Dressings can prevent pressure ulcers: fact or fallacy? - Wounds ...

Clinical REVIEWDressings can prevent pressureulcers: fact or fallacy? The problemof pressure ulcer preventionIn part one of this two-part article, the authors discuss the aetiology of pressure ulcers, the means ofidentifying those patients at risk, the range of clinical intervention strategies implemented to try and preventtheir formation and the problems faced by clinicians in developing cost-effective solutions to pressure ulcerprevention. Part two will set out the scientific evidence to support the use of dressing materials to preventpressure damage, discuss the clinical realities faced by clinicians and explore if the use of wound dressingmaterials has any part in a modern pressure ulcer prevention strategy.Martyn Butcher, Geoffrey ThompsonKEY WORDSPressureShearPressure damageGuidelinesEvidence-based practicebeen largely overlooked is the potentialbenefit of using wound care materials notto treat damage, but to help prevent it inthe first instance.Pressure ulcers as an issuePressure ulcers are an all too commonproblem that occur in both hospital andcommunity environments (Weir, 2007;Stotts and Wu, 2009) and are reportedworldwide by numerous authors andagencies (European Pressure UlcerAdvisory Panel [EPUAP], 2003; Clarket al, 2004; National Institute for Healthand Clinical Excellence [NICE], 2005).US estimates of pressure ulcerThe development of pressureulcers in vulnerable, at-riskindividuals is a significant burdenon healthcare resources and it has beenstated that their development can beviewed as an indicator of poor qualitycare (Department of Health, 1993;Olshansky, 2005). Despite position papersindicating some pressure ulcers maybe unavoidable (Wound, Ostomy andContinence Nurses Society [WOCNS],2009), there is still a stigma surroundingtheir formation and a drive to affectimproved preventative strategies. Manydifferent approaches to care have beenadopted to prevent their developmentand yet pressure ulceration remains oneof the most significant issues in healthcare today. One approach which hasMartyn Butcher is an Independent Non-medical Prescriber,Independent Tissue Viability and Wound Care Consultant;Geoffrey Thompson is an Infection Prevention/ControlAudit and Research Nurse, Worcestershire Acute HospitalsTrust NHS UK, Independent Tissue Viability Nurse, Trusteemember, Wound Care Alliance UKACFigure 1. Pressure ulcers: A. Moisture damage to the sacrum; B. Presumed full-thickness damage under eschar;C. Blanching hyperaemia to elbows; D. Mixed levels of tissue damage, grades 1, 2, 3 and possibly 4.BD80Wounds uk, 2009, Vol 5, No 4

Clinical REVIEW8 Pressure duration over the pressurepoints which can result in damagefrom high pressure for short intenseperiods, which can be as damaging aslow pressure for prolonged periods(Bell, 2005)8 Collagen function protecting themicrocirculation helps to maintainthe pressures inside and outsidethe cells preventing cell bursting.Collagen levels vary from personto person with lessening protectivequalities with aging (Russell, 1998)8 Autoregulatory processes initiatedwhen external pressure is sensed,leading to increased internal capillarypressure, reduced blood flow andreactive hyperaemia to counteractthe pressure loading.These mechanisms can fail when theexternal pressure exceeds the person’sdiastolic pressure rather than the32mmHg often quoted (Nixon, 2001).The response of tissue to externalforces varies greatly, being dependenton a large number of factors. It istherefore not possible to establish a‘safe level of pressure’. In addition,tolerance to pressure can vary greatlyfrom individual to individual due tothe interplay of external factors listedin Table 1. Given the highly variablenature of pressure transmission, capillaryclosure and the individual’s normal andadaptive responses to pressure stress,the production of time/pressure curves(mathematical models for predicting thetime likely to cause tissue damage whentissue is exposed to specific levels ofpressure [Reswick and Rogers, 1976])may be of little practical benefit to theclinician in everyday practice (Sharp andMcLaws, 2005; Grefen, 2009).Shear is a mechanical stress appliedparallel to the skin. The SFI describes itas: ‘An action or stress resulting fromapplied forces which causes or tends tocause two contiguous internal parts ofthe body to deform in the transverseplane (i.e. “shear strain”)’ (SFI, 2006).This sliding or twisting force occurscontinuously within soft tissues evenwhen perpendicular pressure is applied,but increases greatly when combinedwith lateral movement, as seen when84 Wounds uk, 2009, Vol 5, No 4the body is adapting to the inclinationof the bed or when sitting in a chair. Ifthe skin adheres to the surface support(which is more likely if the skin is moistor wet from environmental factorsor intrinsically from incontinence orsweating) (Weir, 2007; Beldon, 2008), thetissues attached to the gradually movingskeletal frame become distorted which,in turn, distort the blood vessels leadingto their collapse or rupture.Shear forces are generated as aresult of the interplay of friction andpressure (Collier and Moore, 2006).When applied, shear increases theeffects of pressure resulting in vascularocclusion at only half the pressure ofnon-stressed tissues (Bennett and Lee,1986). Shear forces may also have asignificant role in the development ofdeep tissue damage, although this isdifficult to measure in the clinical setting(Russell, 1998). Potentially, shearing isthe most serious extrinsic risk factordue to the rapidity with which it canresult in tissue damage (Sharp andMcLaws, 2005). This is more likely tooccur in the elderly as a result of loose,fragile skin and the ease with which thedifferent tissue types can be sheared offtheir respective attachments (Allman etal, 1995).The edges of ulcers caused by shearforces appear to be ragged with moreuneven wound margins, often withsurrounding epidermal scuffing. Bruisingmay also be a feature (Figure 4).The mechanisms of shear damagehave important consequences for theplanning and delivery of preventativecare interventions, even though thereare few clinical methods to estimateshearing forces or their resultant effectson tissues (Verluysen, 1985). It is hopedthat the work of the SFI will add to thisbody of knowledge.Friction is a complex phenomenonwhich depends on complex physicalscience and engineering concepts. Insimplistic terms, within the context offriction-induced tissue damage, we arereferring to kinetic friction. Kinetic (ordynamic) friction occurs when twoobjects are moving relative to eachFigure 3. Sacral area showing clinical features ofblanching hyperaemia.Figure 4. Shear pressure damage occurring in ayoung woman during childbirth.other and rub together. Bergman-Evanset al (1994) define it as the resistanceto lateral movement. Kinetic friction isdependent on mass, force applied andthe friction co-efficients of the surfacesinvolved. Clinically, the effect of frictionbetween the skin and a support surfacehas important dynamics that can initiatepressure ulcer formation:8 It can cause excessive wear to thecornified layers of the skin withresultant exposure of the underlyingstructures (Read, 2001)8 It can cause the formation of blistersas separation occurs between thelayers of the epidermis leading to

Wound Clinical care REVIEW SCIENCEexposure of the underlying dermis(Butcher, 1999)8 The deformation of skin can leadto further deformation in deepertissues (shear damage).The amount of damage causeddepends on tissue resistance andthe interplay of friction and pressure.Pressure and friction together causemore damage than friction alone and willinduce greater shear forces (Figure 5).MoistureAlthough not directly indicated asa mechanism of pressure damage,the role of moisture is pivotal in thedevelopment of friction damage andso is a secondary factor in shear forces(Beldon, 2008) (Figure 6). Moisturelevels within the cells of the epidermishave a direct bearing on the frictionco-efficient of this tissue. Even atrelatively low levels, moisture causes arise in friction co-efficient making skin‘stick’ to surfaces (Nacht et al, 1981). Inaddition, when exposed to moisture forprolonged periods, the keratinised cellsof the epidermis swell and becomewaterlogged. This reduces their abilityto withstand friction and can result inepidermal stripping.These features have new relevancesince the re-classification of moisturelesions (Bethell, 2003; Butcher, 2005;Beldon, 2008). There is a closeassociation between incontinencedermatitis, moisture-induced damageand superficial pressure ulceration. TheEPUAP have suggested that moistureinduceddamage should be categorisedseparately from pressure ulcers. Inpractice, this differentiation can bedifficult to interpret