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In this issue
Wound infection and colonisation

57-67

production teamss
Managing editor Lisa Berry

A guide to emollient therapy

68-75

Production editor Gary Bell


Art director Ken McLoone

Wound infection and


colonisation
Elizabeth Scanlon RGN, RM,
Cert DN, MSc, is nurse

Scanlon E (2005) Wound infection and colonisation. Nursing Standard.


19, 24, 57-67. Date of acceptance: November 15 2004.

consultant, tissue viability,


St Jamess University Hospital,
Leeds. Email:
elizabeth.scanlon@leedsth.nhs.uk

keywordsss
Bacterial infection
Infection control
Tissue viability
Wounds
These key words are based
on subject headings from the
British Nursing Index. This
article has been subject to
double-blind review.
online archivess
For related articles visit our
online archive at:
www.nursing-standard.co.uk
and search using the key words
above.

summaryss
Many wounds seen by nurses will involve
infection and colonisation. To enable nurses
to correctly assess and manage these
wounds, infection and colonisation are
explained and options for management
discussed.
MOST REGISTERED nurses will, at some time,
be responsible for caring for people with wounds.
The frequency with which they encounter
wounds will vary according to their area of
practice. The majority of district nurses workloads may involve dealing with wounds. Specialist
medical areas such as cystic fibrosis units are
unlikely to encounter wounds on a daily basis
but even these patients may develop pressure
ulcers if they are acutely ill or experience traumatic injuries that require nursing intervention.
The nurses role in wound management is to:
Minimise the impact of the wound on the
patients quality of life.
Promote the healing of the wound by creating the right local environment and optimising the patients general health.
Reduce the risk of complications.
Manage the symptoms of wounds for patients
whose wounds are unlikely to heal or where
concordance with appropriate treatment is
unachievable.
The impact of a wound on a persons quality
of life will vary according to the type and duration of the wound. Nurses should carry out a
thorough patient assessment including factors
such as pain and discomfort, personal hygiene
routines, physical activity, health beliefs and
emotional response to the wound. The plan
of care should aim to reduce the unpleasant
effects of having a wound.
Creating the right local environment entails

keeping the wound warm and moist, preventing


trauma to the wound and reducing the risk of
contamination. Optimising the patients general health by improving nutrition, stabilising
diseases such as diabetes mellitus, respiratory
disorders and anaemia will also promote healing. Reducing the risk of complications includes
preventing haemorrhage, wound breakdown,
trauma and infection. Infection will delay healing and may cause deterioration in a chronic
wound but can result in complete breakdown
of an acute surgical wound. Apart from the
detrimental effect on the wound, infection can
cause unpleasant systemic effects and in some
cases may be fatal.
It is important, therefore, that nurses understand the role of bacteria in wound healing,
how to recognise when problems are occurring and how to manage them.
Bacteria in wound healing
The effects of bacteria in wounds vary according to the:
Type of wound.
Type of bacteria.
Patients immune response.
In acute wound healing by primary intention,
for example, a sutured surgical wound with
skin edges joined, the early inflammatory phase
of the healing process provides many neutrophils (white blood cells which ingest and kill
bacteria), but macrophages, which are more
efficient at dealing with bacteria, do not appear
until several days later and only in small numbers (Kindlen and Morison 1997). The likelihood of these wounds breaking down due to
infection is related to the number of bacteria
at the point of wounding.
In chronic wounds that are subject to a prolonged inflammatory phase, bacterial colonisation will not be detrimental to wound healing

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because of the number of macrophages (Trengove
et al 1996). Notably, there is evidence to suggest that the presence of bacteria in a chronic
wound may stimulate wound healing (Robson
1997).
The type or number of bacteria may influence wound healing. Many chronic wounds
are colonised with Staphylococcus aureus including methicillin-resistant Staphylococcus aureus
(MRSA). These can proceed to normal healing
with no detrimental effect, however, any strain
of S. aureus in an acute wound can lead to
infection and wound breakdown (Emmerson
et al 1996). Streptococcus is a more virulent
bacterium in most of its strains and is responsible for life-threatening infections such as
necrotising fasciitis. Even in low concentrations
beta-haemolytic streptococci is capable of
impeding healing (Schraibman 1990). The presence of four or more groups of bacteria has
been shown to retard healing (Trengove et al
1996).
The patients immune system will significantly
influence the effect the bacteria have on the
wound. Factors that compromise the immune
system include (Scanlon 2003):
Stress (including stress due to illness and
operations).
Nutrition.
Table 1. Definitions of colonisation and infection
Contamination

