continuing professionai deveiopment

Delayed wound healing:

in whom, what, when and why?
PHC117 White R (2008) Delayed wound healing: in whom, what when and why? Primary Health Care. 18. 2,40-46.
Date of acceptance: 18 February 2008.

SummarY
For a variety of reasons, some wounds take longer than anticipated to heal, or do not
heal at all. Delayed or impaired healing may occur with wounds such as leg ulcers, but
can also sometimes be seen with acute traumatic wounds such as pre-tibial lacerations.
This article, using leg ulcers as an example of 'chronic' wounds, provides a guide to
delayed healing and how it can be anticipated, avoided and managed.

Author
Richard White is Professor of Tissue Viability, University of Worcester.
Email: rwhite@worc.ac.uk

Keywords
Chronic wound; Ulcer; Delayed healing
These keywords are based on the subject headings from the British Nursing Index. This
article iias been subject to double-blind review. For related articles and author guidelines visit our online archive at www.pHmaryhealthcare.net and search using the
keywords.

Aims and intended learning objectives

The aim of this article is to introduce and

define the concept of delayed wound healing,
with a focus on venous leg ulceration and to
describe the causes of delayed healing and
interventions to overcome it. After reading this
article, you shouid be able to:
understand what healing rates might be
expected with standard treatment.
relate delayed or prolonged healing to
treatment, medical, biological, psychological
and lifestyle causes.
be aware of guidelines avaiiabie to aid
prediction of vyound chronicity.
appreciate the evidence in support of
interventions to overcome delayed healing.
Introduction
Many wounds that heal by secondary intent,
such as leg ulcers and pressure ulcers, have
historically been referred to as 'chronic', but a
wound is not always inherently 'chronic' simpiy
40 primary health care | Vol 18 No 2 | March 2008

because of its aetiology (Harding 2000). This

label is applied to wounds in which compromised healing is anticipated, usually because
of complex underlying pathologies such as
diabetes (King 2001), vascular disease (Grey et
ij/2006), malignancy (Izadi and Ganchi 2005),
malnutrition {Graue etallOOS) or morbid
obesity (Fife et al 2008). The published literature contains many references to such wounds,
referring to them as 'stunned' (Ennis and
Meneses 2000), recalcitrant (Thomson 2000)
or 'difficult to manage' (Ballard and Baxter
2000). Consideration must be given to the
diagnosis, and to what degree or rate of healing
is anticipated, if any, before any judgement of
delayed healing can be made (Harding 2000,
Cardinal f/i7/2008).
The management of chronic wounds in
the UK has been estimated to cost over l
billion a year (Bennett et al 2004}, with an
additional cost to patients of reduced quality
of life (Charles 2004). What then constitutes a
'chronic' wound and what determines 'delayed'
healing?
Now do Time out 1
Delayed healing

The term 'delayed heaiing' has been defined

as 'heaiing that takes longer than anticipated,
given appropriate therapy' (Ballard and Baxter
2000). Wounds can heal within an 'acceptable' time given appropriate treatment. Thus a
venous leg ulcer, treated with a moist wound
dressing and graduated compression, that does
not show signs of a healing response in four
weeks may be described as 'delayed' or compromised (Phillips et al 2000). This definition
demands that 'appropriate' therapy is provided,
and this will vary according to the aetiology
and condition of the wound.
Predictive leg ulcer healing rates have been
published (Margolis et al 2004, Flanagan
2003) and validated (Cardinal et al 2008).

These provide a benchmark whereby 'normal'

healing rates, as measured by reduction in
wound area over time, can be compared with
those achieved in individual patients. This,
by definition, requires regular assessment
including wound measurement (Langemo et al
2008). Diabetic foot ulcers require the control
of blood glucose, pressure offloading and
debridement if they are to heal (Cavanagh et
iii 2005); predictive healing rates have been
published (Sheehan et at 2003). Similarly,
pressure ulcers need pressure relief as well as
attention to general medicai condition if they
are to heal (Thomas 2006).
It is not only chronic wounds that can be
classed as delayed; acute traumatic wounds
can also fall into this category. A good
example is the pre-tibia! laceration (Warren
et al 1991); these wounds often become static
and fail to respond to treatment (Dunkin et al
2003). In such cases, the patient's underlying
medical condition can be one of the main
reasons (Wood and Lees 1994).
Anticipating a delay in healing

