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Compression Therapy: The Key to Unlocking VLU Healing

Wound care clinicians may be wary of initiating compression therapy when arterial disease is present due to fears for patient safety. This article will instruct providers on appropriate assessment and treatment.


Venous leg ulcers (VLUs) are the most common type of ulcer that develops in the lower extremities.1 Although compression therapy is considered the essential intervention for chronic VLUs,2 this modality appears underutilized and experts agree that healing rates could be improved through increased appropriate use of this therapy.3 The main hesitation with providing compression comes from the fact that this therapy is contraindicated in the presence of severe arterial disease, and many lower leg ulcers are of mixed etiology (venous and arterial components). Clinicians often choose to “play it safe” and avoid compression due to concern that patients could have a level of arterial disease for which compression might be detrimental. This situation has been recognized for years, with the published observation that only 17% of  VLU patients in the United States receive adequate compression.4 A more recent consensus document cites various European studies for which this metric is also reported, and the percentage of patients receiving compression therapy ranges from 10.8-53%.3 This approach, however, does not follow the current guidelines and represents an underutilization of compression, which is detrimental to the large number of patients who would benefit from it. The key issue, therefore, is the appropriate assessment of the patient to determine whether compression is safe, and to choose the proper level of compression (standard or modified). This article will clarify how to make this assessment and seek to empower providers in the outpatient wound clinic to initiate appropriate compression therapy in a timely manner. Several guidelines have been published over the years on how to assess and treat patients living with lower-leg ulcerations. These guidelines have been recently reviewed, compared, and summarized by a panel of experts.5 In addition, recommendations from a panel of experts have been published in a consensus document.3 The authors are also providing here an overview of this work to facilitate implementation in practice.


With any leg ulcer, a comprehensive patient assessment is needed to establish wound etiology and to guide the development of an appropriate treatment plan.3 Key components of the assessment take into account medical history, bilateral lower extremity assessment, vascular assessment, mobility status, pain level, nutritional status, degree of glucose control among patients living with diabetes, and wound characteristics.6,7 Patients with a history of deep vein thrombosis (DVT), traumatic injury, and/or signs and symptoms of acute DVT (eg, unilateral edema in leg, ankle, or foot; pain with ambulation; tenderness; warmth; or redness) must be referred to a vascular specialist for further investigation. A comprehensive lower extremity assessment incudes severity of edema (if present), wound characteristics, condition of the periwound skin, and skin changes consistent with lower extremity venous disease and/or peripheral arterial disease (PAD). The wound assessment takes into account wound size, tissue quality, exudate characteristics, duration or age, and previous treatment response.3 All patients living with nonhealing lower extremity leg ulcers should undergo noninvasive arterial screening to identify the possible presence of arterial insufficiency.5 There are several methods of arterial screening, including transcutaneous oximetry, skin perfusion pressure, and referral to a vascular laboratory for a complete arterial Doppler study. Each method has certain advantages. However, they require relatively expensive equipment and trained staff, are somewhat time-consuming, and may require advance scheduling, which can delay the implementation of needed compression by several days. Delay of effective treatment of venous ulcers increases time in care, and thus the total cost of care. These are serious problems as we approach bundled and capitated payments. However, the ankle-brachial index (ABI) is a reliable, noninvasive screening method6,8 that can be performed in the wound center on the first visit. The ABI guides the amount of compression to be applied and the need for additional arterial testing and/or referral. Because all noninvasive screening tests have limitations, results must be interpreted in conjunction with the history and physical examination, particularly among patients living with diabetes who may have calcified vessels. For example, if an ABI result falls in the normal range, but the patient exhibits intermittent claudication or rest pain and skin changes consistent with PAD, a referral to a vascular specialist is needed prior to initiation of compression therapy. Normal ABI will range from 0.9-1.3; 0.5-0.8 indicates no significant PAD or mild PAD; < 0.5 indicates severe PAD or critical ischemia, in which case compression therapy is contraindicated. If the ABI is > 1.3, the result is unreliable and those patients should also be evaluated before considering compression.

