Snm11460 wound bed - a5
2. The Bacterial Balance within a chronic wound
2.1 Bacterial involvement in a chronic wound and assessment
2.2 Bacterial screening of a chronic wound
2.3 Variables that affect the bacterial burden of a wound
2.4 Bacterial burden, pathogenicity and the presence of
biofilms in wound healing
2.5 Antibiotics and antiseptics in wound infection
3. Management of necrosis
3.1 Surgical and sharp debridement
3.2 Enzymatic debridement
3.3 Autolytic debridement
3.4 Mechanical debridement
4. Exudate Management
4.1 Direct and indirect exudate management
4.2 Wound Dressings
5. Molecular events in wound healing cellular dysfunction
6. Molecular events in wound healing biochemical balance
Vincent Falanga, MD
Professor of Dermatology and Biochemistry, Boston University School
of Medicine; Chairman of Dermatology Department And Training
Program, Roger Williams Medical Center
Rather suddenly, the term "wound bed preparation" has burst into the wound care field
and is already having a tremendous impact on how we approach and think about
chronic wounds. One might argue that the term itself is very simple, and some would
even wonder what is new about it. Yet, there is little doubt that the focus on wound
bed preparation is being successful, for it is galvanising both clinicians and industry into
renewed action for the benefit of our patients. Wound bed preparation as a strategy is
allowing us to break various aspects of wound care into individual components, while at
the same time maintaining a global view of what we wish to achieve. In this
comprehensive compendium on wound bed preparation, the various aspects needed
for achieving it are discussed in detail and should provide clinicians with a very
substantial working knowledge of the field. In this preface, I have the opportunity to
comment on wound bed preparation, why it has become so important, and how it will
evolve in the next several years. I regard wound bed preparation as the global
management of the wound to accelerate endogenous healing or to facilitate the
effectiveness of other therapeutic measures. Specifically, with my comments, I want to
differentiate wound bed preparation from wound debridement alone, suggest the need
for a more prolonged, maintenance debridement phase, and discuss the importance of
eliminating wound exudate. I believe that, ultimately, wound bed preparation will also
involve the correction of the wound's biological microenvironment. This may require the
elimination of phenotypically abnormal cells and correction of corrupt matrix
Chronic wounds have always lived in the shadow of acute wounds. Scientific
breakthroughs, therapeutic measures would generally first be developed or envisioned
for wounds caused by trauma, scalpel, or other types of acute injury. The whole
cascade of wound-healing events for which we now have a seemingly endless number
of diagrams is really an attempt to explain what happens after acute injury to the skin or,
for that matter, to other organ systems. Inevitably, lessons learned about acute injury
were extrapolated to the care of chronic wounds, which have often been seen as an
aberration of the normal process of tissue repair. There are many examples of how this
reliance on acute wounds worked out. For instance, stimulation of re-epithelialisation by
dressings providing moist conditions was first observed experimentally in acute wounds.
Later, this lesson was extrapolated to the care of chronic wounds. The acceleration of
healing by peptide growth factors was first formally demonstrated in experimental acute
wounds in animals. These observations provided proof of principle for the effectiveness
of topically applied growth factors, and led to testing and commercialisation of these
agents in chronic wounds. There are many other examples, but the point is that
knowledge accumulated about acute injury has been the anchor on which we have relied
for developing a scientific and therapeutic strategy for chronic wounds. However, there
are problems with this rather simplistic approach and, as I will explain, "wound bed
preparation" is a vehicle for chronic wounds to regain their independence from models of
Let us analyse how reliance on acute wounds, while helpful, has influenced the
management of chronic wounds in ways that are not always realistic. For example,
if one starts with the same perspective used for acute wounds, one common error is to
view wound bed preparation as the same as wound debridement. In acute wounds,
wound debridement is a good way to remove necrotic tissue and bacteria. After that is
done, one should have a clean wound that can heal with relative ease. This is not the
case for chronic wounds, where much more than debridement needs to be addressed
for optimal results. For one, defining the necrotic material in chronic wounds is not so
easy. Chronic wounds have what I call "necrotic burden", consisting of both necrotic
tissue and exudate. Chronic wounds can be intensely inflammatory, e.g., venous ulcers,
and thus produce substantial amounts of exudate that interfere with healing or with the
effectiveness of therapeutic products, such as growth factors and bioengineered skin.
So, in the context of wound bed preparation, not only do we need to concern ourselves
with removal of actual eschars and frankly non-viable tissue, but also with the exudative
Another important aspect of chronic wounds, which makes them different from acute
wounds in the context of wound bed preparation, is the possible need for a "maintenance
debridement" phase. Somehow, we have always thought of debridement, whether it be
done by surgical, enzymatic, or autolytic means, as a procedure or a therapeutic step
with defined time frames. That may be true of acute wounds that have become
colonised and necrotic, and thus need to be revitalised. However, with chronic wounds,
we are generally unable to fully remove the underlying pathogenic abnormalities; necrotic
material, non-viable tissue, exudate, i.e., the necrotic burden, continues to accumulate.
This notion of an initial debridement phase followed by a maintenance debridement
phase is one that we should seriously study and consider adopting within the context of
wound bed preparation. It might very well be that we have not paid enough attention to
this problem. For example, clinicians will agree that, after initial debridement of chronic
wounds, one may observe a temporary positive outcome on wound closure. However,
there is often a healing arrest, with a return to a poor wound bed. One explanation is
that, because of the underlying and uncorrected pathogenic abnormalities, there is
continued accumulation of necrotic tissue and exudate which now cause the healing
arrest. Rather than always starting from the beginning, with therefore periodic
debridement and exudate control, one might consider a steady state removal of the
necrotic burden that should go on throughout the life of the wound.