To predict, or anticipate, the chronicity of a

wound at an early stage is clearly of great clinical benefit as it allows timely intervention with
cost-effective treatments. To that end, attempts
have been made to list various indicators (Boyd
et al 2004, Gohel et al 2005). These authors
have established an expert working group to
consider factors tbat might adversely effect
wound healing. Their findings can be summarised as follows:
Local factors - for example, foreign
bodies, scar tissue, peri-ulcer maceration,
incontinence, undermining.
Regional factors - venous or arterial disease,
perfusion, neuropathy, lymphoedema,
oedema.
Systemic factors - diabetes, malnutrition,
chemotherapy, pain, rheumatoid disease,
psychosocial issues, smoking.
These factors may be ranked as 'severe chronicity', 'high to moderate chronicity', 'mild
chronicity', and, 'unlikely to become chronic'.
Figure 1 provides an assessment framework to
assist in the prediction of wound chronicity.
Now do Time out 2
Avoiding delayed healing

in effect, avoiding delayed healing constitutes

'optimising' healing. The positive steps begin
with detailed and regular holistic assessment.
Treatment should be evidence-based and

meet with current gold standards, such as an

optimum moist wound environment and appropriate compression for venous ulcers. Where
local delaying factors exist, steps must be taken
to overcome them by, for example, debriding
slough and necrotic tissue, removing foreign
bodies and avoiding maceration and consequent wound enlargement (Cutting and White
2002a and b).
Regional factors may be more difficult to
overcome. Venous disease and lymphoedema
can often be counteracted hy compression
(Stephen-Haynes 2006), while arterial disease
may require bypass grafting. Neuropathy,
a factor in diabetic foot ulceration, cannot
be treated and requires long-term protective
measures for patients 'at risk' of ulceration
(Cavanagh e/fl/2005).
Systemic factors, once recognised, can be
addressed with appropriate treatment. For
example, diabetes can be managed by blood
glucose control and pain by analgesia, although
not all such factors are manageable (for
example, malignancy, smoking and alcohol
misuse).

What are the

differences between
acute and chronic
wotmds in terms of time
to heal? How might wound
chronicity be predicted?

For a patient with

a venous ulcer, which
of the foliowing factors
would help predict chronicity:
maceration, congestive heart
failure, depression, exposed
tendon, varicose eczema,
hypothyroidism.

Biological factors

The cellular and biochemical environment

can prevent wound healing (Douglass 2003),
although it is not directly observable. Clues
to biological abnormalities can be gained by
observing the tissues in the wound bed and
surrounding skin (Harker and Moore 2004).
These aspects can be monitored, assessed
and documented by the use of either applied
wound management (AWM) or wound bed
preparation, known by the acronym TIME
(tissue, inflammation or infection, moisture, edge or epithelium) (Gray et al 2006,
Schultz et al 2003). The colour of tissues in
the wound, whether black, green, yellow, red
or pink (or combinations of these) is a key to
wound assessment (Gray et al 2005). Harker
and Moore (2004) have described the relationship of wound pathophysiology to observed
features.
Healing in chronic wounds is regarded as
being 'stuck' at the inflammatory stage (Moore
2004). This is attributable to many different
factors:
Infection or bacterial critical colonisation.
High levels of protease enzymes.
Altered growth factor and cytokine function.
Neutrophil accumulation.
Changes in lymphocyte and macropbage
populations.
primary health care | VoMS No 2 | March 2008 41

delayed wound healing

Microbial factors in delayed

wound healing
Wound infection or critical
colonisation (KIngsley 2001)
Bacteria consume the vital
nutrients needed for tissue
regrowth
Increased exudate volume
(Cutting 2004) and purulent
exudate
Toxins from bacteria damage cells
(Cooper 2003)
Proteases damage the
extracellular matrix and other
vital tissue cotnponents
Odour: malodour is attributed to
anaerobic bacteria
Biofilm formation inhibits healing
(James et at 2008)
Slough/necrosis provides an ideal
environment for bacterial growth