The presence of bacteria before multiplication takes place

Colonisation

The presence of multiplying bacterial with no overt host


(immunological) reaction (Ayton 1985) or clinical
symptoms

Critical colonisation

The point at which the host defences are unable to


maintain the balance of organisms at colonisation
(Kingsley 2001)

Infection

The presence of multiplying bacteria overwhelms the host


defences, which results in spreading cellulitis
(Kingsley 2001)

Table 2. Signs and symptoms of infection


Classic criteria

Additional criteria

Abscess

Delayed healing

Cellulitis heat, pain,


oedema and erythema

Discolouration usually appears dull and dark red


Fragile tissue which bleeds easily
Unexpected pain or tenderness

Increased discharge:
Serous
Seropurulent
Haemopurulent
Pus

Bridging of soft tissue


Pocketing at wound base
Abnormal smell
Wound breakdown
Necrotic/sloughy tissue, which is not explained by
pressure damage

(Adapted from Cutting and Harding 1994)

58 nursing standard february 23/vol19/no24/2005

Circulatory system.
Metabolic disorders such as diabetes.
Increasing age.
Concurrent infections.
Immunosuppressant drugs such as steroids.
In an extensive epidemiological study of surgical wounds, Cruse and Foord (1973) identified a number of factors associated with the
risk of infection. In addition to the above factors, they identified:
The site of the wound groin, axillae and
skinfolds where high levels of bacteria usually exist.
Body build adipose tissue impedes haemostasis which results in haematoma, and has a
poor blood supply. Both of these factors
increase the risk of infection, which becomes
more of a problem in people who are overweight.
Hypovolaemia a reduction in the circulating blood volume is associated with dehydration.
Malignancy.
Mertz and Ovington (1993) used an equation to represent the probability of a wound
infection:
Infection = Dose x virulence
Host resistance
It can be seen therefore, that a healthy individual with nothing to compromise his or her
immune system, will be able to tolerate higher
numbers of bacteria in the wound compared
with someone who has an illness which compromises the immune system.
The transition of the wound from being
colonised to being infected is a process that is
specific to the individual patient and the particular bacteria in the wound at the time.
Wound colonisation and infection
It is helpful to define colonisation and infection before each state is described.
Colonisation is a normal state for which there
are no unusual signs or symptoms (Table 1). The
point of critical colonisation beyond which the
patient will experience the detrimental effects
of bacteria would be useful to recognise and
many researchers are still working on this.
The classic signs and symptoms of infection
are the presence of pus with cellulitis (localised
inflammation of the tissues). However, these
signs are less obvious when assessing chronic
wounds. It must also be remembered that the
older or immunosuppressed patient including those taking anti-inflammatory drugs
may not present with the classic signs. Cutting
and Harding (1994) proposed several additional
criteria to assist the practitioner in identifying
infection (Table 2).
It has been suggested that the presence of
additional criteria may be an indication of
critical colonisation (Cutting and Harding 1994).
Reducing the risk of infection Given the
problems associated with wound infection,

