1 INTRODUCTION

Pressure ulcers (PUs) are localised damage to the skin and/or underlying tissue, because of pressure, or pressure in combination with shear.¹ There are a number of important papers that have addressed the extent of the existence and emergence of PUs in health care, giving an indication of the scale of this problem for patients, families, health care workers, and services. In an extensive systematic review by Moore, Avsar,² 79 articles were reviewed with a first-time in-depth exploration of the prevalence of PUs in Europe. They found that the median prevalence was 10.8% (SD: 7%; range: 4.6–27.2%) across the 79 reviewed studies. The incidence of PUs in observational studies was assessed in a global systematic review and meta-analysis by Afzali Borojeny, Albatineh.³ Inclusion criteria were met by 35 studies, and all were included in the review. The incidence rate of PUs was 12% (95% CI: 10–14). Additionally, a systematic review by Chaboyer, Thalib⁴ found that the 95% CI of cumulative incidence and prevalence of PUs were 10.0–25.9% and 16.9–23.8% among patients in intensive care units.

It is widely recognised that early and effective risk assessment and PU detection are important. Evidence indicates that decreased mobility/excess abnormal movement and the presence of pressure/shear are central to PU formation.^{5, 6} The European Pressure Ulcer Advisory Panel recommends a structured risk assessment and comprehensive skin assessment for each patient.¹ The most common method of assessing skin is using visual skin assessment (VSA), which has been shown to vary greatly in terms of reliability, meaning that in practice, there is generally only moderate agreement among staff when assessing the same patient for evidence of PU development.^7-12 Further, assessment of early evidence of PUs, before the skin is broken, is even more challenging, particularly among individuals with darker skin tones.¹⁰ This is a real problem for clinical practice, as skin assessment is fundamental to determine an individual's responses to pressure and shear, in addition to their responses to prevention strategies offered.

Considering the burden that PUs and their prevention place on a health care system and the individual, it seems illogical to use an evaluation tool that is inconsistent. This highlights the need for an alternative tool that can consistently predict the onset of PU. However, existing risk assessment tools include several risk factors, all weighted the same, diluting the importance of immobility as a risk factor. This poses a challenge in the clinical battle to prevent PU in the first place. Furthermore, visual skin assessment, the gold standard, is unable to detect damage which is manifesting beneath the skin, which, if left unnoticed, can progress to irreversible visible tissue damage.^{5, 6}

SEM is a biophysical marker (product of the leak of plasma after the inflammation process increases local vasculature permeability). After tissue damage occurs, local microscopic oedema (or sub-epidermal moisture) and the local increase of moisture change the electrical capacitance of the tissues which can be measured using an electrical bio-impedance device. As SEM is related to deeper layers, it is not influenced by environmental changes, yet is directly related to inflammation.^{5, 6} Elevated SEM has been shown to be an indicator of early-stage PU damage and when detected can direct staff to anatomical areas of the patient which are at risk, thus enabling the targeting of interventions to combat this risk. Early PU detection can be performed with the use of an SEM Scanner.^{5, 6, 13-17} The SEM Scanner manufactured by Bruin Biometrics, is a low frequency, handheld bioimpedance device which uses measures of capacitance to assess changes in SEM in the tissues of patients. Research has demonstrated consistency in the detection of changes in SEM and the development of subsequent PUs 1 week later. Further, the use of the SEM Scanner has been shown to have high inter-rater reliability and accuracy in early PU detection.^18-20

No previous study has investigated if identifying elevated SEM in patients at risk of PU, and correspondingly implementing enhanced skin care interventions, reduces the incidence of PU when compared with a control group receiving usual care. This study, therefore, sets out to assess the usefulness of measuring SEM in prompting targeted preventative wound care interventions, impacting PU incidence.

2 METHODS

2.4 Data collection

To ensure participants believed confident in their decision to become part of the study, the principal researcher approached each individual and supplied them with both verbal and written information about the study. Following a 24-hour cooling off period, the principal researcher approached the potential participants and if they were receptive, obtained informed consent. Then, the principal researcher recorded the participants' demographic details: gender, age, current medical condition, and past medical history.

All participants had the following information recorded every day by the principal researcher with day one information considered to be the baseline (see Figure 1):

• SEM measurements from right heel, left heel, and sacrum.
• VSA observed on right heel, left heel, or sacrum.
• Braden Score.
• Mobility assessment.
• Continence status; Application of barrier cream.
• Pressure relieving mattress use; Pressure relieving cushion use.
• Dietician, occupational therapist, and/or physio input.
• Increased repositioning schedule.
• Where the participant was (in bed or sitting out).

