Clinical PRACTICE DEVELOPMENT Wound bed preparation: TIME in practice

Wound bed preparation is now a well established concept and the TIME framework has been developed as a practical tool to assist practitioners when assessing and managing patients with wounds. It is important, however, to remember to assess the whole patient; the wound bed preparation ‘care cycle’ promotes the treatment of the ‘whole’ patient and not just the ‘hole’ in the patient. This paper discusses the implementation of the wound bed preparation care cycle and the TIME framework, with a detailed focus on Tissue, Infection, Moisture and wound Edge (TIME).

Caroline Dowsett, Heather Newton

dependent on one another. Acute et al, 2003). Wound bed preparation wounds usually follow a well-defined as a concept allows the clinician to KEY WORDS process described as: focus systematically on all of the critical Wound bed preparation 8Coagulation components of a non-healing wound to Tissue 8Inflammation identify the cause of the problem, and Infection 8Cell proliferation and repair of implement a care programme so as to Moisture the matrix achieve a stable wound that has healthy 8Epithelialisation and remodelling of granulation tissue and a well vascularised Edge scar tissue. wound bed.

In the past this model of healing has The TIME framework been applied to chronic wounds, but To assist with implementing the he concept of wound bed it is now known that chronic wound concept of wound bed preparation, the preparation has gained healing is different from acute wound TIME acronym was developed in 2002 T international recognition healing. Chronic wounds become ‘stuck’ by a group of wound care experts, as a framework that can provide in the inflammatory and proliferative as a practical guide for use when a structured approach to wound stages of healing (Ennis and Menses, managing patients with wounds (Schultz management. By definition wound 2000) which delays closure. The et al, 2003). The TIME table (Table 1) bed preparation is ‘the management epidermis fails to migrate at the wound summarises the four main components of a wound in order to accelerate margins, which interferes with normal of wound bed preparation: endogenous healing or to facilitate cellular migration over the wound bed 8Tissue management the effectiveness of other therapeutic (Schultz et al, 2003). 8Control of infection and measures’ (Falanga, 2000; Schultz et inflammation al, 2003). The concept focuses the In chronic wounds there appears 8Moisture imbalance clinician on optimising conditions at to be an over production of matrix 8Advancement of the epithelial edge the wound bed so as to encourage molecules resulting from underlying of the wound. normal endogenous healing. It is an cellular dysfunction and disregulation approach that should be considered for (Falanga, 2000). Fibrinogen and fibrin The TIME framework is a useful all wounds that are not progressing to are also common in chronic wounds practical tool based on identifying the normal wound healing. and it is thought that these and other barriers to healing and implementing a macromolecules scavenge growth plan of care to remove these barriers Wound healing is a complex series factors and other molecules involved and promote wound healing. of events that are interlinked and in promoting wound repair (Falanga, 2000). Chronic wound fluid is also It is important to understand wound Caroline Dowsett is Nurse Consultant in Tissue Viability, biochemically distinct from acute wound bed preparation and TIME within the Newham Primary Care Trust, London, and Heather Newton fluid; it slows down, and can block the context of total patient care. If a wound is Nurse Consultant in Tissue Viability, Royal Cornwall proliferation of cells, which are essential fails to heal there is often a complex Hospital Trust, Cornwall for the wound healing process (Schultz mix of local and host factors which

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Table 1 TIME – Principles of wound bed preparation

Clinical observations Proposed pathophysiology WBP clinical actions Effect of WBP actions Clinical outcome Tissue non-viable or deficient Defective matrix and cell Debridement (episodic or Restoration of wound base Viable wound base debris impair healing continuous): and functional extracellular 8Autolytic, sharp surgical, matrix proteins enzymatic, mechanical or biological 8Biological agents Infection or Inflammation High bacterial counts or Remove infected foci Low bacterial counts or Bacterial balance and prolonged inflammation Topical/systemic: controlled inflammation: reduced inflammation Inflammatory cytokines 8Antimicrobials Inflammatory cytokines Protease activity 8Anti-inflammatories Protease activity Growth factor activity 8Protease inhibition Growth factor activity

Moisture imbalance Desiccation slows epithelial Apply moisture-balancing Restored epithelial cell Moisture balance cell migration dressings migration, desiccation avoided

Excessive fluid causes Compression, negative Oedema, excessive fluid maceration of wound margin pressure or other methods controlled, maceration of removing fluid avoided