Clinicians in the outpatient wound clinic setting should be trained and equipped to measure ABI in a reliable manner. This should be an expected competency, as this test does not need to be performed at a vascular center. ABI measurement is performed using a continuous-wave Doppler (the handheld probe intensifies the sound of the pulse), a sphygmomanometer, and pressure cuffs to measure brachial and ankle systolic pressures. Specific instructions on how to do this have been issued by the Wound, Ostomy and Continence Nurses Society and published in the Ankle
Brachial Index: Quick Reference Guide for Clinicians.
8 The procedure takes 15-20 minutes, but is worth the time, in the opinion of the authors, if compression can be initiated by the end of the visit, as opposed to being delayed by several days (or perhaps weeks) while waiting for other types of assessment. This test has high sensitivity and specificity, and accuracy in diagnosing lower extremity arterial disease is well established.9 The few contraindications for ABI measurement include excruciating pain and the presence of DVT (a duplex ultrasound study can exclude this possibility).


Venous duplex scanning may be necessary to evaluate venous obstruction and valve incompetence, but compression does not need to be delayed.3

Implementation of compression:

Once equipped with the information provided by the assessment, treatment decisions can be made. For an ABI > 0.8 and < 1.3, standard compression (30-40 mmHg) is recommended.3, 10

Experts agree that with a clinical assessment not indicative of severe arterial disease and an ABI > 0.8 and < 1.3, standard compression can be started if the patient can tolerate it. Alternatively, modified (light) compression (20-30 mmHg) can be used first. For an ABI > 0.5 and < 0.8 without claudication or rest pain, modified [light] compression is recommended. If the ABI is > 0.5 and < 0.8, the arterial component does not contraindicate compression. Modified (light) compression can be started, and the patient should be referred to a specialist for further investigation. If pain is present (intermittent claudication or rest pain), compression should not be initiated and the patient should be referred for further evaluation, or the clinician may consider an invasive vascular study.

When not to use compression:

1) When ABI < 0.5.

In cases where the ABI is < 0.5, no compression should be used because there is PAD, and compression could be detrimental to these patients. They should be referred to a vascular center.

2) When ABI > 1.3.

If the ABI is > 1.3, the reading is likely not reliable due to calcified arteries, and other tests should be performed. This typically happens with diabetes; toe pressure determinations will more accurately reflect perfusion.8,11 The direct toe systolic pressure (or toe-brachial pressure index) is more reliable because the digital arteries are rarely heavily calcified.6 These patients should also be referred to a vascular center. Other possible contraindications to compression include acute cellulitis (should be treated with antibiotics for 24 hours before compression), acute congestive heart failure (or myocardial infarction), and acute DVT prior to initiation of anticoagulation.


Various products are available to provide compression; this topic has been reviewed in the literature.12,13 A 2013 Cochrane review14 has concluded that compression is better than having no compression for healing outcomes and that multicomponent compression bandage systems are better than single-component compression. Compression options include dynamic (intermittent pneumatic compression pumps and sleeves) and static compression (stockings and wraps). Specific to static compression wraps, which are used for management of venous hypertension, lymphedema, and venous ulcers to reduce edema and aid return of venous blood to the heart, there are plain and paste bandages, as well as multilayer systems (with two, three, or four layers).14 

Compression bandages are classified as short stretch or long stretch, depending on their elasticity. Sub-bandage pressure (the compression pressure under the bandage) is different, depending on the type of wrap. Short-stretch bandages are made of fibers that stretch 30-60%, and are therefore considered inelastic. They provide low resting pressure and high working pressure. This means the rigid sleeve does not compress the leg at rest, but provides resistance to the expansion of the calf muscle when the patient is walking. Since the pressure is low when the patient is at rest, patient comfort is increased. During patient movement and activity (ie, “work”), the high-dynamic working pressure supports the calf muscle pump, reducing edema and improving venous return.13,15 This is considered the ideal compression bandage (low resting pressure and high working pressure). Long-stretch bandages (made of elastic fibers that can stretch 140-300%) have the opposite effect. They provide high resting pressure when the patient is at rest, because their ability to stretch and tendency to recoil back to the original length exerts a sustained squeeze on the tissue.13 Conversely, they provide low working pressure when the patient is walking or moving because they stretch along with the activity of the calf muscle instead of exerting pressure on it. Due to their limited resistance to calf muscle contraction, long-stretch bandages provide poor edema management.15 These different modes of action are illustrated in the Figure on page 22
Multicomponent bandage systems may contain both high-stiffness (inelastic/short stretch) and low-stiffness (elastic/long stretch) components. 