As already mentioned, in the context of wound bed preparation the exudative
component of the "necrotic burden" is not to be underestimated. Chronic wound fluid,
in contrast to fluid obtained from acute wounds, has been shown to slow down or block
the proliferation of key cells, such as keratinocytes, fibroblasts, and endothelial cells.
Chronic wound fluid contains a number of metalloproteinases that can break down or
corrupt essential matrix material needed for optimal movement of cells and for re-
epithelialisation. Moreover, there is evidence that macromolecules present in the wound
fluid and accumulating in the wound bed can bind or trap growth factors and render
them unavailable to the healing process. By focusing on management of wound
exudate, and not only on removal of necrotic tissue, we hope to find more effective
ways to control the exudate. Also, because of the many deleterious effects of wound
exudate on growth factors and matrix material, we are then beginning to place
emphasis upon correcting the biological microenvironment of the wound.
The biological microenvironment of chronic wounds is clearly not understood,
and we might feel that for now we have limited weapons to address it properly.
As we read this manual on wound bed preparation, however, we will find that many of
the approaches we use to treat chronic wounds may have very beneficial effects on this
more elusive component of wound bed preparation. For example, optimal compression
therapy for venous ulcers will decrease the amount of exudate, and thus clear the
macromolecules that may be trapping growth factors. Similarly, correction of the
bacterial burden decreases the possibility of infection but also diminishes the ongoing
inflammation that often characterises many chronic wounds. It has been said that some
chronic wounds are "stuck" in one of the phases of the normal healing process, such as
the inflammatory or proliferative phase. Eliminating the bacterial burden, by the use of
debridement or slow-release antiseptics, can help this situation. As another example,
appropriate debridement will remove tissue and therefore cells that have accumulated
and are no longer responsive to signals required for optimal wound healing. In this
respect, it has been shown that fibroblasts from chronic wounds, including venous and
diabetic ulcers, have become senescent and are unresponsive to certain growth factors.
I have used the term "cellular burden" for these cells. When we debride wounds, we
are removing this cellular burden and restoring wound responsiveness. In time, we
might develop chemical or biological means for normalising these cells, rather than
Realistically, one can regard this manual on wound bed preparation as a living
document. I say that because we should recognise that the field will continue
to evolve, and undoubtedly new approaches for wound bed preparation and its different
components will become available. However, I feel that a major hurdle has been
overcome. Specifically, we are now beginning to recognise that chronic wounds have a
complex life of their own, and that they are not simply an aberration of the normal
healing process. The concept of wound bed preparation allows us to dissect the
different components that need to be addressed in chronic wounds, and to develop
long-term strategies for the more complex issues that lead to failure in healing.
Throughout the last decade new and innovative technologies, such as topically applied
growth factors and bio-engineered skin products (see Table 1), have been at the
forefront of the drive to treat chronic non-healing wounds. Unfortunately, despite these
exciting and technologically advanced therapies, there remains a lack of knowledge
within the medical community of wound healing, with wound bed preparation frequently
underestimated. Furthermore, while standards and guidelines are available to clinicians
and nurses for wound management these are either frequently not followed or only
place emphasis on specific components of wound care, such as wound debridement or
control of infection. Therefore, it remains critically important that clinicians provide
thorough wound care, and ensure that appropriate wound bed preparation is
undertaken, in order to derive the maximum benefit from today's advanced wound care
products (Falanga 2000a).
Table 1. Commercial skin substitutes and growth factors/cytokine treatments currently employed in wound healing (Falanga 2000a)
Growth factor/Cytokine preparations
Regranex® recombinant human PDGF
Leucomax® recombinant human GM-CSF
Procurren Solution® platelet-derived wound healing formula (PDWHF)
Dermagraft® - human fibroblasts in an absorbable matrix
Transcyte® - devitalised fibroblasts on a nylon mesh
Biobrane® - a cellular dressing consisting of collagen bound to nylon fabric
Epicel®- autologous epidermal graft
Alloderm® - a cellular, allogenic dermal graft
Integra®- dressing consisting of bovine collagen and chrondroitin-6-sulphate
Composite Cultured Skin® - human fibroblasts and keratinocytes in a bovine collagen sponge
Apligraft® – human fibroblasts and keratinocytes in a bovine collagen matrix
This booklet aims to provide an explanation of the concept of wound bed preparation,
and to act as a step-by-step guide on preparing the wound bed, emphasising the key
elements of local wound care - bacterial balance, management of necrosis, biochemical
balance, exudate management and cellular dysfunction - in order to obtain optimal
healing (see algorithm in Figure 1).
Figure 1. This algorithm demonstrates an approach to wound bed preparation
2. The Bacterial Balance within a chronic
A major influence on wound care practice has been the clinicians' fear of wound
infection. However, all chronic wounds contain bacteria, and their presence in the
wound does not necessarily indicate that infection has occurred or lead to impairment
of wound healing (Kerstein 1997; Dow et al 1999). Furthermore, it has also been
suggested that the presence of certain bacteria within a chronic wound may actually
facilitate the healing process (De Haan et al 1974; Pollack 1984). This would appear to
be supported by the observation of Louis Pasteur over 100 years ago, "The germ is
nothing. It is the terrain in which it is found that is everything" (Pasteur 1880).
2.1.1 Defining bacterial involvement in the wound
Bacterial involvement within a wound can be divided into three categories -
contamination, colonisation and infection (see Dow et al 1999; Sibbald et al 2000).
