Moisture-associated skin damage (MASD) can result when the skin has prolonged or continuous exposure to excessive moisture. If the skin experiences too much moisture, it becomes overhydrated and is prone to maceration. This makes it easier for irritants and microorganisms to penetrate the skin, reduce its integrity to mechanical forces and disrupt its protective acid mantle. The condition can greatly affect patient wellbeing. MASD is a collective definition and it has four main causes: incontinence-associated dermatitis, periwound skin damage, intertriginous dermatitis and peristomal moisture-associated dermatitis. Practitioners can use tools such as the Skin Moisture Alert Reporting Tool (S.M.A.R.T.) to identify its aetiology, which informs its management. Management of MASD involves assessment, addressing the underlying cause, and implementing a structured skin care regimen to treat it and prevent its recurrence. Case studies illustrate the use of a structured treatment strategy using Medi Derma barrier products and the principles of Total Barrier Protection to provide a cost-effective solution for the prevention and management of skin compromised by MASD.

Chronicity in wound healing is a challenge for health services financially and scientifically, with negative consequences on patients' lives. This paper seeks to explore why chronic wounds fail to heal in relation to the inflammatory cellular dysfunction associated with biofilm development. Findings demonstrate an association between chronic wounds failing to heal, the presence of devitalised tissue and abnormal immune cell activity with a consequential excessive release of harmful matrix metalloproteases (MMPs). This process perpetuates the cycle of wound chronicity and extracellular matrix destruction, which prolongs the inflammatory response, fuelling biofilm formation. Evidence suggests that 'trapping' MMPs may increase new tissue growth but, while devitalised tissue is present, phagocytic cells continue to secrete MMPs and chronicity persists. Consequently, by removing the trigger and implementing effective, sustained debridement of devitalised tissue, both MMP and biofilm production will be diminished, with positive healing outcomes.

Compression therapy is widely used as the gold standard for management of chronic venous insufficiency and venous leg ulcers, and the amount of pressure applied during the compression therapy is crucial in supporting healing. A fibre optic pressure sensor using Fibre Bragg Gratings (FBGs) is developed in this paper to measure sub-bandage pressure whilst removing cross-sensitivity due to strain in the fibre and temperature. The interface pressure is measured by an FBG encapsulated in a polymer and housed in a textile to minimise discomfort for the patient. The repeatability of a manual fabrication process is investigated by fabricating and calibrating ten sensors. A customized calibration setup consisting of a programmable translation stage and a weighing scale gives sensitivities in the range 0.4–1.5 pm/mmHg (2.6–11.3 pm/kPa). An alternative calibration method using a rigid plastic cylinder and a blood pressure cuff is also demonstrated. Investigations are performed with the sensor under a compression bandage on a phantom leg to test the response of the sensor to changing pressures in static situations. Measurements are taken on a human subject to demonstrate changes in interface pressure under a compression bandage during motion to mimic a clinical application. These results are compared to the current gold standard medical sensor using a Bland–Altman analysis, with a median bias ranging from −4.6 to −20.4 mmHg, upper limit of agreement (LOA) from −13.5 to 2.7 mmHg and lower LOA from −32.4 to −7.7 mmHg. The sensor has the potential to be used as a training tool for nurses and can be left in situ to monitor bandage pressure during compression therapy.