AWSA 2025

INFLAMMATION vs INFECTION:Wound climate change

We understand that most of you have heard about the famous George Winter and his study of wound healing which essentially changed the way we approached wounds from 1963 onwards. For some health care professionals however, it seems the understanding of moist wound management has moved just too far in the moist spectrum and we are faced with too many wet wounds.

Our speakers come from scientific laboratory work to functional product design and components of the most common wound care products. You will be encouraged to discuss what you are finding and considerations for how we collectively can make changes to ensure wound care is based on the tissue, the exudate and the aims—amongst other areas.

Do some products cause inflammatory responses and hence wound becomes wetter? Do microorganisms proliferate in a moist environment? Do health professionals have in depth knowledge of wound healing, tissue assessment and settings aims? Do clinicians consider how the product works and how it behaves in different environments and by environment we do not just mean the weather today! Does sitting in a recliner chair- “Princess chair” allow enough airflow or does it create more heat in certain areas and so dressings behave differently?

Moisture management is more than exudate control. What other factors can assist in managing inflammation? Oedema and fibrosis will influence dressing behaviour.

These are just some aspects to be considered and discussed when we look at the current problem of ‘wet’ wounds.

Look forward to you all helping to stimulate health discussion to change the future of the way we look at wounds, set aims and select products.

Continue the discussion during the AWSA 2025 program on Friday 14 February at 9.00am

HIGH RISK FOOT: Beyond just the DFU

When we talk about the high-risk foot many immediately think of Diabetes Related Foot ulcer. However, the high-risk foot encompasses any foot condition or disease complication that increases the risk of trauma, ulceration, infection, or amputation.

The IWGDF refer to “prevention of foot ulcers in at-risk patients with diabetes”. This definition highlights a specific patient demographic of those at risk of ulceration, aligning closely with the concept of “high-risk foot” which is often the result of complications stemming from various pathologies or diseases.

High-risk factors are more prevalent in certain populations such as diabetes, cardiovascular disease, kidney disease, arthritis, scleroderma, or those who are immunocompromised. Inflammatory conditions such as rheumatoid arthritis, psoriatic arthritis, and reactive arthritis in the foot can also serve as significant risk factors. These conditions lead to degenerative joint changes, bone erosions, soft-tissue swelling and joint-space loss. All these risk factors impact on foot structure and function which result in increased plantar pressures on the foot and toe deformities heightening the risk of ulceration. Additionally, medications used to treat inflammatory arthritis, such as corticosteroids, disease-modifying agents, can significantly impact wound healing.

Then add to the mix the Charcot foot, a condition that combines inflammatory and degenerative disease, presenting multiple challenges in the treatment and management.

In this session, we will delve into common high-risk foot conditions, from the perspective of researcher, podiatrist, orthotist and podiatric surgeon. The focus will be the challenge of early diagnosis, prevention and management strategies, access to resources in the community, and referral pathways.

Continue the discussion during the AWSA 2025 program on Saturday 15 February at 8.30am

OEDEMA: more than just fluid.

So … What is oedema?

A very simple definition used by many of us to our patients is:
a build-up of fluid in the body which causes the affected tissue to become swollen and tight. The consequences of uncontrolled oedema can lead to devastating skin changes, wounds, pain, depression and lack of mobility or organ function.

Some of us may look further or deal with patients who have interstitial oedema and this definition gets a bit more complex- Interstitial oedema ought to be considered an early stage of severe oedema that was shown to develop when the extracellular matrix loses its integrity due to fragmentation of the proteoglycan components beyond a critical threshold.

A small amount of protein exists in the interstitium and forces some fluid out of capillary walls. This force is the interstitial oncotic pressure. Together, these factors contribute independently or cooperatively to form oedema.

What are these proteoglycan components, what affects the critical threshold and what makes the ECM lose it integrity? What basic science teaching will help to explain this to our patients? Do we talk about acute oedema and chronic oedema rather than all lymphoedema?

Should we be talking about diet and exercise and if so how do we bring meaning to it without prejudice? What methods of managing acute and chronic oedema work and what does not work? Swelling in some acute injuries is normal, perhaps some consider it even beneficial, the protective mechanisms of the human body, BUT if not resolving within a certain timeframe action should be taken-so what modalities are best.

Prevention should be revisited by all health professionals. Is surgery one area where we should revisit the texts of old? Support therapy or binders were the mainstay -- where are they now?

Correct assessment of the cause of swelling from fluid or fat should be openly discussed and we seek your opinion on strategies to get this subject to the health care sector

Continue the discussion during the AWSA 2025 program on Saturday 15 February at 3.15pm