Implementing TIMERS: the race against hard-to-heal wounds
2019; Mark Allen Group; Volume: 28; Issue: Sup3a Linguagem: Inglês
10.12968/jowc.2019.28.sup3a.s1
ISSN2052-2916
AutoresLeanne Atkin, Zofia Bućko, Elena Conde Montero, Keith Cutting, Christine Moffatt, Astrid Probst, Marco Romanelli, Gregory S. Schultz, William H Tettelbach,
Tópico(s)Diagnosis and Treatment of Venous Diseases
ResumoJournal of Wound CareVol. 28, No. Sup3a Free AccessImplementing TIMERS: the race against hard-to-heal woundsLeanne Atkin, Zofia Bućko, Elena Conde Montero, Keith Cutting, Christine Moffatt, Astrid Probst, Marco Romanelli, Gregory S Schultz, William TettelbachLeanne AtkinVascular Nurse Consultant. Mid Yorkshire NHS Trust/University of Huddersfield, EnglandSearch for more papers by this author, Zofia BućkoHead of Non-Healing Wounds Department, Centrum Medycznym HCP, Poznań, PolandSearch for more papers by this author, Elena Conde MonteroSpecialist in Dermatology. Hospital Universitario Infanta Leonor, Madrid, SpainSearch for more papers by this author, Keith CuttingClinical Research Consultant, Hertfordshire, Honorary, Tissue Viability Specialist, First Community Health and Care, Surrey, EnglandSearch for more papers by this author, Christine MoffattProfessor of Clinical Nursing Research, University of Nottingham, and Nurse Consultant, Derby Hospitals NHS Foundation Trust Lymphoedema Service, EnglandSearch for more papers by this author, Astrid ProbstAdvanced Nurse Practitioner Wound Care, Klinikum am Steinenberg/Ermstalklinik, Reutlingen, GermanySearch for more papers by this author, Marco RomanelliPresident WUWHS, Associate Professor of Dermatology, Department of Clinical and Experimental Medicine, University of Pisa, ItalySearch for more papers by this author, Gregory S SchultzResearcher, Professor of Obstetrics and Gynaecology, University of Florida, Gainesville, Florida, USSearch for more papers by this author, William TettelbachAssociate Chief Medical Officer, MiMedx, Georgia. Adjunct Assistant Professor, Duke University School of Medicine, Durham, North Carolina. Medical Director of Wound Care and Infection Prevention, Landmark Hospital, Salt Lake City, Utah, USSearch for more papers by this authorLeanne Atkin; Zofia Bućko; Elena Conde Montero; Keith Cutting; Christine Moffatt; Astrid Probst; Marco Romanelli; Gregory S Schultz; William TettelbachPublished Online:5 Mar 2019https://doi.org/10.12968/jowc.2019.28.Sup3a.S1AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareShare onFacebookTwitterLinked InEmail ForewordIn July 2018, the authors of this document met in the Royal Borough of Windsor to discus hard-to-heal wounds. The two-day meeting resulted in this consensus document. It is a very difficult area to examine; even the starting point is complicated. What is a non-healing wound? Or is that a chronic wound? Or a hard-to-heal wound? Is this different for every wound type? Does the definition vary by aetiology? Probably. By region? Possibly. A favourite was wanting to ask the panel if there is such a thing as a chronic, hard-to-heal or non-healing wound, or are they wounds that haven't been assessed and treated with a good standard of care (SoC) from the beginning? Then there were the difficult ethical questions, such as should you stop treating the wound of a non-adherent patient?Over the two days, these questions and many others were examined at length. Here we are going to try and summarise the main points of this consensus. In terms of what to call these wounds, it was decided hard-to-heal was the most appropriate—not wanting to put the emphasis on non-healing, that all starts off a little negative. There is also a body of literature out there, and in the document, on when you would consider a wound to be hard-to-heal. This was quite a tough one;in diabetic foot ulcers (DFU) <50% reduction over four weeks is considered hard-to-heal. In venous leg ulcers (VLU) the value is <40% and in pressure ulcers (PU) the value is 60.8,9,10 A percentage of wounds may not heal completely for a year or more,11,12 and this places a significant burden on health-care systems and economies. In the context of this consensus statement, complete healing means full epithelial resurfacing and discharge, or transition to patient-management strategies to prevent recurrence.Hard-to-heal wounds consume disproportionate amounts of medical products—devices and medicines—and the time of health professionals. Despite the relative standardisation of management for chronic wounds, healing rates vary considerably.13,14,15,16,17,18 DFUs classified as stage 4 according to the Wound, Ischemia, and foot Infection (WIfI) system19 may take up to a mean of 190 days to heal.20 VLUs properly managed with 12 weeks of compression have healing rates of 32 to 55%; at 24 weeks, up to 68% may heal.21,22,23,24 Furthermore, between 12% and 47% of VLU patients managed over 