Honey is an ancient remedy for the treatment of infected wounds and was first recognised as a topical antibacterial agent in 1892 (Molan, 2001). !ere are now many published reports describing the effectiveness of honey products in all phases of wound healing, with no adverse effects on the healing process. !is made easy describes the role of Medihoney dressings in the management of hard-to-heal wounds.
Why does healing stall in some wounds?
Normal wound healing is a staged process that comprises inflammation, cell proliferation and tissue remodelling. The inflammatory phase has an essential role in cleaning the wound of bacteria and debris and in initiating the later stages of wound healing.
Most wounds heal uneventfully and in a timely manner, requiring minimal input from clinicians. However, some wounds have the potential to become chronic, where healing is stuck in the inflammatory stage (Boyd et al, 2004). This may be due to the patient’s age and the presence of co-morbidities, as well as factors related to the wound itself such as high bioburden, size, depth, location and duration of the wound (EWMA, 2008).
For wounds that are not progressing, wound bed preparation is essential for effective management. It enables clinicians to remove the barriers that may lead to delayed wound healing, by identifying the presence of infection, devitalised tissue or moisture imbalance (Falanga, 2004).
What are MedihoneyTM dressings?
The MedihoneyTM antibacterial range of dressings include: MedihoneyTM Antibacterial Medical Honey; MedihoneyTM Wound Gel; MedihoneyTM Gel Sheet; MedihoneyTM Apinate Dressing; MedihoneyTM Tulle Dressing and MedihoneyTM Barrier Cream. All products within this range of medical honey dressings are derived from Leptospermum scoparium (manuka).
Additionally, MedihoneyTM Wound Gel contains natural waxes and oils and MedihoneyTM Barrier Cream contains coconut oil, German chamomile flower extract, evening primrose oil, aloe vera and vitamin E. MedihoneyTM Apinate Dressing is a calcium alginate dressing impregnated with manuka honey and MedihoneyTM Tulle Dressing is a non-adherent wound contact dressing with manuka honey. MedihoneyTM Gel Sheet is a flexible dressing with manuka honey and sodium alginate.
All products are sterilised by gamma irradiation, which does not affect the antibacterial properties of honey.
MedihoneyTM products can be considered for use as part of a wound bed preparation protocol to:
- Promote a moist wound environment
- Debride sloughy wounds
- Reduce inflammation
- Reduce bioburden
- Reduce malodour
- Stimulate the immune system.
- How does Manuka honey work?
The role of honey in the management of wounds is based on its antimicrobial properties and its ability to influence wound healing (Molan, 1999). This is achieved in a number of ways:
In laboratory studies, manuka honey has been shown to have an antibacterial action against a broad spectrum of bacteria and fungi, including:
- Staphylococcus aureus (Cooper et al, 2002; Blair et al, 2009)
- Pseudomonas aeruginosa (Cooper and Molan 1999; Blair et al, 2009)
- MRSA, vancomycin-sensitive and vancomycin-resistant enterococci (Cooper et al, 2002; George and Cutting, 2007).
Antibiotic-sensitive strains and their respective antibiotic-resistant strains have also demonstrated similar susceptibility to manuka honey.
Although undiluted honeys possess broad spectrum antibacterial activity due to their high sugar content and lower water content, not all exhibit similar activity on dilution (Cooper and Jenkins, 2009). Manuka honey has a distinctive, heat stable antibacterial component, known as methylglyoxal (MGO) (Mavric et at, 2008). It is formed from dihydroxyacetone, which is typically found in the nectar of manuka flowers (Adams et al, 2008). This allows it to maintain its antibacterial activity even when it comes into contact with wound fluid and becomes diluted.
Structural changes observed by electron microscopy indicate that manuka honey prevents bacterial cell division in Staphylococcus aureus (Henriques et al, 2010) and also in MRSA (Jenkins et al, 2011). The inability to divide, limits the potential of bacteria to establish an infection. Loss of integrity to cell surfaces leading to cell lysis has been reported in Pseudomonas aeruginosa cells exposed to manuka honey (Henriques et al, 2011).
Removal of biofilms and MRSA
Biofilms are now recognised to impede wound healing and there is a need to inhibit their development in wounds (Phillips et al, 2011). Honey containing a high value of MGO (i.e. equivalent to manuka honey) has been shown to inhibit Staphylococcus aureus biofilms (Jervis-Bardy et al, 2011), while laboratory tests have shown that the concentration of manuka honey required to prevent biofilm formation is lower than that required to disrupt established biofilms (Cooper et al, 2011). Inhibition of Pseudomonas aeruginosa biofilms was found to be dependent on contact time and concentration of manuka honey (Okhiria et al, 2009).
Eradication of MRSA from colonised wounds following topical application of manuka honey has been reported in patients with leg ulcers (Dunford et al 2000; Natarajan et al, 2001; Gethin and Cowman, 2005; Chambers 2006), paediatric oncology patients (Blaser et al, 2007) and in patients with maxillofacial wounds (Visavadia et al, 2006). The removal of MRSA from wounds reduces the risk of systemic infection and cross-infection to other individuals.
Reduction in malodour
Patients with exuding and/or infected wounds may experience maladour. The ability of honey to eliminate unpleasant odours from wounds may be due to the inhibition of anaerobic bacteria that are able to ferment amino acids to malodorous organic amines. Honey contains a range of sugars that may be metabolised by bacteria to many odourless products and glucose is used preferentially by most bacteria. Honey has been shown to have a rapid deodorising effect in patients with malodorous fungating wounds, with a reduction in odour within 24 hours (Molan and Betts, 2004; Segovia, 2010) and in leg ulcers (Gethin et al, 2008).
Patients presenting with a wound containing slough and eschar are at increased risk of infection as the devitalised tissue provides a focus for bacteria and is a significant barrier to healing. Wounds that are not progressing require repeated debridement to remove necrotic and sloughy tissue to establish a healthy wound bed (Falanga, 2004).
Honey provides an autolytic debriding effect whereby the osmotic action of honey encourages lymph fluid to rehydrate devitalised tissue, helping to remove sloughy and necrotic tissue by moving fluid away from the wound bed (Gethin et al, 2008).
Chronic wounds have increased inflammation, giving rise to elevated levels of proteases that appear to degrade the extracellular matrix components, growth factors and receptors that are essential for healing. Manuka honey has a low pH, which may help to achieve sub-optimal levels at the wound surface to control protease activity in the wound (Gethin, 2007). This may promote healing, with evidence that a low pH wound environment may be associated with a reduction in wound size (Gethin et al, 2008). It is likely that the antioxidants in honey also confer anti-inflammatory influences by scavenging free radicals that arise in both acute and chronic wounds (Henriques et al, 2006).
Manuka honey stimulates the immune system to produce pro-inflammatory cytokines, which are important for wound healing. It is likely this stimulation of the immune system helps to promote progression towards healing (Tonks et al, 2007).