3/30/2016

Burnwoundinfectionandsepsis

OfficialreprintfromUpToDate
www.uptodate.com2016UpToDate

Burnwoundinfectionandsepsis
Authors
GerdGGauglitz,MMS,
MD
ShahriarShahrokhi,MD,
FRCSC,FACS

SectionEditor
MarcGJeschke,MD,
PhD

DeputyEditor
KathrynACollins,MD,
PhD,FACS

Disclosures:GerdGGauglitz,MMS,MDNothingtodisclose.ShahriarShahrokhi,MD,
FRCSC,FACSNothingtodisclose.MarcGJeschke,MD,PhDNothingtodisclose.Kathryn
ACollins,MD,PhD,FACSNothingtodisclose.
Contributordisclosuresarereviewedforconflictsofinterestbytheeditorialgroup.When

Alltopicsareupdatedasnewevidencebecomesavailableandourpeerreview
processiscomplete.
Literaturereviewcurrentthrough:Feb2016.|Thistopiclastupdated:Dec14,
2015.
INTRODUCTIONInfectionremainsthemostcommoncauseofmorbidityand
mortalityinburnpatients.Thediagnosisandmanagementofburnwoundinfection
remainschallengingduetothemanyphysiologicfeaturesuniquetoburninjury.A
varietyoffactorsincreasetheriskofdevelopingburnwoundinfection,and
individualswhosustainasevereburnhaveaparticularlyhighriskforburnwound
sepsis.
Anyrapidchangeintheburnwoundappearanceortheclinicalconditionoftheburn
patientmayheraldburnwoundinfectionorsepsis.Thedifferentcategoriesofburn
woundinfectionarecharacterizedbasedonclinicalfeaturesanddepthofinvasion,
whichisdeterminedthroughculturesandhistopathologyoftissueobtainedbyburn
woundbiopsy.Adiagnosisofburnwoundinfectionreliesonthedemonstrationof
>105bacteriapergramtissue(orrecoveryofmoldoryeastbyculture).Specific
criteriathatincludethepresenceofmicrobialinvasionintoadjacentnormaltissue,
amongothercriteria,havebeensuggestedbytheAmericanBurnAssociation
(ABA)todefineburnwoundsepsis.
ThemostcommonorganismsremainStaphylococcusandPseudomonashowever,
theepidemiologyofburnwoundinfectionshaschangedwithtimeandalsodepends
ongeography.Itisimperativetobeawareofthefloraandsusceptibilityof
organismsineachburnunittobeabletotreatburnwoundinfectionseffectively.
Dependingupontheburnwoundcategory,treatmentofburnwoundinfection/sepsis
consistsofacombinationofwoundcleansing,debridement,topicalorsystemic
antimicrobialtherapy,andburnwounddebridementorexcision.
Theclinicalmanifestations,diagnosis,andtreatmentofburnwoundinfectionand
sepsisarereviewedhere.Sepsisrelatedtootherconditionsisreviewedelsewhere.
(See"Sepsissyndromesinadults:Epidemiology,definitions,clinicalpresentation,
diagnosis,andprognosis".)
EPIDEMIOLOGYANDRISKFACTORSTheincidenceofburnwoundsepsis
hasdeclinedfrom6to1percentsincethepracticeofearlyburnwoundexcision
however,forpatientswithtotalbodysurfacearea(TBSA)burns>15percent,the
ratehasremainedthesame[1,2].Thehighestratesofsurgicalburnwound
infectionsoccurinthelowerextremities,butspecificorganismsorclassesof
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organismsarenotconfinedtooneparticularanatomiclocation[3].
Patientswithburnwoundsalsohavehighratesofothertypesofinfection,suchas
catheterrelatedinfection[4,5].Inaseriesof175patientswithsevereburns,
infectionsprecededmultiorgandysfunctionin83percentofpatientsandwere
consideredthedirectcauseofdeathin36percentofthosewhodied[6].
RiskfactorsAvarietyoffactorsincreasetheriskofdevelopinginvasiveburn
woundinfection(burnwoundsepsis).IndividualswhosustainaTBSAburn>20
percentareatparticularlyhighriskhowever,burnwoundinfectionandsepsiscan
occurinsmallerburns[4,68].Otherriskfactorsincludedelaysinburnwound
excision,extremesinage(veryold,veryyoung)andimpairedimmunity.Microbial
factors,suchastypeandnumberoforganisms,enzymeandtoxinproduction,and
motility,alsocontribute[4,913].Butitisimportanttorememberthatburnwound
infectionandsepsiscanoccurinsmallerburns.
Inthemanagementofburnwounds,topicaltherapyisassociatedwithahigher
incidenceofburnwoundinfectionandgraftlosscomparedwithearlyexcisionand
grafting.Delayingburnwoundexcisionincreasesbacterialloadsandgramnegative
colonization.Whenbacterialcountsexceed105organismspergramoftissueinthe
burneschar,woundsshouldbeconsideredatriskfordevelopinginvasiveburn
woundinfections,evenwhenthewoundsareexcised.Despitetheabilityofburn
woundexcisiontodecreasebacterialcounts,burnwoundswithhighcountsareat
riskofdevelopingburnwoundsepsisbothbeforeandaftersurgery[14].(See
'Woundcolonization'belowand"Principlesofburnreconstruction:Overviewof
surgicalprocedures".)
PATHOGENESISBurninjuryisassociatedwithprofoundalterationsin
metabolicandhostdefensemechanismsandimmunefunction,whichpredisposes
burnpatientstolocalandsystemicinvasionbymicrobialpathogens[1518].The
burnwoundisalsosusceptibletoopportunisticcolonizationbyendogenousand
exogenousorganisms.Thespectrumofmicroorganismscausinginfectioninburn
patientsvariesnotonlywithgeographicallocation,butalsohaschangedwithtime,
andthus,itisnecessarytoreviewthebacterialfloracolonizingburnpatientsona
regularbasis[19,20].(See'Woundcolonization'below.)
Anintact,healthyskinsurfacehasbacteriostaticpropertiesthatnormallylimitthe
