All open wounds become contaminated by microorganisms, which can rapidly progress to colonisation.1 This contamination process may include the formation of biofilm, which can form on the wound surface within 24–48 hours and, when established, increases the risk of delayed healing, infection and sepsis.2,3 Biofilm is a major factor in wounds failing to heal in a timely fashion, and it can be found in the vast majority of hard-to-heal wounds.4
Consequently, effective wound care involves the disruption and removal of biofilm to initiate and support healing.3 One vital part of an antibiofilm strategy is debridement, the removal of tissue that is infected, damaged or dead (necrosis). This can be achieved with a variety of methods, each with its advantages and disadvantages. Options include autolytic debridement with hydrogel and hydrocolloid wound dressings, which are widely used but may not be effective at removing biofilm,5 as well as a range of active debridement techniques (for example, surgical, sharp, mechanical and enzymatic) that are more effective against biofilm.6
This article explores the risk factors associated with biofilm development and reformation, the impact this has on wound healing and the various debridement techniques available for clinicians to address this.
The burden of hard-to-heal wounds
Hard-to-heal wounds are wounds that fail to heal with standard therapy in an orderly and timely manner.7 This term—synonymous with chronic, non-healing or recalcitrant wounds or failure to heal—can describe wounds of any type or aetiology, whether acute or chronic, that fail to heal within the normal healing trajectory.
Hard-to-heal wounds present a major challenge for health professionals, with the potential for poor patient health and quality-of-life outcomes and substantial costs to healthcare systems.8-10
A meta analysis11 of 11 papers put the global prevalence of hard-to-heal wounds per 1000 population at 1.67 (confidence intervals (CI): 0.83–2.80), although this was 1.51 in reports on leg ulcers alone and 2.21 in reports covering various aetiologies. The limited number of studies and heterogeneity in study design and data collection means that the data should be considered with caution.12
Managing hard-to-heal wounds is expensive. According to a cohort study of the approximately 3.8 million patients with a wound managed by the NHS in 2017/18, £5.6 billion of the NHS's £8.3 billion annual wound management cost was associated with unhealed wounds, compared with £2.7 billion for healed wounds.13 Healing rates were lower in those with (45%) than without (59%) evidence of infection in hard-to-heal wounds, although this did not affect healing rates in acute wounds.13 Healing rates affected the average 12-month management cost of surgical wounds, which were £6000 in healed and £13 700 in unhealed wounds.14 This average cost was also linked to evidence of infection, which was £2000 in its absence and £5000–£11 200 in its presumed presence.14 An earlier report from the same study series looked at the mean 12-month cost of pressure ulcers in the NHS. This was only £1400 for ulcers of the lowest severity (category 1), compared with >£8500 for ulcers of all other categories, and it was £12 300 for unhealed ulcers, 2.4 times more than the £5140 for healed ulcers.15
Controlling the ever-increasing costs of hard-to-heal wounds will require more resources, better education and greater continuity of care. Cost-effective healing can also be facilitated with earlier and faster wound bed preparation, assisted by the availability of appropriate debridement techniques to a wider range of clinicians.
Risk factors and assessment of hard-to-heal wounds
The chance of delayed wound healing is increased by a number of risk factors (Box 1).8 These can be related to the wound itself, to any comorbidities or ongoing treatments or to the patient's demographic profile.8 Some comorbid conditions often present with a variety of risk factors for hard-to-heal wounds, such as chronic kidney disease, which often involves hypertension, diabetes mellitus, vascular disease, obesity, malnutrition and chronic inflammatory states.16 Identifying and addressing these risk factors is essential to promoting and maintaining effective wound healing.
To identify these risk factors, health professionals should conduct a thorough assessment of the patient and their wound. This should include an in-depth assessment of the wound itself, which may involve measuring its depth, location and size, as well as wound culture or biopsy to identify infection and bioburden. Understanding the underlying aetiology and pathophysiology can help identify what caused the wound in the first place or may be presenting significant barriers to healing. For example, this could reveal an endogenous tissue-breakdown mechanism that is preventing the wound from following the normal healing trajectory, which is associated with tissue-destructive enzymes (principally matrix metalloproteinases), an oxidative environment (caused by reactive oxygen species) or impaired endogenous control mechanisms (which modulate enzyme activities).
