Chapter 20 Treatment of Venous Ulcers

Venous ulcers affect 2% of the adult population. Millions of dollars are spent each year on the care of this difficult condition. There is as yet no consensus on the best therapy; the main treatment strategy has been compression therapy.

In this chapter, the etiology is examined from a hemodynamic and cellular aspect. Adjunctive treatments, both medical and surgical, are discussed. Finally, a new treatment option—terminal interruption of the reflux source (TIRS)—is introduced. First, all venous ulcers have a common denominator. The commonality is increased ambulatory venous pressure. A pressure above 45 mm Hg increases the risk of ulceration. The higher the pressure, the greater is the risk of eventual venous ulceration.¹ The increased pressure may be due solely to reflux at some point in the venous system or coexist with other factors.²

When evaluating a patient with a venous ulcer, an understanding of venous pathophysiology and the complex interaction at the cellular level must be understood. The etiology of the increased venous pressure should be documented. This may be from a superficial, deep, or perforating vessel or a combination of any of the three. There may be other contributing factors such as abdominal outflow compression or problems with venous or arterial capacity.

The eventual goal, if possible, is to provide relief of the increased venous pressure. This will ensure the best possible outcome and help reduce further ulcerations. Most therapy is directed at the local level when the patient is first seen. This is in the form of compression therapy.

Compression therapy with either elastic or inelastic dressings has been the historical treatment.^3,4 As compliance increases, so do the healing rates. However, with compression alone, there is still a high recurrence rate.^4,5

Other adjuncts to improving ulcer healing have been described. Medical therapy has included rutosides, aspirin, and pentoxifylline.^6–8 Of course, local wound care is essential and irrigation and debridement of devitalized tissue are essential.

At the Midwest Vein and Laser Center, debridement is often carried out using a 3- to 10-mL syringe with saline connected to a 30-gauge needle. This technique in effect sends a high-pressure stream of saline that is directed at the ulcer base. This is very effective and better tolerated by the patient.

Many dressings have been advocated for the active ulcer. These range from simple gauze to impregnated foam dressings. Silver-impregnated dressings are used in our clinic when there is evidence of infection locally. However, there is no evidence of the superiority of one dressing over the other in promoting wound healing.

Skin grafts have been used as an adjunct in wound healing for venous ulcers. These grafts include full-thickness punch grafts, xenografts, or allografts. To date, in an updated review on skin grafting for venous ulcers, bilayer artificial skin used in association with compression dressings increased ulcer healing compared to compression alone.^9,10 In the study by Falanga et al.,⁹ healing at 6 months was only 63% with allogenic human skin equivalent compared to 43% with compression alone.⁹

Surgical techniques such as stripping the great saphenous vein,^10,11 subfascial perforator ligation,^12,13 endoluminal thermal ablation,¹⁴ and minimally invasive perforator therapy¹⁵ have been used as adjuncts in the treatment of venous ulcers. Nontargeted foam sclerotherapy has also been mentioned as a treatment modality.^15–17 Except for foam sclerotherapy, none of these procedures has proved to increase the healing rate of venous ulcers. These adjunctive procedures are mostly directed at preventing future occurrences.

Recently, the TIRS technique was introduced.¹⁸ The TIRS technique targets only those vessels in close proximity to the venous ulcer.

The basis of this theory is that venous ulceration is a local manifestation of a systemic problem. The high venous pressure in a vein or veins draining the ulcer bed, or in some instances a perforator directly in continuity with the ulcer, is responsible for the local phenomenon of ulceration. If the venous hypertension is relieved, then healing should accelerate.

When using the TIRS technique, patients at Midwest Vein and Laser Center had rapid healing of ulcers compared to compression alone or compression with other adjunctive procedures. In a series of 20 patients treated with the TIRS technique, healing occurred in 90% of patients within 8 weeks. All patients had been compliant with compression for 18 to 24 months prior to treatment.¹⁸

The exact mechanism of action at the microscopic level is as yet unknown in the TIRS technique. The genesis of ulceration at the microscopic level is generally believed to be an inflammatory response. According to this theory, continuous high-pressure leads to eventual necrosis. The necrosis is mediated by complex interaction at the cellular level. Rapid healing observed after occluding these high-pressure venous effluents with foam sclerotherapy must be related to a marked reduction in ambulatory venous pressure at the local level. Unfortunately, there is no reliable means to measure pressures in those smaller distal venous channels or, for that matter, at the tissue level. Hence, an assumption is made that healing is mediated through a local reduction of venous pressure at the ulcer site. The response has been rapid in most patients; however, there may be other mechanisms that are also contributing that are so far not known.

The TIRS technique requires good interpretive ultrasound skills and the ability to safely deliver the foamed sclerotherapy with the aid of ultrasound guidance. Only the most distal venous branches draining the area of the ulcer are identified. In some patients, especially those with anterior calf ulcers, a perforator leading directly to the ulcer bed may be identified (Figs. 20-1 and 20-2). The proximal source of reflux (i.e., saphenous vein, classic posterior tibial perforator, or other source proximally) is ignored. Only the distal vessel or vessels are targeted initially (Fig. 20-3 through 20-13).

Fig 20–1 Anterior leg ulcers secondary to chronic venous hypertension.