Edge of wound — Non-migrating keratinocytes Re-assess cause or consider Migrating keratinocytes Advancing edge of wound non-advancing or Non-responsive wound cells corrective therapies: and responsive wound cells. undermining and abnormalities in extra- 8Debridement Restoration of appropriate cellular matrix or abnormal 8Skin grafts protease profile protease activity 8Biological agents 8Adjunctive therapies

will need to be assessed and treated. treatments. Assessment and treatment The TIME table has been designed A full and detailed patient assessment of the underlying condition is essential to help the clinician make a systematic will highlight the underlying aetiology as the type of wound bed preparation interpretation of the observable of the wound and other factors that implemented may vary with wound characteristics of a wound and to may impede wound healing such as type. For example, sharp debridement decide on the most appropriate pain and poor nutrition (Dealey, 2000). is common in the management of intervention: With this in mind the wound bed patients with diabetic foot ulceration, preparation ‘care cycle’ was developed while compression therapy is the T — for tissue: non-viable or deficient in 2004 (Dowsett, 2004) to provide recommended treatment for patients I — for infection/inflammation a care programme that includes the with venous leg ulcers (European M — for moisture imbalance TIME framework. It focuses both on Wound Management Association, E — for edge, which is not advancing the patient and on the wound in an 2004). The cycle moves from patient or undermining. attempt to address all factors that assessment and diagnosis to assessing influence wound healing. and treating the wound using the T — Tissue TIME framework. The importance The specific characteristics of the Wound bed preparation care cycle of assessment in terms of evaluating tissue within a wound bed play a very The care cycle (Figure 1) starts with the effectiveness of the treatment is important role in the wound healing the patient and their environment of highlighted in the cycle. Those patients continuum. Accurate description of this care. Individual patient concerns need who have healed come out of the cycle tissue is an important feature of wound to be addressed as well as quality of life into a ‘prevention programme’ and assessment. Where tissue is non-viable issues in order to achieve a successful patients who have not progressed to or deficient, wound healing is delayed. care programme. Patients need to healing or who have palliative wounds It also provides a focus for infection, understand the underlying cause of remain in the cycle and are reassessed, prolongs the inflammatory response, their wound and the rationale for using TIME. mechanically obstructs contraction

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Wound bed preparation - TIME in contex be realised. In the majority of clinical cases there is a need to remove the Start with devitalised tissue through a process of the patient debridement, however, it is important No to assess the blood flow to the affected area first, particularly if the wound is on the lower leg or foot. In cases where Identifying the limb requires revascularisation, it Prevention Yes Healed wound may not be appropriate to undertake Wound bed aetiology tissue debridement until the viability of preparation the limb is determined. Care cycle Debridement Debridement is the process of removing devitalised tissue and/or Treat & evaluate Perform TIME foreign material from a wound and TIME assessment it may occur naturally. However, in interventions Agree goals some cases the patient may have an underlying pathology which affects the ability of the body to naturally debride the wound. In a chronic wound, debridement is often required more Figure 1. The wound bed preparation care cycle. than once as the healing process can stop or slow down allowing further dark grey appearance and, when devitalised tissue to develop. Where dried out, is tough and leathery to debridement is an option for clinicians touch. Wound eschar is full thickness, the following methods may be used: dry, devitalised tissue that has arisen 8Surgical through prolonged local ischaemia 8Sharp (Gray et al, 2005). It is derived from 8Autolytic granulation tissue after the death of 8Enzymatic fibroblasts and endothelial cells and 8Larval may also contain inflammatory cells 8Mechanical. (Thomas et al, 1999) which increases the risk of chronic inflammation of Surgical and sharp debridement Figure 2. Fixed yellow slough on a wound bed. the wound and delays extracellular Surgical and sharp debridement are matrix formation. Necrotic tissue the fastest methods of removing acts as a physical barrier to epidermal devitalised tissue and have the benefit and impedes re-epithelialisation cell migration, and hydration at of converting a non-healing chronic (Baharestani, 1999). Necrosis, eschar, the wound interface is significantly wound to that of an acute wound and slough are terms that describe reduced. within a chronic wound environment non-viable tissue, however, little is (Schultz et al, 2003) Surgical known about their constituents. Slough is adherent fibrous material debridement is normally performed derived from proteins, fibrin and where there is a large extent of Work undertaken by Thomas et al fibrinogen (Tong, 1999). It is usually devitalised tissue present and where (1999) found that devitalised tissue has creamy yellow in appearance and can there are significant infection risks. a defined structure similar to human be found dehydrated and adhered to dermis, however, there are areas of the wound bed (Figure 2) or loose and Sharp debridement is more scattered, degraded or disrupted stringy when associated with increased conservative, but it still requires the tissue present. For epidermal cells wound moisture. skills of an experienced practitioner. to migrate across a wound surface Clinical competencies such as a well built extracellular matrix is The presence of devitalised tissue in knowledge of anatomy, identification required. Therefore, early interventions a wound is often a challenge to health of viable or non-viable tissue, to remove devitalised tissue are an care professionals. It is difficult to ability and resources to manage essential part of wound management. accurately assess the depth of a wound complications such as bleeding and that is covered or filled with necrotic the skills to obtain patient consent Necrosis or eschar on a wound is or sloughy tissue and, until removed, are all essential before undertaking usually identified through its black/ the true extent of the wound may not this procedure.