Likewise, measuring biochemical parameters, such as blood glucose, renal function and inflammatory markers, can help identify relevant comorbidities so that they can be managed.17 This clinical assessment should be accompanied by a holistic assessment of the patient's medical history, covering any known comorbidities and ongoing treatments, as well as any relevant personal demographic, social and psychological information. The results of this in-depth, holistic assessment can then be used to guide the selection of interventions that optimise healing outcomes in hard-to-heal wounds.8
Initial assessment should be followed by a consistent cycle of reassessment to monitor outcomes. This is essential to determine the response to any interventions and enable any appropriate and timely changes to the treatment plan.18
Biofilm and hard-to-heal wounds
One of the most significant risk factors for hard-to-heal wounds is bioburden, including the presence of biofilm. Biofilm refers to a collection of microorganisms that have formed an extracellular polysaccharide substance, a protective environment that makes them difficult to eradicate with antimicrobial agents.19 These complex colonies of microorganisms can be diverse, including bacteria, proteins and DNA, and they can survive attached to a living or non-living surface.20
Biofilms typically cause and maintain ongoing inflammation and low-level infection, and they have been shown to have a negative impact on wound healing.20,21 Wound biofilm increases risk of infection, and this risk can be multiplied where there are increased microbial virulence, antibiotic/antimicrobial resistance or impaired host defences, such as in diabetes and obesity.22 Bacteria that form biofilm are sessile (fixed in place) as opposed to planktonic (freely moving). However, the biofilm cycle has been shown to involve the release of planktonic bacteria, which can cause acute infection and increase the risk of wound chronicity.21 According to an in vitro analysis of the efficacy of antimicrobial agents against the same bacterial strain either in a planktonic state or within a biofilm, it could not be guaranteed that an agent would be able to penetrate deep enough to eradicate the planktonic bacteria in a complex biofilm scenario.23
Risk factors for hard-to-heal wounds
| Wound-related |
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| Comorbidity-related |
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| Treatment-related |
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| Patient-related |
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According to a systematic review and meta-analysis, biofilm is present in over 70% of all hard-to-heal wounds.24 However, there is no point-of-care diagnostic test for wound biofilm, and it is not possible to definitively diagnose it with the naked eye.2 Therefore, the presence of biofilm must be assumed after eliminating other possible causes of non-healing. Observation of the wound bed characteristics does enable the clinician to assess the possible presence of biofilm, as well as identify the type of tissue present, such as devitalised or non-viable tissue (Table 1).3,20,25,26 To reduce any persistent inflammatory state, bioburden should be managed following local biofilm pathways.
Assessing the wound bed to determine the identification of devitalised or non-viable tissue and possible presence of biofilm (Harker and Moore, 2004; World Union of Wound Healing Societies, 2008; Percival et al, 2015; International Wound Infection Institute, 2022)
| Tissue colour | Characteristics | Cause | Biofilm or local infection | Risks and issues |
|---|---|---|---|---|
| Red | Appearance of granules (healthy granulation tissue) | Budding or growth of new vessels into the tissue | Unlikely | Some colonisation likely, so healthy granulation should be maintained and biofilm development prevented |
| Dark red | Friability, bleeds easily | Likely localised biofilm presence | Likely | Likely presence of inflammation/biofilm increases risk of wound infection and prevents advancement of wound edges and wound contraction |
| Red over granulation | Overgranulation or raised tissue (proud of wound) without presence of granules | Presence of a foreign body, prolonged inflammation, biofilm, local infection, rubbing of dressing, over use of occlusive dressings or malignancy | Likely | Likely presence of inflammation/biofilm increases risk of wound infection and prevents epithelialisation and wound contraction; malignancy should be suspected if there is no response to biofilm strategies |
| Yellow | Slough (which can be dry, fibrinous or wet) | Clearance of cellular debris containing waste products | Likely | Obscuration of true wound depth; obstructed wound contraction; impeded epithelialisation; provision of area of attachment for microbes and biofilm formation; slough likel to continue to develop in presence of biofilm |
