Index: WOUNDS. 2013;25(4):94–103.
Abstract: Wound dressings have been successfully explored for use in prevention of pressure ulcers in individuals who are at clinical high-risk for developing ulcers. Methods. In this study, application of a recently described body analog test fixture and method is used to evaluate performance features of 8 clinically available dressings for prophylaxis. Documenting dressing performance is essential to defining the proper use and limits to application of dressings for ulcer prevention. These in vitro studies were undertaken to characterize the impact on the microclimate generated by the application of a dressing to the surface of the skin. Results. The measurement of moisture trapped next to the skin, moisture escaped from the dressing, and heat trapped by the dressing show that some dressings are more suited for skin protection. Conclusion. It is evident that an optimal performance band for microclimate management exists in the application of dressings for prophylaxis, and that dressings should be evaluated for proper performance prior to implementation in a pressure ulcer prevention program.
For 3 decades, pressure ulcer research has focused on pressure and ischemia to develop models for prevention and treatment of pressure ulcers.1,2 Current evidence indicates these efforts have not generated noticeable reductions in incidence.3-5 It was recently demonstrated by multiple authors that a dressing placed on skin at risk for ulceration can significantly reduce the rate of ulceration.6-8 While sacral pressure ulcer dressings have not typically been applied preventively, it seems intuitive that a dressing that redistributes forces or mitigates the microclimate could provide some preventive benefit. Recognizing the impact of moisture on the generation of friction, which results in shear forces delivered to the skin, suggest that microclimate requires investigation. Ohura et al’s9 demonstration of the reduction of both shear and axial pressure forces by a dressing on the surface of porcine skin,9 combined with the impact of moisture on friction,10 suggests the need to examine microclimate in dressing-based prevention.11 Microclimate is defined as the temperature and humidity found in the interface between the body and the support surface.12 Its proper management will maintain a favorable temperature and moisture level at the skin surface.11 Skin moisture levels govern elasticity, tensile, and yield properties,16 and thus, resistance to injury. Limited testing of the impact of pressure and shear of dressings8,13 leaves the effect of dressings on microclimate unresolved. Brienza and Geyer14 outlined tissue damage due to temperature exposure, heat flux, specific heat, perspiration, incontinence, skin pH changes, and the moisture vapor transmission rate. Dressings add the need to characterize moisture vapor transmission and the trapping of moisture next to the skin. The classic thermodynamic model considers the body a heat source, and each layer on it a resistor to the escape of heat or moisture.17 This model predicts the addition of a dressing to the skin will raise the temperature. Making characterization of dressing prophylaxis important, especially in consideration of these in deep tissue injury prophylaxis.18 Given that moisture-accentuated shear forces may contribute to deep tissue injury, and force applied to the skin results in internal loads that are as much as 2 times greater in the deep tissues,19 further examination is required. Two methods have been developed for measuring the heat and water vapor characteristics of support surfaces in the laboratory: the method proposed by Nicholson et al22 and the Body Analog Method (US ANSI RESNA draft standards), which is based on the method published by Ferguson-Pell et al.23 The Nicholson method yields engineering values for heat transfer in watts/m2 and gm H2O/m2, units unrecognized by clinicians, and tests a small portion of the surface without typical body loading. The Body Analog method was selected for its recognizable temperature and humidity report under typical use conditions. The body analog method utilizes the L5 to Femoral Epicondyles (approximate) segment of a model of a 50th percentile male human. An inner tank is filled with circulating water held at 37° C. An outer shell of the rig is filled with water that escapes through a “sweating membrane,” so that only water vapor is delivered to the test surface mimicking the moisture vapor delivered by a human subject. This assembly is placed on a support surface such as a mattress and weight is applied until the load on the surface is the same as a 50th percentile human male. The test rig is allowed to deliver heat and humidity at the same rate as that of a 50th percentile male for 3 hours while the temperature and humidity are monitored at the interface. For the purposes of this study, the authors placed the dressing being tested on the surface of the indenter as though it were covering the sacrum of a patient. The moisture-dependent viscosity, elasticity, and resilience of skin, particularly in the aging individual, make shear the most significant of ulcerating mechanical forces.15 This concept is supported by Wildnauer et al16 who demonstrated significant changes in skin properties based on skin moisture content. Knowing the protective effect of dressings raises the following questions:6,20,21 how do prophylactic dressings impact the forces reaching the underlying tissue and what characteristics of prophylactic dressings impart the observed protective effect?22 This research was undertaken to characterize these impacts using bench tests for microclimate properties of 8 commercially available dressings.