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Autolytic debridement Autolytic debridement is a highly Table 2. selective process involving macrophage Risk factors for infection in chronic wounds and endogenous proteolytic enzymes Local factors Systemic factors which liquefy and separate necrotic Large wound area Vascular disease tissue and eschar from healthy tissue (Schultz et al, 2003) The natural Deep wound Oedema process is further enhanced by the High degree of chronicity Malnutrition use of occlusive and semi-occlusive dressings and those which interact Anatomic location, e.g. anal region Diabetes mellitus/rheumatoid arthritis to create a moist environment. Presence of necrotic tissue Smoking/alcoholism Phagocytic activity is enhanced and increasing the moisture at the wound High degree of contamination Previous surgery or radiotherapy interface promotes tissue granulation. Reduced tissue perfusion Use of corticosteroids/immunosuppressants

Enzymatic degradation Enzymatic debridement is a less common method of debridement, however, it is effective in the removal of hard necrotic eschar where surgical debridement is not an option. Exogenous enzymes are applied to the wound bed where they combine with the endogenous enzymes in the wound to break down the devitalised tissue. (Schultz et al, 2005).

Larval therapy Larval therapy is a quick, efficient method of removing slough and debris from a wound, however, not all patients or staff find this debridement method socially acceptable. Sterile larvae secrete powerful enzymes to break down devitalised tissue without destroying healthy granulation tissue Figure 3. Clinically infected wound. (Thomas et al, 1998). of care. All wounds contain bacteria healing include co-morbidities and Mechanical debridement at levels ranging from contamination, medication such as steroid therapy Mechanical methods of debridement through critical colonisation (also and immunosuppressive drugs. Local such as irrigation and wet to dry known as increased bacterial burden factors at the wound bed, such as dressings are rarely used as they can or occult infection), to infection. The necrotic tissue and foreign material cause increased pain and can damage increased bacterial burden may be such as fragments of gauze and newly formed granulation tissue confined to the superficial wound dressings, also affect healing and the (NICE, 2001). bed or may be present in the deep risk of infection. compartment and surrounding If debridement is effective, the T of tissue of the wound margins. Several When a wound is infected (Figure 3) TIME is removed and wounds can systemic and local factors increase the it contains replicating micro-organisms progress through the remaining phases risk of infection (Table 2). Emphasis is which elicit a host response and cause of wound healing. often placed on the bacterial burden, injury to the host. In an acute wound, but in fact host resistance is often the infection is met by a rapid inflammatory I — infection/inflammation critical factor in determining whether response which is initiated by Infection in a wound causes pain and infection will occur. Host resistance complement fixation and an innate discomfort for the patient, delayed is lowered by poor tissue perfusion, immune response followed by the wound healing, and can be life poor nutrition, local oedema and release of cytokines and growth factors threatening. Clinical infections as well other behavioural factors such as (Dow et al, 1999). The inflammatory as having serious consequences for smoking and drinking excess alcohol. cascade produces vasodilation and a the patient can add to the overall cost Other systemic factors that impair significant increase of blood flow to

