Volume 45 Number 3

Introduction

Venous leg ulcers (VLUs) are among the most common chronic wounds affecting the lower limbs, arising as a complication of chronic venous insufficiency (CVI).¹ The gold standard for VLU treatment involves compression therapy combined with appropriate skin and wound management.² However, VLUs are prone to recurrence, recalcitrant healing and infection due to factors such as inadequate or noncompliance with compression therapy, suboptimal wound care, and poor biofilm management.³

In Singapore, the prevalence of VLUs was 15 per 100,000 people in 2017, increasing to 38 per 100,000 among those aged 50 and older.¹ A recent study revealed that the cost of compression therapy for VLUs ranged from SGD 80 to SGD 41,713.07, depending on the complexity and duration of treatment.⁴

International best practice guidelines have recommended the use of antimicrobial wound products, such as topical silver-impregnated dressings, to manage infections and promote healing.^2,5,6 Nanocrystalline silver dressings (NCSD) have demonstrated high efficacy in treating local wound infections caused by highly resistant bacteria or antibiotic-resistant organisms.⁷

In recent years, global concerns about antimicrobial resistance have grown, alongside increased awareness of how to address this critical issue. While much of the discussion has centered on the proper use of antibiotics, it is essential to ensure the appropriate use of all antimicrobials to minimise the risk of silver resistance.⁷ A step-up or step-down approach is recommended for antimicrobial wound product usage.^5,6 Clinicians are advised to regularly assess and reassess wounds to ensure antimicrobial treatments remain clinically beneficial and are used for an appropriate duration, typically two to four weeks.^5,6,8 While NCSD is recommended as an early intervention for managing local infections and potentially reducing the duration of antibiotic therapy for patients,^7,8 concerns remain about the cytotoxic effects, which may inhibit fibroblast activity—an essential process for wound healing.^9,10

This single case study aims to evaluate the efficacy of bio-electric dressings (BED) in healing an infected, recalcitrant VLU. This case study was guided by the CARE guidelines framework.¹¹ The intervention served as a step-down approach following surgical debridement and four weeks of treatment with NCSD, during which the healing process fluctuated between periods of progress and stagnation.

Background

The patient, a 77-year-old female living alone, uses a walking stick and has kyphosis. She has had a left lower limb VLU since 2017 and previously underwent a VenaSeal procedure for long saphenous vein (LSV) insufficiency. She experienced recurrent ulcer episodes, intermittently managed with 2-layer and 4-layer bandages. Her medical history includes hypertension, hyperlipidemia, hyperthyroidism, leiomyosarcoma, lichen amyloidosis and stasis dermatitis. On 10 October 2022, a CVI scan revealed great saphenous vein (GSV) tributary reflux with popliteal vein reflux. The patient’s wound care included povidone iodine-impregnated dressing and 2-layer compression bandaging, leading to complete healing of the VLU. Following this, Class II compression stockings were prescribed for maintenance. On 23 November 2023, a repeat CVI scan revealed GSV reflux. However, the wound recurred on 18 March 2024, prompting treatment with hydrogel dressing and the reintroduction of two-layer compression bandaging. On 15 April 2024, the wound care regimen was updated to hydrofiber silver dressing combined with two-layer compression bandaging. By 10 June 2024, the VLU was fully healed.

Presentation

On 28 August 2024, the patient’s VLU recurred, leading to admission for surgical wound debridement. The left anterior ankle wound presented with sloughy, greyish-tinged tissue. Debridement was performed until healthy bleeding tissue was achieved, and wound tissue was sent for aerobic culture. The anterior ankle wound measured 7.1cm x 5.5cm, revealing a pinkish-red fibrotic wound bed with a thin layer of fibrin slough (Figure 1). While waiting for the wound culture results, the wound was managed with Cadexomer-iodine ointment dressing only.