clinically. Defloorand Schoonhoven (2004) and Deflooret al (2005) identified that reliabilityof the EPUAP tool was low whenused to differentiate moisture lesionsand superficial pressure ulcers fromphotographic evidence. Indeed, writerssuch as Houwing et al (2007) argue thatsuch a distinction should not be madeas it distracts clinicians from the needto implement appropriate pressureulcer prevention strategies, and, asMcDonagh (2008) points out, these twophenomena can co-exist within a clientat a given point in time.Aetiological pathwaysControversy exists as to the aetiologicalroute by which pressure ulcers formand progress. It is acknowledged thatpressure ulcers are primarily causedby sustained mechanical loading,however, prevention of ulcer formationby reducing the degree of loadingalone remains difficult to achieve. Thisis mainly due to poor understandingof the underlying pathways wherebymechanical loading leads to tissuebreakdown (Bouten et al, 2005).Three theories have been postulatedto explain this process:1. Pressure ulcers form via the topto-bottommodel2. Pressure ulcers form via the bottomto-topmodel3. Pressure ulcers form via a middleapproach model.Theory 1Pressure and shear induce localischaemia, and impaired drainageimpairs the transport of oxygen andnutrients to and metabolic wasteproducts away from the cells within theaffected tissues. Eventually this leadsto cell necrosis and the formation ofan ulcer. There are sound argumentsfor damage to muscle tissue as it ismetabolically more active than skin.Theory 2This model states that when pressureis relieved from the compressed tissuesby patient repositioning or the useof an alternating pressure-alleviatingmattress (APAM), it is the restorationof blood flow after the load-removalrather than impaired blood flow duringpressure loading that is the mechanismof tissue necrosis. It is claimed that it isan over-abundant release of oxygenfreeradicals during pressure off-loadingthat causes the damage.Theory 3In the third model, tissue damage maystart anywhere between the skin andthe underlying bone, but can includethe skin surface and bone interface,concurrently or haphazardly, to producea pressure ulcer.Prevalence and incidence of pressure ulcersUnless correctly identified and treated,pressure ulcers can have a significanteffect upon the patient’s quality of lifeFigure 5. Shear and friction damage to stump from badly fitting prosthesis.Figure 6. Sacral region showing clinical features ofmoisture damage combined with shear and pressure.86 Wounds uk, 2009, Vol 5, No 4

Clinical REVIEWand may, under certain circumstances,prove fatal. The deaths of thousandsof patients are attributed to pressureulcers and their complications everyyear (Agam and Gefen, 2007). Datarelating to incidence (a statisticalmeasurement of the number ofindividuals developing a condition) andpressure ulcers varies considerably. Arecent literature review investigatedpressure ulcer prevalence and incidencein intensive care patients. The analysis ofdata from published papers highlightedthese variations with pressure ulcerprevalence (the number of individualswith pressure ulcers as a percentageof the total defined population at onepoint in time) in intensive care settings,ranging from 4% in Denmark to 49% inGermany, while incidence ranged from38% to 124% (Shahin et al, 2008). Ina Canadian study in 2004 the nationalprevalence figure across all care settingswas estimated at 26% (Woodbury andHoughton, 2004). More specifically,a recent study has shown that theprevalence of pressure ulcerationwithin the population receiving healthcare in Bradford, UK was 0.74 peoplewith a pressure ulcer per 1000population (95%, CI 0.6–0.8) (Vowdenand Vowden, 2009).Cost of pressure ulcers to health carePatients with pressure ulcers place aburden on health care as they require asignificant amount of medical resourcesto treat. A recent survey evaluatedthe impact of wound care in Bradfordand Airedale NHS Primary Care Trustin the UK (Vowden et al, 2009), andshowed that the prevalence of patientswith a wound was 3.55 per 1000population. The estimated cost to theUS hospital sector is $11 billion perannum (Bales and Padwojski, 2009). Thishas been considered unsustainable andunacceptable. In an effort to controlcosts and raise quality standards, theCenters for Medicare and MedicaidServices (CMS) has determined itwill no longer reimburse hospitals