Protecting Edges of Venous Ulcers: An Evidence-Based Approach

  Healthy wound edges are described as pink or pearl colored and attached to the underlying tissue. The term “open” is used to describe a wound edge that is capable of generating cells for healing. Movement of cells from the wound edge can be halted when the wound edge closes prematurely. Cell migration can also be compromised when the wound edge is open but excessively hydrated. Due to their unique pathophysiology, venous ulcers are at high risk for moisture-associated skin damage at the wound edge and within surrounding skin. ³

  This article will provide a review of the underlying mechanisms for the changes that are seen at the wound edge and adjacent periwound skin as a result of excessive exposure to moisture. Strategies for skin protection will also be discussed.

The Problem With Moisture

  The stratum corneum is the uppermost layer of the epidermis and provides significant barrier protection. The ideal state for this epidermal layer is dry. When the stratum corneum is exposed to excessive moisture, corneocytes swell, soften, and take on a “soggy” texture with a distinctive color change to white or gray.^4,5 Structural changes cause alterations in stratum corneum permeability. This condition has traditionally been described as maceration; more recently the concept of periwound moisture-associated skin damage (MASD) has been introduced.⁶ Extended overhydration can cause significant structural damage including cracking and fissuring. A reduction in natural moisturizing factor (necessary for barrier health) is observed⁷ and the normally acidic pH of skin shifts into an alkaline range. The net effect of these changes is a compromise of intrinsic skin barrier competence. This potentially increases the likelihood of penetration by irritants, allergens, and microbes. Composition of exudate is also believed to be a factor. Exudate from venous ulcers has been shown to be rich in matrix metalloproteinases and other pro-inflammatory chemicals capable of causing damage independent of moisture.^5,8,9 In addition, overhydrated skin is more susceptible to damage from frictional forces and secondary infection.¹⁰   Not surprisingly, wound exudate is the primary source for excessive epidermal moisture. For venous ulcers, volume of exudate is not only related to local inflammation, but the magnitude of edema as well. Large amounts of exudate can be expected early in the treatment process or when compression is absent or inadequate. As such, periwound MASD can be a likely consequence.¹¹

  Fluid-handling capabilities of compression materials can be another factor contributing to maceration. Most traditional three- and four-multilayer compression systems incorporate a cotton or a synthetic fibrous wrap as the base layer that contacts skin. These materials were originally intended for cast padding and do not wick or transfer fluid. Instead, moisture can be trapped against the skin. The potential for damage can be exacerbated if the clinician does not use a primary dressing and relies on the base layer alone for exudate management.

  Dressing materials, dressing application technique, and dressing change frequency can also promote wound edge and skin damage. Moisture-related skin changes can result when a primary dressing is used but is poorly suited to the volume of drainage. A dressing that is properly selected but improperly prepared or applied can also expose the edge and skin to excess moisture as the dressing absorbs exudate. If not changed at an appropriate interval, absorbent dressings can serve as a source of wetness. Finally, failure to protect the wound edge and adjacent periwound skin with a moisture barrier leaves the skin vulnerable to excessive hydration.¹²

Preventing Periwound MASD

  The significance of edge condition on healing is underscored by inclusion of edge assessment and management in wound bed preparation models.^2,13 Once established, periwound MASD around a venous ulcer may be difficult to resolve, especially if exposure has been prolonged and skin changes are severe. For that reason, prevention should be the focus with the primary clinical objective being reduction and management of exudate. Effective compression is the primary approach to venous ulcer management addressing edema and impacting exudate volume. A conformable low-profile, two-layer system (Coban™ 2 Layer Compression System, 3M™) can provide sustained short-stretch compression that is effective for both ambulatory and sedentary patients.

  Prior to application of the compression bandage, the wound and periwound skin should be cleansed. Cleansing the surrounding skin is essential to remove debris such as exudate, dead skin, crust, or dressing residue. A primary dressing should then be applied over the ulcer for exudate absorption.¹³ Moderate to heavily draining wounds are best managed with absorbent dressing materials. Tegaderm™ High Performance Foam Non-Adhesive Dressing (3M) and Tegaderm™ Silicone Foam Border Dressing (3M) are examples of open-cell polyurethane foam dressings that can be used as primary or cover dressings. They are ideally suited for exudating wounds due to technology that enables rapid wicking and fluid management.