degreeofskincolonizationbypathogensandnoninvasiveresidentmicrobes.Low
levelsofbacteriathatcolonizetheburnwoundstimulatetheinflammatory
response,activatemacrophages,andproducegrowthfactorsandcytokinesthat
aidinwoundhealing.Theyalsopreventovergrowthofnonresidentbacteria.(See
'Microbiology'below.)
Burnedpatientslosetheirprotectiveprimarybarrier(skin)toenvironmental
microorganisms.Theburnalsoconsistsofavascularnecrotictissue(eschar)that
providesaproteinrichenvironmentfavorabletomicrobialcolonizationand
proliferation[9,10,14].Theavascularityoftheescharimpairsmigrationofhost
immunecellsandrestrictsdeliveryofsystemicallyadministeredantimicrobial
agents,whiletoxicsubstancesreleasedbyeschartissueimpairlocalhostimmune
responses[10].
MICROBIOLOGYThespectrumofmicroorganismscausinginfectionsinburn
patientsvarieswithtimeandlocation(table1).Theorganismscausingburnwound
infectiontypicallyappearatvaryingstagespostburninjury(table1)[4].
Immediatelyafterburning,themicrobialpopulationoftheburnwoundissparseand
includespredominantlygrampositivebacteriathatsurvivedthethermalinsult,such
asstaphylococcilocateddeepwithinsweatglandsandhairfollicles[4,11].Within
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thefirstweekpostburn,burnwoundsarecolonizedwithothermicrobes,suchas
grampositivebacteria,gramnegativebacteria,andyeastsderivedfromthe
patientsnormalgastrointestinalorupperrespiratorytractflora,andfromthe
hospitalenvironment[4,911].Thepredominantgrampositiveorganismsfoundin
burnwoundinfectionsremainStaphylococcusaureus,followedbyEnterococcus
species,whicharefoundindecreasingnumbers(table1).Gramnegative
pathogensdominateafterthefifthdayofatypicallyprotractedinhospitalstayand
haveemergedasthemostcommonetiologicagentsofinvasiveinfectionbyvirtue
oftheirlargerepertoireofvirulencefactorsandantimicrobialresistancetraits
[10,21].Pseudomonasaeruginosaremainsthemostfrequentgramnegative
microorganismisolatedfromburnwounds,followedbyE.coli.
Withsevereburnassociatedimmunedeficiencyand/ordelayedorinadequate
treatment,microbialinvasionofviabletissueoccurs,whichrepresentsthehallmark
ofaninvasiveburnwoundinfection[10].Fungi(eg,Candida,Aspergillus,
Fusarium,Mucorspecies)andmultiresistantorganisms(eg,Methicillinresistant
Staphylococcusaureus[MRSA],vancomycinresistantEnterococcus[VRE],
Acinetobacter)appearlateinchronologicalappearance,andtypicallyoccurafter
useofbroadspectrumantibioticsand/oraprolongedhospitalstay[10].Candidasp.
isthemostcommonfungusisolatedfromburnwoundsandthefourthmost
commoncauseofburnwoundinfectionsoverall[7],andHSV1remainsthemost
commonviralorganisminburnwounds[10].Thecharacteristicphysicalfindingsof
thesecommonorganismsaredescribedinthetable(table2).Emergingmultidrug
resistantstrainsofbacteriaandfungihavecausedanunanticipatedriseinburn
woundinfections,sepsis,andassociateddeathworldwide[7,2225].Inrecent
years,infectionswithMRSA,S.maltophilia,andAcinetobactersp.havebecome
morefrequentandincreasinglymoredifficulttotreatasthesespeciesare
becomingmoreoftenresistanttotheantibioticstraditionallyusedtotreatthem
[19,20].(See'Burnwoundappearance'below.)
CLINICALFEATURESArapidchangeintheclinicalconditionoftheburn
patientmayindicatethatburnwoundinfection,andpotentiallyburnwoundsepsis,
ispresent.
Patientswithinvasiveburnwoundinfections(burnwoundsepsis)mayhavefever,
othersignsofsepsis,changesinwoundappearance(eg,purulentdrainage,
erythema,tenderness),orincreasedpain.Patientswhohadpreviouslytolerated
enteralfeedingsmayshowsignsofintolerance(eg,abdominaldistention,increase
inresidualvolumetwotimesthefeedingrateinadultsand>150mL/hrinchildren,
uncontrollablediarrhea>2500mL/dayforadultsand>400mL/dayforchildren).
(See'AmericanBurnAssociationcriteriaforburnwoundsepsis'below.)
PhysicalexaminationBurnwoundinfectionsaremostoftenrecognizedbased
uponthegrossappearanceoftheburnand/orskingraftdonorsite,andalterations
inclinicalmeasurements(eg,vitalsigns,abdominaldistention).Theburnwounds
shouldbecarefullyexaminedwitheachdressingchange,particularlyinthosethat
willnotbechangedonadailybasis.
BurnwoundappearanceEarlydiagnosisandtreatmentofburnwound
infectionreliesonrecognitionofaninfectedburnwoundsite.Themostcommon
clinicalfeatureisarapidchangeintheappearanceofthewound,whichmay
includeconversionofapartialthicknessinjurytofullthicknessinjury,orlossof
previouslyviabletissueorskingraft.
Acutebacterialinfectionmanifestswiththedevelopmentofdiscoloration,pain,
purulentexudate,edema,tenderness,swelling,drainage,ormalodorfromaburnor
burnrelatedwound(previouslyreepithelializedgraftedburnsite,skindonorsite).
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Theappearanceofinfectionmayinvolveonlyaportionoftheburnwound.A
surroundingcellulitiscanoccurandischaracterizedbyerythemainvolving
uninjuredskin,andwhichmayalsoexhibitlocalizedpainandtenderness,swelling,
