13.04.

2016

PeritonitisandAbdominalSepsis:Background,Anatomy,Pathophysiology

PeritonitisandAbdominalSepsis
Author:BrianJDaley,MD,MBA,FACS,FCCP,CNSCChiefEditor:JulianKatz,MDmore...
Updated:Feb23,2015

Background
Peritonitisisdefinedasaninflammationoftheserosalmembranethatlinesthe
abdominalcavityandtheorganscontainedtherein.Theperitoneum,whichisan
otherwisesterileenvironment,reactstovariouspathologicstimuliwithafairly
uniforminflammatoryresponse.Dependingontheunderlyingpathology,the
resultantperitonitismaybeinfectiousorsterile(ie,chemicalormechanical).Intra
abdominalsepsisisaninflammationoftheperitoneumcausedbypathogenic
microorganismsandtheirproducts. [1]Theinflammatoryprocessmaybelocalized
(abscess)ordiffuseinnature.(SeePathophysiology.)
Peritonitisismostoftencausedbyintroductionofaninfectionintotheotherwise
sterileperitonealenvironmentthroughorganperforation,butitmayalsoresultfrom
otherirritants,suchasforeignbodies,bilefromaperforatedgallbladderora
laceratedliver,orgastricacidfromaperforatedulcer.Womenalsoexperience
localizedperitonitisfromaninfectedfallopiantubeorarupturedovariancyst.
Patientsmaypresentwithanacuteorinsidiousonsetofsymptoms,limitedand
milddisease,orsystemicandseverediseasewithsepticshock.(SeeEtiology.)
Peritonealinfectionsareclassifiedasprimary(ie,fromhematogenous
dissemination,usuallyinthesettingofanimmunocompromisedstate),secondary
(ie,relatedtoapathologicprocessinavisceralorgan,suchasperforationor
trauma,includingiatrogenictrauma),ortertiary(ie,persistentorrecurrentinfection
afteradequateinitialtherapy).Primaryperitonitisismostoftenspontaneous
bacterialperitonitis(SBP)seenmostlyinpatientswithchronicliverdisease.
Secondaryperitonitisisbyfarthemostcommonformofperitonitisencounteredin
clinicalpractice.Tertiaryperitonitisoftendevelopsintheabsenceoftheoriginal
visceralorganpathology.(SeeClinicalPresentation.)
Infectionsoftheperitoneumarefurtherdividedintogeneralized(peritonitis)and
localized(intraabdominalabscess).Thisarticlefocusesonthediagnosisand
managementofinfectiousperitonitisandabdominalabscesses.Anabdominal
abscessisseenintheimagebelow.

A35yearoldmanwithahistoryofCrohndiseasepresentedwithpainandswellingintheright
abdomen.InfigureA,athickenedloopofterminalileumisevidentadherenttotherightanterior
abdominalwall.InfigureB,therightanteriorabdominalwallismarkedlythickenedand
edematous,withadjacentinflamedterminalileum.InfigureC,arightlowerquadrantabdominal
wallabscessandentericfistulaareobservedandconfirmedbythepresenceofenteralcontrast
intheabdominalwall.

Thediagnosisofperitonitisisusuallyclinical.Diagnosticperitoneallavagemaybe
helpfulinpatientswhodonothaveconclusivesignsonphysicalexaminationorwho
cannotprovideanadequatehistoryinaddition,paracentesisshouldbeperformed
inallpatientswhodonothaveanindwellingperitonealcatheterandaresuspected
ofhavingSBP,becauseresultsofaerobicandanaerobicbacterialcultures,usedin
conjunctionwiththecellcount,areusefulinguidingtherapy.(SeeWorkup.)
Thecurrentapproachtoperitonitisandperitonealabscessestargetscorrectionof
theunderlyingprocess,administrationofsystemicantibiotics,andsupportive
therapytopreventorlimitsecondarycomplicationsduetoorgansystemfailure.
(SeeTreatmentandManagementandMedication.)
Earlycontrolofthesepticsourceismandatoryandcanbeachievedoperativelyand
nonoperatively.Nonoperativeinterventionsincludepercutaneousabscessdrainage,
aswellaspercutaneousandendoscopicstentplacements.Operativemanagement
addressestheneedtocontroltheinfectioussourceandtopurgebacteriaand
toxins.Thetypeandextentofsurgerydependsontheunderlyingdiseaseprocess
andtheseverityofintraabdominalinfection.