Materials and Methods
A sweating thermodynamic rigid cushion loading indenter (TRCLI) as described by Ferguson-Pell et al23 was employed for prophylactic dressing testing. Dressings were tested by applying them to the approximasacral location of the TRCLI, and placement was done to reflect typical application and functional anatomy for dressings applied to the body while supine in bed (Figure 1). Each dressing was centered on the TRCLI and positioned to cover the typical sacral location. The TRCLI is intended to test a larger surface area than the dressings covered, so each dressing was placed as previously described, and the remaining TRCLI test surface was left unmodified. This arrangement was also selected to provide a microclimate comparable to that created by the body when lying supine on a support surface. A photograph of the dressing placement is shown in Figure 1. Eight commercially available dressings (Table 1) were tested in triplicate. Dressings as close to the same size as possible were obtained, however, due to differences in dressing design, intended function, and manufacturer offerings, there were significant differences in size of the dressings. All trials were conducted in a temperature and humidity controlled laboratory maintained at 23° C +/- 2° C and 50% RH +/- 5% as per International Organization for Standardization 554-1976(E).24 The TRCLI was charged with a 50/50 ethylene glycol/water solution and a circulating water bath (Forma Scientific Model 2095) maintained circulation through the indenter at a constant temperature of 37° C +/- 0.1° C. The TRCLI has been shown to deliver 3.6 grams of insensible water vapor per 3-hour trial, and the resolution of the system is 1% relative humidity and 0.1° C.23 The TRCLI was brought to set point and held for 60 minutes to allow for equilibration prior to each trial. The sweat chamber of the TRCLI was charged with deionized water and recharged following each test to ensure that the starting sweat volume was identical for each trial. The charged, dressed, and equilibrated TRCLI was loaded onto a mattress surrogate consisting of a water-impermeable mattress cover over a high resilience-45 (firm) foam mattress analog. Temperature and humidity data were logged using a Sensirion EK-H3 system (Sensirion Inc, Westlake Village, CA) with 11 combined thermistor-based temperature and silicone wafer humidity sensors from the same company. Sensors were calibrated prior to use with the saturated salts method.25 Duplicate sensors were placed at each of the following 5 locations, one inside and one outside the dressing; right and left ischial tuberosities, the perineum and the right and left thigh. When dressing size limited the number of sensors that could be placed under the dressing, the compliment of sensors was reduced to 3 locations, the right and left ischial tuberosities and the perineum. Each test consisted of a 60-minute equilibration period, a 180-minute test period, then a 45-second raising of the indenter intended to represent the repositioning of the patient, followed by a 15-minute replacement in the test position. The apex of the TRCLI was placed 13 cm from the edge of the support surface surrogate so that no edge effect would confound the test data. The 11 sensors were continuously sampled with data logged at a rate of 0.5 Hz throughout the test period. Data was stored in a comma-delimited format that allowed it to be imported into a spreadsheet for analysis. The average temperature, average relative humidity, difference between pairs of sensors both inside and outside the dressing, and the difference between the dressing and the support surface surrogate were calculated.
Tests utilizing the dressings showed a significant difference in the amount of heat and moisture transpired through or being trapped in a particular dressing (Tables 2 and 3). Table 2 shows the average temperature difference from inside the dressing to outside the dressing. It should be noted that the tight range in the confidence intervals of the means is due to the very large data sets that were generated by logging temperature at 0.5 Hz throughout the 3-hour and 15-minute test period. Note that there is not a direct correlation between thickness and temperature. In addition, as moisture built up in the moisture management bed, some dressings lost the ability to transpire as the moisture level in the dressing increased (see dressings 3 and 8 in Table 3.) Dressings 3 and 8 also demonstrate negative moisture escape values, indicating that the moisture management of these 2 dressings absorbed more moisture than was delivered by the test fixture, presumably from the ambient laboratory conditions. P-values are shown in Table 4 and Table 5 for the moisture that escaped the dressing, and moisture trapped inside the dressing, respectively.