Utceration of the lower limb:

common differential
diagnoses
Many differential diagnoses for
ulceration of the lower limb exist
(Tillman 2004). All can delay
or impair healing and need to
be excluded at the outset and
throughout the treatment period:
* Venous leg ulcer
Arterial ulcer
Complex or mixed venous/arterial
aetiology ulcer
Pyoderma gangrenosum (Bull
1997)
Necrobiosis lipoidica
Rheumatoid ulcer (Firth 2006)
Malignant ulcer (Marjolin's ulcer)
(Enoch ef al 2004)
Bullous pemphigoid

Although all wounds that heal by secondary

intent are colonised by bacteria, the presence of
micro-organisms in the wound can, in certain
circumstances, give rise to impaired/delayed
healing (Bowler et ai 2001) (Box 1). Indeed, the
presence of opportunistic pathogens has been
postulated as an important factor in non-healing (Bjarnsholt et al 2007). In an attempt to
clarify how the bioburden influences healing,
Kingsley (2001) has devised the wound infection continuum.
Protease enzymes, notably matrix
metalloproteases (MMPs), are the product
of neutrophils (endogenous) and bacteria
(exogenous). In chronic wounds, the levels of
proteases are raised (Agren 1994) and their
natural inhibitors are diminished, which leads
to uncontrolled destruction of the extracellular
matrix.

Low tissue oxygen levels compromise

healing because of, for example, microvascular
disease in diabetic foot ulceration, arterial
ulceration accompanied by atherosclerosis,
venous hypertension and lipodermatosclerosis
in venous ulceration, and, in pressure ulcers,
vascular occlusion and ischaemia.
Pulse oximetry has been successfully applied
to patients with leg ulcers; this is a measure
of arterial oxygen and, consequently, tissue
perfusion (Bianchi 2008). Impaired perfusion
can be alleviated in some patients by exercise,
limb position, compression therapy (this
improves venous return, reduces oedema and
thereby raises arterial perfusion). If these
fail, or are inappropriate, surgery for arterial
grafting or endarterectomy is indicated.

In normal healing, specific proteins known

as growth factors and cytokines regulate the
movement and growth of the key cell types:
keratinocytes, fibroblasts and endothelial cells
(Broughton et al 2006a and b). In chronic
wounds, these are either reduced or absent,
probably because of the proteolytic action of
MMPs. The mechanisms that 'orchestrate' the
tissue repair and reconstruction processes are
thus impaired; this can manifest as delayed
healing, overgranulation or scarring (Moore
2004).

Having established the chronicity of a wound,

either prospectively using the indicators listed
above or retrospectively from the patient's
history, the next question is how to counteract these factors. By reference to Figure 1, the
clinician can differentiate the severe, moderate
and mild factors, and appreciate why each is so
ranked. By using the venous ulcer as a paradigm, we can illustrate how each factor may be
addressed with current therapeutic interventions.

The extracellular matrix (ECM) is essentially

the dermal component of the skin. It comprises
fibrous proteins such as collagens and elastin,
and protein-carbohydrate complexes known
as glycosaminogtycans (GAGs). The most
important GAG is hyaluronan, previously
known as hyaluronic acid. The ECM provides
the skin with its strength and resilience, as well
as forming a foundation for the regrowth of
epidermis and a scaffold matrix for the growth
of blood vessels and nerves. In wounds that
heal by secondary intent, the replacement of
EGM is central to tissue repair (Midwood et
al 2004). In chronic wounds, many factors
conspire to prevent these processes occurring in
an orderly fashion, thus impairing the healing
process (Baum and Arpey 2005).

Leg ulcers that faii to heal

Perfusion

The blood supply to the wound bed and surrounding tissues brings vital oxygen, nutrients,
white cell subpopulations, drugs (such as antibiotics) and hormones. Where perfusion is poor,
tissue ischaemia and an increased risk of infection are barriers to healing (Hunt et al 2000).
42 primary health care | Vol 18 No 2 | March 2008