fortreating a range of hospital-acquiredconditions including pressure ulcers(Bergquist-Beringer et al, 2009). Thisis having a serious impact on UShealthcare management and serviceprovision and has lessons for the UK88 Wounds uk, 2009, Vol 5, No 4healthcare sector. The majority ofwounds were surgical/trauma (48%),leg/foot (28%) and pressure ulcers(21%). Prevalence of wounds amonghospital inpatients was 30.7%. Of these,11.6% were pressure ulcers, of which66% were hospital-acquired. Furthercases have received attention; over$3 million was awarded by a Floridacourt in 2008 (Legal Eagle, 2008),while the Supreme Court of Mississippiapproved a $1 million award against anursing home (Legal Eagle, 2007).In a study undertaken on patientsdeveloping a pressure ulcer to estimatethe annual cost of treating pressureThe direct costs of patienttreatment are not theonly area of expense.Increasingly, the spectreof the threat of legalaction is taking a greaterplace in pressure ulcermanagement.ulcers in the UK, the actual costs werederived from a bottom-up methodology,based on the daily resources required todeliver protocols of care reflecting goodclinical practice. The results showedthat at this time the cost of treatinga pressure ulcer varied from £1,064(grade/stage 1) to £10,551 (grade/stage4). Costs increase with ulcer grade/stagebecause the time to heal is longer andbecause the incidence of complicationsis higher in more severe cases. At thetime of writing, the total cost in theUK was estimated at £1.4–£2.1 billionannually (4% of total NHS expenditure).The study also showed that most of theassociated cost was related to nursetime (Bennet et al, 2004). Vowden et al(2009) also concluded that the mostimportant components are the costsof wound-related hospitalisation andthe opportunity cost of nurse time (theindirect cost incurred to the healthcareprovider by the nurse undertakingcare for this individual which wouldotherwise be utilised caring for otherpatients). In total, 32% of patients treatedin hospital accounted for 63% of totalcosts, of which the development ofhospital-acquired pressure ulcers werea significant component and focus forpotential cost reductions.Legal issuesThe direct costs of patient treatmentare not the only area of expense.Increasingly, the spectre of the threatof legal action is taking a greaterplace in pressure ulcer management.In a US study, hospital stays for thetreatment of pressure ulcers havebeen estimated to be in the regionof $37,800 (Weir, 2007). It has beenshown that these patients require 50%more nursing time, remain hospitalisedfor significantly longer periods, andincur higher hospital charges (Bradonand Endowed, 2008). Pressure ulcersare the leading iatrogenic causes ofdeath reported in developed countries,second only to adverse drug reactions(Barczak et al, 1997).In November 2000 the State ofHawaii convicted an individual ofmanslaughter in the death of a patientat a nursing home for permittingthe progression of decubitus ulcerswithout seeking medical help, andfor not bringing the patient back to adoctor for treatment of the ulcers (DiMaio and Di Maio, 2002). A number ofauthors have highlighted the increasein litigation associated with malpracticerelated to pressure ulcers not only inthe US (Bennet et al, 2000; Levine et al,2008; Meehan and Hill, 2009), but alsoin Europe (Cherry, 2006). It thereforemakes clinical and economic sense totakes measures to minimise pressureulcer risk by taking preventative actions(Meehan and Hill, 2009).Standard preventative interventionsPossibly due to the emphasis ofscientific research on the role ofpressure within pressure ulcer aetiology,most effort appears to have goneinto strategies to reduce or attemptto eliminate pressure in the clinicalsetting. Over the past thirty years manymanufacturers have developed a widevariety of support surfaces, principallymattresses, aimed at this particularendpoint. With such a wide range ofproducts there can be confusion overproduct selection for a given pressure