Both groups had SEM deltas and VSA recorded daily for a maximum of 5 days using the SEM Scanner (Bruin Biometrics LLC, Los Angeles, California), on three sites: the sacrum, the right heel, and the left heel, as these are the most common sites for PUs to occur.^{4, 21-28} Results of the SEM measurement were not shared with staff caring for participants in the control group.

2.4.1 Measurement tools

Recording measurements with the SEM scanner

SEM measurement detects changes in fluid contents of human skin and subdermal tissues, by measuring “capacitance.” The capacitance of tissues, called “biocapacitance,” is impacted by the amount of fluid in the tissue.^{15, 29} To take SEM measurement using the SEM Scanner the operator performs several readings from each site: six readings from the sacrum and three to four from the heel depending on the level of callous present. The SEM Scanner automatically compares the values in each set of measurements and pinpoints the maximal and minimal values within the set. The variance between the maximal and minimal values is displayed as the SEM-delta. The SEM-delta is a measure of the difference between the capacitance at a tissue site that may contain subsurface damage in comparison with healthy (reference) tissue sites. For this study, and in keeping with previous works,^{6, 30} an SEM delta was considered abnormal if the value was ≥0.5.

In the current study, despite having their SEM deltas recorded daily, these were not shared with the participants or the staff caring for them, and the participants in the control group had usual care used in the hospital. They received prevention care based on the SSKIN bundle with indication for the use of the bundle being based on their risk assessments and visual skin assessments. The participants in the intervention group received SSKIN bundle care based on their daily SEM delta, if they had an abnormal delta, the researcher requested the participant's nurse to arrange additional enhanced interventions as appropriate. These interventions included.

• Application or increase in pressure relieving mattresses/cushions.
• Application of barrier cream if sacral SEM raised and they were incontinent.
• Increase in reposition schedule and/or offloading of heels.

The Braden Scale

The Braden Scale³¹ was used from day one (baseline) and every day thereafter on all participants. The Braden PU risk assessment scale uses six subscales to assess an individual's risk of developing a PU: sensory perception, moisture, activity, mobility, nutrition, and friction/shear. Each subscale is marked from 1 to 4 apart from friction/shear, which is from 1 to 3. The scores are accumulated to give a total score that ranges from 6 to 23. A lower Braden Scale Score indicates a lower level of functioning and, therefore, a higher level of risk of PU development. A score of 19 or higher indicates that the patient is at low risk, with no need for immediate treatment.

There are numerous PU risk assessment tools including the Norton Scale,³² Gosnell Scale,³³ Waterlow scale,³⁴ Braden Scale,³¹ and the Risk Assessment Pressure Score Scale.³⁵ Pressure ulcer risk assessment tools are varied and inconsistent in their inclusion of different risk factors,³⁶ an issue that has prompted substantial research into their reliability and validity.^37-40 The Braden Scale was selected as it has been shown to have moderate to high validity and reliability among varied patient cohorts including trauma/ICU patients,^40-42 paediatric patients,^{43, 44} long term care patients,^{45, 46} patients with spinal cord injuries,⁴⁷ and elderly patients.⁴⁸ The inter-rater reliability of the Braden Scale was substantial in every ward versus not good in orthopaedic and spinal surgery wards for the Norton Scale and not good in the orthopaedic wards for the Waterlow Scale. These were the key reasons that underpinned the use of the Braden Scale in this study.

Mobility assessment

Mobility assessment was carried out prior to patients being included in the study. Mobility assessment occurred daily for all participants in the control and treatment groups. The mobility assessment tool used was a simple statement:

‘Does the person regularly reposition themselves without assistance, every few minutes (including during sleep, when seated and persons with sensation deficits).”

If Yes, the patient is not at risk, if No the patient is at risk.

Individuals who are immobile or unable to reposition effectively are susceptible to developing a PU despite any other traditional risk factor being present, as mobility is the highest predictor.^{6, 49-51}

3 RESULTS

3.1 Flow of participants through the study

Following the application of the inclusion criteria, 204 people were invited to participate, 149 consented, an additional 50 people refused to consent, and 5 people were excluded. Postrandomisation the treatment group had 78 participants and the control group had 71 participants. Data were collected over several months, thus participants were commencing the study and left on many different dates. Both groups were followed up for a maximum of 5 days and only participants with an abnormal SEM delta reading in the treatment group received targeted treatments (See Figure 2).

3.6 SEM Scanner deltas at baseline

3.6.1 SEM

The mean SEM delta right heel at baseline was 1.02 (SD: 0.8) in the control group and 1.0 (SD: 0.8) treatment group. The mean SEM delta left heel was 0.9 (SD: 0.77) in the control group and 1.01 (SD: 0.75) in the treatment group. Finally, mean SEM delta sacrum was 0.6 (SD: 0.54) in the control group and 0.55 (SD: 0.48) in the treatment group (see Figure 3).