However, when applied to a leg, a multicomponent system usually functions as a high-stiffness system (eg, Coban 2 Layer Compression System; 3M,Maplewood, MN).3 The authors suggest the use of Coban 2 Compression System for patients with an ABI between 0.8 and 1.3, and the use of Coban 2 Layer Lite Compression System for patients with an ABI ≥ 0.5 who need a modified, lighter compression (or those who are new to compression or may not initially tolerate standard compression). This system can also help these patients gradually become more comfortable with compression. The safety of lighter compression provided by inelastic systems in patients with an ABI between 0.5 and 0.8 has been demonstrated and published.16-19 The technology behind Coban 2 Compression System and Coban 2 Lite Compression System is based on the use of two layers that combine to create a thin, lightweight, breathable inelastic sleeve conforming to the limb contour and providing a consistent proper pressure profile to reduce edema.20 In addition, these products display a low profile, allowing patients to wear their regular shoes, and offer less slippage,21 encouraging compliance. 


Despite the numerous clinical guidelines advocating the use of compression therapy as the “gold standard” for VLU treatment, many patients do not receive appropriate compression or do not receive it in a timely manner.22 This is a serious problem for VLU management. The reasons for this include lack of knowledge and/or confidence by clinicians.3,23 The situation can be effectively addressed through training programs, which will in turn improve the healing time of  VLUs.24

Various pathologies may cause chronic leg ulcers. It is estimated that 70% or more of these ulcers are related to venous disease (chronic venous insufficiency), while approximately 20% are caused by arterial insufficiency or mixed arteriovenous disease.6 Leg ulcers are notoriously slow to heal and, even when best practices are implemented, only 50-75% heal in six months.6 Chronic venous insufficiency is caused by abnormalities in the venous valves, resulting in venous reflux. Compression therapy is effective because it improves venous return, and thereby helps to reduce the effects of chronic venous insufficiency. It also reduces edema by opposing leakage of fluid from capillaries into tissue and by encouraging lymphatic drainage. This improves skin blood flow, which in turn aids healing.3 Lack of compression or nonadherence to therapy are listed as factors that delay healing (along with large wound size, long ulcer duration, involvement of all three venous valvular systems, older age, being overweight, and a history of DVT).6,25 On the other hand, if a leg ulcer is caused by arterial insufficiency, compression would be contraindicated because it could further reduce distal blood flow. In reality, many leg ulcers have both a venous and an arterial component with venous and arterial disease present simultaneously. When the venous component dominates and the arterial component is not severe, compression therapy is still beneficial. In fact, several studies have been published on the safe use of modified compression for mixed arteriovenous disease, reflected by an ABI between 0.5 and 0.8.16-19 


Clinical judgment based on findings from a comprehensive assessment and patient history should guide the treatment decision. If the ABI is adequate and no “red flags” have emerged in the clinical assessment as contraindications for compression therapy, standard or modified (light) compression can be initiated while waiting for the results of further investigations. The earlier that compression therapy can be initiated, the better the outcome will be for the patient. As stated in the 2015 consensus recommendations,3 “Compression therapy is an active therapy that is generally underused. But when used on the right patient in the right way so that concordance is maintained, it is the key to healing active ulceration.” Since the duration of an ulcer has been consistently identified as a risk factor associated with delayed healing,25 timely implementation of the appropriate therapy is simply good practice. 

Stéphanie Bernatchez is a scientific and medical writer for 3M. Lynn Peterson is product service specialist at 3M. Caroline E. Fife is chief medical officer at Intellicure Inc.; executive director of the U.S. Wound Registry; medical director of St. Luke’s Wound Clinic, The Woodlands, TX; and co-chair of the Alliance of Wound Care Stakeholders.


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2. Thomas DR. Managing venous stasis disease and ulcers. Clin Geriatr Med. 2013;29(2):415-24.

3. Harding K, Dowsett C, Fias L, et al. Simplifying venous leg ulcer management. Consensus recommendations. Wounds Int. 2015;6(2):54.

4. Fife CE, Carter MJ, Walker D. Why is it so hard to do the right thing in wound care? Wound Repair Regen. 2010;18(2):154-8.