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nurses have a role to play in minimising risks
in the management of patients with wounds.
White et al (2001) suggest some tissue viability principles to reduce the risk of infection
(Box 1).
Managing colonisation and
infection
It has been shown that colonisation and infection may be a common feature in wound management. It is part of the nurses role, when
these have been identified, to correctly manage them. To avoid ambiguity, definitions of
the terms antimicrobial, antiseptic, disinfectant and antibiotic are provided in Table 3.
Box 1. Reducing the risk of wound infection
Identify the aetiology of the wound
Remove continuing intrinsic and extrinsic causative factors such as venous
hypertension and shearing pressure
Eliminate or reduce factors that may impair healing such as malnutrition,
hyperglycaemia and anaemia, among others
Initiate the most effective therapy at the outset; do not use holding or wait and
see treatments just because they are more convenient
Use universal infection control precautions to prevent cross-contamination from
the wound
Remove all necrotic and foreign material
Allow drainage of wound exudate or pus, in particular from sinuses
Observe closely for signs of change at all dressing changes, in particular those
representing a delay in healing or infection
Construct a care plan that details expected progress so that delays can be
detected at the earliest opportunity
Use a framework to guide decision-making for undesired events
(Kingsley 2001)

Table 3. Antimicrobial definitions


Term

Definition

Antimicrobial

Substances, including antibiotics, disinfectants and antiseptics,


that are used to treat infections and kill micro-organisms

Antiseptic

General term used to describe chemical agent used to limit


infection in living tissues
Toxic to viable tissues (depending on agent, concentration and
contact time)
Unlike antibiotics, not able to act selectively

Disinfectant

A non-selective agent (sometimes combined with detergent)


that destroys, removes or inactivates potential pathogens on
inert surfaces. It is used particularly on instruments, work
surfaces and equipment

Antibiotic

Substances capable of destroying or inhibiting pathogens and


either derived from micro-organisms or synthetically
manufactured
Able to selectively target bacteria rather than viable tissue, so
can be used in low concentrations
Less toxic than antiseptics

(Adapted from White et al 2001)

60 nursing standard february 23/vol19/no24/2005

The algorithm in Figure 1 has been designed


to aid decision-making when managing a
colonised or infected wound.
The management of infected wounds with
antibiotics requires the involvement of a medical practitioner or an extended nurse prescriber
and is not discussed further here.
If a wound is identified as having additional
criteria (Table 2), topical antiseptics are appropriate. In recent years there have been significant advances in the development of topical
antiseptics for wound healing. The increase in
resistance to antibiotics has driven this resurgence. Traditionally, antiseptics are used to
cleanse wounds. To be effective within a short
contact time, concentrations need to be high
and can therefore be toxic to tissues with the
risk of delaying healing if use is prolonged.
Modern dressings have much lower concentrations, often with a slow release antiseptic
that maintains antimicrobial control with minimum damage to healthy tissue. There is little
evidence of systemic toxicity from modern antiseptics (Lansdown 2004), which may be due
to the low levels of absorption or to the lack
of research on toxicity.
There have been even fewer in vivo studies
into the effects of these antiseptics in the wound
environment and on wound healing. Although
it has been shown that some antiseptics, in certain doses, are toxic to keratinocytes and fibroblasts in laboratory and animal studies (Brennan
and Leaper 1985, Gibbins 2003), the publication of a high quality randomised controlled trial
is still awaited. Topical antiseptics should therefore only be used where clinically indicated and
for limited periods unless by specialist guidance.
Table 4 summarises the more commonly available topical antiseptics and their clinical use.
For more detailed information see the individual product information leaflets.
The majority of antiseptics are effective against
most of the bacteria that affect wounds. The
decision regarding which antiseptic to use will
usually depend on:
The type of wound, for example, deep cavities, superficial ulcers.
The size of wound, some iodine preparations
cannot be used in large quantities, for example, Iodosorb.
The level of exudate some antiseptics may
be too dry on dry wounds as they work best
when released into exudate solution, others
are water-based creams which may be too
wet on highly exuding wounds.
The frequency of dressing change some
are more effective if left in place for up to
seven days, for example, Acticoat.
The secondary dressings required, for example, compression bandaging, absorbent foams.
Patient preference and quality of life pain
levels and ease of removal.
Conclusion
Bacteria are present in most wounds. The number, virulence and host defences dictate the effect

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Figure 1. Management of infected and critically colonised wounds
* If wound progress is not seen, critical colonisation or other causes of delayed healing not identified may be present in the wound
Refer to a specialist, for example, tissue viability nurse, vascular surgeon or dermatologist
Patients with diabetes who have foot wounds or ulcers should always be referred to a diabetes specialist or podiatrist

Assess wound

Is wound healing
delayed?