Overcoming delayed healing

Leg ulcers are a major health problem in the

UK, with a prevalence of between 1.1 and 3.0
per 1,000 (Gallam et al 1985). Although most
(60 to 80 per cent) are associated with venous
disease {RGN 1998, SIGN 1998), nurses need
to recognise rarer lesions of the lower leg (Box
2). These often need different treatments from
leg ulcers and referral to a specialist. Guidelines suggest that patients should be referred
for biopsy if the appearance of the ulcer is
atypical, or if there is deterioration or failure
to progress after 12 weeks of active treatment
(SIGN 1998).
Published data on healing rates vary.
Typically, the figure given is the percentage
healed in 12 weeks. While this may at first
sight seem impressive, it is the percentage not
healed that will present the clinical challenge
to the practitioner. This group will also be the
most expensive to manage, as treatment can
often be protracted for many months or years.
Figure 2 shows the percentage of venous ulcers
healed, taken from data from 27 published
clinical trials of compression therapy. This

FIGURE 1
Wound chronicity chart (reproduced from Wounds-UK)

LOCAL FACTORS
Bone, tendon, cartilage
Viscera visible
Foreign bodies, dirt

Chart completed by

Date

Patient Identity

Severe
chronicity factors

High to moderate
chronicity factors

Mild
chronicity factors

Not
relevant

LOCAL FACTORS
No bone, tendon cartilage
No viscera in wound
No foreign bodies, dirt

Sinus/fistula

No sinus/fistula

Undermining

No undermining

Scar tissue
Radiotherapy
Lipodermatosclerosis
Atrophe blanche
Calcification
Malignancy (wound bed)
Poor peri-wound tissue
Incontinence

No scar tissue
No radiotherapy
No lipodermatosclerosis
No atrophe blanche
No calcification
No malignancy (wound bed)
Healthy peri-wound tissue
No incontinence

Wound bed trauma

No wound bed trauma

REGIONAL FACTORS

REGIONAL FACTORS

Venous disease

No venous disease

Arterial disease

No arterial disease

Lymphoedema

No lymphoedema

Neuropathy
Oedema

No neuropathy
No oedema

SYSTEMIC FACTORS

SYSTEMIC FACTORS

Poor organ function

Normal organ function

Sleep disturbance
Diabetes
Malnutrition
Poor respiratory function
Acute illness episode
Pain
Malignancy
Medications-chemotherapy
Medications-Steroid therapy
Rheumatoid disease

No steep disturbance
No diabetes
No malnutrition
Normal respiratory function
No acute illness episode
No pain
No malignancy
No medications-steroid
therapy
No rheumatoid disease

SLE, vasculitis, pyodeima etc

No SLE, vasculitis, pyoderma etc

Negative psychosocial ^ifkjences

Positive psychosocial influences

Smoking
Drug misuse
Alcohol misuse

No smoking
No drug misuse
No alcohol misuse

TOTALS
count number of tick?
entered in each cotumn
Pale colouring indicates where
chronicity Is not applicable.

primary health care | Vol 18 No 2 | March 2008 43

delayed wound healing

FIGURE 2
Percentage ol venous leg ulcers that heal over time with compression therapy:
meta analysis data (Rippon eta/2006)
120
100

80
a
V

60

40 20

[\>^ ^
//

[
y = 16.878Ln(x) + 8.5838
R^ = 0.5997

c)

20

40

60

80

100

120

Time (weeks)

graph shows that more than 40 per cent of

ulcers are unhealed at 20 weeks and more than
20 per cent still unhealed at 70 weeks (Rippon

Therapy

Exposed bone and tendon may be treated by

either hydration with a hydrogel (Scardillo and
Seeley 1996), occiusive dressings (Omidi and
Nahass 1996) or cultured epidermal grafts
(Bolivar-Flores and Kuri-Harcuch 1999),
as re-epithelialisation will not occur where
there is dry tissue. Lipodermatosclerosis and
related atrophie blanche present maior hurdles
to healing, and treatment is either invasive,
by excision and grafting (Schmeller and
Gaber 2000), or conservative by compression
(Kirsner et al 1993). Malignancy, as basal cell
or squamous cell carcinoma (Marjolin's ulcer),
occurs in more than 2 per cent of leg ulcers
{Yang etal 1996). The older a leg ulcer, the
greater the likelihood of malignancy; where
ulcers are of greater than 12 weeks' duration
(Figure 3), or malignancy is suspected on other
criteria, urgent referral is essential (Enoch et
al 2004).
The condition of the skin surrounding the
ulcer can have an impact on healing. Where
skin becomes exposed to chronic wound fluid,
maceration and the consequent deterioration/
enlargement of the wound is a risk (White
and Cutting 2003). Optimal moisture control
is central to good wound care (Bishop et al
2003). The simple precautions of protecting
the peri-wound skin, use of emollients for
44 primary health care | Vol 18 No 2 | March 2008