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Table 3 Sibbald et al (2000) suggest that Differentiating between superficial and deep infection diagnosis should differentiate between superficial and deep infection as Superficial infection Deep infection outlined in Table 3. Non-healing Pain: other than usually reported Treatment of infection should Friable granulation tissue Increased size first of all focus on optimising host Exuberant bright granulation tissue Warmth resistance by promoting healthy eating, encouraging smoking cessation Increased exudate Erythema > 1–2cm and addressing underlying medical New areas of necrosis in base Probes to bone or bone exposed conditions such as diabetes. Systemic Wound breakdown antibiotics are not necessarily the most appropriate way of reducing bacterial Odour (Sibbald et al, 2000) burden in wounds, particularly because of the threat of increasing bacterial resistance and should only be used where there is evidence of deep the injured area. This also facilitates the clinical diagnosis. The classic signs of infection or where infection cannot be removal of micro-organisms, foreign infection in acute wounds include: managed with local therapy (Schultz bodies, bacterial toxins and enzymes 8Pain et al, 2003). Local methods include: by phagocytic cells, complements, and 8Erythema debridement to remove devitalised antibodies. The coagulation cascade is 8Oedema tissue; wound cleansing; and the use activated isolating the site of infection 8Purulent discharge of topical antimicrobials such as iodine in a gel matrix to protect the host 8Increased heat. dressings and silver. (Dow et al,1999). In a chronic wound, however, the continuous presence For chronic wounds it has been There is renewed interest in the of virulent micro-organisms leads to suggested that other signs should be selective use of topical antimicrobials a continued inflammatory response added: as bacteria become more resistant to which eventually contributes to host 8Delayed healing antibiotics. Studies show that some injury. There is persistent production 8Increased exudates iodine and silver preparations have of inflammatory mediators and steady 8Bright red discolouration of bactericidal effects even against multi- migration of neutrophils which release granulation tissue resistant organisms such as methicillin- cytolytic enzymes and oxygen-free 8Friable and exuberant tissue resistant Staphylococcus aureus (MRSA) radicals. There is localised thrombosis 8New areas of slough (Landsdown, 2002; Romanelli et al, and the release of vasoconstricting 8Undermining 2003; Sibbald et al, 2003). Where metabolites which can lead to tissue 8Malodour and wound breakdown infection in the wound has extended hypoxia, bringing further bacterial (Cutting and Harding, 1994). beyond the level that can be managed proliferation and tissue destruction with local therapy, systemic antibiotics (Sibbald et al, 2003). These criteria have now been should be used. Systemic signs of modified according to wound type infection, such as fever, and cellulities The presence of bacteria in a (Cutting et al, 2005) and are the subject extending at least 1cm beyond the chronic wound does not necessarily of a position paper (EWMA, 2005). In wound margin and underlying deep indicate that infection has occurred this document, Cutting et al describe structures, will require systemic or that it will lead to impaired wound the results of a Delphi approach as a antibiotic therapy (Schultz et al, 2003). healing (Cooper and Lawrence, 1996). method of developing consensus on Micro-organisms are present in all the criteria for identification of wound M — moisture imbalance chronic wounds and low levels of infection. The results of the study Creating a moisture balance at certain bacteria can facilitate wound indicated that cellulities, malodour, pain, the wound interface is essential if healing as they produce enzymes such delayed healing or deterioration in the wound healing is to be achieved. as hyaluronidase which contributes to wound/wound breakdown are criteria Exudate is produced as part of the wound debridement and stimulates common to all wounds, but other body’s response to tissue damage and neutrophils to release proteases (Stone, changes should be noted in different the amount of exudate produced is 1980). wound types. The Delphi process dependant upon the pressure gradient identified the criteria for six different within the tissues (Trudgian, 2005). A Diagnosis of infection is primarily wound types and should be used as a wound which progresses through the a clinical skill and microbiological data guide when diagnosing infection in both normal wound healing cycle produces should be used to supplement the acute and chronic wounds. enough moisture to promote cell

