Julie Hewish Senior Tissue Viability Nurse Community .

Julie HewishSenior Tissue Viability NurseCommunity Tissue Viability.

Questions What is a wound? Give me a definition.What is the definition of wound healing?When does an acute wound become a chronic wound?Are chronic wounds the same as Hard to heal wounds?Are wound types treated differently i.e. A pressureulcer differently to a leg ulcer? Do we assume the wound will heal unless convincedotherwise? Isn't it about the dressings? If we had MORE choice,we’d heal the wounds quicker!

A wound - definition A wound may be defined as the interruption ofcontinuity in a tissue, usually following trauma. Skin ispredominantly affected although any tissue, whethernerve, bone or organ, may be wounded.

Wound healing - definitions the process of returning to health; the restoration ofstructure and function of injured or diseased tissues. Wound healing, is an intricate process in which theskin (or another organ-tissue) repairs itself after injury. Wound healing can be defined as the physiologicalprocess by which the body replaces and restores thefunction of damaged tissue. (Flanagan 1997)

Chronic wounds or Hard to Heal –are they the same?

Chronic wounds - definitionTypically they have a duration of more than4 weeks and are characterised by the failureto progress through the normal stages ofwound healing (Menke, 2007)

Hard to Heal definition One that fails to heal with standard therapy inan orderly and timely manner (Troxler, Vowden & Vowden, 2006)

Its all about timing Hard to heal definition can be applied to bothacute and chronic wounds and is independent ofthe wound type and aetiology Many wounds are challenging to manage Delayed healing occurs in a variety of wound types Although common, delayed healing is frequentlynot recognised early enough

The human costs

Wounds the patients view ‘Pain was terrible.God almighty, the painwas terrific.it was unrelenting.’‘I couldn’t walk about.I packed up driving.I was on crutches.I couldn’t take the kidsswimming.I didn’t go out.’ ‘You get the feeling that other people [wonder]what the hell is that dog doing down there, whenthe dog goes past everyone else, you know.’

The patients view ‘.and when they used to come twice a week todo my legs, sometimes three, if I did want togoout, I couldn’t go out ‘cos they held me in. Youdon’t know what time they are going to call somy life was round the district nurse.’ ‘I am very conscious of it, if its there I thinkto myself I can smell myself, somebody elsecan.’

The patients view ‘But what made me angry, really, all the time was,nobody ever seemed to be really doing anything. Justone dressing off, put another one on There you go,see you in two to three days’ time ’ Exudate ‘Stench’, ‘dirty’, ‘unpleasant’, ‘horrible’,‘obnoxious’, ‘rotten’, ‘terrible’ ‘My friends say, come on But I say when you are inpain all the time, it’s miserable. I feel better sat athome quietly ’

Glass half empty .Treat all wounds aspotentially hard toheal

Facts chronic wounds: Affect 1 – 2% of the population (Anderson, 2006) Costs the UK 1 Billion per year As nurses we spend 40 – 50% of our time supportingPts with chronic wounds They have a detrimental impact on a Pts QoL Lost working days Social isolation Depression/ anxiety Increased stress leads to further non healing

General differences between acute &chronic woundsAcuteChronicShort durationNot healed by 6 weeksNo underlying pathologyUnderlying pathologyNormal inflammatory stageProlonged inflammatory stageUsually heals without complicationA variety of complications may ariseAcute wound fluid supports proliferationCWF does not support proliferationWound fluid doesn’t damage peri- wound skinCWF damaging to peri-wound skinNeutrophil, elastase and MMP levels normalNeutrophil, elastase and MMPs levels highFibrinectin intactFibrinectin degradedNormal remodelling of ECMDefective remodelling of ECMNormal growth factor levelsLower levels of GFsNormal levels of inflammatory cytokinesIncreased levels of pro-inflammatory cytokines

How do wounds heal? Normal healing process is a well orchestrated, complexand interlinked series of four well recognisedoverlapping phases

Understanding normal healingFour phases of wound healing:1. Vascular response (or coagulation)2. Inflammation3. Proliferation4. MaturationNot all wounds follow this initial stage as this dependsupon the nature of the wounding (i.e. pressure ulcers orC6 stage leg ulcers)The normal process can be interrupted at any stage and isvulnerable to a variety of intrinsic and extrinsic factors

Extra cellular matrix Largest component of normal skinGel like matrixComposed ofpolysaccharides, water andcollagen proteinsServes as a scaffold for cellsRegulates cellular functionsLubricates cellsProvides a transport systemfor nutrients and wasteproducts

Wound healing analogy

Vascular response Trauma Bleeding Air initiates clotting processsupported by plateletaggregation (clumping) Coagulation cascade –formation of fibrin meshwhich closes woundtemporarily – dries to formscab Blood and serous fluid helpsto cleanse wound surface.

Inflammation 1 Release of inflammatorymediators (protaglandin &histamine) from mast cells Blood vessels adjacent toinjured area become morepermeable (vasodilation) Presence of heat,erythema, discomfort andfunctional disturbance. Increase in exudate due toincreased permeability ofcapillary walls. This is richin nutrients, growthfactors and enzymes(MMPs)

Inflammation 2 Neutrophils arrive within a few hours of injuryPrimary role is 1st linedefence against infectionPhagocytotic action,killing bacteria andbreaking down foreignmaterials and devitalisedtissueProduce and releaseinflammatory mediatorswhich recruit and activatefibroblasts and epithelialcellsShort life span.