Heat. When lying on a support surface the insulated nature of the surface traps body heat at the interface.17 This trapped heat generates the following physiologic responses; increased transpiration, increased perspiration, increased metabolic stress on cells (due to the Arrhenius Effect), increased friction, and thus, shear due to the increased moisture present, and heat-accelerated moisture softening of the hyaluronic acid intracellular bonds increasing the potential for skin failure. Kokate et al26 showed that elevation of skin temperature under identical loading conditions increases the rate of ulceration in swine. The average temperature differences observed are just under 0.4° C (Table 2). According to the Arrhenius Effect, temperature over time begins to have a significant impact on tissue at approximately 1.0° C - 2.0° C.17, 27 While the authors anticipated this effect with the application of dressings to the skin, the heat-trapping effect of the dressing is low enough that it does not have a significant negative impact on the skin (Table 3). Therefore the authors conclude that the use of a dressing does not elevate the tissue temperature to the point of injury. It is important to observe that typical interventions to reduce pressure risk to the tissue also tend to mitigate heat accumulation, such as turning and offloading, both of which produce an inrush of air that washes the heat from the region at risk, as well as improved exposure to room temperature air (21° C - 23° C). The mechanism of the beneficial effect of reducing skin temperature supports this discussion as described by Tzen and colleagues.28 Moisture. In 1981, Reuler and Cooney29 indicated the presence of moisture from either incontinence or perspiration resulted in a 5-fold increase in risk of ulceration. In measuring the validity and reliability of the Braden scale, it was shown that the presence of excess moisture on the skin is 1 of 4 risk factors predictive of ulceration.30,31 Clark32 found that the relative humidity between the body and support surface was higher for subjects who developed ulcers. In the examination of blister formation, results showed that wet skin is less susceptible to friction and shear-based damage; however, moist skin has a greater risk due to the increase in friction caused by the presence of moisture in quantities too low to be lubricious, but high enough to increase the surface tension between the skin and the contacting surface.33 Moisture management by dressings has been examined and the role of moisture wicking, storage, and evaporation in relation to dressing design described.34 Wildnauer et al16 demonstrated that, as moisture in the skin increases, skin strength decreases. Results in the author’s laboratory indicate all of these conditions are changed when a dressing is applied to the skin. An aggressive moisture-trapping bed can draw too much moisture from the skin in the early phase of use, while dressings that do not breathe adequately will trap moisture and compromise skin viability due to overhydration. In the extreme, these changes will result in undesirable changes in skin properties.16,35 Managing these changes by retaining adequate moisture in the skin to optimize elasticity and minimize maceration, excoriation, and cell stripping is an essential function of a prophylactic dressing. This suggests that the optimal performing dressings are those found in the midrange of the results shown in Table 3. In the case of dressing 3 and dressing 8, both the moisture transmission and the thermal resistance characteristics altered significantly after 90 minutes of exposure to test conditions (Table 6). Grams of moisture trapped in the dressing verses grams of moisture escaping the dressing provides strong evidence of a dressing’s ability to moderate the skin/dressing microclimate and to potentially provide a prophylactic benefit. It should be noted that some references suggest skin moisture should not drop below prescribed levels in order to preserve the skin’s elasticity and protective barrier properties.36 The moisture management demonstrated by dressings in the lower midrange of test results appear to support the observation that moisture in the skin environment not be allowed to fall below 40% relative humidity,36 thus protecting the skin from both dehydration and overhydration. The authors theorize that overhydration exhibited by dressing 3 and dressing 8 will amplify the issues identified by Breuls et al,37 Ceelen et al,38 and Gawlitta et al.39 Overly hydrated cells are more sensitive to compression and shear loading due to reaching the distortion limit at lower forces.37,38,39 This becomes the argument that there is an “optimal band” of moisture for prevention of pressure ulcers using dressings prophylactically (Table 7). Confirming the estimate of the upper limit of this band now becomes the focus in dressing-related prophylaxis. Overhydration of the skin is also responsible for increasing sensitivity to irritants.40 Use of a dressing on the surface of the TRCLI raises the temperature at the interface of the dressing and the TRCLI, as predicted by the Interface Model, except where the dressing’s moisture management bed is saturated. When this occurs, the heat conduction increases and the thermal resistance of the dressing is overcome. At least 3 of the tested dressings maintained a moisture environment comparable with other work that defines a minimum relative humidity in the skin environment that ensures adequate elasticity and strength to respond to typical loading and shear that skin is exposed to in the bed-bound patient.15,35 At least 2 of the dressings (Table 6) retained moisture at a level that will challenge the integrity of the skin exposed to observed moisture levels based on the characterization of skin strength and elasticity shown by Wildnauer16 and Wilkes.35 The ability of a dressing to handle the transdermal water vapor loss of the skin under the dressing appears to play a pivotal role in managing the microclimate of the protected skin. The dressings tested did not follow the classical thermodynamic model for resistance to heat flow based on the thickness of the resistor, which indicates that the specific heat and thermal conduction of each dressing is unique and dependent upon the material of construction; the number of layers; the presence of perforations or micropores in the films used; the concentration of thermally dense polymers; air entrapment in foams; and changes in all of these factors based on the accumulation of moisture in the moisture management bed.
Test data shows a continuing moisture trapped/escaped curve suggesting that the test period should be lengthened to allow the time/moisture escaped curve to approach equilibrium, or to reach the point that would be considered a typical use period for a dressing, for example, 24 hours. It is believed that the size of the dressing does play a role in the outcome of these tests. This belief is based on the test forces being applied to a dressing structure that reacts to the loading as a cohesive unit, dispersing the test load over the responding area of the dressing. Since it was not possible to match the various manufacturers’ dressings to the same size, it seems appropriate to explore the proper methods of standardizing for size and repeating these tests.