– is defined as the presence of non-replicating microorganisms
within the wound and encompasses the majority of the microorganisms present in a
– is defined as the presence of replicating microorganisms
adherent to the wound in the absence of injury to the host. This would include skin
commensals such as Staphylococcus epidermis
whose presence has been shown to increase the rate of wound healing (Rodeheaver
– is defined as the presence of replicating microorganisms within a
wound with subsequent host injury. A pathogenic micro-organism may initially
colonise a wound without inducing host injury, however as the bacterial burden
increases, the colonised wound is subtlely transformed into a covert infection
(Thompson and Smith 1994), which although not involving extensive tissue invasion is
sufficient to inhibit wound healing. Ultimately, as the bacterial burden increases yet
further, evident wound infection or systemic dissemination (sepsis) can occur (Dow et
The various diagnostic approaches of screening infection within a chronic wound are
described in Table 2. However, for routine assessment of the bacterial burden,
semiquantitative bacteriology remains the most practical means and correlates well to
the gold standard quantitative biopsy results first described by Levine et al (1976) (see
Dow et al 1999).
Table 2. Techniques for assessing infection in chronic wounds (Dow et al1999)
Tissue is biopsied,
Evaluates for the
Invasive procedure. Primarily
weighed, placed in a
reserved for clinical
sterile tissue grinder
trials and other
with a known volume
within tissue as
homogenised to free
microorganisms from evaluate surface
tissue matrix. The
homogenate is seriallydiluted and plated. After incubation, colonies are enumerated and identified and colony counts are calculated.
Swab is twirled over
a 1 cm2 surface area
study to define role.
of the wound and
agitated in 1 mL of
but less rigorously
Then serially diluted
colony countsobtained byquantitative biopsyby 1 log.
Swab is rolled across
choice under most
bed and inoculted
on standard media
in petri dish, then
wound bed results
in excess presence
of surface colonisers.
A rapid technique
sample collection be identified.
diluted 10-fold and
Technique is highly
closure or delayed
A 0.02 mL aliquot
is placed on a slide,
stained. A single
bacterium per total
may be identified.
to >105 CFU/gm of tissue.
non-invasive culture quantitate
technique to serve
and then cultured.
as an alternative to biopsy.
While semi-quantitative bacteriology is a relatively quick and inexpensive diagnostic
technique, and is the procedure utilised most frequently in clinics, there can be a loss of
specificity (Sapico et al 1980). Furthermore, if the wound bed is inadequately prepared,
the clinician may be provided with confusing or nonsignificant results (Sibbald et al
There are a number of variables that should be considered by the clinician which are
known to affect the bacterial burden of a wound and increase the risk of infection in a
wound. These include the amount of necrotic or sloughy tissue in the wound, the
number of organisms, bacterial pathogenicity and host factors. The following equation
indicates that although bacterial quantity and virulence are important factors in
assessing a wound for infection, host resistance is clearly of critical importance (Dow et
al 1999; Sibbald et al 2000).
= dose x virulence
"Host resistance is the single most important determinant of wound infection and must
be meticulously assessed in every situation where a chronic wound fails to heal". (Dow
at al 1999) Host resistance can be determined by examining any local or systemic
factors that will lead to reduced wound healing in a patient.
2.3.1 Local and systemic factors that can affect host resistance
Local factors relate to those local wound characteristics (such as wound size, depth
and duration) that will increase the likelihood of wound infection. Table 3 lists a number
of local factors that are related to an increased risk of infection in chronic wounds.
For instance a larger wound is associated with greater host impairment during wound
healing and consequently, a greater risk of infection. The location of the wound over a
bony prominence such as a shin and subsequent soft tissue destruction can be
indicative of osteomyelitis (Dow at al 1999).
Equally important is the vascular status of the wound, as it has been shown that
wounds with a reduced arterial pressure will remain unhealed (EWGCLI 1991; Carter
1993). The extent of wound perfusion is also important, as an inadequately perfused
wound is unlikely to show the typical signs of inflammation. Host resistance can also be
compromised by systemic factors (Table 3) such as metabolic disorders (diabetes
mellitus – raised blood sugar levels may indicate local or systemic infection), underlying
Table 3. Systemic factors that increase the risk of infection
vascular disease or oedema, or patient malnutrition. Also, patient compliance with
regard to smoking, drug and alcohol abuse can have a detrimental effect upon host
resistance (Dow et al 1999).
The use of immunosuppressive drugs are also an important factor to be considered
when assessing wound infection, as they may mask signs of localised or systemic
sepsis (Dow et al 1999). Therefore, host monitoring is a critical feature of wound
assessment and management.
It is clear that an increased bacterial load within a chronic wound can lead to reduced
healing or indeed, no healing whatsoever! Experimental evidence indicates, that
regardless of the type of organism, substantial impairment of healing occurs, when there
is between 10 and 10 organisms per gram in a wound bed (see Dow et al 1999),
although, it has also been shown that many chronic wounds with a bacterial load
greater that 10 will heal without incident (Robson et al 1973). However, it is also
thought that the number of organisms in a wound may not necessarily be as critical as
the type and pathogenicity of the organism in the wound; for example, low numbers of
Streptococcal organisms may cause problems. Furthermore, with an increased
bacterial load and/or infection, there may be an increased rate of wound exudate; this
will require removal so that it does not provide a focus for increased bacterial infection.
In his presentation Falanga (2000b) has also suggested that the presence of sheets of
soft adherent material or "bio-films" are an important element in wound infection and
that more attention should be paid to their presence. These biofilms represent highly
organised bacterial communities that allow individual organisms to interact socially with
each other providing a means to exchange nutrients and metabolites. The biofilms
represent protected foci of infection and bacterial resistance within the wound and the
biofilm itself affords the bacteria protection from the effects of antimicrobial agents
especially antibiotics and antiseptics (Davey and O'Toole 2000).
Antibiotic resistance has developed as a result of the genetic elasticity of bacteria, which
have developed enzymes that can dismantle the antibiotics either before or after
entering the bacteria. Others can actively pump the antibiotics out of the cell or alter
the shapes of the molecule to which the antibiotic binds. Thus, the actual or potential
increase in the occurrence of bacterial resistance has become a major concern when using
antibiotics for treating infections. Consequently, it has become essential to restrict the use
of antibiotics to situations where they are absolutely necessary. Furthermore it is also
important to use the narrowest spectrum of antibiotic possible (see Sibbald et al 2000).