Using an independent samples t test at baseline, there was no statistical difference between the study groups in terms of mean SEM delta right heel (t [147] = 0.242; P = .80), left heel (t [147] = −0.778; P = .43), and sacrum (t [147] = 0.695; P = .48).

3.7 Results for the primary outcome

3.7.1 Difference in all mean SEM deltas from baseline to end of the study

Figure 4 outlines the mean SEM deltas at end of the study across each anatomical area, in addition, to the total SEM deltas. Analysis of the data determined the mean difference in SEM deltas from baseline to end of the study.

The mean SEM delta at baseline in the control group was 0.88 (SD: 0.42) and at end of the study, this mean SEM delta was 0.98 (SD: 0.36). The mean difference (MD) is 0.09 (95% CI: 0.22 to 0.04; P = .19). In the treatment group, the mean SEM delta at baseline was 0.88 (SD: 0.40) and at the end of the study, this mean SEM delta was 0.49 (SD: 0.28). The MD is 0.40 (95% CI: 0.29 to 0.51; P = .0001).

Further analysis determined the difference in mean SEM deltas at study completion between the control and treatment group. The MD is 0.49 (95% CI: 0.59, 0.39; P < .0001). These results indicate that the mean overall SEM delta was statistically significantly lower in the treatment group at the study end.

3.7.2 Incidence of SEM PU (sustained SEM ≥0.5, developed during the study period, any anatomical site)

SEM readings were recorded daily and were considered elevated if they were ≥0.5, and they were considered sustained if they were elevated for two or more days over any anatomical site, after day 1. Of the total participants, 30% (n = 45/149) had a SEM PU ≥0.5 from day two onwards on any anatomical site, 38% (n = 27/71) of the control group, and 23% (n = 18/78) in the treatment group.

The mean time to SEM PU ≥0.5 developing over any anatomical site was 2.44 days (SD: 0.69; min 2 days; max 4 days). In total, five participants developed more than one SEM PU ≥0.5, with 2 participants developing the SEM PU on both right and left heels, and 3 participants developing the SEM PU on the left heel and the sacrum.

Analysis of the data was undertaken to explore the odds ratio (OR) of SEM PU ≥0.5 between the study groups. The OR of SEM PU ≥0.5 was 0.59 (95% CI: 0.24 to 1.00; P = .05), indicating a 49% reduction in the odds of SEMPU ≥0.5 in the treatment group and this finding is statistically significant.

3.7.3 Abnormal SEM delta scores (≥0.5) at baseline and sustained through the study period

At baseline, there were 330 abnormal SEM deviations (≥0.5) recorded across all three anatomical sites. Of these, 50% (n = 166) were in the treatment group and 50% (n = 164) were in the control group. In total, 65% (n = 213) were sustained during the study follow-up period, of these, 36% (n = 76) were in the treatment group and 64% (n = 137) were in the control group.

By the end of the study, 35% (n = 117) of all readings returned to normal by the end of the study follow-up period, 54% (n = 90) in the treatment group, and 36% (n = 27) in the control group. The OR of readings returning to normal by the end of the study period is 6.01 (95% CI: 3.60 to 10.04; P = .0001). This indicates that the treatment group is 6 times more likely to have an SEM reading return to normal at the end of the study, and this finding is statistically significant.

4 DISCUSSION

It is widely accepted that tissue damage begins at a cellular level.⁵⁷ In individuals with normal sensation, mobility, and cognition, exposure to protracted pressure prompts a reaction that results in a change in body position.⁵² However, when the feedback response is deficient or missing, sustained pressure/shear ultimately occurs leading to ischaemia, cell deformation, and necrosis.^{58, 59} Ischaemic damage caused by occlusion of blood vessels can take several hours to develop, however, cell deformation occurs within minutes when tissue is exposed to high pressure strains.^{57, 60-62} This rapid onset of pressure/shear induced damage highlights the importance of prompt detection and initiation of effective prevention strategies.

