Etiology and Treatment of Venous Ulcers

11/26/12

Ronald Bush, MD, FACS

Peggy Bush, APN

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Treating venous leg ulcers is time-consuming and affects patients’ quality

of life. Venous ulcers affect approximately 2 percent of the adult population.

Millions of dollars are spent each year on the care of venous ulcers. At this time,

there is no consensus on the best therapy. Compression therapy has been the

main treatment strategy.

In this discussion, the etiology from a hemodynamic and cellular aspect

will be examined. Adjunctive treatments both medically and surgically will be

outlined. Finally, a new treatment option will be introduced known as ‘Terminal

Interruption of the Reflux Source,’ (TIRS). This technique was published in

Perspectives in Vascular Surgery and Endovascular Therapy, 2010.

The common factor for venous ulcers is increased ambulatory venous

pressure. A pressure above 45 mmHg increases the risk of ulceration. The

higher the pressure, the greater is the risk of eventual tissue necrosis.(1) The

increased pressure may be due solely to reflux at some point in the venous

system or co-exist 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 increase venous pressure should be

documented. This may be from a superficial, deep, perforating vessel or a

combination of any of the three. Other contributing factors such as abdominal

outflow compression or problems with venous or arterial capacity may be

present.

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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 in the clinic and this is usually 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.

Even 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 aspirin, rutosides, and pentoxyphine. (6) (7) (8) As always, local wound

care is essential and irrigation and debridement of devitalized tissue is essential.

At the ‘Midwest Vein and Laser Center’, Dayton, Ohio, debridement is

often carried out using 3 ‐10cc syringes with saline connected to a 30‐gauge

needle. This technique in effect directs a high-pressure stream of saline that is

directed at the ulcer base. Debridement is very effective and easily tolerated by

the patient.

Countless dressings have been advocated for ulcers and these range

from 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 in the literature 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. Grafts include full thickness punch grafts, xenografts, or allografts. To

date, in an updated review on skin grafting for venous ulcers; bi-layer artificial

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skin, used in association with compression dressings, increased ulcer healing

compared to compression alone. (10) (11) In the study by (Falanga et, al, 1998),

healing at 6 months was only 63% with allogenic human skin equivalent

compared to a 43% with compression alone. (10)

Surgical techniques such as, stripping the greater saphenous vein (11), (12),

subfascial perforator ligation, (13) endoluminal thermal ablation, (15) and minimally

invasive perforator therapy, (16) have been used as adjuncts in the treatment of

venous ulcers. Non‐targeted foam sclerotherapy has also been mentioned as a

treatment modality. (16)(17) Except for foam sclerotherapy, none of these

procedures have proven to increase the healing rate of venous ulcers. The above

adjunctive procedures are mostly directed at preventing future occurrences.

Recently, a technique, ‘Terminal Interruption of the Reflux Source (TIRS)

has been 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 phenomena 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 when compared to compression alone, or

compression with other adjunctive procedures. In a series of twenty patients

treated with the TIRS technique, healing occurred in ninety percent of patients

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within 8 weeks. All patients had been compliant with compression for 18-24

months prior to treatment. (Bush, 2010)

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- pressured 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 smaller

distal venous channels, or for that fact 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 which as yet are 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. 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.

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Vessels under the ulcer bed, somehow you must get the foam here, by direct puncture or by introducing it through a superior or inferior vessel close to the circumference of the ulcer. When these vessels clot, this equates to an internal compression, which is more effective than external compression. Copyright 2011 by www.bushvenouslectures.com

Using ultrasound guidance, these vessels are cannulated with needle

penetration through normal skin, as far from the ulcer margin as possible. A 3 cc

syringe and a 22‐gauge needle are used in our clinic. Cannulation is done

superior to the ulcer if chronic skin change exist inferiorly. After penetrating the

target vessel, the foam is slowly injected.

