62 february 20 :: vol 22 no 24 :: 2008 NURSING STANDARD

THERE ARE MANY classifications of wounds.

These may be based on the depth of tissue injury,
for example, grading in pressure ulcers; how
wounds heal, for example, by primary or
secondary intention; or the underlying pathology,
for example, diabetic foot ulcers (Figure 1). A
frequently used general description that crosses
all of these typologies classifies wounds as either
acute or chronic.
Acute wounds include:
Surgical wounds (Figure 2).
Traumatic wounds (Figure 3).
Burns (Figure 4).
Chronic wounds include:
Pressure ulcers.
Leg ulcers.
Diabetic foot ulcers (Figure 1).
Fungating wounds (Figure 5).
This is, however, not straightforward because
there are no accepted definitions of the terms
acute and chronic.
Classification as acute or chronic can
sometimes be unhelpful (Schultz et al 2004). It is
often assumed that the difference between the
two relates to the time taken for a wound to heal
and therefore acute wounds heal quickly and
chronic wounds take much longer to heal. In most
cases even extensive surgical or traumatic
wounds will heal in a timely and ordered way.
Those deemed as chronic, however, seem to take
extended periods to heal, for example, the
standard definition of a leg ulcer is time-bound:
a wound below the knee which fails to heal in
four weeks (Cullum et al 1997), and it is not
unusual for patients to have chronic wounds for
months or even years.
Troxler et al (2006) define chronic wounds as
those that fail to heal with standard therapy in
an ordered and timely manner. The allocation of
wound aetiologies to the time-bound definition,
however, reveals only part of the definition of
chronic wounds and raises several contradictions.
If a patient has a surgical wound to the abdomen,
which becomes infected, dehisces (breaks down)
and takes several months to heal, does it remain
an acute wound because it is a surgical wound or
Differences between acute and
chronic wounds and the role of
wound bed preparation
Fletcher J (2008) Differences between acute and chronic wounds and the role of wound bed
preparation. Nursing Standard. 22, 24, 62-68. Date of acceptance: November 27 2007.
&
art &science tissue viability supplement
Summary
There are major differences in the way acute and chronic wounds
heal. An understanding of these differences enables practitioners to
plan more appropriate care and management for patients. A simple
framework such as wound bed preparation can be used to identify
problems and plan realistic and appropriate outcomes of care.
Author
Jacqui Fletcher is principal lecturer, School of Nursing and
Midwifery, University of Hertfordshire, Hatfield, Hertfordshire.
Email: j.fletcher@herts.ac.uk
Keywords
Dressings; Tissue viability; Wound bed preparation
These keywords are based on the subject headings from the British
Nursing Index. This article has been subject to double-blind review.
For author and research article guidelines visit the Nursing Standard
home page at www.nursing-standard.co.uk. For related articles
visit our online archive and search using the keywords.
FIGURE 1
Diabetic foot ulcer
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p62-68w24 14/2/08 1:06 pm Page 62
does it become a chronic wound because it has
taken a long time to heal? Equally, is a wound to
the lower leg on a patient who clearly has
underlying venous disease an acute wound until
it has been present for four weeks? This is a
common occurrence when patients knock their
legs and sustain a skin tear because of fragile
skin. It is evident that other factors need to be
considered in classifying a wound as acute or
chronic.
Wound healing
Flanagan and Fletcher (2006) suggest that in
chronic wounds the usual orderly process
of healing that occurs in acute wounds
haemostasis, inflammation, proliferation and
remodelling is disrupted at one or more points
in the process, resulting in delayed healing or
failure to heal. Various authors identify different
factors that may interrupt the wound healing
process (Table 1). These factors need to be
considered when assessing and planning the
management of wounds because, where possible,
they should be alleviated to aid timely healing. This is not always possible because some factors,
particularly concomitant disease, cannot be
rectified. However, acknowledging their
presence allows more realistic objectives and
time scales to be set. In addition to the inability to
rectify the problems, identification of some of the
factors that cause delayed healing is not possible
because diagnostic tests to identify particular
cellular markers such as matrix
metalloproteinases (MMPs) (Box 1) do not exist
in a form that is easily usable in clinical practice.
It could be asked therefore, what is the clinical
benefit of knowing about these cellular
differences?
The identification of potential to heal is an
essential part of clinical and cost-effective wound
management. While the management of even
extensive acute wounds is generally a
straightforward process, the smallest of chronic
wounds frequently presents practitioners with a
considerable challenge (Troxler et al 2006).