andwarmth.Infectionmayalsoleadtoischemia,necrosis,orlossofsyntheticor
biologiccovering.
Localsignsandcharacteristicsofburnwoundinfectionscausedbyfungiinclude
unexpectedlyrapidseparationoftheeschar,presumablyduetofatliquefaction,and
rapidspreadofsubcutaneousedemawithcentralischemicnecrosis(table2)[26].
Vesicularlesionsthatappearinhealingorhealedseconddegreeburnsandthe
presenceofcrustedserratedmarginsofpartialthicknessburnsoftheface,
particularlythoseinvolvingthenasolabialarea,arecharacteristicofburnwound
infectionscausedbyherpessimplexvirustype1(HSV1)[27].
Themostreliablelocalsignofinvasiveburnwoundinfection(burnwoundsepsis)is
conversionofanareaofpartialthicknessinjurytofullthicknessnecrosis,orthe
necrosisofpreviouslyviabletissueinanexcisedwoundbedorskingraft.Such
necrosisappearsasfocal,multifocal,orgeneralizeddarkbrown,black,or
violaceousdiscolorationofthewoundorgraft,orasovertsloughingofapreviously
adherentgraft[28].
Othercharacteristicsofinvasiveburnwoundinfectioninclude[4,911,26,28]:
Edemaand/orviolaceousdiscolorationatthemarginoftheburnand/or
unburnedskin
Hemorrhagicdiscolorationofsubeschartissue
Separationordiscolorationoftheburneschar
Presenceofgreenpigment(pyocyanin)insubcutaneousfat(indicativeof
Pseudomonasinfection)
Presenceofinitiallyerythematousandlaterblacknecroticnodularlesions
(ecthymagangrenosa)inadjacentunburnedskin
Exophthalmosmaybethefirstsignofmucormycosisinmidfaceburns
(retrobulbarspaceinvolvement)
SystemicsignsSeverelyburnedpatientslosetheirprimarybarrierto
invasionbymicroorganisms,andassuch,theyareconstantlyexposedtothe
externalenvironment.Suchexposureleadstosubstantialelevationsinthewhite
bloodcell(WBC)count,makingleukocytosisapoorindicatorofsepsis[22].
Systemicsignsofsepsisincludetachycardia,tachypnea,hypotension,oliguria,
unexplainedhyperglycemia,thrombocytopenia,andmentalstatuschange(eg,
confusion).Thefollowingsystemicfindingsareassociatedwithinvasiveburn
woundinfection(burnwoundsepsis)(see'AmericanBurnAssociationcriteriafor
burnwoundsepsis'below):
Temperature>39Cor<36.5C
Progressivetachycardia(eg,adults>90beatsperminutechildren>2
standarddeviations[SD]aboveagespecificnormalvalues)(table3andtable
4)[29]
Progressivetachypnea(eg,adults>30breathsperminutechildren>2SD
aboveagespecificnormalvalues)(table3andtable4)[29]
Refractoryhypotension(eg,adults:systolicbloodpressure<90mmHgora
decrease>40mmHg,ormeanarterialpressure<70mmHgchildren<2SD
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belownormal)
Thecontinuousreleaseofinflammatorymediatorsaltersthebaselinemetabolic
profileoftheburnpatient.Baselinetemperatureisresettoabout38.5C,and
tachycardiaandtachypneapersistformonthsinpatientswithextensiveburns
[30,31].Patientswhohaveonlysignsofhypermetabolismwithoutothersignsof
sepsismustbedistinguishedfromtypicalchangesassociatedwiththe
hypermetabolicresponsetothermalinjury.(See'Hypermetabolicresponseto
thermalburn'below.)
Inoneretrospectivereviewof110patientsadmittedtoaburnunitwithawide
rangeofburnwounds,56patients(50percent)developedearlyinfectionand18
developedearlysepsis[12].Logisticregressionidentifiedmaximumtemperature
39CandFiO2>25percent(surrogatemarkerforrespiratoryproblems)as
significantpredictorsofburnwoundsepsiswithinthefirst10daysofinjury.In
addition,predictorsofearlysepsis(within10daysofburn)includedheartrate110
bpm,systolicbloodpressure100mmHg,andintubation.
LaboratoryfindingsForpatientsintheintensivecareunit,routinelaboratory
studiesaretypicallyobtainedatleastdaily,butforthosebeingcaredforinaless
intensesetting,oftenonlyasneeded.(See"Postoperativefever",sectionon
'Procalcitonin'.)
Thefollowinglaboratoryalterationsinbloodtestscanbefoundinpatientswithburn
woundsepsis:
GlucoseFastingserumbloodglucoselevels>110mg/dL(6.1mmol/L)inthe
absenceofpreexistingdiabetesmellitus.(See"Hypermetabolicresponseto
severeburninjury:Recognitionandtreatment",sectionon'Glucose
metabolism'.)
WhitebloodcountLeukocytosis(>12,000cells/microL,adults,>2SDabove
thenormallevelforchildren(table3),orleukocytopenia<4000cells/microL.
PlateletcountPlateletcount<100,000/microL(adults),<2SDbelowthe
normallevelforchildren.(table5)
ProcalcitoninForpatientswithsevereburns,dailymeasurementsofserum
procalcitonin(PCT)maybeusefulformonitoringtheeffectivenessof
antibiotictherapy.ThevalueofserumPCTconcentrationfordifferentiating
bacterialinfectionfromothercausesofpostoperativefeverhasbeenexplored
inpatientswithburnwoundsepsis[32,33].However,postoperativePCT
concentrationsarequitevariable,particularlyinpostoperativepatients,andas
aresult,aspecificthresholdvalueisdifficulttodetermine[34].Ina
systematicreviewthatidentified566PCTsamplesamongburnpatientsin
ninetrials,cutoffvaluesabovewhichapositiveresultwasdefinedranged
from0.53to3ng/mL.Forsimilarcutoffvalues,thesensitivityandspecificity
ofPCTalsovariedwidely[32].