Employing the TRCLI to characterize dressing performance yields a sensitive test method for temperature and humidity and moisture escape from the body analog. Historically, the average differences in temperature and humidity are small yet the test system provides adequate resolution to observe significant differences between the dressings tested in this system. The use of a dressing prophylactically alters the skin surface microenvironment for both temperature and humidity. For temperature, the increase is less than half of the estimated threshold for potential heat stress-related ulceration risk. For humidity, the impact can be either negative or positive based on the nature of the dressing and the performance of the fluid handling bed. Two of the dressings tested create environments that are thought to be in the range of risk to the tissue. This was due to high relative humidity where the ultimate relative humidity under the dressing reaches ≥ 70% as seen with dressing 5 and dressing 7. Another area of potential concern is where a dressing’s performance changes due to fluid loading in the dressing’s moisture-management bed; this is a potential risk for dressing 3 and dressing 8. The materials of each dressing’s construction were found to have a significant influence on the temperature of the TRCLI (body analog) under the dressing, particularly when foam was present. These temperature differences did not reach the point of inducing temperature-related injury, which has been a point of potential concern based on the classic thermodynamic model. The significance of the microclimate challenge represented by this study is seen in the heat and relative humidity data where the support surface is a dramatically larger resistor to heat and moisture loss; yet, in this study, it did not obscure the observed results. This is due to the fact that temperatures were measured both inside and outside the dressing, and thus were able to treat the dressing as one of the resistors to heat loss in the system. These measurements were independent of the largest resistor, the support surface. Because there is no direct relationship between dressing thickness and resistance to heat flow through the dressing, it is not possible to use marketing literature or dressing specifications to determine the ability of a dressing to support prophylaxis without testing. The authors recommend dressings be characterized prior to use in a pressure ulcer prevention program.
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Validity and reliability of the Braden scale and the influence of other risk factors: A multi-centre prospective study. Int J Nurs Stud. 2000;37(4):313-319. 32. Clark M. The etiology of superficial sacral pressure sores. In: Leaper D, Wound Management Association, eds. Proceedings of the 6th European Conference on Advances in Wound Management. Amsterdam: McMillian Magazines; 1997:167-170. 33. Mulvaney M, Harrington A. Cutaneous trauma and its treatment. In James WD, ed. Military Dermatology: Textbook of Military Medicine. Part III. Disease and the Environment. 1st ed. Washington DC: Office of the Surgeon General, US Department of the Army; 1994:145. 34. Thomas S. The Role of dressings in the treatment of moisture-related skin damage. World Wide Wounds. 2008. http://www.worldwidewounds.com/2008/march/Thomas/Maceration-and-the-role-of-dressings.htmlmarch/Thomas Accessed March 28, 2013. 35. Wilkes GL, Brown IA, Wildnauer RH. The biomechanical properties of skin. CRC Crit Rev Bioeng. 1973;1(4):453-495. 36. Pressure Ulcers in Adults: Prediction and Prevention: Clinical Practice Guideline Number 3. (AHCPR Publication NO 92-0047). Rockville, MD: Agency for Health Care Policy and Research, United States Department of Health and Human Services; 1992. 37. Breuls RG, Bouten CV, Oomens CW, Bader DL, Baaijens FP. Compression induced cell damage in engineered muscle tissue: an in vitro model to study pressure ulcer aetiology. Ann Biomed Eng. 2003;31(11):1357-1364. 38. Ceelen KK, Stekelenburg A, Loerakker S, et al. Compression-induced damage and internal tissue strains are related. J Biomech. 2008;41(16):3399-3404. 39. Gawlitta D, Li W, Oomens CW, Baaijens FP, Bader DL, Bouten CV. The relative contributions of compression and hypoxia to development of muscle tissue damage: an in vitro study. Ann Biomed Eng. 2007;35(2):273-284. 40. Basketter D, Gilpin G, Kuhn M, Lawrence D, Reynolds F, Whittle E. Patch tests versus use tests in skin irritation risk assessment. Contact Dermatitis. 1998;39(5):252-256. Evan Call, MS; Brian Bill; and Craig Oberg PhD are from the Weber State University, Ogden, UT. Justin Pedersen is from the University of Utah, Salt Lake City, UT. Martin Ferguson-Pell, PhD is from the University of Alberta, Edmonton, Canada. Address correspondence to: Evan Call, MS Department of Microbiology Science Lab Building Floor 3M Weber State University 2506 University Circle Ogden, UT 84408 firstname.lastname@example.org