Effective wound management relies on accurate
assessment. If assessment is superficial it is likely
that underlying factors will not be identified and
therefore the management plan will fail to
address the perpetuating factors resulting in less
than optimal results.
Wound bed preparation
Wound bed preparation (WBP) has been
described as: the desire to provide an optimal
64 february 20 :: vol 22 no 24 :: 2008 NURSING STANDARD
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FIGURE 4
A burn on the forearm
FIGURE 2
Surgical wound on the abdomen
FIGURE 5
FIGURE 3
Traumatic wound to the head
Fungating wound on the lower lip
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environment by producing a stable wound bed
with minimal exudate (Dowsett 2002) and the
acceleration of endogenous healing to facilitate
the effectiveness of other therapeutic measures
(Schultz et al 2003).
WBP links treatment to cause by focusing
on three components of local wound care
debridement, bacterial balance and moisture
balance (Sibbald et al 2000). Because chronic
wounds relate to an underlying pathology that
slows the acute phases of healing, other factors
such as infection or ischaemia alter the molecular
and cellular environment so that the healing
process does not progress in a straightforward
way. The changes in the molecular and cellular
environment for healing are underpinned by
ever-increasing knowledge of the biological
micro-environment within a chronic wound and
centre on the interrelationship of functionally
abnormal cells, bacterial balance, inappropriate
biochemical messages and dysfunctional wound
matrix components (Vowden and Vowden
2002). This complex biological micro-
environment makes wounds chronic. Assessment
of the cause of the wound (underlying pathology)
is therefore crucial before starting local wound
management interventions (Schultz et al 2004).
The three central components of WBP can be
easily related to the factors identified in Table 1
and appear much more practical.
Debridement In addition to preventing the full
extent of the wound from being seen, the
presence of necrotic tissue, slough and other
debris acts as a barrier to healing, providing a
focus for infection, prolonging the inflammatory
phase and obstructing contraction and
re-epithelialisation (Baharenstani 1999).
Prolonging the inflammatory phase causes
neutrophils, mast cells and macrophages to enter
the wound in an attempt to remove the necrotic
tissue. This in turn then initiates a further
inflammatory response as the by-products of this
activity include proteases and pro-inflammatory
cytokines (Schultz et al 2004).
In acute wounds debridement may be carried
out to remove devitalised or damaged tissue to
create a neat edge or a clean wound bed. Once it
has been performed it is unlikely to be required
again. However, in chronic wounds the increased
february 20 :: vol 22 no 24 :: 2008 65 NURSING STANDARD
TABLE 1
Factors that interrupt or delay the wound healing process
Doughty and Sparks-
Defriese (2007)
Underlying pathology
Prolonged inflammatory
phase
High levels of proteases
Deficiency of growth factor
receptor sites
No initial bleeding event to
trigger fibrin production and
release of growth factors
Cellular senescence
Flanagan and Fletcher
(2006)
Underlying pathology
High levels of pro-
inflammatory cytokines
Increased proteases in
wound fluid
Medina et al
(2005)
Growth factors
Serine proteinases
Matrix
metalloproteinases
Adult stem cells
Chemokines
Replicative cell
senescence
Integrins
Moore (2005)
Complicated by local or
systemic factors:
Infection
Ischaemia
Concomitant disease
Fixed persistent state of
inflammation
Abnormal deposition of
extracellular matrix
Failure to epithelialise
Fibroblasts and endothelial
cells fail to form granulation
tissue
Falanga (2004)
Bacterial burden and
biofilms
Growth factor
trapping
Wound fluid and
metalloproteinases
Impaired blood flow
and hypoxia
The pathophysiological
status of the wound
BOX 1
Glossary
Extracellular matrix (ECM): a protein matrix laid
down in the wound which comprises proteins such as
collagen, elastase and fibrin. A functioning ECM is
essential as new cells migrate across this structure in a
granulating wound.
Integrins: a protein that links the outside of a cell to
its interior.
Matrix metalloproteinases (MMPs): proteinases are
enzymes capable of breaking down proteins. MMPs
have specific activity against the proteins of the ECM.
Tissue inhibitor of matrix metalloproteinases
(TIMPs): TIMPs inhibit the activity of MMPs and
prevent the matrix being broken down once debris is
removed in acute wounds. Down regulation of TIMPs
allows MMPs to carry on unchecked and can lead to
break down of the wound.
