colonization

february 23/vol19/no24/2005 nursing standard 57

Wound infection andcolonisation

Elizabeth Scanlon RGN, RM,

Cert DN, MSc, is nurse

consultant, tissue viability,

St James’s University Hospital,

Leeds. Email:

[email protected]

MOST REGISTERED nurses will, at some time,be responsible for caring for people with wounds.The frequency with which they encounterwounds will vary according to their area ofpractice. The majority of district nurses’ work-loads may involve dealing with wounds. Specialistmedical areas such as cystic fibrosis units areunlikely to encounter wounds on a daily basisbut even these patients may develop pressureulcers if they are acutely ill or experience trau-matic injuries that require nursing intervention.

The nurse’s role in wound management is to: ■ Minimise the impact of the wound on the

patient’s quality of life. ■ Promote the healing of the wound by cre-

ating the right local environment and opti-mising the patient’s general health.

■ Reduce the risk of complications.■ Manage the symptoms of wounds for patients

whose wounds are unlikely to heal or whereconcordance with appropriate treatment isunachievable.

The impact of a wound on a person’s qualityof life will vary according to the type and dura-tion of the wound. Nurses should carry out athorough patient assessment including factorssuch as pain and discomfort, personal hygieneroutines, physical activity, health beliefs andemotional response to the wound. The planof care should aim to reduce the unpleasanteffects of having a wound.

Creating the right local environment entails

keeping the wound warm and moist, preventingtrauma to the wound and reducing the risk ofcontamination. Optimising the patient’s gen-eral health by improving nutrition, stabilisingdiseases such as diabetes mellitus, respiratorydisorders and anaemia will also promote heal-ing. Reducing the risk of complications includespreventing haemorrhage, wound breakdown,trauma and infection. Infection will delay heal-ing and may cause deterioration in a chronicwound but can result in complete breakdownof an acute surgical wound. Apart from thedetrimental effect on the wound, infection cancause unpleasant systemic effects and in somecases may be fatal.

It is important, therefore, that nurses under-stand the role of bacteria in wound healing,how to recognise when problems are occur-ring and how to manage them.

Bacteria in wound healing The effects of bacteria in wounds vary accord-ing to the:■ Type of wound. ■ Type of bacteria. ■ Patient’s immune response.In acute wound healing by primary intention,for example, a sutured surgical wound withskin edges joined, the early inflammatory phaseof the healing process provides many neu-trophils (white blood cells which ingest and killbacteria), but macrophages, which are moreefficient at dealing with bacteria, do not appearuntil several days later and only in small num-bers (Kindlen and Morison 1997). The likeli-hood of these wounds breaking down due toinfection is related to the number of bacteriaat the point of wounding.

In chronic wounds that are subject to a pro-longed inflammatory phase, bacterial coloni-sation will not be detrimental to wound healing

keywordsss

■ Bacterial infection■ Infection control■ Tissue viability■ Wounds

These key words are based on subject headings from theBritish Nursing Index. This article has been subject to double-blind review.

online archivess

For related articles visit ouronline archive at:www.nursing-standard.co.ukand search using the key wordsabove.

summaryss

Many wounds seen by nurses will involveinfection and colonisation. To enable nursesto correctly assess and manage thesewounds, infection and colonisation areexplained and options for managementdiscussed.

Scanlon E (2005) Wound infection and colonisation. Nursing Standard. 19, 24, 57-67. Date of acceptance: November 15 2004.

Wound infection and colonisation 57-67

A guide to emollient therapy 68-75

production teamssManaging editor Lisa Berry

Production editor Gary Bell

Art director Ken McLoone

In this issue

p57-67w24 17/2/05 12:27 pm Page 57

58 nursing standard february 23/vol19/no24/2005

because of the number of macrophages (Trengoveet al 1996). Notably, there is evidence to sug-gest that the presence of bacteria in a chronicwound may stimulate wound healing (Robson1997).

