Member’s update – February 2011

Member’s update – February 2011

The Executive is very pleased to present the first update for 2011. This update is focusing on two topics; an article on wound treatment and the major initiative by AMHA with its interlab programme.

Best wishes

The AMHA Executive

Wound treatment –

Two years ago an agent of AMHA met a retired nurse who had extensive experience in wound treatment. His initial meeting with her reminded him of the value of experience, education and a commitment to the patient. He walked away from the meeting re-enthralled with the prospects for product development with Manuka honey in this area, and he also learned that successful application could only be achieved by a clinician who understands wound treatment, the complications involved with wounds and that Manuka dressings would not be appropriate in all situations. The wound treatment plan is only one part of a total care plan for the patient.

He found it exciting that yet another health professional independent from the honey industry was using Manuka honey in a wound treatment plan. In this update we have printed an article written by that nurse. This article was prepared to help support the work already done and research published in this area. It’s the gathering of this knowledge that will assist in determining areas to target for research. This article has been printed as received

Interlaboratory Programme

The AMHA initiative of having laboratories set up in the UK and Singapore is still on track. We have just confirmed all the permits to transfer product from country to country and laboratory to laboratory. This is very useful to not only ensure we are testing to the same standard but for calibration of future laboratories. We have also had contact with a laboratory in Australia, they have been testing using the Bio and Chemical assays since 2009 and are very keen to become part of the programme. We are working through a contract with a statistician to ensure we test the appropriate number of samples to establish equivalency.

Use of Manuka Honey in the Treatment of Wounds

by Marilynne T. Laidlaw Biggs

Registered general nurse, orthopaedic nurse, intensive care trained nurse and midwife. Trained in Scotland 1961-1966. Travelled extensively overseas as a nurse.   Came to New Zealand in 1973. Became interested in wound care 1979. Became charge nurse at Middlemore Emergency Department 1982-1996. Also became clinical nurse specialist for the Emergency Department. This seven module programme included a three day course on wound management.

In the early 1980’s our wound dressings were very basic – paraffin tulle, gauze and SSD cream. Then the advent of interactive dressings began. The advantages of these dressings were:

  • maintain correct humidity at wound interface
  • meeting physiological needs of damaged and healing tissue – that is to:
    • remove excess exudate
    • reduce bacterial load
    • be impermeable to bacteria
  • allow gaseous exchanges
  • provide thermal insulation
  • reduce pain (keep nerve endings moist)
  • allow removal without causing additional trauma
  • create an acidic environment

This was so welcomed as paraffin tulle (a passive dressing) could not cope with large amounts of exudate and strike-through to the outer dressing could produce a channel for infection as well as maceration of surrounding skin. This moisture evaporation through wet dressings cools the wound and lowers wound temperatures, slowing down white blood cell/metabolic activity. Paraffin dressings will only attain temperatures of 25-27°C, with water vapour admission rate of over 3000g per square metre per day.

I trialled many of these new dressings. When I left Middlemore I worked at a private A-M clinic but lectured to many practice groups and St. Johns ambulance service, wrote articles for magazines and spoke at seminars.

11/3/2003 – 4/9/2005 I was a wound care nurse at the Hyperbaric Oxygen Centre in Auckland, treating long term chronic wounds. Comvita wound care Manuka honey was first produced in a tube and I used it on small acute wounds using adaptic as its carrier and covered with a film dressing.

During my period in the Hyperbaric Unit I used Manuka honey on chronic wounds with good results. There were only two patients who could not tolerate this treatment which had now expanded into actual dressings. This was due to pain and itching which they experienced. The new Comvita dressing had an alginate type of backing or carrier for the Manuka honey and helped to cope with exudate from the wound.

Spooning Manuka honey from your breakfast jar is not good practice.

Wound care nurses require highly developed wound assessment skills as well as the ability to determine concomitant medical problems or drugs which may interfere with healing.

Be cognisant with the stages of wound healing, recognise these stages and the progression or regression of a wound. There are many components of wound assessment which include history, wound location, surrounding skin, the wound edges, size, depth and the particular characteristics of the wound bed e.g. necrosis, odour exudate, slough, infection, granulation tissue.

This allows the nurse to plan their approach for wound treatment and chose an appropriate dressing in a structured and rational approach.

Treatment of chronic wounds is aided by the concept of wound bed preparation to promote healing and correct the chemical and cellular dysfunctions which are a barrier to healing. This was devised by prominent Professors engaged in research in wound healing.

The acronym “TIME” defines four fundamental principles for wound bed preparation:

  • tissue
  • infection
  • moisture balance
  • edge of wound – non-advancing or undetermined

Put succinctly it advocates removing all necrotic, damaged or defective tissue by either debridement or use of specific dressings.

Lowering the bacterial count through dressings, antibiotics and controlling the inflammatory effects of cytokines and proteases. This will help to increase growth factor activity.