Topical antiseptic agents can also be used in wounds. Although certain of these agents
can display cytotoxic properties, if used correctly they maybe extremely effective
antibacterial agents (see Sibbald et al 2000). Furthermore, in contrast to antibiotics, which
have a more specific mode of action, and are effective against a narrower range of
bacteria, antiseptic agents such as iodine (in cadexomer iodine) provide antibacterial
action across three target areas – the cell membrane, cytoplasmic organelles and the
bacteria's nucleic acid. This multi-target antibacterial effect suggests that bacterial
resistance to such a topical agent is less likely to develop.
Whatever the antibacterial agent used, it is important to realise that without appropriate
use of these antibiotic and antiseptic agents, wound bed preparation will remain
inadequate and bacteria will continue to thrive in the wound and delay healing.
3. Management of necrosis
Debridement of devitalised tissue is an essential mandatory step to the success of
wound management (Bergstrom et al 1994), provided adequate blood supply to the
wound is present. "A nidus for infection, necrotic tissue prolongs the inflammatory
response, mechanically obstructs contraction and impedes re-epithelialisation"
(Baharestani 1999)-without debridement the healing process cannot start. Table 4 lists
the consequences of not debriding necrotic tissue. Although debridement occurs
naturally within the wound, studies have indicated that if this process is accelerated, then
the process of wound healing will be more rapid (Steed et al 1996). The clinician has the
choice of four different methods of debridement, however, the decision to use a particular
method depends upon a number of factors (Falanga 2000b; Sibbald et al 2000) (Table 5).
Table 4. Consequences of not debriding tissue (after Baharestani 1999)
Establishment of an optimum substratum for bacterial growth with increased risk of infection,
amputation, sepsis or death
Imposition and perpetuation of metabolic load on the wound and added psychological stress
Ongoing inflammation and leukocyte infiltration with delayed progression to the proliferative
and remodelling phases of wound repair
Compromised restoration of the structure and function of the skin
Potential masking of underlying fluid collections or abscesses
Inability to evaluate actual wound depth
Protein losses through wound drainage
Prevention of wound apposition secondary to the splinting effect of necrotic tissue
Increased risk in burns for hypertrophic scarring with delayed healing and suboptimal
Table 5 . Key factors in choosing which method of debridement to use in wound repair
(after Sibbald et al 2000)
Surgical and sharp debridement methods are the fastest and most effective ways
to remove debris and necrotic tissue. In essence, the scalpel in both these methods
acts as an antimicrobial agent, decreasing the bacterial burden and removing "the
cellular burden" (ie cells that have become old and senescent and so interfere with
wound closure). Surgical debridement is normally performed where the need is
extensive: the degree of undermining and tunnelling cannot be determined, there is
widespread infection, bone and infected tissue must be removed and/or the patient is
septic (Sieggreen and Makelbust 1997). Although, there are a number of advantages to
surgical debridement (see Table 6) this method can also lead to a high risk of pain,
bleeding (although this allows platelet release of growth factors), transient bacteraemia
and damage to tendons and nerves (Baharestani 1999). Importantly, surgical
debridement cannot be employed for all patients or in all settings (see Table 7). In
contrast to surgical debridement, sharp debridement can be performed in the home or
clinic environment. However, in patients with terminal disease, where comfort
management is of greater importance, these approaches can be too aggressive. This
form of debridement must be performed by an experienced, trained clinician.
Table 6. Advantages of surgical debridement (Drager and Winter 1999)
Most rapid and effective technique to remove necrotic tissue, toxic debris and bacteria
Local perfusion can be immediately improved
Risk of infection is significantly diminished
Minor bleeding after debridement leads to the release of several cytokines that have
considerable influence on the initial process of wound repair
Table 7. Contraindications for surgical debridement (Sibbald et al 2000)
Lack of expertise in the procedure
Nonhealable ulcer (ie insufficient vascular supply to permit healing)
Septicaemia in the absence of systemic antibacterial coverage
Medically unfit patient
Patient on anticoagulants
Home care setting
Enzymatic debridement – relies upon the topical application of exogenous enzymes to
the wound surface. These agents work synergistically with endogenous enzymes.
Sinclair and Ryan (1994) have stated that "the role of proteolytic enzymes in wound
healing can no longer be seen as mere wound debridement. Rather it should be
considered as a single, but important player in the wound healing orchestra". The most
characterised exogenous enzyme is bacterial collagenase from Clostridium histolyticum
which displays great specificity for the major collagen types in the skin (type I and type III
collagen) (Drager and Winter 1999; Jung and Winter 1998). It has been successfully
used as an enzymatic debrider for over a quarter of a century and has a number of
distinct advantages (Drager and Winter 1999) (see Table 8). Other enzymes such as
fibrinolysin/deoxyribonuclease and papain have enjoyed limited success in comparison to
bacterial collagenase. Furthermore, in addition to its unique debriding action, bacterial
collagenase has been shown to enhance macrophage chemotaxis and activation within
the wound itself (see Table 9). (Radice et al, 1996) (Herman and Shujath, 1999)
Table 8. Advantages of enzymatic debridement with collagenase (Drager and Winter 1999)
Selective removal of dead tissue
Painless and bloodless
Easily used in long-term care environments and in home-care
Can be used in combination with sharp and mechanical debridement
Enhances granulation tissue formation
Attracts inflammatory cells and fibroblasts to the wound
Reinforces the body's own healing mechanisms
Table 9. Mode of action of enzymes used in wound debridement (Baharestani 1999)
Breaks down fibrin Acts on DNA of
Degrades native collagen
alone, indiscriminate Does not attract fibrin
and requires urea
may act chemotactically on macrophages, fibroblasts and keratinocytes
This occurs naturally to some extent in all wounds, where it is a highly selective process
involving macrophages and endogenous proteolytic enzymes that liquify and
spontaneously separate necrotic tissue and eschar from healthy tissue. Moist
interactive dressings such as hydrogels, hydrocolloids etc can also provide an optimal
environment for debridement by phagocytic cells and help to create an environment
capable of liquifying slough and promoting tissue granulation (Kennedy et al 1997;
Mechanical debridement is a non-discriminatory method that physically removes debris
from the wound. Examples of non-selective mechanical debridement include: wet-to-
dry dressings, wound irrigation and whirlpool therapy.