Clinical REVIEWulcer risk (Rithalia, 1996), and thereis a need for an understanding ofthe difference between the mattressand cushion classes (Finucane, 2006).Standard interventions to preventpressure ulcer formation have includedthe use of specific redistributivesurfaces as either pressure-reducingappliances or pressure-relievingmattresses or cushions.Pressure-reducing support surfacesvary from relatively simple foam andslashed foam constructions to gel,fluid, and air-filled systems. There arealso more complex dynamic pressurereducinglow airloss systems anddynamic foam (Thompson, 2006;Gray et al, 2008), or forms of ‘air-float’(Thompson et al, 2008) in whichpressure at the interface between thedependent skin and the support surfaceis reduced through the use of theconforming support surface, therebyspreading load and reducing pressureper square centimetre.In addition, the materials that used tocover such devices have become moretechnically advanced with non-stretchPVC covers giving way to two- andthree-way stretch which encouragesgreater conformity between the bodyand the mattress/cushion. Improvedvapour permeability with PU materialsalso reduces the risk of moisture buildupat the interface, with the aim ofreducing the friction/shear co-efficient(Jay, 1995).It stands to reason that if one ofthe major components of pressureulcer formation is the application ofunrelieved pressure, then the reductionof this pressure to sub-morbid levelsis a key factor in pressure damageprevention. Pressure redistributionthrough offloading provides tissues withthe time needed for cellular repair andthe restoration of normal cellular activity.In its basic form, this is achieved byoffloading tissues through either manualrepositioning or the use of splints,wedges and other repositioning devices(Guttmann, 1955, 1976).Cyclical offloading teamed with theuse of a conforming interface is one90 Wounds uk, 2009, Vol 5, No 4approach to this problem. This approachis adopted by those using APAMswhere load is supported by alternating,conforming air cells. These cellsperiodically change their pressure profilein a pre-set cycle, thereby altering thearea of tissue exposed to compressionstresses. However, some clinicians preferconstant low pressure support surfaces,such as those found in air fluidised andlow air loss systems. Unfortunately, thereis little data to indicate which approachis preferable.Reduction of friction and shearWhile friction and shear are cited asthe other mechanisms of pressuredamage, due to technical and ethicalissues little research has beenundertaken in this area (Ohura et al,2005). For this reason, the reduction ofthese components in clinical practicehas generally been undertaken basedon anecdotal evidence. Due to therisk of increasing shear forces, previouspractices such as massage of highrisk tissues have been indicated asdangerous (Dyson, 1978; Pritchardand Mallett, 1993; Buss et al, 1997;Shahin et al, 2009), and so have beenlargely abandoned. Clinicians havebeen advised to use care in positioningpatients to minimise shear force,(Maklebust, 1987; AWMA, 2001) andto use low-friction turning/repositioningaids to minimise skin and soft tissuedamage (Butcher, 2005). Some writershave also indicated that the use ofdressings and skin sealants may help inreducing friction and therefore reducethe risks of friction damage and shearforces (AWMA, 2001; Black, 2004;Butcher, 2005).The practice of using simpleadhesive dressings to minimise frictionis accepted by many authorities ascommonplace among healthcareworkers and the general public. Howmany of us have used adhesive tapeor wound plasters on our heels toprevent new footwear from rubbingand producing painful blisters? (Is thisany different from the concept of usingdressings to prevent pressure ulcers?)The effects of ‘rubbing’ are to producefriction which is, by definition, one ofthe primary mechanisms of pressureulcer formation. However, somewound care practitioners continue towarn that dressings do not preventpressure damage and, as such, their useis neither scientifically validated norcost-effective.This is a contentious issue whichdemands further inspection. Itsrelevance cannot be overstatedwhen one considers that while theclinical community is aware of themechanisms of pressure damageand enormous amounts of moneyhave been invested in pressureredistributive surfaces, particularlythe dynamic devices, pressure ulcersremain such a common occurrence(Vangilder et al, 2008).In the second part of this paperin a subsequent issue of Wounds UK,the authors will look at the evidenceavailable to support the use of dressingsto prevent pressure ulcer formation, andwhat properties such products mightneed to make them an effective tool inclinical use. 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