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Table 4 If a wound produces excessive amounts Exudate types of exudate the wound bed becomes saturated and moisture leaks out onto the peri-wound skin causing maceration Description of exudate Components of exudate and excoriation. This in turn could lead Serous Clear and watery. Bacteria may be present to an increased risk of infection. Fibrinous Cloudy. Contains fibrin protein strands Exudate assessment Purulent Milky. Contains infective bacteria and inflammatory cells Assessment of the exudate is an Haemopurulent As above but dermal capillary damage leads to the presence of red cells important part of wound management. Haemorrhagic Red blood cells are a major component of the exudate The type, amount and viscosity of (Vowden and Vowden, 2004) the exudate should be recorded and dressings selected based on the exudate’s characteristics. If a wound is too dry, rehydration should be the principle of management, unless contraindicated as in the case of ischaemic disease. Occlusive dressing products promote a moist environment at the wound interface. As wounds heal, the level of exudate gradually decreases. The management of excess exudate in chronic wounds, however, presents a challenge to many health care professionals. Vowden and Vowden (2004) suggest that an understanding of the systemic and local conditions influencing exudate production and knowledge of the potential damaging chemical constituents of exudates should inform management strategy. Figure 4. Evidence of irritant dermatitis following dressing application. Dressing selection When selecting a dressing, proliferation and supports the removal and endothelial cells. Increased levels consideration should be given to the of devitalised tissue through autolysis. If, of proteolytic enzymes and reduced volume of exudate and the viscosity as however, the wound becomes inflamed growth factor activity all contribute some dressings absorb a higher volume and/or stuck in the inflammatory to a poorly developed extracellular of fluid than others and some are more phase of healing, exudate production wound matrix. This in turn affects the efficient when dealing with viscous increases as the blood vessels dilate. ability of the epidermal cells to migrate exudate. There are a variety of dressing across the surface of the wound to products available for the management A description of the types of complete the healing process. of exudates ranging from foams, exudates can be found in Table 4. hydrocolloids, alginates, hydrofibres, Factors such as the underlying cadexomer iodine to capillary action Evidence suggests that there are condition of the patient, the pathology dressings. All play a role in the removal significant differences between acute of the wound and the dressing of fluid away from the wound surface, and chronic wound fluid (Park et selection all affect the production of however, many of the products, through al,1998). Acute wound fluid supports exudate (White, 2001). Moisture in a their ability to gel on contact with the stimulation of fibroblasts and the wound enhances the natural autolytic wound exudates, maintain a moisture production of endothelial cells as process and also acts as a transport balance on the wound surface itself. it is rich in leukocytes and essential medium for essential growth factors nutrients. Chronic wound fluid, during epithelialisation. If a wound bed VAC therapy or total negative however, has been found to contain becomes too dry, however, a scab will pressure is a therapy which draws high levels of proteases which have form which then impedes healing and exudates from the wound bed through an adverse effect on wound healing wound contraction. The underlying application of sub-atmospheric pressure by slowing down or blocking cell collagen matrix and the surrounding via an electronic pump (Mendez- proliferation (Schultz et al, 2003) in tissue at the wound edge become Eastman, 2001). Compression bandages particular keratinocytes, fibroblasts desiccated (Dowsett and Ayello, 2004). also play a role in the removal of excess

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fluid in the lower limbs in patients with venous leg ulcers and lymphoedema. The condition of the surrounding skin is also important as vulnerable skin can react to excess exudate and cause maceration, excoriation, and irritant dermatitis (Figure 4). Early application of a protective skin barrier film can minimise these risks. It is important to remember to treat the underlying clinical condition when addressing moisture imbalance in a wound (Newton and Cameron, 2003).