Figure 1. Anterior ankle VLU post-surgical debridement

On 30 August 2024, tissue culture results identified three bacterial pathogens: Pseudomonas aeruginosa, Group B Streptococcus, and Escherichia coli. The patient was discharged on 31 August 2024, with instructions to continue Cadexomer iodine ointment dressing and a two-week antibiotic course of oral Ciprofloxacin and Clindamycin. On 2 September 2024, vascular surgeons and a vascular specialty nurse reviewed the patient. The wound care regimen was updated to NCSD with a superabsorbent pad, and 2-layer (40mmHg) compression bandaging was reinitiated. The patient was scheduled for weekly dressing and compression bandage changes with the vascular speciality nurse.

Discussion/interventions

The patient underwent weekly dressing changes at the outpatient wound clinic, maintaining the same treatment modality for four weeks. Wound care was consistently managed by the same vascular specialty nurse during each visit.

Chronic VLUs often experience delayed healing due to elevated inflammatory mediators, rather than a lack of growth factors.¹² Addressing the bioburden is essential to prevent further wound deterioration and increase the efficacy of wound care modalities.⁵ While wound bed preparation, including wound cleansing and debridement, is critical for promoting healing by enabling the development of a functional extracellular matrix^12,13, it can also disrupt and prevent biofilm reformation. The vascular wound nurse incorporated two wound management strategies for managing this complex venous leg ulcer: the TIME framework and wound hygiene.

To support this practice, conservative sharp wound debridement was performed using a scalpel, along with thorough cleansing of the wound bed and peri-wound skin at each dressing change. Then 2-layer compression bandage was applied and pressure was maintained via the UrgoK2® layer system, which comprises inelastic and elastic bandages: the first layer is a soft-padded short stretch, and the second layer is a cohesive long stretch, delivering a compression pressure of 40mmHg.

After 32 days of treatment, the anterior ankle wound measured 5.5cm x 3cm (Figure 2). During the outpatient clinic visit on 30 September 2024, the patient expressed distress over the slow wound recovery, despite adherence to compression bandaging (maintaining dry bandages and elevating the legs during rest). A new treatment approach was proposed and agreed upon by the patient. The dressing was switched to BED covered with a superabsorbent dressing, and secured with 2-layer compression bandaging.

Figure 2. Anterior ankle VLU after 32 days of NCSD prior to the use of BED

Within seven days, the VLU wound presented with a few islands of epithelial tissue over the wound bed. The wound measured 4.9cm x 3.1cm (Figure 3a,b,c). The patient was on the BED dressing in total for 21 days. Patient tolerated the dressing changes well. During the use of BED, patient was comfortable and did not experience any adverse events. During each dressing change, the patient said pain was tolerable during the procedure. The anterior ankle VLU epithelialised and measured 6cm x 5cm. A large area of new epithelial skin was present over the wound bed, suggestive of total wound closure being achieved. Patient was discontinued from the BED dressing. The healed wound was moisturised with emollient and the patient was placed on Class II compression stockings. Patient was reviewed again after a week at the wound clinic. The VLU has fully healed, leaving a scar with minimal residual hyperpigmentation and hyperkeratosis at the anterior ankle (Figure 4).

Figure 3a. Anterior ankle VLU after seven days use of BED;
3b. Anterior ankle VLU after 14 days; 3c. Anterior ankle VLU after 21 days

Figure 4. Anterior ankle VLU healed

Wound healing is a complex process that requires comprehensive management for effective care. A holistic approach to wound care should focus on reducing bioburden, creating an optimal healing environment, and supporting the host’s natural healing response.⁵

