thrombosis, primary or secondary pathological venous valves or weakened muscle pump to 60-90 mmHg. This high pressure causes responsible for the later complications anatomical, physiological and histological changes of the vessels.

The most important changes caused by venous hypertension relate to the vein valves. Thrombosis causing venous hypertension and destroy with the venous valves, so the high pressure persists even when, for example, a recanalization. The result is a so typical for the medical vicious circle. The vessel wall changes due to high pressure cause further damage to valves and thus the high pressure gets itself

Under physiological conditions, the capillary bed is protected from strong pressure changes, as precapillary arterioles can be contracted by reflex. This reflex seem to have lost patients with chronic elevated venous pressure, however, namely that with changes in body position changes in pressure are passed directly to the capillary bed.

With long-term elevated venous pressure caused changes that affect the capillary walls. This includes an expansion and extension of the capillary bed, increased endothelial surface, increased deposition of collagen IV in the basement membrane and pericapillary deposition of fibrin. The interaction of elevated venous pressure and abnormal capillaries with increased permeability lead to a flushing out of water, large proteins and red blood cells in the interstitium. The accumulating fibrin seems to be less easily solved. At the same time leads to a reduced gas exchange, ie, cutaneous hypoxia. This leads among other things to leukocyte activation. The interaction of these pathological conditions leads to local tissue proliferation, inflammatory processes and Kapillarthrombosen.

Clinic

Clinically, chronic venous insufficiency is divided into three stages according to Widmer ( inter alia ):

  • Stage 1: Reversible edema, Corona Phlebectatica (dark blue veins of the skin changes in the med and lat border of the foot ), perimalleoläre Kölbchenvenen
  • Stage 2: persistent edema, hemosiderosis and purpura of the skin of the lower leg, and Dermatosklerosen lipodermatosclerosis, atrophy blanche, stasis dermatitis, cyanotic skin color.
  • Stage 3: leg ulcer

Diagnostics

Most of the lesions described are enough sufficient for the diagnosis. Nevertheless, it is important in some cases to carry out a more extensive diagnostics to determine the etiology and possible further action. Ascending phlebography is here though gold standard but invasive and expensive. So one usually uses the duplex sonography. By B- mode ultrasound to changes in the vein wall and surrounding structures can be detected by the Doppler altered flow conditions. In order to exclude an arterial vascular disease, since then the compression treatment would rule, one should also determine the ABI ( ankle -brachial index).

Therapy

Symptomatic

  • Elevating the legs for 30 minutes 4-5 times per day is already clearly reduced the tendency to edema and improves microcirculation. Alone, of course, this is only sufficient in mild stages, and for busy people, it is probably difficult times hochzulagern legs on the day.
  • Manual Lymphatic Drainage
  • Compression therapy: Compression therapy, for example, with compression stockings is an important part of therapy. How exactly this works is not entirely clear, it is usually to improve the cutaneous hemodynamics, reduce the rate of blood flow in the deep veins, the lymphatic flow and venous pressure. You should even increase fibrinolysis and thus counteract the vascular sclerosis. It reduces the incidence of edema and ulceration. Most ranges from Class 2 (30 mm Hg ankle pressure). In patients with massive obesity and edema compression stockings may be ineffective. Here one uses, for example, pneumatic compression pumps. Contraindications are: AVK with ankle pressure < 80 mmHg, congestive heart failure and unstable angina pectoris.
  • Antiseptics for wound healing
  • Drug therapy: coumarin ( α - benzopyrones ), flavonoids ( γ - benzopyrones ), horse chestnut extracts ( saponosides ) as well as aspirin and pentoxifylline are used for therapy, although the data available for the benefit of these materials is partly contradictory.

Invasive

Sometimes underlying diseases, such as a varicose veins must be treated accordingly interventional or surgical.

Endothelium Stroma (animal tissue) Gold standard (test) Medical guideline
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