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DIAGNOSISWhenburnwoundinfectionissuspectedclinicallybaseduponthe
clinicalfeaturesdiscussedabove,qualitativewoundculturescanidentifythe
presenceofflora,butquantitativewoundcultures(numberofbacteriapergramof
tissue)andhistopathologyobtainedbybiopsyofthewound,arerequiredtoconfirm
thediagnosisofburnwoundinfection(algorithm1).Inaninfectedburnwound,
bacteriaarepresentatconcentrations>105bacteriapergramoftissue[35,36].The
presenceofbacteriaatconcentrations>105bacteriapergramoftissueinadjacent
unburnedtissuedefinesinvasiveburnwoundinfection.Systemicsymptomsare
usuallypresentinpatientswithburnwoundsepsisrelatedtoinvasiveburnwound

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infection.

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TissuebiopsyandhistopathologyTheonlyreliablewaytodifferentiate
noninvasivefrominvasiveburnwoundinfectionisbyhistopathologyfromaburn
woundbiopsy[4,14,36,37].Tissuehistopathologyallowsforquantificationand

evaluationofinfectiondepthandextentofinvolvement[10].Thetissuebiopsy
1Pack,100seeds/
samplesshouldbeobtainedfromseveraloftheaffectedareasoftheburnwound
pack,RussianGiant
SweetPepperSeeds
andshouldbeapproximately1to2cminlengthand1.5cmdeepandextendinto
thesubcutaneoustissue,orweighapproximately0.5gram.Althoughapresumptive
diagnosisofinfectioncanbemadewhenbacterialcountis>105organismsper
gramoftissue,quantitativeculturesaremorehelpfulforconfirmingtheabsenceof
woundinfection(<105organismspergramoftissue).Thecorrelationsbetween
negativecultureresults(<105bacteriapergramoftissue)andnegative
AcrylicKnitting
5bacteria
histopathologyis96percenthowever,positivequantitativecultures(>10
NeedlesFuchsia
1.6mm(...
pergramoftissue)correlatewithtissueinvasioninonly36percentofcases[36].
Thespecifichistologicalsignofinvasiveburnwoundinfectionisthepresenceof
microorganismsinadjacentnormal,unburnedtissue[4,10,14,36,37].

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Otherhistologicalfindingsindicativeofinvasiveburnwoundinfectionarethe
presenceofhemorrhageinunburnedtissue,smallvesselthrombosisandischemic
OneplusOneTwo
necrosisofunburnedtissue,markedinflammatorychangesinunburnedtissue,
PremiumTempered
densebacterialgrowthinthesubescharspace(asiteofmicrobialproliferationprior
GlassScreen...
toinvasion),andintracellularviralinclusionstypicalforHSV1infections(table2).
Aninvasivefungaldiseaseisdiagnosedbyidentifyinghyphaeormelanizedyeast
likeformsusinghistopathologic,cytopathologic,ordirectmicroscopicexamination
ofabiopsyorneedleaspirationspecimen[38].Thesefindingsareaccompaniedby
histopathologicevidenceofassociatedtissuedamageorrecoveryofamoldor
1PcsComb
yeastbycultureofaspecimenobtainedfromanormallysterilesite,orbya
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radiologicalabnormalityconsistentwithaninfectiousdiseaseprocess.

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WoundcolonizationSurfacewoundculturesareusefulforidentifying

predominantorganismsoftheburnwoundflora.Swabculturesassistinthe
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surveillanceofthebacterialfloracolonizingburnpatients[19,20,35,36].Burn
woundsareswabbedonadmission,andagainifthereareanyconcerningchanges
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inappearance.Intheabsenceofchanges,weeklysurveillanceswabsare
suggested.Colonizationispresentwhenbacteriaareculturedfromtheburnwound
surfaceatconcentrations<105bacteriapergramtissue,intheabsenceofclinical
orhistopathologicevidenceofinfectionorinvasionofunburnedtissue[10].
Semiquantitativecultureofwoundexudateortissuewilldetermineifthereisgrowth
withinlessthan24hoursformostmicroorganisms[39].Colonizationdoesnot
generallyimpairwoundhealing.Forpatientswithconcerningchangesandsystemic
signs,awoundbiopsywouldbebeneficial,whichistypicallyperformedduringthe
operativeexcisionofanynecroticorinfectedtissue.(See'Tissuebiopsyand
histopathology'above.)
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BurnwoundcategoriesThecategoriesofburnwoundinfectionare
characterizedbaseduponclinicalfeatures,andextentanddepthofmicrobial
invasion[22].

