Abstract：

This series of four case studies focuses on patients with difficult-to-debride wounds who were treated with Manuka honey dressing , which is impregnated with 100% pure, medical-grade manuka honey. Manuka honey dressing is indicated for autolytic debridement of necrosis and slough, to encourage granulation and epithelialisation, and can be used on wounds with any level of exudate when used with an appropriate secondary dressing.

Keywords：

 Antimicrobial activity, Debridement, Manuka honey dressing, Necrosis Slough

Introduction：

The three main considerations for optimal wound bed preparation are regular debridement to reduce devitalised tissue and encourage formation of healthy granulation tissue, restoration of bacterial balance and promotion of a moist wound-healing environment through exudate management. Honey provides a moist wound-healing environment, and is antimicrobial, de-odourising, anti-inflammatory/ antioxidant and debriding — all of which address the key issues in wound bed preparation and bioburden management to promote healing in chronic wounds. Honey’s multimodal action justifies its use in a variety of wounds, addresses multiple clinical factors and eliminates the need for multiple products, making it a safe and easy treatment option.

The biochemical and antimicrobial components of various honeys differ depending on factors such as floral source, climate and harvesting conditions . Medical-grade honeys designed for clinical use are specially treated to destroy bacteria and contaminants, are from specific, traceable sources and have proven antimicrobial activity . Clinicians should be aware that the antimicrobial potency of honey products varies .

Honey facilitates autolytic debridement by creating moist conditions, although it has also been suggested that the sugar content of honey is involved in activating proteases, which aid the debridement process . Honey may also promote autolytic debridement by causing an enzymatic action that activates plasmin, which disintegrates blood clots that bind necrotic tissue to the wound bed .

A particular kind of honey made from the nectar of the manuka plant (Leptospermum scoparium) found in New Zealand has been shown to be particularly effective in wound bed preparation. Manuka honey is particularly useful in facilitating wound cleansing and autolytic debridement due to its high osmolarity, promoting a moist wound environment and creating an acidic environment conducive to healing .

Case1： 

Ms B, a 70-year-old woman, presented to accident and emergency following a prior mass bowel resection and colostomy formation that had resulted in a dehisced abdominal wound.

The wound was 3 weeks old and measured 18 cm × 10 cm, and the colostomy was at risk of leaking into the wound. Wound pain was rated 5 on a visual analogue scale (VAS; 1–10). Slough covered 75% of the wound bed, with some necrotic tissue and granulation tissue also present. Surgical sutures were visible. Exudate levels were moderate. Antibiotics were initiated; however, they loosen the colostomy discharge, which then poses greater risk of leakage and infection.

To lift the slough and ready the wound for negative pressure wound therapy,  Manuka honey dressing was initiated along with a gel adhesive hydrocellular foam dressing to protect the periwound area and achieve a protective seal from potential colostomy leaks. Dressing changes were scheduled every 2 days, or more frequently if colostomy leakage occurred. After 1 week, wound size remained the same, however the slough had reduced and was beginning to lift from the wound and necrotic tissue now comprised 50–75% (Figure 1a). Wound-related pain was rated as 3 on the VAS. The dressing regimen was deemed effective and continued unchanged. In addition, a colostomy nurse was scheduled to address the leakage before the next wound assessment.

At week 2, the wound appeared larger due to the debridement of all necrotic tissue. Slough covered just over 50% of the wound, and the rest was granulation tissue. The patient reported no pain, and said that she was feeling much happier due to the improvement in the wound and the resolution of colostomy leakage. The dressing regimen was deemed effective and continued unchanged, with dressing changes extended to every 3 days.

After 3 weeks, wound size reduced to 12cm × 8cm (47% reduction since presentation), exudate levels were low, there was no wound- or dressingrelated pain and the wound remained infectionfree despite occasional leakage from the colostomy. Granulation tissue covered two-thirds of the wound bed and slough the remaining third (Figure 1b). The dressing regimen continued unchanged.

After 4 weeks, the wound measured 9cm × 5cm (75% reduction since presentation), with >75% granulation tissue and minimal slough (Figure 1c). As the goals for its use had been achieved, Manuka honey dressing 

was discontinued and alignate fibre dressing was initiated to manage the low exudate level and promote further granulation and wound closure.

Case2：

Ms W is a 74-year-old woman who was immobile due to a stroke. She had well-controlled diabetes, and her diet was good. She developed a sacral pressure ulcer (PU) from a wheelchair cushion that was not fit for purpose during the course of a day out.

On presentation, the PU was ungradable due to nectrotic tissue obscuring the extent of the ulcer (ultimately judged to be category IV). The PU was 2 weeks old and measured 6 cm × 7 cm. There was no pain associated with the wound, which had previously been treated with a hydrocolloid dressing . The wound area comprised >75% necrotic tissue that was lifting at the edges and the rest was slough. It was determined that Manuka honey dressing should be initiated to debride the wound. A gel adhesive hydrocellular foam dressingwas used as a secondary dressing to manage exudate. A barrier film was applied to protect the periwound area. Dressing changes were scheduled for every 3 days, or more frequently depending on exudate levels. Ms W’s blood sugar levels were closely monitored.

After 1 week, the wound size had not changed and necrotic tissue remained at >75% of the wound bed but was lifting. The dressing regimen continued unchanged. The clinician reported that the dressing was easy to apply after it had been wetted, although it was sticky, meaning that gloves may have needed changing before applying the secondary dressing.

At week 2, necrosis made up 25% of the wound bed and was lifting, with approximately 50% slough and the remaining quarter granulation tissue (Figure 2a). The wound size remained the same. The dressing regimen was maintained, but the secondary dressing was changed to an absorbent foam adhesive dressing to achieve a better seal. After 3 weeks, the wound had increased in size due to the lifting of almost all the necrotic tissue, with granulation tissue in 50% of the wound bed and <25% slough. To complete debridement, the dressing regimen was maintained, but with dressing changes extended to every 4 days.