dry skin, topical corticosteroids where

indicated, avoidance of contact allergens,
modern dressings to manage exudate, control
of bioburden where indicated, carefully
selected dressing/bandage wear time, suitable
compression, leg elevation and management
of infection are all important in this
respect (Nelson et al 2005). With respect to
bioburden control it is important to recognise
those wounds which require treatment
with antimicrobials and avoid unnecessary
treatment in those which do not (White et al
(2006). Inappropriate use of antimicrobial
dressings such as silver- or iodine-containng
products, or antibiotics, is wasteful and may
select for bacterial resistance.
The underlying pathology, venous disease,
responds to compression therapy (Nelson
et al 2005). This has justifiably become the
mainstay of treatment and shouid be the first
choice in every case.
Wound and patient assessment

The key to managing wounds is to assess

systematically and frequently, so that appropriate treatments can be implemented in a timely
fashion and any deterioration recognised early.
The tools exist to predict delayed healing
(Flanagan 2003), and to assess the wound systematically. In the latter case, the two systems

in widespread use are AWM and TIME (Gray

et al 2006, Schultz et al 2003). Accurate diagnosis is a prerequisite to effective treatment.
Leg ulcers should be diagnosed according to
the defined criteria, and a Doppter ankle-brachial pressure index is essential (RCN 1998,
SIGN 1998). Recently, pulse oximetry has
been shown to be valuable in assessing the vascular status of patients with leg ulcers before
compression therapy (Bianchi and Douglas
2002, Bianchi 2005).
The systemic factors involved in chronicity
of venous leg ulcers include:
Diabetes (venous leg ulcers, as opposed to
foot ulcers, in patients with diabetes).
Pain.
Psychosocial factors.
Smoking.
Drug or alcohol misuse.
Now do Time out 3

Having established the factors

contributing to chronicity in a patient
with venous leg ulceration, decide
vtfhich may easily be addressed and which
may not

Each of these factors can be addressed. Pain

will delay healing and have an impact on quality of life (Mangwendeza 2002). Published
guidelines on pain assessment and management strategies exist (EWMA 2002), White
and Harding 2006). Pain is often associated
with the dressing change procedures, for
example, with trauma on removal of a dressing (Romanelli and Dini 2006). The means to
overcome this are now well known and must be
adopted (Hofman 2006). Among the psychosocial factors is patient concordance, which can
be addressed through the application of several
measures, including education, communication, pain management and a social model
(Goode 2004, Moffatt 2004a, Briggs 2005,
Seymour 2005, Price 2006).
Interventions to address bioiogicai factors
in venous leg uiceration

The use of the 'new generation' of what might

be best termed biological treatments is in its
infancy. Various compounds and living tissues
for topical use or replacement therapy exist,
and clinical data are being accumulated, for
example, specific growth factors, avaiiabie
in topical formulation, for application to the

ulcer bed (Enoch et al 2006). Tissue replacements for dermal and epidermal components
are available. These are either autograft or allograft materials (Owen et al 2006). Extracellular matrix components have been developed
for topical use on hard to heal wounds, and
biological chemicals such as GAGs, hyaluronan
(Colletta et al 2003) and integrins have been
evaluated in clinical trials (Mirastschijski et al
2004). Control of inflammation is achieved by
using agents designed to inhibit MMP activity (Moore 2004). In general, these are more
expensive than orthodox dressings, and health
economic data are needed to support their use
in specific cases of delayed healing.
Clinical setting of care
The precautions and guidance set out here are
not restricted to secondary care. Communitybased practitioners, although they do not have
direct access to many of the essential services
and treatments needed, may still manage and
refer as appropriate. For example, awareness of
differential diagnoses can be invaluable in the
case of 'unusual' or idiosyncratic, non-healing
leg ulcers. Failure to recognise malignancy can
be costly; according to Walsh (2002) 'as most
patients in the UK are assessed and treated by
community nurses, the nurse has a vital role in
referring patients for further detailed assessment'. The rate of referral to specialist skin ulcer clinics has historically been very low (Dorman et al 1995). which is likely to have resulted
in unnecessary morbidity. With the advent of
telemedicine, community practitioners need no
longer be isolated from local expert opinion
(Newton et al 2000, Ameen et at 2005).
Conclusion
Through education and the implementation
of clinical guidelines nurses responsible for
leg ulcer care can recognise or predict delayed
healing and instigate appropriate treatment or
referral accordingly. It is in recognition of such
wounds that the key to appropriate management lies. Clinicians must be aware of the factors that contribute to delayed healing, and to
interventions intended to overcome chronicity
factors. Where necessary, referral to specialist clinics will identify other pathologies and
ultimately reduce morbidity.
It is no longer acceptable, or ethical, to allow
non-healing wounds to escape the due clinical
diligence and modern treatments that patients
deserve
Now do Time out 4