NoninvasiveinfectionNoninvasiveburnwoundinfectionispresentwhen
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therearetypicalclinicalfeaturesofinfectionwithoutsystemicsigns,andthe
bacterialcountis>105bacteriapergramoftissue(orrecoveryofmoldoryeastby
culture)obtainedfromaburnwoundorescharwithnoinvasivecomponent(ie,no
microbialinvasionintounburnedtissue)asidentifiedbytissuehistopathology.This
bacterialburdenresultsinimpairedskinandtissuegrafttake,andpromotes
systemicinfection.

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Subcategoriesofnoninvasiveinfectionsincludethefollowing:
BurnwoundcellulitisBurnwoundcellulitisispresentwhenclinicalfeatures
ofinfectionextendintohealthy,uninjuredskinandsofttissue,andthe
bacterialcountis>105bacteriapergramoftissue(orrecoveryofmoldor
yeastbyculture)withnoinvasivecomponent(ie,nomicrobialinvasioninto
unburnedtissue)identifiedbytissuehistopathology.
BurnrelatedsurgicalsiteinfectionBurnrelatedsurgicalsiteinfectionis
presentwhentherearetypicalclinicalfeaturesofinfectionwithoutsystemic
signs,andthebacterialcountis>105bacteriapergramoftissue(orrecovery
ofmoldoryeastbyculture)obtainedfromanexcisedburnwound,orskin
donorsitesthathavenotyetreepithelializedwithnoinvasivecomponent(ie,
nomicrobialinvasionintounburnedtissue)identifiedbytissuehistopathology.
BurnwoundimpetigoBurnwoundimpetigoisthelossofepitheliumdueto
aninfectionatapreviouslyreepithelializedsurface,suchasagraftedburn,a
partialthicknessburnallowedtohealbysecondaryintention,orahealedskin
donorsite.Itisnotrelatedtoinadequateexcisionoftheburn,mechanical
disruptionofthegraft,orhematomaformation.
InvasiveinfectionInvasiveburnwoundinfectionispresentwhenthereare
typicalclinicalfeaturesconsistentwithburnwoundinfectionassociatedwith
systemicsigns,andbacterialcountis>105bacteriapergramoftissueobtained
fromaburnwoundorescharwithaninvasivecomponent(ie,microbialorfungal
invasionintounburnedtissue)identifiedbytissuehistopathology.Necrotizing
infections,whichareaggressiveinfectionsinvolvingthedeepertissueswiththe
potentialtocauseextensivetissuenecrosis,canoccur.
Adiagnosisofaninvasiveburnwoundinfectionandsepsisshouldbemadebased
upontheAmericanBurnAssociation(ABA)consensuscriteriagivenbelow.
Althoughthereareotherexcellentcriteriaforthediagnosisofinfectionandsepsis
inmostpatients,thestandarddiagnosisisnotoptimalforburnpatients[22].
Standardizeddefinitionsforsepsisandinfectionthatarespecificallyapplicableto
theburnpatientweredevelopedin2007[22].Theburnsepsisdefinition
distinguishesthechangeinpatientstatusasaresultofamicrobialinfectionfrom
changesthatoccursecondarytothehypermetabolicresponseoftheburnitself.
(See'Differentialdiagnosis'below.)
AmericanBurnAssociationcriteriaforburnwoundsepsisTheABA
criteriaareasfollows[22,30,31]:
Fulfillmentofoneofthefollowingthreecriteria:
Pathologicinfectionisconfirmedonaculture(eg,wound,blood,urine),
or
Pathologictissuesourceisidentified(ie,>105bacteriaonquantitative
woundtissuebiopsyormicrobialinvasiononbiopsy),or
Improvementintheclinicalsettingisattributedtoantimicrobial
administration
Andatleastthreeofthefollowingparameters:
Temperature>102.2F(39C)or<97.7F(36.5C)
Progressivetachycardia(eg,adults>90beatsperminutechildren>2
standarddeviations[SD]aboveagespecificnormalvalues[29])(table3
andtable4)
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Progressivetachypnea(eg,adults>30breathesperminutechildren>2
SDaboveagespecificnormalvalues[29])(table3andtable4)
Refractoryhypotension(eg,adults:systolicbloodpressure<90mmHg
oradecrease>40mmHg,ormeanarterialpressure<70mmHgchildren
<2SDbelownormal)(table3)
Leukocytosis(eg,adult>12,000whitecells/microL,children>2SD
abovenormal)orleukocytopenia(eg,<4000whitebloodcells/microL)
(table3).
Thrombocytopeniathatoccursthreedaysafterresuscitation(eg,adults
<100,000plateletspermicroliterchildren<2SDbelowagespecific
normalvalues)(table5)
Hyperglycemia>110mg/dL(6.1mmol/L)intheabsenceofpreexisting
diabetesmellitus
Inabilitytotolerateenteralfeedingsformorethan24hoursbasedupon:
Abdominaldistention
Residualvolumes(twotimesthefeedingrateinadultsand>150
mL/hrinchildren)
Uncontrollablediarrhea(>2500mL/dayforadultsand>400mL/day
forchildren)
Improvingtheabilitytorapidlyidentifyburnsepsis(orthoseatrisk)isthesubject
ofongoingstudy.Onegroupidentifiedsixvariables(heartrate>130beatspermin,
meanarterialpressure<60mmHg,basedeficit<6mEq/L,temperature<36C,use
ofvasoactivemedications,andglucose>150mg/dL)thatmayhelpwithearly
predictionofburnwoundsepsis[40].
DIFFERENTIALDIAGNOSISThedifferentialdiagnosisofburnwoundinfection