| Black | Black tissue (which can be wet or a dry eschar) | Localised ischaemia causing death of tissue, as a result of hypoxia, pressure or infection | Likely | Obscuration of true wound depth; obstructed wound contraction; impeded epithelialisation; provision of area of attachment for microbes and biofilm formation; potential to mask fluid collection or abscess; wound malodour |
Wound-bed preparation
Once a patient with a hard-to-heal wound has been assessed, the wound bed should be prepared to encourage conditions that are conducive to healing.27 This can be achieved with clear and focused guidance from a structured framework, such as TIMERS, TIME and DIME (Box 2).8 In TIMERS, interventions should aim to treat the underlying cause and risk factors, based on diagnosis and holistic assessment, as well as address social and patient-related factors. This mnemonic should help clinicians ensure effective wound bed preparation, select the most appropriate interventions and maintain a holistic approach to care (Table 2).8
The TIMERS framework (Atkin et al, 2019)
Applying the TIMERS framework in hard-to-heal wounds (Atkins et al, 2019)
| Aspect | Observation | Treatment options | Outcome |
|---|---|---|---|
| Tissue | Devitalised tissue | Debridement (autolytic, sharp, surgical, mechanical, hydrosurgical, debridement pads, enzymatic, larval, ultrasound or laser), CO2, concentrated surfactants | Clean wound bed, debrided devitalised tissue |
| Inflammation and infection | Signs of inflammation and/or infection, bioburden | Antimicrobials, antibiotics, biofilm pathway, bacterial binding dressings, fluorescence biomodulation, gas plasma, oxygen therapy (hyperbaric and topical), MMP/TIMP management, surfactants | Controlled inflammation, infection and biofilm |
| Moisture balance | Incorrect moisture balance | NPWT, compression, absorbent dressings | Managed moisture; wound environment conducive to healing |
| Edge | Edge rolled, epibole or callus; poor advancement of wound edge | Debridement, cyanoacrylate periwound protectants, excision of sclerosed margins, fluorescence biomodulation, wound fillers (for example, collagen) | Reduced wound size, epithelialisation |
| Tissue regeneration | Slow/stalled closure failing conservative therapy | Amnion/chorion membrane, ECM scaffolds, growth factors, PRP, bioengineered substitutes, NPWT, oxygen therapy (hyperbaric and topical), stem cell therapy, autologous skin graft | Wound closure, tissue repair |
| Social and patientrelated factors | Social situation, patient choice, psychosocial state | Engaging the patient with the care plan; patient, family and/or caregiver education; active listening, motivational literacy, psychoeducation | Understanding patient's belief system, adherence patient's own goals |
| Abbreviations: ECM: extracellular matrix; MMP: matrix metalloproteinases; NPWT: negative-pressure wound therapy; PRP: platelet-rich plasma; TIMP: tissue inhibitor of metalloproteinase | |||
This structured approach can be enhanced by providing patients and their families with bespoke education and involving them in decision-making regarding the interventions. This active communication can improve adherence to treatment plans.
Wound bed preparation is required on a day-to-day basis. Devitalised tissue and biofilm need to be removed at the point of need for the patient, rather than having to wait for specialist intervention—this is in keeping with the guidance that health professionals should be doing the right thing at the right time for the right patient.28 Appropriate management of barriers to healing, such as devitalised tissue, would expedite wound healing, prevent infection, reduce antibiotic resistance, prevent hospital admissions, minimise the economic burden of wounds and improve quality of life for patients.29,30
Debridement
A key tool in wound-bed preparation to promote healing is debridement. Debridement (distinct from wound cleansing) is the removal of adherent, contaminated or devitalised (non-viable or necrotic) tissue from the wound, including the wound bed, wound edges and periwound skin.31
Debridement is especially important as part of an antibiofilm strategy. This is because the tissue removed is likely to be harbouring bacteria and biofilm. Compared with planktonic bacteria, biofilm is more resistant to treatment with antibiotics and topical therapies. Therefore, debridement, which can remove biofilm, can enhance the activity of biocides and create a clean wound bed that is receptive to antimicrobial therapies.32-34
Moreover, timely and effective debridement should physically disrupt and suppress the constant cycle of biofilm formation and reformation, preventing planktonic bacteria becoming sessile and establishing biofilm nearby or elsewhere in the body.33,35,36
Before undertaking debridement, practitioners must have completed any relevant training in the chosen technique, and not all practitioners will be competent in the use of surgical and/or sharp debridement methods. Moreover, prior to commencing any type of debridement, capable practitioners must consider a range of factors (Box 3). If there is any concern regarding debridement, a senior member of healthcare staff should be referred to for advice.