5. Franks PJ, Barker J, Collier M, et al. Management of patients with venous leg ulcers: challenges and current best practice. J Wound Care. 2016;25(6 Suppl):S1-S67.

6. Alavi A, Sibbald RG, Phillips TJ, et al. What's new: management of venous leg ulcers: approach to venous leg ulcers. J Am Acad Dermatol. 2016;74(4):627-40.

7. Harding K. Challenging passivity in venous leg ulcer care - the ABC model of management. Int Wound J. 2016;13(6):1378-84.

8. WOCN Clinical Practice Wound Subcommittee, 2005. Ankle brachial index: quick reference guide for clinicians. J Wound Ostomy Continence Nurs. 2012;39(2 Suppl):S21-S29.

9. Grenon SM, Gagnon J, Hsiang Y. Video in clinical medicine. Ankle-brachial index for assessment of peripheral arterial disease. N Engl J Med. 2009;361(19):e40.

10. Ratliff CR, Yates S, McNichol L, Gray M. Compression for primary prevention, treatment, and prevention of recurrence of venous leg ulcers: an evidence-and consensus-based algorithm for care across the continuum. J Wound Ostomy Continence Nurs. 2016;43(4):347-64.

11. Sacks D, Bakal CW, Beatty PT, et al. Position statement on the use of the ankle brachial index in the evaluation of patients with peripheral vascular disease. a consensus statement developed by the standards division of the society of interventional radiology. J Vasc Interv Radiol. 2003;14(9 Pt2):S389.

12. Partsch H. Compression therapy in leg ulcers. Rev Vascular Med. 2013;1(1):9-14.

13. Woo KY, Cowie BJ. Understanding compression for venous leg ulcers. Nursing. 2013; 43(1):66-8.

14. O'Meara S, Cullum NA, Nelson EA, Dumville JC. Compression for venous leg ulcers (review). Cochrane Database Syst Rev. 2013(3):1-196.

15. Bjork R. The long and short of it: understanding compression bandaging. what you need to know about long-stretch and short-stretch compression bandaging in patients with peripheral arterial disease. Wound Care Advisor. 2013;2(6):12-5.

16. Schuren J, Annelies V, Allen JO. Venous leg ulcer patients with low ABPIs: how much pressure is safe and tolerable? EWMA Journal. 2010;10(3):29-34.

17. Ladwig A, Haase H, Bichel J, Schuren J, Jünger M. Compression therapy of leg ulcers with PAOD. Phlebology. 2014;29(1 Suppl):7-12.

18. Mosti G, Iabichella ML, Partsch H. Compression therapy in mixed ulcers increases venous output and arterial perfusion. J Vasc Surg. 2012;55(1):122-8.

19. Mosti G. Compression in mixed ulcers: venous side. Phlebology. 2014;29(1 Suppl):13-7.

20. Schuren J, Bernatchez SF, Tucker J, Schnobrich E, Parks PJ. 3M coban 2 layer compression therapy: intelligent compression dynamics to suit different patient needs. Adv Wound Care (New Rochelle). 2012;1(6):255-8.

21. Moffatt CJ, Edwards L, Collier M, et al. A randomized controlled 8-week crossover clinical evaluation of the 3M coban 2 layer compression system versus profore to evaluate the product performance in patients with venous leg ulcers. Int Wound J. 2008;5(2):267-9.

22. Vowden P, Vowden K. Are we fully implementing guidelines and working within a multidisciplinary team when managing venous leg ulceration? Wounds UK. 2013;9(2):17-20.

23. Ylönen M, Stolt M, Leino-Kilpi H, Suhonen R. Nurses' knowledge about venous leg ulcer care: a literature review. Int Nurs Rev. 2014;61(2):194-202.

24. Mooij MC, Huisman LC. Chronic leg ulcer: does a patient always get a correct diagnosis and adequate treatment? Phlebology. 2016;31(1 Suppl):68-73.

25. Parker CN, Finlayson KJ, Shuter P, Edwards HE. Risk factors for delayed healing in venous leg ulcers: a review of the literature. Int J Clin Pract. 2015;69(9):967-77.

Feature Article
Stephanie F. Bernatchez, PhD; Lynn Peterson, RN, BSN, WOCN; & Caroline E. Fife, MD, FAAFP, CWS, FUHM
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