includesmainlyburnwoundcolonization,butmayalsoincludeotherconditionsthat
canaffecttheskinincriticallyillpatients.Colonizationoftheburnwoundsis
distinguishedfromburnwoundinfectionandinfectionrelatedproblemsbythe
absenceoftheaccompanyingclinicalfeaturesdiscussedabove,inspiteofthe
presenceofbacteria,whichwillhavelowcounts.(See'Woundcolonization'
above.)
MedicationrelatedmucocutaneousreactionsReactionstomedications
superimposedonburnwoundsmightbeconfusedasburnwoundinfectionor
sepsishowever,inmostcasesdermatologicreactionsarewidespread(ie,would
alsoinvolveunburnedskin)andgenerallyinvolvethemucousmembranes.
StevensJohnsonsyndrome(SJS)andtoxicepidermalnecrolysis(TEN),are
examplesofsuchmucocutaneousreactions(table6).Theskinchangesare
characterizedbywidelydistributedcutaneouserythematousmaculesorpatches,
and/ordiffusecutaneouserythema(picture1AD).TENbeginswithaprodromeof
feverandmalaise,highfever(102.2F[39C]).Intheearlystages,skinpainmay
beprominentandoutofproportiontoclinicalfindings.Theskinlesionscan
progresstofullthicknessepidermalnecrosis.(See"StevensJohnsonsyndrome
andtoxicepidermalnecrolysis:Pathogenesis,clinicalmanifestations,and
diagnosis".)
HypermetabolicresponsetothermalburnBurnwoundsepsisshouldnotbe
confusedwiththenormalhypermetabolicresponsetothermalinjury.Followingburn
injury,thecontinuousreleaseofinflammatorymediatorsaltersthebaseline
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metabolicprofileoftheburnpatientbaselinetemperatureisresettoapproximately
101.3F(38.5C),andtachycardiaandtachypneapersistformonths[22,30,31].
Themetabolicrateincreasesinproportiontothesizeoftheburn,withincreasing
energyexpenditure.Asanexample,adultswitha25percenttotalbodysurface
area(TBSA)burninjurydevelopametabolicratebetween118to210percentofthe
predictedbasalmetabolicratechildrenwithburninjuriesgreaterthan40percent
TBSAdevelopametabolicrateof180percentofthepredictedbasalmetabolic
rate.(See"Hypermetabolicresponsetosevereburninjury:Recognitionand
treatment".)
OthercauseofsepsisBurnwoundsepsisneedstobedistinguishedfromother
causesofsepsis,andfromnoninfectiousentitiesthatcanmimicmanyofthe
systemicfeaturesofsepsis(table7).Physicalexaminationorisolationofa
pathogeninbloodorurineculturesmaysuggestanalternativesourceforsepsis
(table8).(See"Evaluationandmanagementofseveresepsisandsepticshockin
adults",sectionon'Identificationofthesepticfocus'.)
Burnsepsismustalsobedistinguishedfromsepsisrelatedtoassociatedissues
thataffectcriticallyillpatients(eg,centralcatheterrelatedinfection,urinary
infection,pneumonia,othersinthosewithcombinedburntraumainjury).(See
"Epidemiology,pathogenesis,microbiology,anddiagnosisofhospitalacquired,
ventilatorassociated,andhealthcareassociatedpneumoniainadults"and
"Catheterassociatedurinarytractinfectioninadults"and"Epidemiology,
pathogenesis,andmicrobiologyofintravascularcatheterinfections".)
TREATMENTThetreatmentstrategyforburnwoundinfectioncanbedivided
intoinitialtreatment,systemictherapies,andlocalburnwoundmanagement.
StabilizationTheinitialmanagementofinvasiveburnwoundinfection(burn
woundsepsis)isaimedatstabilizingthepatientandrestoringperfusion.
(See"Septicshock:Rapidrecognitionandinitialresuscitationinchildren".)
(See"Evaluationandmanagementofseveresepsisandsepticshockin
adults".)
SystemicantimicrobialtherapySystemicantimicrobialtherapyisreservedfor
patientsdemonstratingsepsisorsepticshocktolimittheriskofsuperinfection
withresistantmicroorganisms[4].Antibioticchoicesaredependentonthe
antibiogramoftheindividualinstitution.Attheauthorsinstitution,forburnwound
sepsisweinitiateempiricantimicrobialtherapywithpipercillin/tazobactamor
carbapenem,+/vancomycinifthereissuspicionformethicillinresistant
Staphylococcusaureus(MRSA),+/anaminoglycosideifthereissuspicionfor
multidrugresistantPseudomonasaeruginosa.Forpatientswithburnwound
cellulitis,weinitiatetreatmentwithintravenousCefazolinorClindamycinor
VancomycinifthereissuspicionforMRSA,+/anoralfluoroquinoloneforburns
involvingthelowerextremityorfeetorburnsinpatientswithdiabetes.
Systemicantimicrobialtherapyisunnecessaryforpatientswithburnwound
colonizationornoninvasiveburnwoundinfection.Intheabsenceofotherclinical
symptomsandsignsofburnwoundinfection,antimicrobialtherapytotreatfeveris
discouragedgiventhatburnpatientshaveincreasedbodytemperaturesecondaryto
thesystemicinflammatoryresponsetoburninjury.Althoughtheadministrationof
systemicantibioticsperioperativelyinlargepercentagetotalbodysurfacearea
burnsisassociatedwithareducedrateofsurgicalburnwoundinfections,therehas