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Using ultrasound to demonstrate vessels draining ulcer bed -‐ Copyright 2011 by www.bushvenouslectures.com

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Local anesthesia to skin delivered with 30-‐gauge needle with tumescent solution -‐ Copyright 2011 by www.bushvenouslectures.com

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Percutaneous puncture of target vessel -‐ Copyright 2011 by www.bushvenouslectures.com

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Aspirating blood after puncture to confirm needle placement -‐ Copyright 2011 by www.bushvenouslectures.com

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Injecting Sotradecol foam -‐ Copyright 2011 by www.bushvenouslectures.com

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Injecting Sotradecol foam -‐ Copyright 2011 by www.bushvenouslectures.com

In our clinic, a 4:1 mixture of Sotradecol and C02 is used. After

injecting the foamed solution, compression is applied and local wound care is

done. The patient is rescanned at weekly intervals and foam injections are

repeated if necessary. A 1 percent concentration is used, unless extenuating

circumstances, such as concurrent anticoagulation or high flow exists. A 3

percent foamed solution of Sotradecol is then used.

Definitive treatment of the proximal reflux source such as thermal ablation

of the saphenous vein or perforator interruption is done at a later date, to help

prevent future ulcer occurrences. In some cases, concurrent treatment can be

done. However, many times insurance requirements must be addressed and the

more definitive procedures are done 6-‐8 weeks after the first ultra sound guided

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treatment. Most patients have had rapid healing by this time and local infection

and pain have abated.

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Venous Ulcers: The TIRS Technique Through a Percutaneous Approach

69- year old male with recurrent venous ulceration right lower leg; the

patient had a previous saphenous vein ablation three years ago with foam

injection of the ulcer bed 8 weeks before the procedure. The ulcer healed

completely before the ablation.

Now, presents with recurrent venous ulcer inferior to the old site. Popliteal

vein shows no reflux, posterior tibial vein shows no reflux, but there is an

incompetent perforator that drains the ulcer bed. This can be seen in figures 1-3.

The ulcer bed has been injected once before percutaneously with a 25-gauge

needle. This is a quick and relatively painless way to deliver foam into the

underlying ulcer bed.  

In almost all patients, a small superficial venous tributary can be found in

close proximity to the ulcer. This has now become my preferred method of

performing the TIRS Technique. It is also much more comfortable for the patient.

This provides excellent access to the ulcer bed. Make sure there is good blood

return in your tubing before injecting the foam. Foam is much safer to inject and

much more effective than liquid. This can be seen in Figure 4. Figure 5 shows

the foam in the ulcer bed after the percutaneous injection with the 25-gauge

needle.

The patient should be seen in one week and any patent vessels under the

ulcer bed are obliterated with foam. Foam sclerotherapy provides an excellent

internal compression dressing. In Fact, this patient had a reduction of one half of

the original ulcer size in 2-weeks.

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11/26/12

The above US shows the clotted vessels under the ulcer bed, post 2nd injection. The ulcer continues to heal rapidly. The perforator is still patent, but is no longer in continuity with the vessels that are draining the ulcer bed.

As long as these vessels remain thrombosed, rapid ulcer healing will occur. I may have to target the perforator by standard US guided techniques in the future. However, if the ulcer heals and there are no further problems, I will leave the perforator alone at this time.

As you can see from the US image, the clotted vessels form a barrier to the increased pressure in the deep system.

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1/12/13

8-weeks post Percutaneous TIRS Technique

Venous Ulcer 8-Weeks Post Percutaneous TIRS Technique - Copyright 2013 by www.veinexperts.org

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12/18/12 - Co-existing GSV reflux and posterior tibial perforator in a patient with venous ulcers

Many times I have encountered patients with C5- C6 disease that have both GSV reflux and also a pathologic perforator of the post tibial vein (Cockett’s). It is known that both of these conditions may cause ulcerations. When both co-exist two questions must be answered. What is the primary etiology and what abnormality should be addressed first.

The answer is illustrated in the following case. This case may be the best illustration of the pathogenesis of both GSV reflux and post tibial perforator occurring together.

Remember, a perforator that is abnormal is usually a secondary occurrence. However, once abnormal, it may become the primary origin of C5 – C6.

In the following presentation, you can see that GSV reflux occurred to the ankle level. Communicating veins then course under the indurated, inflamed ulcer to connect to a large post tibial perforator. There is also a smaller perforator at the ankle level.

The inderated-inflamed area is in continuity with the large posterior perforator. The post tibial vessels are normal in size until the origin of the perforator.

Above this level, they are also normal. This picture is one of secondary pathology due to superficial venous overload.

The GSV is treated first, and if syptoms persist which they usually do, then the perforator is addressed.