Inflammation 3 Macrophages andlymphocytes becomeprominent in the wound bedand help with the clean up byregulating phagocyticactivity. They also encourageproduction of enzymes(growth factors) andcytokines. Cytokines are usedextensively in intercellularcommunication (Projectmanager!) These cells control thetransition from inflammationto proliferation – preparing forrepair men!

Proliferation 1 - ECM Production of newgranulation tissuethrough collagenproduction (Scaffolding)and angiogenesis (newblood supply) Fibroblasts are key cellsin this phase (beingresponsible forproduction of collagen)but they also produce theExtra cellular matrix(ECM)

Proliferation 2 Provisional wound matrix isremodelled and replaced withscar tissue which partiallyrestores structure & functionof tissues. Migration and proliferation ofepithelial cells and fibroblastsfrom uninjured tissue andstem cells circulate to woundsite. In normal dermis fibroblastsare slow and sparselydistributed, in provisionalwound matrix they arenumerous and active migratingin response to cytokines(communication cells) andgrowth factors released

Migration of fibroblasts Moves by binding tomatrix components such ascollagen While one end remainsbound the cell extends acytoplasmic projection tofind another binding site When found, theattachment to the originalsite is broken by proteasesecreted by the fibroblast Cell uses its cytoskeletalnetwork of fibres to pullitself forward.

Fibroblasts

Maturation Wound becomes less vascularisedCollagen fibres arereorganised lying at rightangles to the wound margins.Collagen is constantlydegraded and new collagensynthesised.Highest activity occursbetween 14 – 21 days.Scar tissue is graduallyremodelled and becomescomparable to normal tissueafter a long period of time.Can take 12 – 18 months andfull tensile strength notregained (Approx 80%)

MMPs (Matrix metalloproteinases) Part of a larger family of Metalloproteinases that playan important role in wound healing. They are produced by inflammatory cells (Neutrophils& macrophages) and wound cells (epithelial,fibroblasts and vascular endothelial cells). When first synthesised, MMPs are latent. They areactivated by other proteases. 23 MMPs have been identified. MMP – 1, 2, 8 & 9 arerelated to wound healing.

Matrix Metalloproteinases (MMPs) Essential for the migration of cells through the ECMThey remove collagen and otherECM components that weredenatured during injuryImportant because collagenmolecules must interact witheach other to form a fibril (Finefibre)Partially degraded matrix willnot bind resulting indisorganised, weak ECMDegraded collagen must beremoved by the controlledaction of MMPsHole in the wall image

MMPs ctd MMPs “Chew back” the denatured matrix to reachintact functional matrix It must be carefully controlled by tissue inhibitors ofmetalloproteinases (TIMPS) to prevent MMPs fromdegrading intact functional matrix This controlled action of proteases on ECM plays a keyrole in regulating angiogenesis and other aspects ofnormal wound healing.

MMPs in normal wound healingRole of MMPsMain phase of healing Removal of damaged ECM andbacteriaInflammation Degradation of capillary basementmembrane for angiogenesis (temporarybreakdown of the ECM) Migration of epidermal cellsProliferation Contraction of scar ECM Remodelling of scar ECMMaturation/ remodelling

Why do MMPs cause problems? MMPs present in a wound bed at too high a level fortoo long a time begin to degrade proteins such asgrowth factors and ECM proteins essential for healing.This ultimately impairs healing. Evidence has found that MMPs in general are highlyelevated in wounds with delayed healing compared toacute healing wounds.

How do we know that MMPs arecausing healing problems? Ability to heal is affected by a wide range of intrinsicand extrinsic factors. However, Regardless of underlying cause of the delay, H2Hwounds generally share similar characteristics,including: Elevated inflammatory markers High levels of proteases Diminished growth factor activity Reduced call numbers in the woundHostile wound environment, wounds are stuck inthe inflammatory phase of healing

How do we as nurses know? Wounds are failing to progress Wounds appear ‘inflammatory’ Cycles of local wound bed infection Less than 40% wound area reduction in 4 – 6 weeks isa significant indicator A protease testing kit has been developed.

Vicious circle of delayed wound healing

Assessment

How can we improve healing rates?

Putting the patient at the centre ofwound care Holistic approach Identifying reasonsfor non concordance Quality of life/wellbeing Joint care planning Outcome driven Timely referral Social model Audit

So how do we do this?Holistic approach

Holistic assessment3 Groups Patient related factors – Intrinsic Patient related factors – Extrinsic Wound related factorsWhat are these?

Patient related factors - Extrinsic Non concordance Social isolation Financial/ employment issues Environmental Nurse/ pt relationship Is a carer for others Cultural/ religious beliefs Previous experiences Lifestyle choices

Wound related factors Long wound durationLarge wound ( 100cm²)Full thickness wound (Exposed tendon or bone)Underlying osteomyelitisFailure to progress by 40% at 6 weeksPresence of devitalised tissuePresence of local infectionPresence of systemic infectionHigh exudate levelsWounds over a moveable jointWounds that are in close proximity to an ‘orifice’ (ie anus, stoma)Inflammatory/ excoriated or macerated peri wound skinPresence of oedemaHistory of previous damage to same siteMalignancy

Wound bed assessment- tissuetype Assessing the tissue in the wound bed informs thephase of healing a wound may be in and aidsdiagnosis. Part of your management plan should bebased on wound bed status.Is the wound bed

Necrotic

sloughy

granulating

epithelialising

Assess for Infection Wound infection is a problem because it delays healingDefining the term infection is importantThe presence of bacteria does not necessarilyconstitute infectionWound swabs will not diagnose infectionIdentification of clinical signs of infection is essentialfor diagnosisNot all clinical signs are associated with a woundinfectionFollow your local guidelines