No

Yes

Is there evidence of
increased exudate or
cellulitis?
(Table 2)

No

Is there evidence of
additional factors?
(Table 2)

Yes

Yes

No

Is the patient unwell,


for example:
feverish
pyrexial

Take a swab or
sample of pus (give
full details of patient
and wound history
and treatment or any
antibiotic therapy on
the pathology form)

Choose appropriate
topical antiseptic and
treat (see Table 4)
Reassess frequently*

Consider other
factors that may
delay healing

Yes

Liaise with doctor or


microbiologist re
results/treatment and
most effective route
for treatment

Consider topical
antiseptics, in
addition, if the patient
is at high risk of
developing infection
or has severe oedema
and/or arterial
insufficiency

Treat with
appropriate antibiotic
with or without
antiseptic
Reassess frequently*

Start broad spectrum


antibiotics before
swab results
confirmed

Discuss need for


intravenous or oral
antibiotics

62 nursing standard february 23/vol19/no24/2005

A low adherent viscose sheet


impregnated with povidone-iodine
ointment 10%

Water-based ointment containing


weight/volume povidone-iodine 10%

These have identical properties, Iodosorb


is an ointment, Iodoflex is a paste or
powder. Choice will depend on personal
preference or ease of application. The
product contains 9mg/g (0.9%) iodine as
cadexomer, which is a modified starch
hydrogel. The ointment is in a base of
polyethylene glycol

Dressings containing nanocrystalline


silver, either in multi-laminate layers or as
absorbent combined with calcium
alginate

Activated charcoal cloth combined with


silver

Hydrofibre sheet or ribbon impregnated


with ionic silver

Film dressing or alginate island dressing


containing controlled release polymers of
silver

Polyurethane foam impregnated with


silver

Polyurethane foam or hydrocolloid


dressing impregnated with silver

Inadine (J&J)
Poviderm (SSL)

Betadine (SSL)

Iodosorb
ointment Iodoflex
paste or powder
(S&N)

Acticoat (S&N)
Acticoat 7
Acticoat
absorbent
(S&N)

Actisorb Silver
220 (J&J)

Aquacel Ag
(ConvaTec)

Arglaes island
(Unomedical)

Avance (SSL)

Contreet foam
Contreet
hydrocolloid
(Coloplast)

Iodine
Effective
against most
bacteria and
fungi

64 nursing standard february 23/vol19/no24/2005


Hydrocolloid suitable for low to moderate
exudate on shallow wounds
Foam suitable for moderate to high levels
of exudate

Moderate to highly exuding wounds

Shallow, low-exuding wounds or moderate


to heavy exudate with island dressing

Moderate to heavily exuding acute and


chronic wounds

Suitable for moderate to highly exuding


deep or shallow wounds, also reduces
odour and absorbs endotoxins

Suitable for moderate to highly exuding


deep or shallow wounds

Moderate to heavily exuding wounds,


ulcers, pressure ulcers, etc

Patients with known sensitivity to dressing


or its components

Patients with known sensitivity to dressing


or its components

Patients with known sensitivity to dressing


or its components

Patients with known sensitivity to dressing


or its components

Patients with known sensitivity to dressing


or its components

Patients with a known allergy to silver

As above

As above

Where there is known iodine


hypersensitivity (allergy)
Before and after the use of radioactive
iodine (until permanent healing)
If there is renal disease
In pregnant or lactating women
In cases of Duhrings disease (dermatitis
herpetiform)

Contraindication

Foam is available with or without


adhesive border

Requires secondary dressing

Requires secondary dressing

Acticoat 7 has a longer sustained


release action, up to seven days
Requires secondary dressing

Not suitable for large wounds.