The type or number of bacteria may influ-ence wound healing. Many chronic woundsare colonised with Staphylococcus aureus includ-ing methicillin-resistant Staphylococcus aureus(MRSA). These can proceed to normal healingwith no detrimental effect, however, any strainof S. aureus in an acute wound can lead toinfection and wound breakdown (Emmersonet al 1996). Streptococcus is a more virulentbacterium in most of its strains and is respon-sible for life-threatening infections such asnecrotising fasciitis. Even in low concentrationsbeta-haemolytic streptococci is capable ofimpeding healing (Schraibman 1990). The pres-ence of four or more groups of bacteria hasbeen shown to retard healing (Trengove et al1996).

The patient’s immune system will significantlyinfluence the effect the bacteria have on thewound. Factors that compromise the immunesystem include (Scanlon 2003):■ Stress (including stress due to illness and

operations).■ Nutrition.

■ Circulatory system.■ Metabolic disorders such as diabetes.■ Increasing age.■ Concurrent infections.■ Immunosuppressant drugs such as steroids. In an extensive epidemiological study of sur-gical wounds, Cruse and Foord (1973) identi-fied a number of factors associated with therisk of infection. In addition to the above fac-tors, they identified: ■ The site of the wound – groin, axillae and

skinfolds where high levels of bacteria usu-ally exist.

■ Body build – adipose tissue impedes haemosta-sis which results in haematoma, and has apoor blood supply. Both of these factorsincrease the risk of infection, which becomesmore of a problem in people who are over-weight.

■ Hypovolaemia – a reduction in the circulat-ing blood volume is associated with dehy-dration.

■ Malignancy. Mertz and Ovington (1993) used an equa-tion to represent the probability of a woundinfection:

Infection = Dose x virulenceHost resistance

It can be seen therefore, that a healthy indi-vidual with nothing to compromise his or herimmune system, will be able to tolerate highernumbers of bacteria in the wound comparedwith someone who has an illness which com-promises the immune system.

The transition of the wound from beingcolonised to being infected is a process that isspecific to the individual patient and the par-ticular bacteria in the wound at the time.

Wound colonisation and infectionIt is helpful to define colonisation and infec-tion before each state is described.

Colonisation is a normal state for which thereare no unusual signs or symptoms (Table 1). Thepoint of critical colonisation beyond which thepatient will experience the detrimental effectsof bacteria would be useful to recognise andmany researchers are still working on this.

The classic signs and symptoms of infectionare the presence of pus with cellulitis (localisedinflammation of the tissues). However, thesesigns are less obvious when assessing chronicwounds. It must also be remembered that theolder or immunosuppressed patient – includ-ing those taking anti-inflammatory drugs –may not present with the classic signs. Cuttingand Harding (1994) proposed several additionalcriteria to assist the practitioner in identifyinginfection (Table 2).

It has been suggested that the presence of‘additional criteria’ may be an indication ofcritical colonisation (Cutting and Harding 1994).Reducing the risk of infection Given theproblems associated with wound infection,

art&sciencetissue viability supplement

Contamination The presence of bacteria before multiplication takes place

Colonisation The presence of multiplying bacterial with no overt host(immunological) reaction (Ayton 1985) or clinicalsymptoms

Critical colonisation The point at which the host defences are unable tomaintain the balance of organisms at colonisation(Kingsley 2001)

Infection The presence of multiplying bacteria overwhelms the hostdefences, which results in spreading cellulitis(Kingsley 2001)

Table 1. Definitions of colonisation and infection

Classic criteria Additional criteria

Abscess Delayed healing

Cellulitis – heat, pain, Discolouration – usually appears dull and dark redoedema and erythema Fragile tissue which bleeds easily

Unexpected pain or tenderness

Increased discharge: Bridging of soft tissue■ Serous Pocketing at wound base■ Seropurulent Abnormal smell■ Haemopurulent Wound breakdown■ Pus Necrotic/sloughy tissue, which is not explained by

pressure damage

(Adapted from Cutting and Harding 1994)

Table 2. Signs and symptoms of infection

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nurses have a role to play in minimising risksin the management of patients with wounds.White et al (2001) suggest some tissue viabil-ity principles to reduce the risk of infection(Box 1).

Managing colonisation andinfectionIt has been shown that colonisation and infec-tion may be a common feature in wound man-agement. It is part of the nurse’s role, whenthese have been identified, to correctly man-age them. To avoid ambiguity, definitions ofthe terms antimicrobial, antiseptic, disinfec-tant and antibiotic are provided in Table 3.