  Wounds with greater depth or drainage may require the addition of an absorbent wound filler such as a calcium alginate dressing (Tegaderm High Integrity Alginate Dressing, 3M). This type of absorbent fibrous dressing should be sized appropriately to the wound margins according to manufacturer’s instructions to prevent overlap of moist or wet dressing onto periwound skin. Hydrating dressing materials such as hydrogels are seldom appropriate. If preferred, wound fillers may be covered with a superabsorber dressing (Tegaderm Superabsorber Dressing, 3M). Both the compression bandage and the dressing should be changed at an interval sufficient to prevent strikethrough or saturation.

  Finally, a protective moisture barrier should be applied to the wound edge and any surrounding skin exposed to wetness.^11,14 Traditionally, moisture barrier creams and ointments containing petrolatum and zinc oxide have been used. While capable of repelling moisture and irritants, many of these products are occlusive and will interfere with skin’s normal transepidermal water loss (TEWL), potentially worsening the problem.¹⁴ At the time of dressing change, removal of ointments and thick creams, especially those containing zinc oxide, can be uncomfortable for patients and can cause mechanical damage to fragile periwound skin. Removal can also be time consuming for direct-care staff.

  Careful consideration of topically applied products is especially important for the venous ulcer population, where increased risk of allergy to topically applied products has been shown.¹⁵ Not surprisingly, vulnerability to potential allergens can be exacerbated when barrier function is compromised. Multi-ingredient cream formulations can contain common sensitizers (eg, preservatives, fragrances).

  A liquid barrier film provides an alternative and advantageous method of edge and periwound protection. ^{6,12,14,16,17} For periwound protection, a product that is non-cytotoxic, hypoallergenic, and indicated for use on intact or damaged skin should be selected. CavilonTM No Sting Barrier Film (3M) contains a unique terpolymer dissolved in an alcohol-free solvent system. When applied to the skin, the solvent evaporates quickly, leaving the terpolymer as a breathable, transparent protective coating. The film is waterproof, enabling it to repel moisture and irritants. Because the barrier film does not require removal, patient discomfort can be minimized and staff time conserved. In addition, the product offers the advantage of protection from adhesives, which can help to prevent medical adhesive-related skin injuries.¹⁸

What Does the Evidence Tell Us?

  Cavilon No Sting Barrier Film is supported by more than 70 pieces of evidence, with numerous studies evaluating its use specifically for wound edge and periwound protection. A meta-analysis analyzed data from 11 controlled trials and concluded the product is a safe and effective barrier to protect the periwound skin of chronic ulcers with benefits including visibility of wound margins, reduction of erythema, pain control, patient comfort, and reduced staff time.¹⁹ Other findings show significant advantages of the barrier film over zinc oxide containing barriers including greater patient comfort (no removal required versus the scrubbing necessary for the zinc barrier); reduced nursing time; ability to visualize the skin for assessment; and better patient and caregiver friendliness.^20,21 Another trial evaluated the effect of Cavilon No Sting Barrier film on the periwound skin of patients living with venous ulcers. A 45% reduction in TEWL (considered an indicator of barrier function) as compared to baseline was found.²² The clinical effectiveness of the film in combination with multilayer compression has also been demonstrated. In a randomized controlled trial of 98 patients,²³ the average reduction in ulcer area after 12 weeks of treatment was statistically greater in patients treated with Cavilon No Sting Barrier Film (83%) as compared to the control group (72%) (P = 0.046). The study concluded the clinical effectiveness of the multilayer compression bandage as measured by percentage reduction of area was increased by the concomitant use of Cavilon No Sting Barrier Film.

Summary

  Periwound MASD does not have to be an inevitable complication of venous ulcer management or management of any heavily draining wound. With careful assessment and recognition of risk, an effective management plan can be implemented. Effective compression, selection of topical dressings appropriate to drainage volume, and use of Cavilon No Sting Barrier Film for protection of wound margins can provide a comprehensive solution to help prevent this troublesome complication.

References

1. Robson MC, et al. Guidelines for the treatment of venous ulcers. Wound Repair Regen. 2006. 14(6): 640-662.

2. Sibbald RG, Orsted HL, Coutts PM, Keast DH. Best practice recommendations for preparing the wound bed: update 2006. Adv in Skin and Wound Care. 2007; 20(7):390-405.