Now that you have

read this article
you might like to
write a practice profile.
Guidelines to help you can be
found on page 47

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continuing professional development

Practice profile
I do now?
Using the information in section 1 to guide
you, write a practice profile of between 750
and 1,000 words - erisuring that you have
related it to the article that you have studied.
See the examples in section 2.
Write 'Practice Profile' at the top of your
entry followed by your name, the title of the
article, which is: 'Delayed wound healing;
in whom, what, when and why?', and the
article number, which is PHC117.
Complete all of the requirements of the
cut-out form provided and attach it securely
to your practice profile. Failure to do so wiil
mean that your practice profile cannot be
considered for a certificate.
You are entitled to unlimited free entries.
Using an A4 envelope, send for your
free assessment to: Praaice Profile, RCN
Pubiishing Company, Freepost PAM 10155,
Harrow, Middlesex HA1 3BR by March 2009.
Please do not staple your practice profile and
cut-out slip - paper-clips are recommended.
You can also email practice profiles to
practiceprofiie@rcnpublishing.co.uk. You
must also provide the same information
that is requested on the cut-out form. Type
'Practice Profile' in the email subject field to
ensure you are sent a response confirming
receipt.
You will be informed in writing of your
result. A certificate is awarded for successful
completion of the practice profile.
Feedback is not provided: a certificate indicates that you have been successfui.
Keep a copy of your practice profile and add
this to your professional profile - copies are
not returned to you.
1. Framework for reflection
Study the checklist {section 3).
What have i learnt from this article?
To what extent were the intended learning
outcomes met?
What do I know, or can I do, now, that
I did not/could not before reading
the articie?
What can I apply immediately to my practice
or client/patient care?
Is there anything that i did not understand.

need to explore or read about further, to

clarify my understanding?
What else do I need to do/know to extend
my professional development in this area?
What other needs have 1 identified in relation to my professional development?
How might 1 achieve the above needs?
(It might be helpful to convert these to
short/medium/long-term goals and draw up
an action plan.)
2. Examples of practice profile entries
Example 1 After reading a CPD article on
'Communication skills', Jenny, a practice nurse,
reflects on her own communication skills and
re-arranges her clinic room so that she will sit
next to her patients when talking to them. She
makes a conscious decision to pay attention
to her own body language, posture and eye
contact, and notices that communication with
patients improves. This forms the basis of her
practice profile.

Continuing professional
development
Complete this form using a ballpoint
pen and CAPITAL tetters only

1. First name;

5. Full title and date of artic e

Example 2 After reading a CPD article on

'Wound care', Amajit, a senior staff nurse on a
surgical ward, approached the nurse manager
about her concerns about wound infections
on the ward. Following an audit which Amajit
undertook, a protocol for dressing wounds
was established which led to a reduction in
wound infections in her ward and across the
directorate. Amajit used this experience for
her practice profile and is now taking part in a
region-wide research project.
3. Portfolio submission
Checklist for submitting your practice profile
%/ Have you related your practice profile to
the article?
%/ Have you headed your entry with: the title
'Practice Profile'; your name, the title of the
article; and the article number?
%/ Have you written between 750 and 1,000
words?
%/ Have you kept a copy of the practice profile
for your own portfolio?
%/ Have you completed the cut-out form and
attached it to your entry?

Please cut out this form and send

it in an envelope no smaller than
9x6 inches to:
Practice Profile
RCN Pubiishing Company
Freepost PAM 10155
Harrow
MiddiesexHAI 3BR

primary heaith care | Voi 18 No 2 | March 2008 47