Maximum single application is 50g
Weekly maximum must not exceed
150g, length of treatment must not
exceed three months
Requires secondary dressing

Activity persists while brown colour is


maintained
Requires secondary dressing

Fading of colour indicates loss of


antiseptic efficacy. When the distinctive
orange brown colour turns white, the
dressing should be changed
Requires secondary dressing

Guidance on use

12:27 pm

Dry wounds which require hydration and


antiseptic in ulcers, burns, pressure ulcers,
infection control, mycotic and bacterial
skin infections

Shallow wounds with low exudate


Prevention and treatment of infection in
minor burns, minor traumatic skin loss
injuries and as part of the treatment for
ulcerative wounds, abrasions and
lacerations

Indication

17/2/05

Silver
Effective
against most
bacteria and
fungi

Description

Commercial
preparation

Antiseptic

Table 4. Topical antiseptics

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66 nursing standard february 23/vol19/no24/2005

Calcium alginate impregnated with 1%


zinc

Curasorb Zn
(Tyco)

EUSOL
(Edinburgh
Solution of Lime)

Zinc*

Sodium
hypochlorite
Effective
against most
bacteria

Activon Tulle
(Advancis
Medical)

Non-adherent tulle impregnated with


manuka honey (Unique Manuka Factor)
(umf12+)

Water-based cream containing 1.5%


hydrogen peroxide with prolonged
antiseptic action (at least eight hours)

Low to moderate exuding wounds

Often used for wounds that require


debridement and antiseptic

Effective disinfectant, used in preparation


for skin grafting
It is not the first choice for general
antiseptic use due to reported adverse
effects

Suitable for all types of moderate to highly


exuding wounds

Patients with known sensitivity to dressing


or its components
Caution in patients with diabetes, close
monitoring of glucose levels is required
(according to data sheet)

May chemically interact with other topical


medicaments

Adverse effects: delayed healing,


cell toxicity, irritancy, reduced capillary
blood flow, renal failure/Schwartzman
reaction, depressed collagen synthesis,
overgranulation and localised oedema,
hypernatraemia

Patients with known sensitivity to dressing


or its components

Suitable for wet or dry wounds, shallow


Hypersensitivity to silver sulfadiazine or
or some cavity wounds. Active for up to 72 other ingredients
hours

Hypersensitivity to silver sulfadiazine or


other ingredients

Some patients have experienced pain


when honey is applied
Can reduce odour

Requires secondary dressing

Activity reduced in presence of organic


material and in alkaline conditions
Only stable for two to three weeks
once prepared
Requires secondary dressing

Keeps integrity to allow easy removal


Requires secondary dressing

Requires secondary dressing


Wet wounds will require extra
absorbent dressings

Particularly effective against


Pseudomonas. Silver is combined with
an antibiotic
Requires secondary dressing

Guidance on use

MRSA = methicillin-resistant Staphylococcus aureus

(Adapted from Cooper and Lawrence 1996, Morgan 1993, Pike 1983, Scanlon and Stubbs 2002)

*Although zinc is not licensed as an antiseptic, recent research suggests it has antimicrobial properties and may be beneficial in preventing infection (Agren et al 2004, Stubbs and Scanlon 2004)

Honey
Tested against
Escherichia coli,
Proteus,
Pseudomonas,
Staphylococcus
(including
MRSA), and
Streptococcus
pyogenes

Hioxyl cream
(Ferndale)

Non-occlusive polyester mesh


impregnated with hydrocolloid, paraffin,
contains 3.75% silver sulfadiazine

Urgotul SSD
(Parema)

For the prophylaxis and treatment of


infection in burns, an aid to the short-term
treatment of infections in leg and pressure
ulcers, an aid to the prophylaxis of
infection in skin graft donor sites and
extensive abrasions and conservative
management of finger-tip injuries

Contraindication

12:27 pm

Hydrogen
peroxide
Effective
against most
bacteria

Water-based cream containing silver


sulfadiazine 1%

Flamazine (S&N)

Silver
Effective
against most
bacteria and
fungi

Indication

17/2/05

Chlorinated lime and boric acid solution


containing not less than 0.25%
weight/volume available chlorine
May be combined with liquid paraffin to
minimise adherence to wound

Description

Commercial
preparation

Antiseptic

Table 4. Topical antiseptics (continued)