In chronic wound management, appropriate use of silver antimicrobial dressings can effectively treat wound infections, prevent biofilm formation, and potentially reduce the duration of antibiotic use.⁸ NCSD, with their proven antimicrobial efficacy, have demonstrated the ability to reduce antibiotic usage, shorten hospital stays, lower treatment costs, and decrease the prevalence of antibiotic-resistant organisms (Table 1).⁸ However, emphasis should be placed on the recommended 2–4 weeks treatment window, with regular reassessment and evaluation to minimise impact on antimicrobial or silver resistance.^{5, 6, 8} Although there is no strong evidence that silver resistance directly leads to treatment ineffectiveness, the concentration of silver in the dressing needs to be considered. When biofilms form they can exhibit higher tolerance to antibiotics and require 10 to 100 times higher concentrations of silver to eradicate planktonic bacteria effectively.⁷ This means that silver dressings with concentrations less than 60ppm may not be effective for biofilm management.¹⁴ Another consideration is that most silver dressings containing concentrations of above 70ppm, which is cytotoxic to keratinocytes and fibroblasts that contribute to wound healing.¹⁵

In recent years, a novel wound modality, BED, has garnered attention as the only dressing that utilises electrical principles for biofilm management (Table 1).^16,17 BED is a single-layer polyester dressing with a matrix of silver and zinc dots printed on one side. BED generates low-voltage electricity through silver (Ag+) and zinc (Zn+) ions when in contact with moisture or exudate. The Ag+ dots measure 2mm in diameter, while the Zn+ dots are 1mm.¹⁶ When activated by wound exudates or exogenous fluids like normal saline, it delivers a voltage of 0.5–0.9 volts.¹⁸ The micro electrical charges released into the wound bed enhance the electric field to accelerate the wound healing. BED has proven effective in eliminating several multidrug-resistant microorganisms, including Methicillin-resistant Staphylococcus aureus, Klebsiella pneumoniae, and Pseudomonas aeruginosa MDR strains, as well as common Gram-negative and Gram-positive bacteria.¹⁸ Biofilm infections often complicate non-healing skin ulcers, with Pseudomonas aeruginosa playing a key role in delaying the healing of leg ulcers. BED has shown effectiveness in eliminating and disrupting Pseudomonas aeruginosa biofilm.¹⁴

Table 1. Wound products and intended action

BED is non-cytotoxic and utilises weak electrical activity to disrupt biofilm formation and activity, without high silver concentration. BED impedes biofilm formation and aggregation by limiting quorum sensing activities, and it can also suppress planktonic growth.^14,16,19 Additionally, BED features a unique mechanism that accelerates keratinocyte migration, thereby facilitating wound closure.¹⁴ Chronic wound healing is often delayed due to prolonged or persistent inflammation, which is linked to biofilm formation. Nevertheless, BED can limit biofilm formation, reduce inflammation in keratinocytes, and promote migration, ultimately leading to epithelialisation and wound closure.¹⁹ A randomised controlled trial conducted by Chan et al in 2023 has proven and demonstrated that BED significantly accelerates wound healing by reducing and preventing biofilm formation.¹⁷ Similarly, in a case report, BED dressing was used beneath compression bandaging for VLU, achieving complete healing from an initial size of 10cm² before treatment.²⁰ Unlike some silver dressings, BED does not stain wounds and is low-adherent, allowing for non-traumatic removal. However, based on our experience with the use of BED on highly exudative VLUs, it appeared unsuitable likely due to its lower or limited vertical wicking capability or low moisture vapor transmission rate (MVTR), which causes peri-wound maceration, even when superabsorbent or foam dressings were used as secondary dressing. There are currently no studies available that provide evidence or insights into BED’s MVTR or wicking capability. Exploring the wicking capability of BED in future research could yield significant benefits.