This is the simplest form of mechanical debridement and is
used to macerate eschar and induce mechanical separation once the dressing is
removed from the wound bed (Jeffrey 1995). However, there are a number of
detrimental effects to using wet-to-dry dressings, including increased patient dis-
comfort and damage to newly formed tissue (Table 10).
Table 10. Detrimental effects of wet-to-dry mechanical debridement
Increase in patient discomfort when changing dressings
Damage to newly formed granulation tissue and fragile epithelial cells
Potential for wound desiccation and peri-wound maceration
This involves the use of either a high pressure or low pressure
stream of water. High pressure irrigation has been shown to be effective in removing
bacteria, particulate matter and necrotic debris from wounds. However, concerns
exist with regards to driving bacteria further into soft tissue.
Another form of powered irrigation that is used to loosen and
remove surface debris, bacteria, necrotic tissue and wound exudate. Although this
method is suitable for necrotic wounds at the inflammatory phase, it is inappropriate
for granulating wounds which have fragile endothelial and epithelial cells.
4. Exudate Management
The elimination of wound exudate or fluid is an important part of wound management
and wound bed preparation, yet its role still remains under emphasised (Falanga 2000a).
The best-looking wound bed will simply not heal if copious amounts of chronic wound
exudate are associated with it. Furthermore, chronic wound fluid is biochemically distinct
from acute wound fluid (Park et al 1998) and has been shown to consist of a biochemical
milieu that is deleterious to the wound healing process. The presence of chronic wound
fluid leads to the breakdown of extracellular matrix proteins and growth factors, and the
inhibition of cell proliferation (Falanga et al 1994; Ennis and Meneses 2000).
Consequently, for proper wound bed preparation, it is imperative that the build-up of
chronic wound fluid is managed efficiently to prevent negative biochemical implications
occurring (Ennis and Meneses 2000).
For the clinician, the management of wound exudate can be performed either directly or
indirectly. Direct wound exudate management involves the use of compression bandages,
highly absorbent dressings (Sibbald et al 1999) or vacuum based mechanical systems
(Ballard and Baxter 2000), although one of the simplest ways of wound exudate
management is through the cleansing and irrigation of a chronic wound with saline or sterile
water. This not only facilitates healing of the wound through removal of exudate and cellular
debris, but it can also reduce the bacterial burden of the wound and a frequent cause for
Indirect approaches to wound exudate management focus on alleviating the underlying
cause, such as extreme bacterial colonisation. It is important to remember that direct
management of wound exudate using appropriate dressings will remain unsuccessful if
treatment of the underlying cause is neglected (Falanga 2000a).
4 . 2 Wo u n d D r e s s i n g s
Clearly it is important for a wound dressing to protect the wound from either
re-injury or re-infection. Additionally, the use of an appropriate dressing may not only
remove copious amounts of wound exudate, but also may alleviate patient pain and
reduce the costs associated with patient care. Clinicians now widely accept that, by
maintaining a moist wound environment, wound healing can be accelerated by as much
as 50% compared to a dry wound, often with an increased rate of re-epithelialisation
(Geronemus and Robins 1982). Furthermore, as wound healing can be thought of as a
continuum, the choice of dressing at one stage of the wound repair process is likely to
influence subsequent events in the later phases of healing (Kerstein 1997). The recent
recommendations proposed by the Agency for Health Care Policy and Research
(AHCPR) in 1994 (Bergstrom et al 1994) which aimed at advising clinicians regarding
correct wound dressing procedures, have been published by Ovington (1999). These
recommendations consist of seven points and are summarised overleaf (see Sibbald et
1. It is important to use a dressing that will maintain a moist
2. Use clinical judgement to select a moist wound dressing for
the particular wound being treated
3. The dressing chosen by the clinician should be able to keep
the surrounding peri-ulcer skin dry while maintaining the
moisture within the wound
4. The wound dressing chosen should control the wound exudate
and not lead to desiccation of the wound bed: uncontrolled
exudate can lead to maceration of the surrounding skin and
lead to further deterioration of the wound
5. Dressings that are easy to apply and do not require frequent
changes decrease the amount of healthcarer time required
6. When applying the dressing, it is important to fill any cavities
within the wound to avoid impaired healing and increased
bacterial invasion (Stotts 1997): overpacking should be
avoided to prevent damage to newly formed granulation
tissue, which could delay healing; overpacking may decrease
the absorbent capacity of the dressing
7. All dressings should be monitored appropriately, but especially
those applied near the anus as they are difficult to keep intact
None of the many dressings currently available to clinicians address all the
requirements contained within the recommendations, although Table 11 does provide a
guide for choosing the appropriate dressing based upon the appearance of the wound
(Sibbald et al 2000). Of these different categories of wound dressings those employed
primarily for sloughy or exudative wounds are the foams, hydrofibres and crystalline
sodium chloride gauze (Sibbald et al 2000).
Other dressings are also available that maintain a moist environment for wound repair
and can be used at other stages of wound bed preparation. Alginates are excellent for
infected wounds and form a gel upon contact promoting moist interactive healing (Blair
et al 1990; Barnett and Varley 1987). Hydrogels are most appropriate for the treatment
of dry, sloughy wounds with low exudate levels, but have weak anti infective properties
and require changing every 24-72 hours.
