VOL: 96, ISSUE: 49, PAGE NO: 36
Peter Molan, PhD, BSc, is associate professor of biochemistry and director of the Honey Research Unit, University of Waikato, Hamilton, New Zealand
Julie Betts, RGON, AdDipN, is wound resource nurse, community services, Health Waikato Ltd, Hamilton, New Zealand
Honey is increasingly being used as a dressing for infected wounds (Molan, 1999). Interest in its antibacterial properties has arisen mainly as a result of accounts of its inhibitory action against common wound-infecting species of bacteria (Willix et al, 1992; Cooper and Molan, 1999; Cooper et al, 1999), including methicillin-resistant Staphylococcus aureus (Allen et al, 2000).
More general reports of its effectiveness in managing a wide range of wounds (Molan, 1999), particularly where conventional treatments have failed (Dunford et al, 2000), have also contributed to interest in its use.
There is, however, a lack of awareness among clinicians of the wide variations in the antibacterial activity of honey (Molan, 1992), which is often compounded by a failure to use dressing procedures that keep sufficient levels of honey in contact with the wound. In many cases this means that the full potential of the treatment is not realised.
This article aims to pass on the experience gained from the widespread clinical use of honey in New Zealand and the work carried out by the country’s Honey Research Unit.
The ancient physicians apparently knew that only certain types of honey should be used therapeutically (Gunther, 1934). More recent microbiological studies have shown huge differences in the potency of the antibacterial activity of various honeys (Molan, 1992), with the activity of many being no greater than that which can be attributed to their sugar content.
In each of these studies the minimum inhibitory concentration (MIC) of a variety of honeys was tested against the same strain of bacteria, with the resultant values ranging from 25% to 0.25%, 20% to 0.6% and 50% to 1.5%.
In another study the antibacterial activity of various honeys against S. aureus was compared with that of phenol, a standard antiseptic, and found to range from the equivalent of 2% phenol to 58% phenol (Allen et al, 1991).
The main antibacterial component of honey is hydrogen peroxide, which is produced by enzymatic action. But the enzyme responsible is easily deactivated by heating (Molan, 1992), so processed honey often has a low activity. Although the use of hydrogen peroxide as an antiseptic is controversial because of its inflammatory effects, that in honey is continuously produced at a low level - about 1,000th of that in 3% hydrogen peroxide.
Our research also suggests that antioxidant components in honey inhibit the generation of free radicals that is found in hydrogen peroxide antiseptic.
Clinical experience of treating infected wounds with honey shows that the best results are achieved when the honey selected has a high level of antibacterial activity.
Various brands of honey with standardised levels of antibacterial activity are commercially available from manufacturers in New Zealand and Australia. These are all leptospermum honey, commonly known as manuka honey, which has an unusually high level of plant-derived non-peroxide antibacterial activity.
In New Zealand, this natural non-peroxide antibacterial activity is rated on a Unique Manuka Factor scale. For example, UMF 10 is equivalent in antibacterial activity to 10% phenol. Alternatively, a local honey with the highest level of antibacterial activity can be used after its potency has been checked in a microbiology laboratory.
Some nurses may be concerned about the risk of raw honey infecting a wound. Although none of the many reports on the clinical use of honey on open wounds used sterilised honey, its application did not result in any type of infection (Molan, 1999).
There is also a perceived risk of wound botulism resulting from the presence of Clostridium botulinum spores in honey (Mossel, 1980). If clinicians prefer to use sterile products, honey that has been treated by gamma irradiation is available. This processing kills clostridial spores without the loss of antibacterial activity (Molan and Allen, 1996).
No comparative cost analyses have been carried out but experience indicates that although there is not much difference in the unit costs of honey and other treatment regimes, large savings can be made in total treatment costs. This is the result of shorter treatment periods because honey clears infection quickly, speeding up healing.
Dressing the wound
The literature contains little on the methods used to dress wounds with honey, and where details are provided it is apparent that techniques vary widely. The following advice is based on clinical experience gained at the Honey Research Unit and that of associates working in the field.
Amount of honey
The amount of honey needed to treat a wound depends on the amount of exudate, because the beneficial effects are reduced or lost if small amounts of honey are diluted by large amounts of exudate. The deeper the infection, the more honey will be needed to achieve an effective level of antibacterial activity diffusing deep into the wound tissues. Typically, 20ml of honey (25-30g) should be used on a 10cm-square dressing.
Frequency of dressing changes
This depends on how rapidly the honey is diluted by exudate. Dressings are usually changed once a day, but with heavily exuding or infected wounds they may initially need to be changed up to three times a day.
The anti-inflammatory and antibacterial action of honey will reduce the amount of exudate, so within a few days the dressings should need to be changed less frequently. In some cases dressing changes may be reduced to every two to three days.
If the dressing adheres to the wound this usually indicates that it needs to be changed more often. If it continues to adhere to the wound after more frequent changes, a wound contact material should be placed on the wound before the honey dressing is applied.
The choice of non-adherent dressing is important as it must be sufficiently porous to allow the honey to diffuse through to the wound bed. For example, honey will not diffuse through dressings that are impregnated with paraffin.
Honey is runny and sticky, which can make it a difficult medium to handle, but this can be overcome by soaking it into an absorbent wound-contact material, such as gauze and cotton tissue. Wound-contact materials that have been preimpregnated with honey are the most convenient way to apply it to surface wounds. Preimpregnated pads, which use honey with a standardised level of antibacterial activity that has been sterilised by gamma irradiation, are available commercially in New Zealand.
The honey dressing should be cut to a size that extends beyond the edges of the wound, covering any surrounding area of inflammation.
Abscesses, cavities and depressions in the wound bed should be filled with honey before the honey dressing pad is applied, so that honey is always in contact with the wound bed. The most convenient way to do this is to use a tube of irradiated leptospermum honey.
Occlusive or absorbent secondary dressings should be applied to prevent the honey oozing from the wound. Occlusive dressings have been found to keep more of the honey in contact with the wound as absorbent dressings tend to soak it up.
If an adhesive occlusive dressing has not been used, adhesive tape or bandages can be used to hold the dressing in place.
Honey dressings can also be used under multilayer compression bandaging. They usually need to be changed twice a week, particularly in the early stages of treatment until exudate levels have decreased, but daily changes may be necessary if there is heavy exudation.
Further information on the antibacterial properties of honey can be obtained on the internet at: http://honey.bio.waikato.ac.nz
For advice on clinical matters contact Julie Betts by email on: BETTSJ@hwl.co.nz
Other enquiries can be directed to: Peter Molan, Honey Research Unit, Department of Biological Sciences, University of Waikato, Private Bag 3105, Hamilton, New Zealand.