12 months may not heal.10,25,26,27,28 Healing rates with compression bandaging over more extended periods of up to 420 days can reach around 90%12 and over 500 days, 93%.29Up to 10% of patients with diabetes have a DFU and the lifetime incidence is reported to be 19%, but may be as high as 34%.30,31 Furthermore, the prevalence of diabetes is increased in the elderly32 population, resulting in an increase in the prevalence and incidence of DFU. Lower extremity ulcers including DFU may last for up to 13 months with estimates that nearly 40% of patients have a recurrence, within one year of their DFU healing.31 Healing times in more severe DFU are worse than in less severe ulcers19,33 and referral times are longer.34,35Analysis of The Health Improvement Network (THIN) database of patient records managed by primary care in the UK has identified deficiencies in delivery of care for VLU and DFU related to diagnosis1 and appropriate wound management.1,2 Referrals may take place in months rather than the recommended days.36 Over a 12-month period, approximately 50% of PUs may heal. However, the proportion of PUs that heal is inversely proportional to its category. In Guest et al,37 all category I PUs healed over the 12-month audit period, but the likelihood of a category IV or unstageable PU healing was less than 20%.37There may be significant deficiencies in the knowledge among nurses,38,39,40 an issue recognised by many.41 A survey of community nurses in Ireland found that more than half did not use Doppler to assess ankle-brachial pressure index (ABPI) in the assessment of VLU patients.42 Differences43 and deficiencies in referral and care have been noted in other countries.44,45,46Patient engagement is an important part of the equation and may be affected if they cannot understand the reason(s) for the management of their wounds.47 This will likely lead to poor adherence to the care plan and poor healing. Often, the evidence for efficacy of many medical products is limited and of poor quality48 and carers find managing chronic wounds challenging.49There is a variable understanding among general practitioners (GPs) about the underlying causes of chronic wounds and incomplete understanding of the organisation of care pathway structures.50,51 A study from four European countries showed that not all GPs identify specialised practitioners to refer patients to, and many are unaware of clinical guidelines and protocols.50,51 These factors are highly likely to be contributors to poor healing outcomes and to be mirrored in health-care systems worldwide.Patients with chronic wounds suffer increased morbidity and decreased quality of life (QoL).52,53,54,55,56,57,58,59,60,61,62,63,64,65,66,67There have been and are numerous studies assessing the financial cost of hard-to-heal, chronic wounds, of many different types.57,58,59,60,61,62,63,64,65,66,67 These assessed parameters including nursing time and length of stay in hospital, along with how severity increases costs, some examples are shown in Table 1.Table 1. Examples of the cost of hard-to-heal woundsAetiology and situationCostsVLU >grade 1 UK37£7600 (2015/2016)PU >grade 1 UK37£7800 (2015/2016)VLU >grade 1 UK37>£8500 (2015/2016)VLU Community care, Germany€9060 (2014)Chronic wounds Medicare>US$52 billion (2014)Hospital acquired PU USUS$8041 per ulcerDFU61US$44,200 yearlyDFU Europe36€10,000 yearlyVLU—venous leg ulcers; PU—pressure ulcer; DFU—diabetic foot ulcerTable 1. Examples of the cost of hard-to-heal woundsView as image HTML A number of factors may influence the likelihood of a wound healing. Variation in delivery of care affects outcomes. The skill level of the health professional, particularly outside specialist centres, may be insufficient to ensure optimal treatment.68,69,70 Diagnosis,71 referral36 and delivery of a recognised standard of care (SoC) may be suboptimal.10,71,72,73,74 The diagnosis and management of the underlying condition may vary. For example, the application of compression bandages is known to be variable75 and the outcomes in plantar neuropathic DFU are significantly affected by the type of offloading76,77 used, which varies considerably,78 particularly as the foot changes shape.79 Patients with severe ischaemia may not have vascular reconstruction.36 These variations may be compounded by different guidelines that present similar advice on care, but may vary to the point of contradicting each other, leading to confusion in implementation.80,81Patient-related factors that influence outcomes include comorbidities—there is a correlation between the worst wounds and the sickest patients, as patients with multiple comorbidities are the ones that often fail to heal82—severity of the underlying condition, illness beliefs83 and adherence to the care plan. Adherence to the care plan84 is considered a key factor in successful management of chronic ulcers.This