Dry/desiccated wounds slow cell migration. Excessive fluid/exudate can cause severe maceration of surrounding tissue and delay wound healing. Control of oedema – elevation, compression, use of appropriate absorbent dressings, vac therapy system.

Non migrating keratinocytes. Debridement, skin graft, biological agents, adjunctive therapies e.g. hyperbaric treatment.

Wound management over the last 20-30 years has emerged as a dynamic, complex and demanding speciality.

Wound research has provided us with evidence on which we base our wound practice. Dressings are only one component of wound management and nurses working in wound care must have in-depth knowledge of the skin and its structure, physiology of wound healing, accurate assessment of the wound itself (depth, colour, extent of skin damage and infection).

A holistic assessment which provides details of the patient’s health status i.e. diseases they have and/or drugs they are taking should be combines with detailed knowledge of specific dressing products and their actions. By using all this information an effective wound management plan can be implemented and an appropriate wound dressing regime decided upon.

Normal acute wound healing proceeds through an orderly, synchronised and timely reparative process resulting in sustained restoration of anatomic and functional integrity of skin, This amazing phenomenon is an exquisitely regulated orchestration of molecular and cellular interactions in the inflammatory, proliferative (repair) and maturation (remodelling) stages of wound healing. Each stage of wound healing produces cells and substances which influence the following stage.

The following is a simplistic overview of the four phases of wound healing; physiology is a complex subject with many variables.

  • Haemostasis/clot – a platelet plug establishes fibrin giving a provisional wound matrix or foundation for new tissue. Platelets provide initial release of cytokines and growth factors for new tissue.
  • Acute inflammatory stage – mediated by neutrophils and macrophages. Prolonged inflammation retards healing due to excessive levels of proteases and reactive oxygen radicals released from excessive numbers of white blood cells seen in chronic wounds which are stuck in the inflammatory stage.
  • Proliferative stage – this is dependent of the resolution of the inflammatory stage, reduction of wound debris and new tissue growth. New fibroblasts (collagen) and new capillaries develop, producing healthy tissue. Basal epithelial cells proliferate and migrate over the granulation tissue to close the wound.
  • Remodelling – the wound is considered healed. This stage can continue for months. It involves decreases in fibroblast, capillary density, metabolic activity and a restoration of collagen fibres with greater similarity to normal skin. A mature scar does not have the same tensile strength as normal tissue.

The inflammatory stage is a vital stimulant to subsequent events because of its release of white blood cells to remove bacteria, growth factors and vasoactive substances. Macrophage is not only a phagocytic cell but produces many growth factors for the formation of new tissue and is regulated by chemokine and cytokine activities. Inflammatory cells remove damaged tissues by secreting proteases, kill bacteria and secrete oxygen reactive species.

All wounds start as acute wounds but some wounds fail to heal and progress to chronic wounds. Defining the aetiology of a chronic wound is essential as healing is unlikely to be achieved if the causative and contributing wound and patient factors (concomitant illnesses) are not reduced or eliminated. Chronic wounds get stuck in the inflammatory stage and the many cells and substances of normal wound healing become desynchronised and disrupted. Instead of a normal protective healing environment a hostile destructive situation where excessive numbers of cells are generated releasing oxygen radicals, cytokines and proteases in extravagant amounts. This creates a self-perpetuating inflammatory scenario.

Research has shown that in the biochemical analysis of chronic wounds, high levels of proteases and cytokines, low levels of growth factors and poor proliferation of cells. In contrast these levels are the opposite in healthy healing wounds.

To reverse the situation, an in depth, holistic and detailed assessment of the wound is a priority if we are to promote healing in a chronic wound. External factors such as concomitant illnesses e.g. diabetes, nutritional status, age, decreased immune function all require specialist care.

Normal wound healing is a highly integrated series of responses which are activated as a protective mechanism by the body. These responses occur is a sequential manner in the healing process. Each stage produces cells which influence the following stages. In other words the rights cells in the right numbers at the right time provide a healed wound. The rate that cells enter a wound and proliferate determines how quickly the wound will heal.

Any aberration in this sequence of events can impair or delay healing and the causes are many. It can be internal factors of the wound e.g. infection, haematomas, poor blood flow, oedema, slough/necrotic tissue, dehydration or exudate.


Honey provides more than just “carbohydrate filler” in the extracellular matrix. It contains proteins, amino acids, vitamins and minerals as well as sugars.

Some Manuka honeys have an additional Unique Antibacterial Activity that no other honey possesses – the Unique Manuka Factor which prevents and reduces inflammation and bacterial load. Topically applied, this Manuka honey removes bacteria, including antibiotic-resistant strains (MRSA), removes odour, debrides the wound and promotes wound healing. Staph. Aureus is purported to be rendered sterile by Manuka. Acidic pH of honey helps lower the alkaline environment of a chronic wound. A broad spectrum of pathogens – fungi, aerobes, anaerobes, gram positive and gram negative bacteria – are inactivated by Manuka honey.

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