Table 11. Choosing appropriate dressings (Sibbald et al 2000)
Appearance of wound bed
Appearance of granulation tissue
(bleeding) (healthy granulation/
4. Calcium alginate
8. Nonadhesive film
+ = usually appropriate++ = appropriate+++ = highly appropriate
Occlusive dressings such as hydrocolloids change their physical properties upon contact
with the wound exudate to form a linked matrix gel. They are ideally suited to autolytic
debridement, for mild to moderately exudating wounds (Friedman and Wu 1998), and
can promote hypertrophic granulation.
Film dressings are ideally suited for the later stages of wound healing, such as
granulation and epithelialisation, where there is reduced exudate. While permeable to
water vapour and oxygen, they remain impermeable to water and bacteria.
5. Molecular events in wound healing - cellular dysfunction
During the normal process of wound healing, a series of rapid increases in specific cell
populations are responsible for preparing the wound for repair, deposition of the new
extracellular matrix, and eventually complete wound closure. This orderly process of
cellular control appears to be impaired in chronic wounds resulting in a failure to
complete the repair process. For example, wounds such as venous ulcers and leg
ulcers, are characterised by the defective remodelling of the extracellular matrix, a
failure to re-epithelialise and prolonged inflammation (Hasan et al 1997; Agren et al
1999; Cook et al 2000).
Falanga (2000b) has recently demonstrated that the epidermis in chronic wounds (such
as venous ulcers) fails to migrate across the wound tissue, and that there is widespread
hyperproliferation associated with the chronic-wound margins. It is believed that it is
this hyperproliferation that interferes with normal cellular migration over the wound bed
and results from the inhibition of apoptosis, or normal programmed cell death, within
the fibroblast and keratinocyte cell populations (Falanga 2000b). Other researchers
have also described several phenotypic abnormalities associated with fibroblasts from
chronic wounds, including an altered morphology and a reduced rate of proliferation
(Stanley et al 1997; Cook et al 2000). Fibroblasts obtained from chronic ulcers and
cultured in vitro
, also showed a decreased response to an exogenous application of
growth factors such as PGDF-β and TGF-β (Hasan et al 1997; Agren et al 1999). Thisreduction in response is thought to be due to the fact that the fibroblasts from chronic
wounds are senescent and may indicate in vivo
ageing (Mendez et al 1998; Vande Berg
et al 1998). It may also explain why topical application of growth factors to a chronic
wound does not always lead to wound closure (Falanga 2000b).
6. Molecular events in wound healing - biochemical balance
Chronic wounds are "stuck" at a particular phase of the healing process (e.g. venous
and diabetic ulcers, are believed to be stuck in the inflammatory and proliferative
phases respectively [Falanga 2000b]). Understanding the physiological processes
involved in wound healing is essential for the clinician, but it has become apparent that
it is equally important for clinicians to be aware of the molecular events that are intrinsic
to the wound healing process and in particular the events in a chronic wound. In acute
wounds the expression of molecules such as fibronectin and thrombospondin (and
other extracellular matrix molecules) follow a defined temporal course of expression.
However, it has been shown that within chronic wounds there appears to be an
abnormal over-expression of these extracellular matrix molecules. This is believed to
result from cellular dysfunction and disregulation within the wound and may also have
important biological implications (Falanga 2000b). Furthermore, whilst a wound bed
may be visually excellent, on biopsy, numerous proteinaceous molecules are present
which emanate from the circulatory system.
Fibrinogen and fibrin are two molecules commonly observed histochemically in chronic
wounds, particularly venous ulcers. Falanga (2000b) has recently hypothesised that the
presence of these, and other, extravasated macromolecules (such as a2 macroglobulin)
act as scavengers for growth factors and certain signal molecules that promote wound
repair. Hence, whilst there may be abundant growth factors within the wound, they
become trapped or sequestered, and consequently no longer available to the repair
process, because the wound bed has been inadequately prepared. In this regard, use
of compression bandaging helps to remove the wound fluid containing the fibrin and
fibrinogen, thereby releasing the growth factors that can then promote an angiogenic
response leading to complete wound closure (Falanga 2000b).
Therefore, it is becoming increasingly clear that to ensure wound healing progresses it
is vital that the correct biochemical balance is maintained within the wound, and this
can only be achieved through correct wound bed preparation.
Wound treatment has advanced rapidly over the last 20 years, and coupled with the
current rate of progress in treatment technology and our increased understanding of
the biology of chronic non-healing wounds, this advancement is likely to continue.
However, if clinicians and (ultimately) their patients are to derive maximum benefits from
these evolving therapies and technologies, a greater understanding of the basics of
good wound care is essential. In the rush to utilise newer wound treatments, clinicians
have often neglected the basics of good wound care. It is simple – unless the wound
bed has been prepared properly, futuristic therapies such as bioengineered skin,
recombinant growth factors and gene therapy techniques, (all designed to improve
wound healing), will not succeed.
Consequently, it is becoming apparent that guidelines focusing upon proper wound
bed preparation are required to ensure effective wound care. These guidelines should
provide a systematic approach to wound bed preparation and focus collectively, not
individually, upon the critical components of wound bed preparation including
debridement, bacterial balance in the wound, and proper wound exudate
management. They should also emphasise the importance of understanding the
biochemistry of wound repair and the role of the various cell populations in wound
Ultimately, the aim of wound bed preparation is rapid wound healing with the formation
of good quality granulation tissue that will lead to complete closure naturally or through
the use of technologically advanced skin products or grafting. Only after appropriate
wound bed preparation will clinicians achieve the success that they have strived for
when using advanced therapies in healing wounds.