These US images and videos illustrate the most common cause of post tibial perforator pathology- GSV reflux.

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Click on image to see video

Ultrasound of Posterior Tibial Perforator

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The vessels are marked by the red arrow communicate to both the GSV and the vessels under the ulcer bed which then connect to the posterior tibial perforator

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References

1. Payne S, London N, Newland C, et al. Ambulatory venous pressure:

Correlation with skin condition and role in identifying surgically correctible

disease. Eur J Vasc Endovasc Surg. 1996;11:195-‐200.

2. Raju S, Neglen P, Carr-‐White P, et al. Ambulatory venous hypertension:

Component analysis in 373 limbs. Vasc Endovascular Surg. 1999;33:257-‐

266.

3. Fletcher A, Cullum N, Sheldon T. A systematic review of compression

treatment for venous leg ulcers. BMJ. 1997;315:576-‐580.

4. Erickson C, Lanza D, Karp D, et al. Healing of venous ulcers in an

ambulatory

care program: the roles of chronic venous insufficiency and patient

compliance. J Vasc Surg. 1995;22(5):629-‐636.

5. Scriven J, Taylor L, Wood A, et al. A prospective randomized trial of four-‐

layer

versus short stretch compression bandages for the treatment of venous

leg

ulcers. Ann R Coll Surg Engl. 1998;80:215-‐220.

6. Falanga V, Fujitani R, Diaz C, et al. Systemic treatment of venous leg

ulcers

with high doses of pentoxifylline: Efficacy in a randomized, placebo-‐

controlled trial. Wound Repair Regen. 1999;7:208-‐13.

7. Colgan M, Dormandy J, Jones, P, et al. Oxpentifylline treatment of venous

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ulcers of the leg. BMJ. 1990;300:972-‐975.

8. Gohel M, Davies A. Pharmacological agents in the treatment of venous

disease: An update of the available evidence. Current Vascular

Pharmacology. 7(3):303-‐8, 2009 Jul.

9. Jones J, Nelson E. Skin grafting for venous leg ulcers. Cochrane

Database Syst Rev.. 2007;18;(2).

10.Falanga V, Margolis D, Alvarez O, et al. Rapid healing of venous ulcers

and lack of clinical rejection with an allogeneic cultured human skin

equivalent. Arch Dermatol. 1998;134(3):293-‐300.

11.Barwell J, Davies C, Deacon J, et al. Comparison of surgery and

compression with compression alone in chronic venous ulceration

(ESCHAR STUDY): Randomized controlled trial. Lancet.

2008;363(9424):1854-‐1859.

12.Homans J. The operative treatment of varicose veins and ulcers, based on

classification of these lesions. Surg Gynecol Obstet. 1916; 22:143-‐158.

13.Pierik E, Van Urk H, Hop W, Wittens C. Endoscopic versus open

subfascial division of incompetent perforating veins in the treatment of

venous leg ulceration: A randomized trial. J Vasc Surg. 1997;26(6):1049-‐

1054)

14.Glovicski P, Bergan J, Rhodes J, Canton L, Harmsen S, Ilstrup D. Mid-‐

term results of endoscopic perforator vein interruption for chronic venous

insufficiency: Lessons learned from the North American subfascial

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endoscopic perforator surgery registry. The North American Study Group.

J Vasc Surg. 1999;29(3):489-‐502.

15.Rautio T, Ohinmaa A, Perala J, et al. Endovenous obliteration versus

conventional stripping operation in the treatment of primary varicose veins:

A randomized controlled trial with comparison of the costs. J Vasc Surg.

2002;35(5):958-‐965.

16.Poblete H, Elias S. Venous Ulcers: New options in treatment: Minimally

invasive vein surgery. Journal of the Am Coll of Certified Wound

Specialists. 2009;1(1):12-‐19.

17.Hertzman, P, Owens R. Rapid healing of chronic venous ulcers following

ultrasound-‐guided foam sclerotherapy. Phlebology. 2007; 22:34-‐39.

18.Bush R. Terminal interruption of the reflux source for the treatment of

venous ulcers. Presented at the American College of Phlebology. 2009.

19.Bush, R. New technique to heal venous ulcers: Terminal interruption of the

reflux source (TIRS). Perspectives in Vascular Surgery and Endovascular

Therapy. 2010;22(3).

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