TI S SUE VIAB I L I T Y
Figure 2: Provizio SEM scanner
the external strain, will depend on the severity and length of the mechanical load. New perspectives on pressure injury/ulcer development17, 18
indicate that the three key
aetiological factors that contribute to PI/PUs are: l Direct Deformation (primary) l Inflammatory damage (secondary) l Ischaemic damage (tertiary)
Direct deformation in weight bearing soft tissues under bony prominences are the initial factors that begin to inflict cell and tissue damage. With the deformation- inflicted death of the first cells, inflammation is triggered.19
This results in leakage
of plasma fluids from the diluted and permeable blood vessels in the inflamed site into interstitial spaces in tissues, thereby forming oedema, first microscopically and then macroscopically.19 This inflammatory response contributes to the escalation of cell and tissue death.17 Localised oedema, also called sub- epidermal moisture (SEM), is an underlying physiological phenomenon.19 The capacitance of tissues, called ‘biocapacitance’, is strongly affected by the amount of fluid (water) in the tissue. When the first cells die in a forming PU/ PI, inflammatory signaling causes the permeability of blood vessel walls to increase and oedema to develop.19
The biocapacitance, is strongly affected by the amount of fluid (water) in the tissue.
Changes in sub-epidermal moisture is therefore a marker of inflammation and tissue damage.1
Biomedical engineers have
been able to use this progressive build-up of fluid mass in tissues as a ‘biophysical marker’ for detecting initial tissue damage.19 The combined effects of deformation caused by bodyweight or other external forces along with the intensifying effects of oedema and the associated high interstitial pressure, obstruct the blood vessels and impair tissue perfusion causing ischaemia at the damage site.1
The development of a pressure injury/
ulcer often depends on individual tissue tolerance; many physical and environmental risk factors influence this. Although the specific significance of most risk factors has yet to be elucidated1
and underlying disease) can be altered, the significance of other factors, such as excess heat and moisture on the skin, has been clearly established.
Hyperaemic response raises metabolic demand if the skin temperature increases by only 1˚C. This increase will occur at a time when there might be insufficient blood supply by occlusion of the vessel through pressure and shear when higher pressures are encountered.20
This can be especially problematic, and pressure alone can cause an increase in temperature.21
At the same time, increased
heat can cause a natural diaphoretic (sweat) response and create a continually moist
38 l
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atmosphere. Moisture decreases the skin’s tensile strength, resulting in maceration1 an increased risk of exposure to friction.
and
Prevention Prevention begins with the identification of individuals at risk as early as possible in the care pathway, and then taking prompt action to provide the correct intervention1, 22
which
may include early mobilisation.1 Earlier detection
Risk assessment is the first step in pressure injuries/ulcers prevention to identify patients most at risk, plan and implement interventions, and ensure resources are used appropriately23 national24
and international clinical practice and not all (such as age
guidelines.1 The 2019 Clinical Practice Guideline1 recommendation 2.6 states that healthcare practitioners, using their own qualified clinical judgement, should: “Consider using a sub-epidermal moisture/oedema measurement device as an adjunct to routine clinical skin assessment.”
The guideline recommendation 2.7 also states that healthcare practitioners, using their own qualified clinical judgement when assessing darkly pigmented skin, should: “Consider assessment of skin temperature and sub-epidermal moisture as important adjunct assessment strategies. The Provizio SEM Scanner (Figure 1 and 2) is a hand-held wireless scanner
MAY 2021
and is recommended in
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