beennocorrelationwithimprovedmortalityandsuchantibioticusehasincreased
theprevalenceofresistanceofbacteria[41].(See'Hypermetabolicresponseto
thermalburn'above.)
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Systemicantimicrobialtherapyisreservedforpatientsdemonstratingburnwound
cellulitisorsepsis.Wheneverpossible,antimicrobialtherapyshouldbedirected
towardsthespecificorganismsisolatedfromthewound,blood,and/orurine
cultures[4].Whensystemicantimicrobialtherapyisneeded,awarenessshouldbe
heightenedforthepossibilityofsuperinfectionwithresistantorganisms,yeasts,or
fungi.Phycomycoticinfectionsbenefitfrombothtopicalandsystemictherapy
[26,4244].However,systemicantifungalorantiviralagentsshouldonlybe
administeredbasedonaprovendiagnosis.(See'Microbiology'aboveand'Tissue
biopsyandhistopathology'above.)
Specificantimicrobialtherapiesarereviewedelsewhereandinclude:
(See"ClinicalapproachtoStaphylococcusaureusbacteremiainadults".)
(See"Staphylococcusaureusbacteremiainchildren:Managementand
outcome".)
(See"Pseudomonasaeruginosaskin,softtissue,andboneinfections".)
(See"Treatmentofcandidemiaandinvasivecandidiasisinadults",sectionon
'Approachtomanagement'.)
(See"Candidemiainchildren:Treatment".)
LocalburnwoundcareLocalmanagementofinfectedburnwoundsincludes
cleansing,debridement,topicalantimicrobialagents(eg,silversulfadiazine,
combinationantibiotics,chlorhexidine),anddressings(eg,compresses,
biosynthetics,biologics).Thetreatmentforunexciseddeepburnwoundsisalways
excisiontherequireddepthofexcisiondependsonthedepthofmicrobialinvasion.
(See"Principlesofburnreconstruction:Overviewofsurgicalprocedures",section
on'Timingofsurgery'.)
Topicalagentscanbeusedinitiallyforunexcisedburnwoundstominimize
bacterialcolonizationuntiltheexcisioncanbeperformed[45].Burnwoundsthat
arealreadyexcisedthatthenbecomeinfected(ie,burnwoundrelatedsurgicalsite
infection)arealsotreatedwithtopicaltherapy,andpossiblyreexcisiondepending
upontheextentofinvolvement.Thechoiceoftopicalagents,whichrangesfrom
ointmentsandcreamstosolutionsandsilverioncontainingdressings,depends
uponthesuspectedordiagnosedmicroorganismaswellastheavailabilityofthe
agentonformulary[41,4649].Topicalagentsanddressingsarediscussedindetail
separately.(See"Localtreatmentofburns:Topicalantimicrobialagentsand
dressings".)
Themanagementofinvasivewoundinfectionincludesdebridementofwoundstoa
healthytissuebedasdeterminedbyintraoperativebiopsycombinedwithsystemic
antimicrobialtherapy.Invasivefungalinfectionsneedtobetreatedaggressively
withexcision,topicalantifungals,andsystemicantifungaltherapy.Wideexcision
shouldincludealltheinvolvedtissue.Phycomycoticinfectionsmaybesurrounded
byarimofedematoustissue,whichalsomustbeexcised.Theexcisedwounds
needtobeinspectedagainwithin24to48hours,anddebridedagainifnecrotic
tissueispresent,orifthewoundisclean,coveredwithallograftifnoinfected
tissueremainsandthewoundappearsviable[26,4244].(See'Systemic
antimicrobialtherapy'above.)
Burnwoundimpetigoistreatedusingsystemicantimicrobialtherapyandpossibly
topicalglucocorticoids[50].Contactprecautionsshouldbeuseduntil24hoursafter
thestartofantibiotictherapytoavoidspreadofimpetigo[51].(See"Impetigo",
sectionon'Treatment'.)
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MORBIDITYANDMORTALITYItisestimatedthat75percentofthemortality
followingthermalinjuriesisrelateddirectlytoinfections.Nosocomialinfections(eg,
centralvenouscathetersource)andemergingmultidrugresistantstrainsof
bacteriaandfungicontributetoburnwoundinfections,sepsis,andassociated
death[52,53].TheNosocomialInfectionSurveillanceSystemfromtheUSCenters
forDiseaseControlandPrevention(CDC)reportedthatburnintensivecareunits
(ICUs)havethehighestratesofprimarybloodstreaminfectioninpatientswith
centralvenouscathetersamongallICUs[4,5].Inaseriesof175patientswith
severeburns,infectionprecededmultiorgandysfunctionin83percentofpatients
andwasconsideredthedirectcauseofdeathin36percentofthosewhodied[6].
Emergingmultidrugresistantstrainsofbacteriaandfungihaverecentlycausedan
unanticipatedriseinburnwoundinfections,sepsis,andassociateddeath
worldwide[7,2225].Studieshaveshownanincreaseinfungal/Candidaratesin
burnunitsinrecentyears[54,55].However,thesearenotbenigninfections,as
approximately60percentofallwoundinfectionsduetofungi/yeastrequire
regrafting,andotherstudieshaveshownthatCandidacolonizationandcandidemia
areassociatedwithhighmortalityratesinburnpatients[5557].
Infectionofburnwoundsisnotwithoutconsequence.Themostcommonoutcomes
ofburnwoundinfectionsinclude:

