No More Venous Ulcers-What More Can We Do?

Abstract

Venous leg ulcers (VLUs) are the most severe complication caused by the progression of chronic venous insufficiency. They account for approximately 70-90% of all chronic leg ulcers (CLUs). A total of 1% of the Western population will suffer at some time in their lives from a VLU. Furthermore, most CLUs are VLUs, defined as chronic leg wounds that show no tendency to heal after three months of appropriate treatment or are still not fully healed at 12 months. The essential feature of VLUs is their recurrence. VLUs also significantly impact quality of life and could cause social isolation and depression. They also have a significant avoidable economic burden. It is estimated that the treatment of venous ulceration accounts for around 3% of the total expenditure on healthcare. A VLU-free world is a highly desirable aim but could be challenging to achieve with the current knowledge of the pathophysiology and diagnostic and therapeutical protocols. To decrease the incidence of VLUs, the long-term goal must be to identify high-risk patients at an early stage of chronic venous disease and initiate appropriate preventive measures. This review discusses the epidemiology, socioeconomic burden, pathophysiology, diagnosis, modes of conservative and invasive treatment, and prevention of VLUs.

Keywords: burden of illness; compression therapy; conservative treatment; costs; invasive treatment; prevention; recurrent venous ulcer; venous ulcer.

Figure 1

Pathophysiology of venous ulcers.

Figure 2

Different modes of prevention and treatment of venous leg ulcers (CEAP C4—skin damage due to chronic insufficiency; IB—inelastic bandage; ACW—adjustable compression wrap; MCS—medical compression stocking.

Figure 3

The pressure curve of an inelastic bandage exerts a compression pressure of 50 mm Hg. This pressure overcomes the intravenous pressure of about 75 mm Hg (red line) when performing foot dorsiflexion in a standing position and during walking, restoring a kind of valve mechanism; DSI—dynamic stiffness index; SSI—Static Stiffness Index; WPA—walking pressure amplitude.

Figure 4

The pressure curve of an elastic stocking exerts a compression pressure of about 20 mm Hg. The pressure never approaches the intravenous pressure of about 75 mm Hg (red line) when performing foot dorsiflexion in a standing position during walking. Veins are not compressed. DSI—dynamic stiffness index; SSI—Static Stiffness Index; WPA—walking pressure amplitude.

Figure 5

The pressure curve of an elastic bandage applied with full stretch exerts a compression pressure of about 75 mm Hg. Compression pressure is always the same or higher than the intravenous pressure (red line). Veins are always compressed. The bandage becomes painful within a short time. DSI—dynamic stiffness index; SSI—Static Stiffness Index; WPA—walking pressure amplitude.

Figure 6

Invasive methods of superficial venous insufficiency treatment (CHIVA—Ambulatory Conservative Hemodynamic Treatment of Venous Insufficiency; ASVAL—Ambulatory Selective Varices Ablation under Local Anesthesia; PIN—perforation imagination; EVLA—endovenous laser ablation; RFA—radiofrequency ablation; MOCA—mechanochemical ablation).

Figure 7

Invasive treatment of deep venous insufficiency.

Figure 8

Endovascular treatment of the occlusion of the iliac veins. (a,b) Right iliac phlebography shows occlusion of right common iliac vein (CIV) (white arrow) and severe collaterals from right internal iliac vein to contralateral iliac veins (red arrow); (c) balloon dilatation after recanalization of occluded part of right CIV (red arrow shows strong resistance due to scarring in the vein, 15 atm pressure was given); (d) right CIV and external iliac vein (EIV) is stented; (e) phlebography after stenting—vein inflow from CIV restored, all collateral veins disappeared.