Factors to consider before commencing debridement
Types of debridement
An ideal debridement method would be effective, patientspecific, easy to undertake, low-cost, accessible in all clinical settings and available on a regular basis.33 However, each of the range of debridement techniques available has its relative advantages and disadvantages that must be considered when choosing the most appropriate debridement option. This choice should be based on a holistic assessment of the patient and their wound and informed by any relevant clinical guidelines and regulations. However, it will also be influenced by the relative cost and availability of different options and the competency of the workforce to deliver them.31
Surgical debridement
Surgical debridement involves the use of surgical instruments to remove the devitalised tissue. It is the gold standard method of debridement, and its benefits include fast removal of the devitalised tissue and exploration of the underlying tissue and structures. It has been demonstrated to be effective in stimulating the healing of hard-to-heal wounds when combined with advanced therapies.8 Surgical debridement can be performed several times if necessary.
However, surgical debridement is expensive. It must be performed by a multidisciplinary team, including skilled specialist clinicians, usually led by a general, vascular, trauma or plastic surgeon. It also requires a specialist secondary care setting and general anaesthesia, usually meaning hospital admission. Moreover, hospital admission and surgery carry risks of infection, reduced mobility, lung and bladder stasis (causing chest and urinary infections and/or urinary retention) and blood coagulation, as well as surgical trauma, such as damaged nerves and vessels.31
Patients may be unsuitable or unwilling to undergo surgical debridement. This may be due to their general health, quality of life and ability to endure a surgical procedure that may result in a more extensive open wound, as well as their understanding of the risks associated with general anaesthesia and the occurrence of pain.37
Consequently, the implementation of surgical debridement is often limited, and it is usually only considered for the following reasons:
Sharp debridement
Sharp debridement involves the use of scissors, a scalpel or a curette to remove devitalised tissue. Sharp debridement is a fast and extremely efficient way of accurately assessing the extent of the wound, debriding non-viable tissue and managing biofilm.38
Sharp debridement can be performed by a range of healthcare professionals, including nurses, GPs, podiatrists and dermatologists. However, it requires specialist training, and the limited number of nurses with a recognised debridement qualification means that there is often a reliance on medical staff to undertake sharp debridement.
Unlike surgical debridement, sharp debridement can be undertaken in a range of settings, including the patient's home or a local wound, GP or outpatient clinic, and so it does not require hospital admission. However, the need for specialist skills means that it is not always readily available for patients at the point of need and with the regularity needed for biofilm management, especially in community settings.
Sharp debridement comes with the risk of damage to blood vessels, nerves and tendons. It is contraindicated in very large wounds, patients being treated with anticoagulants or an international normalised ratio (INR) above 2.5 (suggesting a raised risk of bleeding).8 Aggressive, excisional sharp debridement should not be conducted in patients with peripheral arterial disease or an ankle brachial pressure index (ABPI) below 0.5,8 because the lack of perfusion and consequent ischaemia compromises the patient's ability to heal, and surgical or sharp debriding is likely to exacerbate the wound.8
Hydrosurgical debridement
Hydrosurgical debridement involves the high-pressure application of a liquid, such as water, saline, polyhexanide or a super-oxidised solution, to wash out the wound (lavage). The effect of high-pressure lavage is similar to sharp debridement, and it can be targeted at a specific area and can remove biofilm.39 However, it can be painful for patients, and it has the potential to increase infection31 or disseminate bacteria into the environment due to aerosolisation.40 Hydrosurgical debridement requires specialist equipment and professional training, and, thus, it is not suitable in all settings.
Autolytic debridement
Autolytic debridement involves the application of a dressing to provide a moist wound healing environment that should facilitate the body's inherent ability to digest and remove necrotic tissue. These dressings have highly absorptive, moisture-retaining, autolytic and occlusive properties and can be made from materials including hydrogels, hydrocolloids and Hydrofiber. Dressing selection should be based on the wound bed and level of exudate and applied according to manufacturer's instruction and clinical need. Contraindications include known sensitivity to the ingredients of the dressing.
Autolytic debridement involves minimal pain and is relatively easy to use for most clinicians in all healthcare settings. This makes it the most commonly used form of debridement in the UK, and it tends to be the initial approach before other methods are tried.37 However, it is time-consuming31 and carries the risk of invasive infection and wound-edge maceration,8,31 and there is limited evidence of its effect on biofilm.33
Autolytic debridement is distinct from use of wet-to-dry gauze to remove devitalised tissue, which has a detrimental effect on granulation tissue and causes pain for the patient and, therefore, is no longer advocated in the UK.