3. Thomas S. The role of dressings in the treatment of moisture-related skin damage. World Wide Wounds. 2008. Accessed online at www.worldwidewounds.com/2008/march/Thomas/Maceration-and-the-role-of-dressings.html.

4. Mayoritz HN, Sims N. Biophysical effects of water and synthetic urine on skin. Adv Skin and Wound Care. 2001;14(6):302-8.

5. Cutting K. Maceration of the skin and wound bed 1: its nature and causes. J of Wound Care. 2002;11(7):275-278.

6. Colwell J, et al. MASD Part 3: peristomal moisture-associated dermatitis and periwound moisture-associated dermatitis. J Wound, Ostomy, Continence Nurs. 2011; 38(5):541-553.

7. Flour M. The pathophysiology of vulnerable skin. World Wide Wounds. Accessed online at www.worldwidewounds.com/2009/September/Flour/vulnerable-skin-1.html.

8. Trengrove NJ, Bielefeldt-Ohmann H, Stacey MC. Mitogeneic activity and cytokine levels in non-healing and chronic leg ulcers. Wound Repair Regen. 2000;8:13-25.

9. Schultz GS, et al. Wound bed preparation: a systematic approach to wound management. Wound Repair Regen. 2003;11:1-28.

10. Foroozan M, et al. Prevalence analysis of fungi in chronic lower extremity ulcers. WOUNDS. 2011;23(3):68-75.

11. Brem H, Kirsner RS, Falanga V. Protocol for the successful treatment of venous ulcers. Am J Surg. 2004; 188(1A Suppl):1-8.

12. Rolstad BS, Bryant RA, Nix DP. Topical Management. In: Bryant RA and Nix DP eds. Acute & Chronic Wounds: Current Management Concepts. 4th ed. St. Louis MO: Elsevier Mosby; 2012: 289-306.

13. Sibbald, Campbell K, Coutts P, Queen D. Intact skin: an integrity not to be lost. Ostomy Wound Manage. 2003 Jun;49(6):27-8, 30, 33 passim, contd.

14. Thomas S. World Wide Wounds. The Role of Dressings in the Treatment of Moisture Related Skin Damage. Accessed online at www.worldwidewounds.com/2008/march/Thomas/Maceration-and-the-role-of-dressings.html.

15. Machet L, et al. Sensitization to topical treatments used in leg ulcers: a meta-analysis (1975-2003) poster presentation. World Union of Wound Healing Societies. (WUWHS). 2008.

16. Lawton, S, Langoen A. Assessing and managing vulnerable periwound skin. Accessed online at www.worldwidewounds.com/2009/October/Lawton-Langoen/vulnerable-skin-2.html.

17. Cutting K. Avoidance and management of peri-wound maceration of the skin. Professional Nurse. 2002;18(1): 33-36.

18. McNichol L, Lund C, Rosen T, Gray M. Medical adhesives and patient safety: state of the science: consensus statements for the assessment, prevention, and treatment of adhesive-related skin injuries. J Wound Ostomy Continence Nurs. 2013;40(4): 365-380.

19. Schuren J, Becker A, Sibbald RG. A liquid film forming acrylate for periwound protection: a systematic review and metal analysis (3M Cavilon No Sting Barrier Film. Int Wound Journal. 2005; 2: 230-238.

20. Coutts P, Queen D, Sibbald RG. Peri-wound skin protection: a comparison of a new skin barrier vs. traditional therapies in wound management. Wound Care Canada. 2003;1(1).

21. Cameron J, Hoffman D, Wilson J, Cherry GJ. Comparison of two peri-wound skin protectants in venous leg ulcers. Wound Care. 2005;14(5):233-6.

22. Dini V, Salibra F, Brillei C, Romanelli M. Instrumental evaluation of the protective effects of a barrier film on surrounding skin in chronic wounds. WOUNDS. 2008; 20(9): 254-257.

23. Serra, N, et al. Effectiveness of the association of multilayer compression therapy and periwound protection with Cavilon (no sting barrier film) in the treatment of venous leg ulcers. Gerokomos. 2010; 21(3):124-130.

Debra Thayer is a senior technical services specialist with 3M Critical & Chronic Care Solutions, St. Paul, MN. She may be reached at 651-733-1447 or dmthayer@mmm.com.