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bacteria will have on the healing process. Most wounds heal with
no adverse effects from bacteria. Harm caused by bacteria ranges
from increase in exudate and odour, delayed healing, local cellulites, to septicaemia or even death.
The need for nurses to recognise what is normal wound healing is vital so they can identify when it is adversely affected by
bacteria. How to manage infection or colonisation is an integral
part of good wound management. Currently there is little reported
resistance to antiseptics. Since the overuse of antibiotics, topical
antiseptics provide a rational alternative to reduce bacteria.
There is still controversy over the use of antiseptics in wound
management (Scanlon and Stubbs 2002). Anecdotal evidence
suggests that prolonged use of antiseptics can also delay wound
healing. While some excellent results have been demonstrated in
individual patients, there is still a lack of rigorous evidence to support the use of antiseptics in wound healing.
Nurses wishing to use antiseptics for wound management should
ensure that they are fully aware of the known risks and benefits.
They should reassess the wounds regularly and only use antiseptics where there are good clinical indications

References
Agren M et al (2004) Topical Zinc
Oxide for Excisional Wounds in
Humans. Oral presentation.
Second World Union of Wound
Healing Societies Conference, July
8-13. Paris, France.
Ayton M (1985) Wound care:
wounds that wont heal. Nursing
Times. 81, 46, 16-19.
Brennan S, Leaper D (1985) The
effect of antiseptics on the
healing wound: a study using the
rabbit ear chamber. British Journal
of Surgery. 72, 10, 780-782.
Cooper R, Lawrence J (1996) The role
of antimicrobial agents in wound
care. Journal of Wound Care. 5,
8, 374-380.
Cruse P, Foord R (1973) A five-year
prospective study of 23,649
surgical wounds. Archives of
Surgery. 107, 2, 206-210.
Cutting K, Harding K (1994) Criteria
for identifying wound infection.
Journal of Wound Care. 3, 4,
198-201.
Emmerson A et al (1996) The Second
National Prevalence Survey of
infection in hospitals: overview of
the results. Journal of Hospital
Infection. 32, 3, 175-190.
Gibbins B (2003) How Much is Too
Much Silver? Oral presentation.
Wounds UK 2003, Harrogate,
November 11-12.
Kindlen S, Morison M (1997) The
physiology of wound healing. In
Morison M et al (Eds) Nursing
Management of Chronic Wounds.
Second edition. London, Mosby.
Kingsley A (2001) A proactive
approach to wound infection.
Nursing Standard. 15, 30, 50-58.
Lansdown A (2004) A review of the
use of silver in wound care: facts

and fallacies. British Journal of


Nursing. 13, 6 Suppl, S6-19.
Mertz P, Ovington L (1993) Wound
healing microbiology.
Dermatologic Clinics. 11, 4,
739-747.
Morgan D (1993) Is there still a role
for antiseptics? Journal of Tissue
Viability. 3, 3, 80-83.
Pike A (1983) Antiseptic use in
wound management. Critical Care
Nurse. 3, 6, 87-93.
Robson M (1997) Wound infection. A
failure of wound healing caused
by an imbalance of bacteria. The
Surgical Clinics of North America.
77, 3, 637650.
Scanlon E (2003) Wound care. In
Lawrence J, May D (Eds) Infection
Control in the Community.
London, Churchill Livingstone.
Scanlon E, Stubbs N (2002) To use or
not to use? The debate on the
use of antiseptics in wound care.
British Journal of Community
Nursing. 8, 10, 12passim.
Schraibman I (1990) The significance
of beta-haemolytic streptococci in
chronic leg ulcers. Annals of the
Royal College of Surgeons of
England. 72, 2, 123-124.
Stubbs N, Scanlon E (2004) Topical
zinc in wound care. Poster
presentation. Second World Union
of Wound Healing Societies
Conference, July 8-13. Paris,
France.
Trengove N et al (1996) Qualitative
bacteriology and leg ulcer healing.
Journal of Wound Care. 5, 6,
277-280.
White R et al (2001) Wound
colonisation and infection: the
role of topical antimicrobials.
British Journal of Nursing. 10, 9,
563-578.

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