The pathophysiological changes that result in PUs are now widely known; blood vessels adjacent to micro-damage sites become more permeable when the inflammatory response to cell death is triggered, allowing immune cells to flee the vasculature and transfer towards these cell death sites, aiming to repair the tissue.⁶² Subsequently, plasma also leaves the leaky vasculature and gradually builds up in the interstitial space, causing oedema. The dielectric constant of the affected tissues becomes like water biocapacitance because of the accumulation of plasma fluids.^{18, 62, 63} It is thus reasonable to conclude that pressure damage begins at a microscopic level.^{18, 20, 62, 63}

The current “Gold Standard” approach of VSA is a macroscopic observation attempting to identify microscopic changes, which identifies existing damage rather than pre-empting it.^{6, 30, 64} A device measuring biocapacitance provides a quantitative assessment of early pressure damage allowing health care professionals to initiate interventions that will reduce or reverse the damage.^{61, 65} The SEM Scanner (Bruin Biometrics, LLC, Los Angeles, California) is a low frequency, handheld bioimpedance device designed for just this use.^{11, 17}

In this study, the mean SEM delta for participants who received targeted interventions were significantly lower than those in the control group, further, the odds of having SEM pressure ulcer ≥0.5 were also lower in the group receiving SEM guided interventions. In addition, the intervention group was 6 times more likely to have a SEM reading return to normal at the end of the study. These findings provide exciting opportunities for improved PU prevention strategies benefiting the individual, the health care professional, and the health care system. PUs' are considered a key performance indicator (KPI) in health care settings, with low incidence representing an example of clinical care being performed well.^{66, 67} Further, PUs can negatively impact financially both the individual and the health care setting,^{68, 69} but more importantly, they can negatively impact a person's quality of life.^{6, 66, 70} Despite the onus on PU prevention, prevalence and incidence rates persist, particularly in hospitals and nursing homes, suggesting that there is a real need to re-think the current approach to the prevention of this prevailing health problem.^{71, 72}

Early identification of pressure damage provides many benefits to care providers and to patients themselves. In terms of litigation, pressure damage can be diagnosed on admission or transfer, this can help attribute “ownership” over the pressure ulcer to the location the patient came from.⁶ Further, timely pressure/shear identification is key to successful PU prevention. When pressure or shear is in progress, the number of ischaemia/reperfusion cycles increases, and there is a corresponding reduction in skin blood flow and oxygenation to the skin.⁷³ The longer durations of ischaemia, followed by reperfusion result in significantly increased tissue oedema (P < .005) and decreased tissue viability (P < .05).⁷⁴ In addition, cell deformation causes immediate cell death, through cell rupture, eliminating the possibility of cell damage reversal. When cell death is present, the deprivation of oxygen and nutrient supply to the affected area serves to accelerate the damage, after 20 hours a large inflammatory response is evident.⁶⁰ The longer the duration of compression, the greater the evidence of cell death, thus time under compression is an important variable.

Therefore, it is essential to know the individual's responses to pressure and shear so care providers can mitigate against allowing the patient to repeatedly load over an area that is adversely responding to pressure and shear. The results highlighted in this study support this concept, as 54% (n = 90) of participants in the intervention group who received targeted interventions had their SEM delta return to normal versus 36% (n = 27) in the control group. This demonstrates that the inflammatory response can be reversed when the original cause is eliminated.

Thus, from a clinical perspective, knowing the patient's individual responses to pressure and shear forces, using technology, such as SEM measurement, will enable the detection of anatomical areas responding adversely. The early detection of tissue damage is beneficial in two different ways. First, it allows practitioners to put interventions into place when the damage is still microscopic and reversible and, thus avoids the knock-on effect of inflammation, especially in the presence of tissue deformation. Secondly, cell death can be avoided when the problem is identified before the cell reaches the point when cell death is present, completely averting the development of a visual PU.

5 LIMITATIONS

Whilst this study has generated new knowledge relating to the identification of early-stage PU damage and the enhanced use of SSKIN interventions, in an Irish acute hospital setting, it does have limitations. The non-inclusion of a qualitative component is something that can be used in future larger scale studies across multiple sites replicating the current study. The use of Braden and counting visual PUs is also something that needs to be explored further, their inclusion in this study, on the one hand, could have been avoided, on the other had their inclusion further highlighted the need for a deeper conversation around there use in practice as the gold standard for risk and predictive assessment.

6 CONCLUSION

The overall purpose of this study was to ascertain if elevated SEM as determined by an elevated SEM delta, which triggered the application of enhanced SSKIN targeted interventions focused on at risk sites, reduced the incidence of PUs in comparison to usual care. In the current study, PU prevention strategies were implemented in the intervention group upon immediate identification of an elevated SEM delta (≥0.05). The interventions included the introduction or upgrading of a pressure redistribution device, the application of barrier cream (where appropriate), and the offloading of heels and/or increasing the repositioning schedule. The use of SEM measurement aided targeted interventions in this study and resulted in a statistically significant reduction in mean SEM delta in the intervention group at the study end in favour of the intervention group. Overall, the results have shown that targeting abnormal SEM deltas with appropriate interventions reduces the SEM delta, thereby reducing the chances of a visible PU occurring resulting in better patient and service outcomes.

CONFLICT OF INTEREST

The School of Nursing & Midwifery has a research collaboration with Bruin Biometrics.