At week 4, the wound had not changed in size but granulation tissue was present in >75% of the wound bed, with some remaining necrosis and no slough (Figure 2b). The dressing regimen was maintained as it was expected that the wound would reduce in size as debridement was completed and granulation progressed to epithelisation.

Case3：

Ms B is a 96-year-old woman who had fractured the neck of her femur and required a hip replacement. She had chronic obstructive pulmonary disease, but had been independent and mobile before the fracture and surgery. After the procedure, she took up residence in a nursing home and a necrotic heel ulcer developed.

On presentation, the wound was ungradable due to nectrotic tissue obscuring the extent of the ulcer. The 4-week-old wound covered the entire heel and had received no prior treatment. The heel was warm and erythema was present around the wound edges. There was no exudate. The patient reported wound-related pain as 9 on a VAS.

To debride the necrosis and address the local infection, Manuka honey gel was initiated. A pad and bandage were used as secondary dressings to absorb exudate that was expected to arise as the necrosis began to lift with gel treatment. Dressing changes were scheduled daily.

After 1 week, the wound size had not changed, and the wound bed was still covered by necrotic tissue (Figure 3a). Wound-related pain and pain at dressing change were both rated 5 on the VAS; the patient was taking paracetamol 4-hourly and Tramadol for analgesia. To accelerate debridement, Manuka honey dressing was initiated in favour of the Manuka honey gel. The secondary dressing regimen was continued. To allow the honey more contact time with the necrotic tissue, dressing changes were decreased to every 2 days.

At week 2, signs of local infection had not reduced, but necrosis had reduced to 75% of the wound bed, with the rest covered by slough (Figure 3b). Wound size, wound-related pain and pain at dressing change were unchanged. The Manuka honey dressing was judged to be easier to keep on the wound and more effective in penetrating the necrotic tissue than the gel had been, so the dressing regimen was maintained, with dressing changes decreased to every 3 days and analgesia increased.

After 3 weeks, the wound size remained static but granulation tissue had appeared at the wound margins. Necrotic tissue had reduced to approximately 50% of the wound bed, with slough comprising the rest (Figure 3c). Wound- and dressing removal-related pain had both reduced to 3 on the VAS, and the patient’s analgesia was reduced. The dressing regimen continued unchanged.

At week 4, wound size remained static but approximately 50% of the wound bed was comprised of granulation tissue and 50% slough. Wound- and dressing change-related pain had not reduced, but the patient no longer required analgesia. The dressing regimen was deemed effective and continued unchanged.

Figure 3. Ms B’s necrotic heel ulcer at (a) 1, (b) 2 and (c) 4 weeks after presentation.

Case4：

Ms H, an 82-year-old woman, is a nursing home resident with multiple sclerosis who developed an ungradable PU on her sacrum. Her diet and general state of health were poor.

On presentation, the PU was 3 weeks old with 100% necrotic tissue coverage. To-date, a hydrogel dressing had been used to treat the wound, exudate levels were moderate and there were no signs of local infection. There was no reported wound-related pain. Manuka honey dressing was initiated, along with a foam secondary dressing to manage exudate, with dressing changes scheduled every 4 days.

After 1 week, wound size had not changed but the necrosis had softened and was moving inward from the wound edges. Although malodour had developed, there were no clinical signs of infection. As a precaution, a swab was taken. The dressing regimen was maintained, with changes scheduled every 3 days, to give the honey more time to exert its effect.

At week 2, the necrosis covered approximately 25% of the wound bed, the rest was slough or exposed wound bed (Figure 4a). Wound size appeared to be increasing due to a reduction in necrosis, exposing its true extent. No culturable organisms were found, so it was determined that the malodour reported could be attributable to the smell of softened necrotic tissue. Manuka honey dressing and change frequency was maintained, but the secondary dressing was changed to an absorbent foam to manage exudate.

After 3 weeks, the malodour resolved, necrotic tissue was no longer present, and slough covered 25– 50% of the wound bed. Granulation tissue was not present, but a clean, healthy wound bed was exposed (Figure 4b). The dressing regimen was continued unchanged, but the secondary dressing was changed to a foam as there was a reduction in the amount exudate.

At week 4, no slough was present and granulation had commenced (Figure 4c). Manuka honey dressing had achieved its purpose and negative pressure wound therapy was commenced to close the wound.

Discussion：

Debridement was successful in all four cases, including in wounds that initially presented with 1% necrosis. Ms B ended the 4-week trial not only fully debrided, but with wound size reduced by 75% from initial presentation. In the case, debridement was effective and the antimicrobial properties of Manuka honey dressing may have helped prevent infection in an anatomical area prone to colonisation. The 100% necrosis cover in Ms B was fully debrided by the end of 4 weeks’ treatment. In Ms H, despite a slow start, the wound was fully debrided and ready to move on to negative pressure wound therapy by the end of the trial.

 In all cases Manuka honey dressing was found to be easy to use and apply, and effective once given time to soften necrotic tissue. Although the dressing is inherently sticky, it did not leave debris in any of the wounds. Furthermore, pain decreased with the use of Manuka honey dressing in the patients who reported wound-related pain.

Conclusion：

Honey is an effective and viable option for debridement and the maintenance of an optimal environment for wound healing. Manuka honey dressing in particular has been shown to safely and effectively debride wounds that are not appropriate for sharp debridement, along with promoting healing in a multimodal fashion. 

Reference：

CALLAGHAN, ROSIE. "Treating difficult-to-debride wounds using a manuka honey dressing: a case study evaluation." Wounds UK 10.2 (2014).