The algorithm in Figure 1 has been designedto aid decision-making when managing acolonised or infected wound.

The management of infected wounds withantibiotics requires the involvement of a med-ical practitioner or an extended nurse prescriberand is not discussed further here.

If a wound is identified as having additionalcriteria (Table 2), topical antiseptics are appro-priate. In recent years there have been signifi-cant advances in the development of topicalantiseptics for wound healing. The increase inresistance to antibiotics has driven this resur-gence. Traditionally, antiseptics are used tocleanse wounds. To be effective within a shortcontact time, concentrations need to be highand can therefore be toxic to tissues with therisk of delaying healing if use is prolonged.Modern dressings have much lower concen-trations, often with a slow release antisepticthat maintains antimicrobial control with min-imum damage to healthy tissue. There is littleevidence of systemic toxicity from modern anti-septics (Lansdown 2004), which may be dueto the low levels of absorption or to the lackof research on toxicity.

There have been even fewer in vivo studiesinto the effects of these antiseptics in the woundenvironment and on wound healing. Althoughit has been shown that some antiseptics, in cer-tain doses, are toxic to keratinocytes and fibrob-lasts in laboratory and animal studies (Brennanand Leaper 1985, Gibbins 2003), the publica-tion of a high quality randomised controlled trialis still awaited. Topical antiseptics should there-fore only be used where clinically indicated andfor limited periods unless by specialist guidance.

Table 4 summarises the more commonly avail-able topical antiseptics and their clinical use.For more detailed information see the individ-ual product information leaflets.

The majority of antiseptics are effective againstmost of the bacteria that affect wounds. Thedecision regarding which antiseptic to use willusually depend on:■ The type of wound, for example, deep cav-

ities, superficial ulcers.■ The size of wound, some iodine preparations

cannot be used in large quantities, for exam-ple, Iodosorb®.

■ The level of exudate – some antiseptics maybe too dry on dry wounds as they work bestwhen released into exudate solution, othersare water-based creams which may be toowet on highly exuding wounds.

■ The frequency of dressing change – someare more effective if left in place for up toseven days, for example, Acticoat®.

■ The secondary dressings required, for exam-ple, compression bandaging, absorbent foams.

■ Patient preference and quality of life – painlevels and ease of removal.

ConclusionBacteria are present in most wounds. The num-ber, virulence and host defences dictate the effect

■ Identify the aetiology of the wound

■ Remove continuing intrinsic and extrinsic causative factors such as venoushypertension 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 andsee’ treatments just because they are more convenient

■ Use universal infection control precautions to prevent cross-contamination fromthe 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 thoserepresenting a delay in healing or infection

■ Construct a care plan that details expected progress so that delays can bedetected at the earliest opportunity

■ Use a framework to guide decision-making for undesired events

(Kingsley 2001)

Box 1. Reducing the risk of wound infection


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 limitinfection in living tissuesToxic to viable tissues (depending on agent, concentration andcontact time)Unlike antibiotics, not able to act selectively

Disinfectant A non-selective agent (sometimes combined with detergent)that destroys, removes or inactivates potential pathogens oninert surfaces. It is used particularly on instruments, worksurfaces and equipment

Antibiotic Substances capable of destroying or inhibiting pathogens andeither derived from micro-organisms or syntheticallymanufacturedAble to selectively target bacteria rather than viable tissue, socan be used in low concentrations Less toxic than antiseptics

(Adapted from White et al 2001)

Table 3. Antimicrobial definitions

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* If wound progress is not seen, critical colonisation or other causes of delayed healing not identified may be present in the woundRefer to a specialist, for example, tissue viability nurse, vascular surgeon or dermatologistPatients with diabetes who have foot wounds or ulcers should always be referred to a diabetes specialist or podiatrist

Figure 1. Management of infected and critically colonised wounds

Assess wound

Is wound healingdelayed?

Yes Yes

No

No

Yes

Yes

No

Is there evidence ofincreased exudate orcellulitis?(Table 2)

Is the patient unwell,for example:feverishpyrexial

Is there evidence ofadditional factors?