Biological debridement
Biological (or larval) debridement involves use of the larvae (maggots) of the green bottlefly to ingest devitalised tissue and microbes and so stimulate wound healing.31 The larvae can be administered free-range (loose) or in a biobag (a special mesh net dressing). Biological debridement is relatively fast and requires limited training, meaning it can be administered in a variety of settings. However, it is comparatively costly, and patients may find it physically uncomfortable and psychologically offputting. Biological debridement is not suitable for very dry wounds or very wet wounds, wounds with exposed blood vessels potentially connected to deep vital organs, malignant wounds or patients with decreased perfusion.41
Ultrasonic debridement
Ultrasonic debridement involves direct or indirect application of low-frequency energy to assist debridement of devitalised tissue. It is painless, can be selective and has been demonstrated to reduce microbial bioburden.42 However, ultrasonic debridement requires specialist training and equipment, and is relatively expensive for continued use. As with hydrosurgical debridement, it also has the potential to disseminate bacteria into the environment due to aerosolisation.40
Mechanical debridement
Mechanical debridement involves use of monofilament cloths, pads or wipes to remove specific tissue types from the wound bed. It should remove slough and devitalised cells, but not necrotic tissue, and it leaves healthy granulation tissue intact.31 It can also be used for the removal of hyperkeratotic tissue in the periwound area.43 Mechanical debridement is widely used by specialists and generalists in all settings, due to its ease of use, relatively low cost and lack of requirement for specialist training. However, it is relatively slow, and it is not suitable for dry eschar.
Enzymatic debridement
Enzymatic (or biochemical) debridement involves topical application of enzymes to dissolve necrotic tissue in a wound. It is suitable for non-surgical patients in a variety of settings and can be effectively combined with the promotion of a moist environment for wound healing. However, it is relatively expensive and not recommended for large wounds and infected wounds. These agents have a specific action based on the enzyme (protease) used and the protein it breaks down, such as collagen (collagenase) and elastin (elastase).44 In many cases, enzymatic debridement (particularly with collagenase) has been shown to work slowly, and this has limited the number of therapies licensed for use in certain jurisdictions, such as the USA.45,46
Chemical debridement
Chemical debridement uses chemical compounds to remove devitalised tissue and biofilm. In contrast to enzymatic debridement, these chemical compounds denature and aggregate proteins using non-specific, non-enzymatic agents, such as hypochlorous acid and methane sulfonic acid.47 Options include ChloraSolv, an amino acid-buffered hypochlorite gel with a chemomechanical action, which selectively softens and removes devitalised tissue and biofilm in hard-to-heal venous leg ulcers or diabetic foot ulcers without causing trauma or bleeding.48 Another option for chemical debridement is Debrichem (DEBx Medical BV, Amsterdam, Netherlands), which has a desiccant action and is covered in detail in the rest of this supplement.
Other therapies providing a debridement benefit
There are other wound-care therapies that provide a benefit similar to debridement.
NPWT removes exudate from the wound, reduces peri-wound oedema, increases local blood flow and promotes angiogenesis, fibrogenesis and leucocyte and macrophage activity.49 It is contrandicated in un-controlled infection or the presence of necrotic tissue, and should be avoided with active bleeding or in the presence of local ischaemia.50 It can be painful for the patient and, therefore, is not always well tolerated, particularly for patients with leg ulcers.
Compression therapy is the gold standard therapy for management of venous leg ulcers,50 and it has been demonstrated to have a debridement effect on the wound, together with softening of lipodermatosclerosis.51,52 However, these wounds typically also require other forms of debridement techniques.
More aggressive debridement techniques have been recommended in the presence of biofilm.53 It has been suggested that a surgical scrub brush could be considered for a wound bed and periwound skin with dry material, especially eschar, that requires a more aggressive tool; however, this may require local anaesthesia and may also remove viable host tissue, and so it must be undertaken by a senior clinician trained in this technique.22
Conclusion
Wound bed preparation and biofilm management need to be ongoing parts of wound management. An ideal debridement method needs to be patient-specific, easy to undertake and available in all settings. Surgical debridement is the gold standard, followed by sharp debridement, but these have limitations, in that they require specialist intervention and are not always suitable for the patient and available at the point of clinical need. Other approaches are limited for various reasons, including availability, cost, competency of the practitioner and infection-control risks.
New approaches for debridement techniques need to be developed to enable this vital intervention to be available at the point of need in all clinical settings.
Regular and consistent biofilm management strategies for hard-to-heal wounds, including debridement, will facilitate evidence- and biofilm-based wound management,32,33 reducing wound chronicity and its subsequent socio-economic and quality-of-life issues. This is particularly important given its role in maintaining a healthy wound bed in hard-to-heal wounds and preventing biofilm re-formation.