Graftlossforexcisedandgraftedburnwounds
Increasednumberofsurgicalinterventions
Increasednosocomialinfections
Increasedlengthofstay
Conversionofdonorsite

PREVENTIONEarlyexcisionandskingrafting(daysonetofive)reducesthe
presenceofpotentiallynecroticandinfectedtissue,andtherebyreducestheriskof
invasiveandnoninvasiveburnwoundinfections[5,8].Earlyexcisionofnecrotic
tissueandclosureoftheburnwoundhasbeenoneofthesinglegreatest
advancementsinthetreatmentofpatientswithseverethermalinjuries,anda
mainstayoftherapy[2224].(See"Principlesofburnreconstruction:Overviewof
surgicalprocedures",sectionon'Earlyexcisionandskingrafting'and
"Hypermetabolicresponsetosevereburninjury:Recognitionandtreatment",
sectionon'Earlywoundclosure'.)
SUMMARYANDRECOMMENDATIONS
Infectionremainsthemostcommoncauseofmorbidityandmortalityinburn
patients.Althoughtheoverallincidenceofburnwoundsepsishasdeclined,
theincidenceofburnwoundinfectionamongthosewithtotalbodysurface
area(TBSA)burn>15percenthasremainedabout6percent.Patientswith
burnwoundsalsohavehighratesofothertypesofinfection,suchas
catheterrelatedinfection.(See'Epidemiologyandriskfactors'above.)
Avarietyoffactorsincreasetheriskofdevelopinginvasiveburnwound
infection(burnwoundsepsis).IndividualswhosustainaTBSAburn>20
percentareatparticularlyhighriskhowever,burnwoundinfectionandsepsis
canoccurinsmallerburns.Otherfactorsincludedelaysinburnwound
excision,extremesinage(veryold,veryyoung)andimpairedimmunity.
Microbialfactors,suchastype,virulence,andbacterialcount(>105
organismspergramoftissue)increasetheriskofaninvasivewound
infection.(See'Riskfactors'above.)
Theorganismsthatcancolonizetheburnwoundandpotentiallygiveriseto
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burnwoundinfectionvarywithtimeandlocation(table1).Weroutinelyswab
burnwoundsforcultureatthetimeofadmission,weekly,andagainifthere
areanyconcerningchangesinappearanceortheclinicalconditionofthe
patient.ThemostcommonorganismsareStaphylococcusand
Pseudomonashowever,theepidemiologyofburnwoundinfectionschanges
overtimeandalsodependsonthespecificburnunit.Abacterialburden>105
bacteriapergramoftissueresultsinimpairedskingrafttake,andpromotes
systemicinfection.(See'Pathogenesis'above.)
Therecognitionofburnwoundinfectionremainschallengingduetothemany
featuresuniquetoaburninjury.Arapidchangeintheclinicalconditionofthe
burnpatient,suchasincreasingpainorchangesinthegrossappearanceofa
burnwoundorskingraftdonorsites,intoleranceofenteralfeedings,or
systemicsigns,isindicativeofburnwoundinfectionandpotentiallyburn
woundsepsis.(See'Clinicalfeatures'above.)
Whenwoundinfectionissuspectedclinicallybaseduponclinicalfeatures,
quantitativewoundculturesandexaminationofhistopathologyobtainedby
biopsyingthewoundarenecessarytoconfirmthediagnosisofburnwound
infection(>105bacteriapergramoftissue),whichmayormaynotbe
invasive(algorithm1).Thecategoriesofburnwoundinfectionare
characterizedbaseduponclinicalfeaturesanddepthofinvasion.(See
'Woundcolonization'aboveand'Noninvasiveinfection'above.)
Mostlaboratorystudiesarenonspecific.Serumprocalcitoninmay
differentiatebacterialinfectionfromnoninfectivecausesoffever
however,aspecificcutoffvalueisdifficulttodefinetrendsmaybe
moreuseful.(See'Laboratoryfindings'above.)
Criteriausedforadiagnosisofsepsisinunburnedpatientsoftendoes
notapplyinburnpatients,particularlyseverelyburnedpatients,dueto
alterationsofthepatientsmetabolicprofilebyinflammatorymediators.
Theburnsepsisdefinitiondistinguishesphysiologicchangesthatoccur
secondarytothehypermetabolicresponseoftheburnitselffromthose
thatresultfrommicrobialinfection.Specificcriteriahavebeen
suggestedbytheAmericanBurnAssociation.(See'AmericanBurn
Associationcriteriaforburnwoundsepsis'above.)
Forpatientswhohaveclinicalchangesand/orsystemicsigns
concerningforburnwoundinfectionorsepsis,webiopsytheburn
woundstypicallyduringtheoperativeexcisionofanynecroticorinfected
tissue.
Dependingupontheburnwoundcategory,treatmentofburnwoundinfection
consistsofacombinationofburnwoundcare(ie,cleansing,dressings),
topicalantimicrobialtherapy,systemicantimicrobialtherapy,andburnwound
debridementorexcision.(See'Noninvasiveinfection'above.)
Noninvasiveburnwoundinfectionischaracterizedbytypicalclinical
featuresofburnwoundinfectionwithoutsystemicsigns,bacterialcount
>105bacteriapergramoftissue(orrecoveryofmoldoryeastby
culture),andnomicrobialinvasionintounburnedtissue.Treatment
consistsprimarilyoftopicalantimicrobialtherapyandburnwound
excisionforunexcisedwoundsandpossiblyreexcisionforexcised
wounds.
Invasiveburnwoundinfectionischaracterizedbytypicalclinical
featuresofburnwoundinfectionandsystemicsigns,bacterialcount
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>105bacteriapergramoftissueobtainedfromaburnwoundoreschar,
andmicrobialinvasionintounburnedtissue.Treatmentisinitiatedwith
systemicbroadspectrumantimicrobialtherapy,andexcisionofall
infectedtissuetohealthytissuebedasdeterminedbyintraoperative
biopsy.Specificantimicrobialtherapyisguidedbytheresultsofburn
woundcultureandhistopathology.
UseofUpToDateissubjecttotheSubscriptionandLicenseAgreement.
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