consensus statement addresses the challenge of long-term, hard-to-heal wounds—those that do not close after care for up to a year or more. Importantly, we emphasise the need to assess patients quickly and intervene early with the optimal SoC to increase the probability that a wound will heal.This working document addresses general principles and provides guidance intended to maximise the likelihood that wounds that have not healed over extended periods will progress. It should be read and implemented in conjunction with the clinician's local guidelines. It brings theory and practice together and offers areas of reflection that allow the reader to review the information and then decide where and how to use it to underpin their own practice.Key pointsHard-to-heal wounds affect the patient's quality of life, as well as being a burden on the health-care systemIncidence of hard-to-heal wounds is rising as the age of the population increasesPatient-related factors that influence outcomes include comorbidities, severity of the underlying condition and adherenceCorrect treatment at an early stage could prevent many hard-to-heal woundsProvider-related factors include awareness of treatment options available, the influence of external wound-healing inhibitors such as biofilm and availability of productsThis document addresses the challenge of long-term, hard-to-heal wounds—those that do not close after care for up to a year or moreSection 2. Identification of hard-to-heal woundsChronic wounds start by either direct trauma to tissue already compromised by underlying pathology or by breakdown of tissue under unbroken skin. Patients with diabetic neuropathy may not be aware of the trauma—pressure, friction, shear or penetrating/other injury—that has led to the wound. Patients with undiagnosed venous disease may notice abrasion or laceration, but not understand the seriousness of the wound. In instances when the wound does not heal and the patient does not understand its seriousness, they may attempt self-care before seeking advice from a health professional. In many cases, that would be a GP or physician who may have limited knowledge of wound care.Wounds can fail to heal due to a lack of understanding/awareness of the importance of establishing and treating the underlying pathophysiology, which has either caused the wound or provides significant barriers to healing. It is important that these factors are addressed or managed to optimise healing outcomes. Crucially, a ‘hard-to heal’ wound needs to be flagged by a health professional before intervention can take place. The key to effective care is application of SoC, including identification of risk factors, monitoring outcomes and recognition of the correct course of action if the wound responds or it does not.Risk factors for hard-to-heal woundsFig 1 summarises the risk factors associated with hard-to heal wounds. Risk factors may be characterised as disease state and pathophysiology specific to the wound aetiology; clinical risk factors not specific to the aetiology; and patient-related and non-clinical risk factors.Fig 1. Risk factors for hard-to-heal wound formation. Note: the more factors a patient has, the more likely the wound will not healDisease state and pathophysiologyDetails of pathophysiology are discussed in section 3 and are summarised here.Venous leg ulcersThe most important risk factor for developing a VLU is underlying chronic venous disease that leads to chronic venous insufficiency, a spectrum of diagnoses of increasing complexity classified by the Comprehensive Classification System for Chronic Venous Disorders (CEAP).85,86 Other classification systems for chronic venous disease have been developed.87Chronic venous disease leads to haemodynamic changes88,89 that increase intravenous blood pressure in the deep, superficial and/or perforator systems. Venous insufficiency or muscle pump deficiency reduce the effectiveness of return of blood to the heart, and defects in the intravenous valves lead to venous reflux and blood pooling in the lower extremities. The high venous pressure caused by pooling stimulates chronic inflammation that eventually makes the skin break down to form a VLU. Effective management of VLU addresses venous hypertension with external compression and potentially venous intervention.Diabetic foot ulcersDiabetes may lead to a number of risk factors for ulcer formation. Key risks are:90Peripheral neuropathy (sensory, motor and autonomic neuropathy)Sensory: reduces or eliminates touch sensation and nociception Motor: foot deformity as a result of distal nerve damage, causing small muscle wasting and muscle atrophy. The protective fat pads over the heel and metatarsal heads become displaced, and atrophy exposing bony prominences to pressure damage and callus formation could lead to ulcerationAutonomic: leads to lack of sweating, dry skin, cracking and