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production of abnormal cells and resulting
cellular debris because of the persistent state
of inflammation lead to a constant cycle of
devitalised tissue production. Therefore,
debridement requires constant maintenance.
Several methods of debridement are available,
including:
Autolysis the use of dressing products to
facilitate the bodys own processes by
providing moisture to the wound.
Sharp debridement the use of scissors or
scalpel to remove dead tissue. This should only
be performed by appropriately trained
personnel.
Surgical debridement the removal of tissue
back to healthy bleeding tissue usually carried
out in theatre. This may be carried out with a
scalpel or with a waterjet (hydrosurgery)
(Gurunluoglu 2007).
Biological or larval therapy the use of
maggots to clean the wound. These may be
either loose or within a bag.
Other types of debridement are described in the
literature, that is, mechanical and enzymatic, but
these are not usually used in the UK (OBrien
2002). Mechanical debridement is usually used
to describe wet to dry debridement and pulsed
lavage, neither of which is considered
appropriate in the UK. In addition, no enzymatic
products are currently available in the UK.
Selection of the most appropriate method should
address what is best for the patient, what is
available in the practice area and what the
practitioner involved is competent to do.
Debridement serves two main functions:
removal of the physical barrier to healing and a
reduction in the microbes, toxins and other
substances which may cause further damage
within the wound.
Bacterial balance The presence of bacteria in
wounds is a normal occurrence until their
number or the action of the toxins they produce
begins to impede wound healing (Box 2).
In chronic wounds the continued presence
and multiplication of bacteria further potentiate
the inflammatory response increasing
production of inflammatory mediators and
recruitment of neutrophils. There may be
localised thrombosis and release of
vasoconstricting metabolites leading to tissue
hypoxia and destruction. This again increases
the amount of necrotic tissue and debris in the
wound, which supports bacterial growth and
the spiral continues.
In patients with chronic wounds the risk of
progressing to infection may be higher because
of the underlying disease process, which may
compromise local blood supply, tissue
oxygenation or the ability to mount a response to
bacterial invasion. These factors may also mask
the signs and symptoms of infection, particularly
in patients who are immunocompromised.
Diagnosis of wound infection should
primarily be based on clinical signs and
symptoms (Cutting and Harding 1994) (Box 3).
In addition to these criteria, Cutting et al
(2005) propose individual collections of signs
and symptoms for specific wound types with
additional criteria for all chronic wounds. These
further signs and symptoms relate to the
progression of the disease process and its impact.
Vowden and Cooper (2006) propose different
stages of wound infection (1-4) based on the
number and severity of signs of infection. They
have also devised an algorithm to determine
treatment of infected wounds based on these
stages. This algorithm identifies when it is
appropriate to manage infection topically and
when systemic treatment is required because the
overriding objective should always be to provide
the optimum conditions for healing. Dowsett
and Ayello (2004) state that the first focus of
management should be on supporting the host
defences, minimising where possible any
conditions which decrease immunity and
removing conditions which support bacterial
growth, such as the presence of devitalised tissue.
Local management with dressings should also
address the additional symptoms caused by the
presence of infection such as odour and increased
levels of exudate.
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BOX 2
Outcomes of host-pathogen interactions
Contamination
All wounds may acquire micro-organisms. If suitable
nutritive and physical conditions are not available for
each microbial species, or they are not able to
successfully evade host defences, they will not multiply
or persist. Their presence is therefore only transient
and wound healing is not delayed.
Colonisation
Microbial species successfully grow and divide, but do
not cause damage to the host or initiate wound
infection.
Infection
Microbial growth, multiplication and invasion into host
tissue lead to cellular injury and overt host
immunological reactions. Wound healing is interrupted.
Local factors can increase the risk of infection.
(Cooper 2005)
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Moisture balance Clinicians are aware of the
problems caused by excessive moisture in wounds
without necessarily understanding the cellular
level detail of what is happening. Wounds with an
excessive exudate leak become malodorous,
cause damage to the surrounding skin both
maceration and excoriation and generally
challenge the practitioner in terms of frequency of
dressing changes. These problems can be related
to what is happening at the cellular level.
Wounds exude for two reasons: the
inflammatory process and as a response to
infection. There may be other reasons related to
systemic factors such as the presence of oedema
but when considering only local factors it is
usually one of these two reasons. The fact that
chronic wound exudate causes so much damage
to the surrounding skin relates to the differences
between acute and chronic wound exudate.