(Table 2)

Take a swab orsample of pus (givefull details of patientand wound historyand treatment or anyantibiotic therapy onthe pathology form)

Choose appropriatetopical antiseptic andtreat (see Table 4)Reassess frequently*

Consider otherfactors that maydelay healing

Liaise with doctor ormicrobiologist reresults/treatment andmost effective routefor treatment

Discuss need forintravenous or oralantibiotics

Consider topicalantiseptics, inaddition, if the patientis at high risk ofdeveloping infectionor has severe oedemaand/or arterialinsufficiency

Treat withappropriate antibioticwith or withoutantisepticReassess frequently*

Start broad spectrumantibiotics beforeswab resultsconfirmed

p57-67w24 17/2/05 12:27 pm Page 62


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r su

lfadi

azin

e or

othe

r in

gred

ient

s

Hyp

erse

nsiti

vity

to

silve

r su

lfadi

azin

e or

othe

r in

gred

ient

s

Patie

nts

with

kno

wn

sens

itivi

ty t

o dr

essin

gor

its

com

pone

nts

Adv

erse

eff

ects

: del

ayed

hea

ling,

ce

ll to

xici

ty, i

rrita

ncy,

redu

ced

capi

llary

bloo

d flo

w, r

enal

fai

lure

/Sch

war

tzm

anre

actio

n, d

epre

ssed

col

lage

n sy

nthe

sis,

over

gran

ulat

ion

and

loca

lised

oed

ema,

hype

rnat

raem

ia

May

che

mic

ally

inte

ract

with

oth

er t

opic

alm

edic

amen

ts

Patie

nts

with

kno

wn

sens

itivi

ty t

o dr

essin

gor

its

com

pone

nts

Cau

tion

in p

atie

nts

with

dia

bete

s, c

lose

mon

itorin

g of

glu

cose

leve

ls is

requ

ired

(acc

ordi

ng t

o da

ta s

heet

)

Gu

idan

ce o

n u

se

Part

icul

arly

eff

ectiv

e ag

ains

tPs

eudo

mon

as.S

ilver

is c

ombi

ned

with

an a

ntib

iotic

Re

quire

s se

cond

ary

dres

sing

Requ

ires

seco

ndar

y dr

essin

gW

et w

ound

s w

ill re

quire

ext

raab

sorb

ent

dres

sings

Kee

ps in

tegr

ity t

o al

low

eas

y re

mov

alRe

quire

s se

cond

ary

dres

sing

Act

ivity

redu

ced

in p

rese

nce

of o

rgan

icm

ater

ial a

nd in

alk

alin

e co

nditi

ons

Onl

y st

able

for

tw

o to

thr

ee w

eeks

once

pre

pare

dRe

quire

s se

cond

ary

dres

sing

Requ

ires

seco

ndar

y dr

essin

g

Som

e pa

tient

s ha

ve e

xper

ienc

ed p

ain

whe

n ho

ney

is ap

plie

d C

an re

duce

odo

ur

*Alth

ough

zin

c is

not

licen

sed

as a

n an

tisep

tic, r

ecen

t re

sear

ch s

ugge

sts

it ha

s an

timic

robi

al p

rope

rtie

s an

d m

ay b

e be

nefic

ial i

n pr

even

ting

infe

ctio

n (A

gren

et

al20

04, S

tubb

s an

d Sc

anlo

n 20

04)

†M

RSA

= m

ethi

cilli

n-re

sista

nt S

taph

yloc

occu

s au

reus

(Ada

pted

fro

m C

oope

r an

d La

wre

nce

1996

, Mor

gan

1993

, Pik

e 19

83, S

canl

on a

nd S

tubb

s 20

02)

An

tise

pti

c

Silv

erEf

fect

ive

agai

nst

mos

tba

cter

ia a

ndfu

ngi

Zin

c*

Sod

ium

hyp

och

lori

teEf

fect

ive

agai

nst

mos

tba

cter

ia

Hyd

rog

enp

ero

xid

eEf

fect

ive

agai

nst

mos

tba

cter

ia

Ho

ney

Test

ed a

gain

stEs

cher

ichi

a co

li,Pr

oteu

s,Ps

eudo

mon

as,

Stap

hylo

cocc

us(in

clud

ing

MRS

A† )

, and

Stre

ptoc

occu

spy

ogen

es

Tab

le 4

. To

pic

al

an

tise

pti

cs (

con

tin

ued

)

p57-67w24 17/2/05 12:27 pm 6

february 23/vol19/no24/2005 nursing standard 67


ReferencesAgren M et al (2004) Topical Zinc

Oxide for Excisional Wounds inHumans. Oral presentation.Second World Union of WoundHealing Societies Conference, July8-13. Paris, France.