E — edge When the epidermal margins of a wound fail to migrate across the wound bed or the wound edges fail to contract and reduce in size, consideration needs to have been given to the T,I, and M first to ensure that all aspects of wound bed preparation have been considered. The final stage of wound healing is epithelialisation, which is the active division, migration, and maturation of Figure 5. Diabetic foot ulcer. epidermal cells from the wound margin across the open wound (Dodds and including hypoxia, infection, desiccation, healing. It is important to select dressing Haynes, 2004). dressing trauma, hyperkeratosis and products which are non adherent, and callus at the wound margin (Moffatt will not dry out or leave fibres in the There are many factors which et al, 2004). For wound healing to be wound bed. need to be present in order for effective, there needs to be adequate epithelialisation to take place. The tissue oxygenation. Decreased In certain clinical conditions such as wound bed must be full of well oxygen levels impair the ability of in diabetic neuropathy, there is an over vascularised granulation tissue in order the leucocytes to kill bacteria, lower production of hyperkeratosis and callus for the proliferating epidermal cells to production of collagen and reduce formation (Figure 5). It has also been migrate. This also ensures that there epithelialisation (Schultz et al, 2003). noted that the epidermis of the skin is adequate oxygen and nutrients to It is important to remember that surrounding venous leg ulcers is thicker support epidermal regeneration. There wounds rely on both macro- and than normal skin and highly keratinised needs to be a rich source of viable microcirculation particularly in the (Schultz et al, 2005). If this proliferative, epidermal cells which can undergo lower limb. thickened tissue is not removed, wounds repeated cell division particularly at will fail to epithelialise. Failure of a the edge of the wound. Where cells A baseline assessment needs to wound edge to migrate is also thought have become senescent the process be undertaken to determine the to be associated with the inhibition of slows down or stops completely. degree of ischaemic disease and the the process of normal programmed cell Wounds that have a significant number ability of the wound to heal without death (apoptosis) which particularly of fibroblasts that are arrested due vascular intervention. Wound infection affects fibrobasts and keratinocytes. to senescence, damaged DNA or as discussed previously is extremely Cells undergo a characteristic series of enduring quiescence do not heal destructive to a healing wound. changes following mechanical damage (Vande Berg and Robson, 2003). Inflammation caused by bacteria to the cell and on exposure to toxic Other factors, such as bacteria or the causes the extracellular matrix to chemicals. Cells become unresponsive presence of devitalised tissue, which degrade and therefore epidermal and die. interfere with epidermal cell growth, cell migration is interrupted. Wounds have the potential to influence the rate become chronic and fail to heal. Undermining or rolling of a wound of wound healing. Dressing products, particularly if edge can also influence the ability of adhered or made of fibrous materials, the wound to heal. Undermining can There are many reasons why the also cause trauma and inflammation of be indicative of a chronic wound and epidermal margin fails to migrate the wound bed which in turn delays in particular, those wounds that are

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also critically colonised with bacteria Key Points Mendez-Eastman S (2001) Guidelines for or infected. Rolled edges can present using negative pressure wound therapy. Adv in wounds that have an inflammatory Skin Wound Care 14(6): 314–22 8 origin such as pyoderma gangenosum The TIME framework has been developed as a practical tool Moffatt C, Morison MJ, Pina E (2004) Wound or in malignancy. Early diagnosis is bed preparation for Venous Ulcers. In: Wound for managing patients with important in these cases as failure to Bed Preparation in Practice. EWMA Position provide the appropriate second-line wounds. Document, MEP, London therapy such as oral steroids or tissue National Institute for Clinical Excellence 8 biopsy and excision can result in poor The wound bed preparation (2001) Guidance of the Use of Debriding Agents healing outcomes. ‘care cycle’ focuses care on the and Specialist Wound Care Clinics for Difficult to patient and their underlying Heal Surgical Wounds. NICE, London condition. Measuring a wound at the start Newton H, Cameron J (2003) Skin Care in of treatment is seen as best practice Wound Management. Medical Communications 8 to enable accurate assessment of the Patient progress and response Ltd. Holsworthy, UK impact of a clinician’s intervention. to treatment should be regularly evaluated. Park HY, Shon K, Phillips T (1998) The effect Subsequent measuring can identify of heat on the inhibitory effects of chronic whether or not a wound is failing to wound fluid on fibroblasts in vitro. Wounds heal or deteriorating. The edge of the 10: 189–92 wound will not epithelialise unless the Dealey C (2000) The Care of Wounds. Romanelli M, Magliaro A, Mastronicola D, wound bed is well prepared. Always Blackwell Science, Oxford Siani S, et al (2003) Systemic antimicrobial consider the elements of T,I, and M first Dodds S, Haynes S (2004) The wound edge, therapies for pressure ulcers. Ostomy Wound to ensure that the use of advanced epithelialisation and monitoring wound management 49(5a Suppl): 25–9 therapies are appropriate and if used healing. A journey through TIME. Wound bed preparation in practice. Br J Nurs Supplement Schultz G, Sibbald G, Falanga V, et al (2003) are applied to a well prepared wound Wound bed preparation: a systematic bed to ensure optimal effect. Dow G, Browne A, Sibbald RG (1999) approach to wound management. Wound Infection in chronic wounds: controversies Repair Regen 11: 1–28 Summary and conclusion in diagnosis and treatment. Ostomy Wound Manag 45: 23–40 Schultz G, Ladwig G, Wysocki A (2005) The management of chronic Extracellular matrix: review of its role in acute wounds has progressed from merely Dowsett C, Ayello E (2004) TIME principles and chronic wounds. World Wide Wounds. assessing the status of the wound of chronic wound bed preparation and www.worldwidewounds.com treatment. 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