Acute wound exudate has a positive function,
including maintenance of the optimum moist
environment necessary for cellular activity and
movement (Winter 1962), carriage of white
cells, part of the primary defence against
invading micro-organisms, and movement of
other key cells such as macrophages which
have a major role in clearing debris from the
wounded area to where they are most needed.
In the normal process of repair where the wound
heals in an orderly fashion, the volume of
exudate gradually diminishes as the wound heals
and fluid conservation may become important
(Thomas 1997). However, in chronic wounds or
where the process of healing is disrupted, for
example, the wound becomes infected, the
exudate level is maintained or may increase and
the constituents of the exudate change.
Although it is generally believed that exudate
plays an essential role in the healing process it is
less clear when the detrimental effects of
exudate begin to outweigh the benefits. Several
studies have investigated the content of exudate
and it is apparent that the constituents and
quantities of individual components vary
between individuals and at particular times
during the healing process (Baker and Leaper
2000). Chronic wound exudate differs from
acute wound exudate in the profiles of proteases
(MMPs and serine proteases) and their
inhibitors with chronic wound fluid being
described as corrosive (Bishop et al 2003).
While MMPs play a positive role in acute
wound healing with regard to the breakdown of
proteins of the extracellular matrix, for
example, collagen and elastin (Box 1), where
they are over-expressed the proteolytic content
of the exudate may be responsible for causing
considerable excoriation to the peri-wound skin
(Cutting and White 2002). Over-expression of
MMPs occurs during prolonged inflammation
or as a response to infection which stimulates
an inflammatory response as seen in chronic
wounds. This becomes a cyclical process
because the now corrosive exudate initiates an
inflammatory response from the wound and
peri-wound skin. This additional inflammatory
stimuli may also be caused by infection and
repeated trauma, for example, trauma from
dressing removal or by hypoxia generated from
applied pressure.
Proactive management of wound exudate can
help to reduce the detrimental effects it causes
without necessarily being able to determine how
much of which MMP is present in the exudate.
Proactive management involves identifying the
cause of increased exudate and where possible
managing this. Oedema in the wound area will
increase the amount of fluid leaking from the
wound. This is not necessarily an increase in
exudate, simply more fluid, and this is more
likely to cause maceration than excoriation, that
is, the wound edges will become white and
appear soggy.
Skin that is bright red, inflamed and may have
superficial breaks suggests that exudate is being
left in contact with the skin surrounding the
wound and the MMPs and other proteases are
causing superficial damage. In this case it is
important to ensure that the dressing used is able
to absorb the amount of exudate being produced
and also retain the exudate within its structure to
prevent it causing further damage. It is unusual
for the exudate from acute or healing wounds to
cause this type of damage because of the
differences in the volume and nature of exudate.
february 20 :: vol 22 no 24 :: 2008 67 NURSING STANDARD
BOX 3
Criteria for wound infection
Traditional criteria:
Abscess.
Cellulitis.
Discharge (serous exudate with inflammation;
seropurulent; haemopurulent; pus).
Suggested additional criteria:
Delayed healing (compared with normal rate
for site and condition).
Discolouration.
Friable granulation tissue that bleeds easily.
Unexpected pain and/or tenderness.
Pocketing at the base of the wound.
Bridging of the epithelium or soft tissue.
Abnormal smell.
Wound breakdown.
(Cutting and Harding 1994)
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Although excessive exudate is the more
common problem it should not be forgotten that
moisture balance is required. A wound that is
dehydrated may also be problematic because all
cells require a moist environment in which to
thrive. A moist environment supports the
movement of cells, the development of the
extracellular matrix and autolytic debridement.
Conclusion
There are many differences between acute and
chronic wounds. Although these may not be
immediately obvious they have a considerable
effect on the potential to heal and risk of
complications occurring in a wound, particularly
infection. Understanding the differences between
acute and chronic wounds should result in a
more appropriate and realistic plan of care.
Much still remains unknown about the healing
process in chronic wounds and much of what is
known cannot be easily demonstrated or
measured in daily clinical practice. It is possible
to relate cellular level information to clinical
reality with careful thought, allowing possible
problems to be identified. To do this clinicians
should ensure that they undertake a
comprehensive assessment of the patient and the
wound before planning care and ensure that
appropriate consideration is given to managing
underlying factors as without this it is unlikely
that care will be effective NS
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