When managing infected or chronic wounds, it is crucial to focus on cleansing, wound bed preparation, wound edge care, and peri-wound skin hygiene before applying dressings.^5,6 Peri-wound skin issues, such as dry skin scales, hyperkeratotic plaques, or calluses with debris, can create an environment conducive to biofilm formation.²¹ In particular, the wound edge often harbors active biofilm. Neglecting proper care of the wound edge and peri-wound area can result in delayed healing, increased wound size, a higher risk of infection, elevated treatment costs, pain or discomfort, and a diminished quality of life. Therefore, effective wound management should encompass thorough cleansing, skin protection, exudate control, and the maintenance of a moist wound healing environment.^21,22

Similarly, an effective management of VLUs requires meticulous care of the wound edge and peri-wound skin, as these areas are crucial for wound size reduction, overall healing progress, and minimising biofilm formation. Thorough cleaning and refashioning of the wound edge to achieve pinpoint bleeding is particularly beneficial.⁶ Following this, implementing a structured skincare regimen, along with measures to protect and prevent damage to the peri-wound area and wound edge caused by wound exudate, is especially important when using compression therapy.^2,21

The efficacy of NCSD in treating this patient’s infected VLU is significant. Following the recommended step-up/step-down antimicrobial wound approach, NCSD was discontinued in week five and replaced with BED, which subsequently healed the ulcer. While the selection of the primary dressing is crucial in treating infected and recalcitrant VLUs, the choice of secondary dressing, wound debridement, management of wound edges, and peri-wound skin care are equally important in promoting healing.

Additionally, proper compression therapy, patient adherence to treatment, and modification of other modifiable risk factors, such as blood sugar optimisation, diet, and adequate rest, are essential. Treatment and follow-up for CVI patients should continue even after the VLU has healed. Patient and caregiver education, regular surveillance, and ongoing compression therapy are vital to prevent recurrence.

What this paper adds

BED holds significant promise in the management of recalcitrant VLUs. By leveraging bioelectric signals, these dressings create a conducive environment for wound healing, promoting cellular activity, reducing inflammation, and addressing microbial challenges that often impede recovery. As an adjunct to standard care, BED offers a novel approach to treating stubborn VLUs, potentially enhancing healing rates and improving patient outcomes, particularly in wounds resistant to conventional therapies.

Conclusion

Based on this case study, BED is effective in accelerating epithelialisation and transitioning wounds from the inflammatory to the proliferative phase. Patients need reliable access to consistent outpatient services for ongoing care and evaluation. Comprehensive investigations and additional interventions are essential for chronic wound care. Education plays a key role, as patients must understand proper wound hygiene, the purpose of specific interventions, and the rationale behind the chosen wound care products. Furthermore, the psychological impact of living with a chronic wound should not be overlooked. Regular assessments should include evaluating mental well-being, with appropriate referrals made to support services as needed.

Acknowledgements

We would like to thank the DMC Clinic Nurses: NC Vir Kaur Gill, ANC Tuang Juan Jang Gracia, SSN Nur Farhana Binte Mohd Ali, PEN Ong Li Li, PEN Teo Mui Huay, PEN Hadigah Bte Mohammed, PEN Nur Amaliyyah Binte Mohd Mocktar and Vascular team doctors for their support. We also like to thank the patient for being supportive of our case study and treatment plans.

Author contribution

Goh Wee Ting and Nanthakumahrie Gunasegaran were involved in conceiving and designing this study, acquiring subjects, collecting data, managing data, and reviewing the manuscript.

Goh Wee Ting and Nanthakumahrie Gunasegaran prepared the manuscript writing.

Fazila Aloweni supervised and reviewed the manuscript.

All authors reviewed and extensively edited the manuscript and approved the final version of this manuscript.

Conflict of interest

The authors declare no conflicts of interest.

Ethics statement

Ethics approval was waived; however, informed written patient consent was obtained for photography.

Funding

The authors received no funding for this study.

Author(s)

Wee Ting Goh
Bachelor of Science (Nursing), Nursing Division,
Singapore General Hospital

Nanthakumahrie Gunasegaran*
Masters of Science (Clinical Leadership), Nursing Division,
Singapore General Hospital
Email nanthakumahrie.gunasegaran@sgh.com.sg

Fazila Aloweni
Masters of Science (Health Research Methodology), Nursing Division, Singapore General Hospital

* Corresponding author

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