Ayton M (1985) Wound care:wounds that won’t heal. NursingTimes. 81, 46, 16-19.

Brennan S, Leaper D (1985) Theeffect of antiseptics on thehealing wound: a study using therabbit ear chamber. British Journalof Surgery. 72, 10, 780-782.

Cooper R, Lawrence J (1996) The roleof antimicrobial agents in woundcare. Journal of Wound Care. 5,8, 374-380.

Cruse P, Foord R (1973) A five-yearprospective study of 23,649surgical wounds. Archives ofSurgery. 107, 2, 206-210.

Cutting K, Harding K (1994) Criteriafor identifying wound infection.Journal of Wound Care. 3, 4, 198-201.

Emmerson A et al (1996) The SecondNational Prevalence Survey ofinfection in hospitals: overview ofthe results. Journal of HospitalInfection. 32, 3, 175-190.

Gibbins B (2003) How Much is TooMuch Silver? Oral presentation.Wounds UK 2003, Harrogate,November 11-12.

Kindlen S, Morison M (1997) Thephysiology of wound healing. InMorison M et al (Eds) NursingManagement of Chronic Wounds.Second edition. London, Mosby.

Kingsley A (2001) A proactiveapproach to wound infection.Nursing Standard. 15, 30, 50-58.

Lansdown A (2004) A review of theuse of silver in wound care: facts

and fallacies. British Journal ofNursing. 13, 6 Suppl, S6-19.

Mertz P, Ovington L (1993) Woundhealing microbiology.Dermatologic Clinics. 11, 4, 739-747.

Morgan D (1993) Is there still a rolefor antiseptics? Journal of TissueViability. 3, 3, 80-83.

Pike A (1983) Antiseptic use inwound management. Critical CareNurse. 3, 6, 87-93.

Robson M (1997) Wound infection. Afailure of wound healing causedby an imbalance of bacteria. TheSurgical Clinics of North America.77, 3, 637–650.

Scanlon E (2003) Wound care. InLawrence J, May D (Eds) InfectionControl in the Community.London, Churchill Livingstone.

Scanlon E, Stubbs N (2002) To use ornot to use? The debate on theuse of antiseptics in wound care.British Journal of CommunityNursing. 8, 10, 12passim.

Schraibman I (1990) The significanceof beta-haemolytic streptococci inchronic leg ulcers. Annals of theRoyal College of Surgeons ofEngland. 72, 2, 123-124.

Stubbs N, Scanlon E (2004) Topicalzinc in wound care. Posterpresentation. Second World Unionof Wound Healing SocietiesConference, July 8-13. Paris,France.

Trengove N et al (1996) Qualitativebacteriology and leg ulcer healing.Journal of Wound Care. 5, 6, 277-280.

White R et al (2001) Woundcolonisation and infection: therole of topical antimicrobials.British Journal of Nursing. 10, 9,563-578.

bacteria will have on the healing process. Most wounds heal withno adverse effects from bacteria. Harm caused by bacteria rangesfrom increase in exudate and odour, delayed healing, local cel-lulites, to septicaemia or even death.

The need for nurses to recognise what is normal wound heal-ing is vital so they can identify when it is adversely affected bybacteria. How to manage infection or colonisation is an integralpart of good wound management. Currently there is little reportedresistance to antiseptics. Since the overuse of antibiotics, topicalantiseptics provide a rational alternative to reduce bacteria.

There is still controversy over the use of antiseptics in woundmanagement (Scanlon and Stubbs 2002). Anecdotal evidencesuggests that prolonged use of antiseptics can also delay woundhealing. While some excellent results have been demonstrated inindividual patients, there is still a lack of rigorous evidence to sup-port the use of antiseptics in wound healing.

Nurses wishing to use antiseptics for wound management shouldensure that they are fully aware of the known risks and benefits.They should reassess the wounds regularly and only use antisep-tics where there are good clinical indications

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