APPENDIX 1. THE WOUND
Wound healing is a dynamic, natural
and efficient process, that involves a
Capillaries and epithelium
complex series of cellular and
biochemical events, which act upon
the damaged tissues – blood vessels,
dermis and epidermis. Although the
biological mechanisms associated with
wound healing are complicated and
still remain unclear, the entire process
Figure 2. The process of wound healing
can be divided into different phases
The phases of wound healing and the factors involved
During coagulation platelets liberate a number of soluble mediators, including
platelet-derived growth factor, which initiate the wound healing process
Coagulation is followed by an early inflammatory phase that is
characterised by vasodilation, increased capillary permeability, complementactivation and polymorphonuclear leucocytes (PMN) and macrophagemigration to the wound
PMNs predominate during the first days of post-wound occurrence with
macrophages becoming the predominant inflammatory cell within 3 days
Macrophages play a key role in regulating the subsequent events in the
wound healing process by attracting further macrophages and inducingthe proliferation of fibroblasts and endothelial cells which, with increasingnumbers, form granulation tissue around 5 days post-injury and heraldthe proliferative phase
Fibroblasts synthesise collagen and other extracellular matrix molecules to
support new cells and the fragile capillary buds, which appear duringangiogenesis. The endothelial buds increase in vascularity, in response tothe large metabolic demand of the repair tissue). Epithelialisationrequires the migration of epithelial cells across the granulation tissue toclose the epidermal defect
Collagen synthesis continues after wound closure, but also undergoes
continual lysis, so a delicate balance exists between the two processes:the final remodelling phase of the wound is accompanied by increasingtensile strength and decreasing cellularity
In healthy individuals, where there are no deleterious factors present, this whole process
takes about 21 days and does not normally require further clinical intervention. However, in
chronic wounds the orderly sequence of events observed during the normal repair process
becomes disrupted or "obstructed" at one or more of the different stages of wound healing.
For the normal repair process to resume it is critical that any "barrier" is removed through
correct wound bed preparation and that the healing process reverts back to an orderly
series of events (Sibbald et al 2000).
To a high degree, wound healing is determined by the general health of the patient.
Therefore, prior to the management of a chronic wound, the clinician should conduct a
holistic assessment of the patient and a diagnosis of the wound.
2.1 Provision of an adequate blood supply to the wound
An important consideration when beginning to manage a wound is to ensure that the wound
has an adequate blood supply as this will ensure that the process of healing can be fully
facilitated (Kerstein 1997; Sibbald et al 2000). It is essential that patients with arterial disease be
diagnosed at the outset of treatment – particularly patients with wounds on the lower extremities
or with a metabolic disorder such as diabetes mellitus (Kerstein 1997; Sibbald et al 2000). A
wound with a poor blood supply will be paler in comparison to the healthy granulation tissue
observed in a well-perfused one. Without adequate wound perfusion, there will be insufficient
nutrients and oxygen delivery, both of which are essential to support the large metabolic
demand associated with the wound repair process. Furthermore, delivery of the cellular
components of the immune system (such as leukocytes and macrophages), which are critical for
healing to progress, is also impaired. Finally, an impaired venous blood supply cannot facilitate
the removal of debris from the wound during the healing process (Kerstein 1997).
A variety of systemic and local factors, diseases, and medications may interfere with wound
healing (see review by Cohen et al 1992) (Table 12). Consequently, it is crucial for proper wound
management to treat the underlying causes (Kerstein 1997; Sibbald et al 2000; Falanga 2000b).
Malnutrition in a patient can be a key factor in wound healing. In particular protein and vitamin
deficiency may deprive the body of essential nutrients required for healing (Kerstein 1997;
Jung and Winter 1998; Sibbald et al 2000). Protein is essential for the formation of new
granulation tissue and severe protein malnutrition results in a decreased rate of wound healing,
decreased immunocompetence and increased susceptibility to infection (Mazzotta 1994). In
the USA, it is recommended that the daily allowance of protein should be increased from 2.0
to 4.0 g/kg/day during wound healing as opposed to the 0.8 g/kg/day recommendation for
healthy individuals (Mazzotta 1994). Protein deficiency in patients is normally measured by
their serum albumin concentration and, although figures vary, an albumin concentration of
below 3.0 g/L will delay wound healing (Mazzotta 1994; Sibbald et al 2000).
Table 12. Systemic and local factors that can interfere with the process of wound repair
– Protein deficiency
– Vitamin deficiency (A, C and E)
– Mineral deficiency (zinc and iron)
Vitamin deficiency, especially of vitamins A and C also impedes wound healing. Vitamin A is
important for each stage of wound repair and a deficiency can lead to a reduction in the
extracellular molecule fibronectin which in turn results in decreased cell chemotaxis, cell adhesion
and epithelialisation. Vitamin C is also important, with poor wound healing being one of the
symptoms of scurvy, whilst deficiency of vitamin C can lead to the breakdown of already healed
wounds (Mazzotta 1994).
Minerals such as zinc and iron also play a pivotal role in the promotion of wound repair. Zinc
deficiency can lead to delayed wound and ulcer closure, it may also result in a reduction in the
number of lymphocytes and an increased susceptibility to recurring infection and hence poor
wound healing. Iron is required as a cofactor for the enzymes involved in DNA synthesis which is
critical for cell division. Consequently, iron deficiency inhibits cellular proliferation especially of the
cells involved in wound debridement and healing (Mazzotta 1994).
2.2.2 The medical history of the patient and their medication
Recording the patient's general medical history and monitoring their ongoing medication is also
critically important for successful wound management. The presence of a major illness or
systemic disease can result in the inhibition of wound healing. Autoimmune diseases such as
rheumatoid arthritis or systemic lupus, and the systemic steroids and immunosuppressive agents
used to control the underlying disease, can interfere with wound healing (Kerstein 1997; Sibbald
et al 2000). The interference of immunosuppression with wound management has become an
increasingly common problem and particularly in patients diagnosed with HIV (Kerstein 1997).