endothelial dysfunctionPeripheral arterial disease (PAD) leading to ischaemiaA history of previous DFU.A number of classification systems for DFU have been developed, including PEDIS (perfusion, extent, depth, infection, sensation),91 by the International Working Group on the Diabetic Foot (IWGDF), SINBAD (site, ischaemia, neuropathy, bacterial infection, area, depth)33 and Wound Ischaemia and Foot Infection (WIfI).92 DFU are, however, generally classified by the Wagner and University of Texas systems.93,94,95 These classification systems effectively stratify the ulcer by the level of risk it presents. Risk stratification for a DFU is a critical input for planning and delivering care.Arterial ulcersThe main risk factor for arterial or ischaemic ulcers is arterial disease manifested as poor blood supply to the extremities and low partial pressure of oxygen in tissue.Pressure ulcersA triumvirate of aetiology-specific factors create critical risks for the formation of PU.96 These are the forces of pressure, friction and shear. Pressure deforms tissue and may occlude blood supply. Pressure causes direct damage to tissue faster than ischaemia does97,98,99 and leads to shear forces, which deform tissue structures over bony prominences. Tissue that has been starved of blood supply may be damaged by reperfusion injury from reactive oxygen molecules when the patient is moved to re-establish blood supply. Shear forces also arise from the effects of friction at the skin surface, which causes lateral skin deformity and shear damage.100 Moisture increases the friction of skin, exacerbating the effects of friction-related deformity.101 A previous PU is a further risk factor for new PU formation. Traditionally, PU are classified by a grading system that takes account of the depth and severity of skin damage.96Clinical risk factorsA wide range of clinical factors not directly related to the aetiology102 of the wound are risks for hard-to-heal wounds. These include: the number of concurrent wounds of any aetiology; obesity; increasing age; poor nutritional status; diabetes; local or systemic hypoxia; ischaemia103 and arterial supply to the lower extremities indicated by the 6-minute walking test; arterial hypertension; dyslipidaemia and metabolic syndrome;104 critical limb ischaemia;105 the presence of biofilm; clinical infection; genetic factors; smoking; lymphatic insufficiency; chronic inflammatory disorders; cancer; immune suppression or immunological disorders; and systemic medications. Wound size greater than 10cm2 and ulcer duration greater than 12 months106 are independent prognostic factors.Non-clinical risk factorsThey include: psychosocial factors;107 educational attainment and its relationship to understanding the care needs of the wound; patient beliefs; dementia; depression; social support; adherence to or concordance with care pathway;108,109 the impact of the care pathway on the patient's activities of daily living (AoDL); patient choice; patient's own goals; quality of life (QoL); previous experience of treatment; mobility; reduced ability to self-care as a result of comorbidities and/or frailty; sleep disorders; environment and living conditions, including distance from the clinical setting and living alone; access to care; and patient's economic situation where, for example, travel to a clinical centre or treatment is self- or part-funded. It may not be possible to address all of the patient's non-clinical risk factors. Patient-related risk factors and their management are addressed in Section 6.Service-delivery factorsThere is increasing evidence for sub-optimal service delivery in which wounds are not managed using best practice. Examples include: inadequate diagnosis; failure to identify the wound type; not using best practice for managing underlying pathology; poor selection of dressings; and lack of adequate, health professional education and training.Patient managementMeasurement of the reduction in wound surface area at four weeks is an accepted marker for progression to wound closure.110,111,112,113,114 Past research involving lower extremity ulcers has demonstrated that a <40% reduction at four weeks for a VLU and <50% reduction at four weeks for a DFU indicates the ulcer is refractory to the current treatment plan.111,112,113,114 Other studies have confirmed that PUs with 40–50% at 4 weeks should be regarded as hard-to-heal and be referred to a specialist wound practitioner or a complex wound clinicSection 3. Pathophysiology of hard-to-heal woundsThe majority of hard-to-heal wounds are associated with risk factors, as discussed in Section 2. In addition to patient-related, non-clinical factors, and to clinical risk factors not directly related to the wound, a critical feature is the presence of an underlying endogenous pathophysiological cause.Acute wounds may be characterised broadly as those with an