Therefore, before wound management can be instigated in autoimmune patients, the heightened
immune response in these patients must be reduced to ensure wound repair can progress
(Sibbald et al 2000).
Treatment with glucocorticoids results in decreased collagen synthesis and a delay in
re-epithelialisation in dermal wounds (Jung and Winter 1998). Impaired coagulation (due either to
the patient's genetic disposition, or the use of anticoagulants such as heparin and warfarin) will
have a negative impact on the earliest stage of wound healing (Kerstein 1997). Furthermore,
metabolic diseases including diabetes mellitus may also lead to an increased incidence of
infection following surgery and may increase the time to complete wound healing (Mekkes and
Westerhof 1995; Levin 1993; DCCTRG 1993).
2.3 Wound assessment
Inherent to effective wound management is
the careful and consistent documentation of
the wound itself which will enable the
clinician to select the appropriate treatment
modalities and evaluate the progress of the
patient (see Figure 3 for an example of a
wound assessment model). The wound
examination includes recording the history,
location, depth and dimensions of the
Figure 3. Wound assessment model (after Kerstein 1997)
wound, evaluation of the wound bed and the
surrounding skin, and an analysis of the wound exudate and associated pain (Kerstein
1997; Sibbald et al 2000).
2.3.1 Wound history
It is important for the clinician to obtain information relating to the duration of the chronic
wound, any previous therapy employed to treat the wound, and if it is a recurrent wound.
The clinician can use such information to address issues concerned with preventing infection,
or to assess whether there are systemic or local factors obstructing the healing process.
This information is also important if the patient is referred and another clinician becomes
responsible for their treatment, as this would help to prevent the repetition of a previous
treatment and also to assist in understanding if a previous diagnosis and treatment were
2.3.2 Wound location and dimensions
The precise anatomical location of the wound on the patient should be recorded (Kerstein
1997; Sibbald et al 2000). This will enable the clinician to assess the time required for the
particular wound to heal and completely close – a wound with an ample blood supply will
heal more rapidly than a wound in a peripheral area of the body – which may have a reduced
blood supply. It is also important to remember that the rate of wound healing can be
affected by skin adherence; for example, a shin wound will be slower to heal than other
wounds because the skin is so tightly adhered to the shin (Kerstein 1997).
The depth and area covered by a wound can also profoundly influence the rate of wound
repair, thus, it is important that the depth of the wound is accurately assessed before
proceeding with wound management. The wound should be checked for the presence of
bone, sinuses or undermining tissue (Kerstein 1997; Sibbald et al 2000).
2.3.3 Condition of the wound bed and characteristics of wound exudate
The condition of the wound bed can indicate how healing within the wound is progressing and
also how effective the treatment has been (see Sibbald at al 2000). The presence of black
eschar is representative of necrotic devitalised tissue and may be soft or firm. If the intention is
to heal the wound then for healing to continue it is essential that this necrotic tissue is removed.
A yellow fibrous wound bed can be firm or soft. A firm base indicates that there
are structures such as fascia, subcutaneous fat or a fibrin base for the future development of
granulation tissue, and does not need to be removed. The presence of soft, sloughy, material
may indicate the presence of infection or degraded fibrin that will require removal for healing to
progress (Sibbald at al 2000).
The appearance of firm, moist granulation tissue, which is salmon red-pink in colour, is a clear
indicator that the treatment regimen employed by the clinician has been effective and healing is
progressing normally. Newly formed epithelialised tissue, pink-purple in colour, normally appears
after this stage, usually at the edges of the wound (Sibbald et al 2000).
When assessing wound exudate clinicians usually describe it based upon quantity,
characteristics and odour (see Table 13). Even if the exudate is clear the presence of a heavy
exudate indicates uncontrolled oedema or an increased bacterial burden or possible infection
within the wound (Sibbald et al 2000).
Table 13. Classification of the exudate in chronic wounds (Sibbald et al 2000)
Descriptions of chronic wound exudate
Exudate quantity – described as scant, moderate
Exudate characteristics – described as serous-serum, sanguinous-blood, purulent-infection,
combination of these
Exudate odour – presence
2.3.4 The wound margin and surrounding skin
It is important for the clinician to also focus upon the wound margin in order to monitor the
patient for signs of erythema, oedema, pain, or maceration of the surrounding skin. The
presence of erythema, swelling and pain can indicate inflammation and infection, or
unrelieved pressure, or adverse reactions to wound care treatments (van Rijswijk 1996;
Sibbald et al 2000). The presence of skin maceration can be the result of prolonged
exposure of the skin to wound exudate indicating that the wound dressing is inappropriate,
or not being changed frequently enough, thereby keeping the wound overly moist.
It is also important to avoid exposure of the wound to allergens as chronic wounds provide
optimal penetration for these substances and their systemic processing by the immune
system (Sibbald et al 2000).
2.3.5 Assessment of wound pain
Wound pain can serve as an important indicator of inadequate wound management.
Therefore, pain should be quantitatively assessed and routinely documented, preferably
using the visual analogue scale (0 = no pain, 10 = worst pain). Chronic wound pain
can be divided into incident pain, recurrent episodic pain, and continuous pain (Krasner
1997). Incident pain results from debridement or trauma to the wound, and can be
relieved through the use of analgesia based upon the WHO pain ladder (Ferris et al
2001). Recurrent episodic pain is frequently experienced by the patient when their
wound dressings are changed.
In such cases, appropriate pain control (administered either locally or systemically)
should be initiated prior to the dressing changes. Continuous pain may indicate that the
underlying cause of the wound has remained untreated, or that the wound has become
extensively infected. It is essential for the clinician to determine whether or not the
continuous pain experienced by the patient originates from the local wound or the
surrounding tissue (Sibbald et al 2000).
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