identifiable acute external cause, little to no causative pathophysiology, and thus a controlled inflammatory response116 and largely predictable healing. In contrast, chronic, hard-to-heal wounds are characterised by a physiological barrier to recovery before the breach in the skin appears, an underlying pathophysiology, chronic inflammation,117,118,119 and a mostly unpredictable healing trajectory. The inflammatory impact of the presence of biofilm120 is overlaid on the patient's pathophysiology. Clinically, these differences mean that acute wounds are usually treated by managing the wound environment and the risk of infection, whereas chronic wounds also require a focus on and management of the underlying pathophysiology and risk factors. Fig 2 shows the major molecular factors that need to be addressed to allow optimal healing.Fig 2. Molecular reasons for hard-to-heal woundsFrom underlying cause to wound: the tissue breakdown pathwayExcellent overviews of the chronic wound pathophysiology may be found in a number of reviews.119,121,122 It is critical to manage the underlying cause to encourage healing. The cycle of relentless chronicity must be broken to manage and reduce the persistent inflammatory state and encourage conditions that are conducive to healing.123Endogenous tissue-breakdown mechanisms, common to all skin ulceration, have three main components:Tissue-destructive enzymes, principally matrix metalloproteinases (MMPs)An oxidative environment caused by reactive oxygen species (ROS)Impaired endogenous control mechanisms that modulate enzyme activities.These mechanisms are capable of destructive tissue breakdown leading to wound formation, the key driver of which is a chronic inflammatory stimulus driven by the nature of the aetiological causes.117,119,124,125 Chronic stimulation of the endothelial lining of blood vessels117 sets up a persistent cycle of leukocyte adhesion to the vessel walls,117 extravasation of leukocytes and accumulation of neutrophils and macrophages, creating a complex, persistent inflammatory state. The expression of inflammatory cytokines and growth factors is disturbed compared with acute wounds,126,127,128 leading to over-expression of several proteases129 such as MMP-1, MMP-9 and MMP-8, elastase and plasminogen activators (PA).130,131,132,133,134 PAs activate plasmin, an important activator of MMP135 and ROS136,137 in tissue. PA is expressed in non-ulcerated skin of patients with chronic venous disease, possibly indicating its role in the development of VLU.138 Exacerbating the effects of the over-expression of proteases capable of degrading dermal extracellular matrix (ECM) is the concomitant down-regulation of the inhibitors that keep the protease activity in check: tissue inhibitor of metalloproteinase-1 (TIMP-1) and TIMP-3.139,140,141,142 Together, the effect of higher levels of proteases and reduced expression of TIMPs contributes significantly to wound chronicity. Fibroblasts become quiescent/senescent143,144 or themselves may have over-express of collagenase, elastase and stromelysin, and reduced levels of TIMP-1 and TIMP-3.145 Fibroblast senescence has been associated with slow healing.146,147 The overexpression of proteinases and ROS is responsible for creating a dysfunctional ECM with reduced integrin binding148 that does not support cell migration and wound healing.Biofilm in hard-to-heal woundsBiofilm is a complex polymicrobial community of microorganisms embedded in a predominantly extracellular polymeric substance (EPS) that protects the microbes from antimicrobial activity (Box 1). Biofilm is now believed to be ubiquitous in chronic wounds,149,150 and once removed, is able to reform quickly,151 unless prevented from doing so. Biofilm has been recognised as an important contributor to the hard-to-heal status of chronic wounds.120 While there is no direct clinical evidence from chronic, hard-to-heal wounds that biofilm is solely responsible for poor or non-healing, there is a wealth of evidence that implicates biofilm in wound chronicity.149 The consensus is that biofilm stimulates chronic inflammation,152 thereby adding to the burden of endogenous inflammatory stimulus. Biofilm expresses inflammatory signals153 that attract neutrophils154,155 and may interfere with neutrophil function, causing inappropriate degranulation releasing proinflammatory cytokines.156 Biofilm inhibits activation of the complement cascade,157 induces microRNAs that inhibit tight junction proteins that maintain skin barrier function,158 reduces the effect of host defences159 and affects pH and local oxygen concentrations.160,161 Preclinical evaluations of healing in wounds with biofilm have shown impaired healing.162 Overall, current opinion supports the importance of biofilm as a mediator of chronicity in hard-to-heal wounds.163 Furthermore, biofilm begins to reform after debridem
Referência(s)