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Anatomy
Theperitoneumisthelargestandmostcomplexserousmembraneinthebody.It
formsaclosedsac(ie,coelom)byliningtheinteriorsurfacesoftheabdominalwall
(anteriorandlateral),byformingtheboundarytotheretroperitoneum(posterior),by
coveringtheextraperitonealstructuresinthepelvis(inferior),andbycoveringthe
undersurfaceofthediaphragm(superior).Thisparietallayeroftheperitoneum
reflectsontotheabdominalvisceralorganstoformthevisceralperitoneum.It
therebycreatesapotentialspacebetweenthe2layers(ie,theperitonealcavity).
Theperitoneumconsistsofasinglelayerofflattenedmesothelialcellsoverloose
areolartissue.Thelooseconnectivetissuelayercontainsarichnetworkofvascular
andlymphaticcapillaries,nerveendings,andimmunecompetentcells,particularly
lymphocytesandmacrophages.Theperitonealsurfacecellsarejoinedbyjunctional
complexes,thusformingadialyzingmembranethatallowspassageoffluidand
certainsmallsolutes.Pinocytoticactivityofthemesothelialcellsandphagocytosis
bymacrophagesallowfortheclearanceofmacromolecules.
Normally,theamountofperitonealfluidpresentislessthan50mL,andonlysmall
volumesaretransferredacrosstheconsiderablesurfaceareainasteadystateeach
day.Theperitonealfluidrepresentsaplasmaultrafiltrate,withelectrolyteandsolute
concentrationssimilartothatofneighboringinterstitialspacesandaproteincontent
oflessthan30g/L,mainlyalbumin.Inaddition,peritonealfluidcontainssmall
numbersofdesquamatedmesothelialcellsandvariousnumbersandmorphologies
ofmigratingimmunecells(referencerangeis<300cells/L,predominantlyof
mononuclearmorphology).
Theperitonealcavityisdividedincompletelyintocompartmentsbythemesenteric
attachmentsandsecondaryretroperitonealizationofcertainvisceralorgans.Alarge
peritonealfold,thegreateromentum,extendsfromthegreatercurvatureofthe
stomachandtheinferioraspectoftheproximalduodenumdownwardovera
variabledistancetofolduponitself(withfusionoftheadjacentlayers)andascends
backtothetaeniaomentalisofthetransversecolon.Thisperitonealfold
demonstratesaslightlydifferentmicroscopicanatomy,withfenestratedsurface
epitheliumandalargenumberofadipocytes,lymphocytes,andmacrophages,and
itfunctionsasafatstoragelocationandamobileimmuneorgan.
Thecompartmentalizationoftheperitonealcavity,inconjunctionwiththegreater
omentum,influencesthelocalizationandspreadofperitonealinflammationand
infections.

Pathophysiology
Inperitonitiscausedbybacteria,thephysiologicresponseisdeterminedbyseveral
factors,includingthevirulenceofthecontaminant,thesizeoftheinoculum,the
immunestatusandoverallhealthofthehost(eg,asindicatedbytheAcute
PhysiologyandChronicHealthEvaluationII[APACHEII]score),andelementsof
thelocalenvironment,suchasnecrotictissue,blood,orbile. [2]
Intraabdominalsepsisfromaperforatedviscus(ie,secondaryperitonitisor
suppurativeperitonitis)resultsfromdirectspillageofluminalcontentsintothe
peritoneum(eg,perforatedpepticulcer,diverticulitis,appendicitis,iatrogenic
perforation).Withthespillageofthecontents,gramnegativeandanaerobic
bacteria,includingcommongutflora,suchasEscherichiacoliandKlebsiella
pneumoniae,entertheperitonealcavity.Endotoxinsproducedbygramnegative
bacterialeadtothereleaseofcytokinesthatinducecellularandhumoralcascades,
resultingincellulardamage,septicshock,andmultipleorgandysfunctionsyndrome
(MODS).
Themechanismforbacterialinoculationofasciteshasbeenthesubjectofmuch
debatesinceHaroldConnfirstrecognizeditinthe1960s.Entericorganismshave
traditionallybeenisolatedfrommorethan90%ofinfectedascitesfluidin
spontaneousbacterialperitonitis(SBP),suggestingthattheGItractisthesourceof
bacterialcontamination.Thepreponderanceofentericorganisms,incombination
withthepresenceofendotoxininasciticfluidandblood,oncefavoredtheargument
thatSBPwasduetodirecttransmuralmigrationofbacteriafromanintestinalor
holloworganlumen,aphenomenoncalledbacterialtranslocation.However,
experimentalevidencesuggeststhatdirecttransmuralmigrationofmicroorganisms
mightnotbethecauseofSBP.
Analternativeproposedmechanismforbacterialinoculationofascitessuggestsa
hematogenoussourceoftheinfectingorganismincombinationwithanimpaired
immunedefensesystem.Nonetheless,theexactmechanismofbacterial
displacementfromtheGItractintoascitesfluidremainsthesourceofmuch
debate.
Ahostoffactorscontributestotheformationofperitonealinflammationand
bacterialgrowthintheasciticfluid.Akeypredisposingfactormaybetheintestinal
bacterialovergrowthfoundinpeoplewithcirrhosis,mainlyattributedtodecreased
intestinaltransittime.Intestinalbacterialovergrowth,alongwithimpaired
phagocyticfunction,lowserumandascitescomplementlevels,anddecreased
activityofthereticuloendothelialsystem,contributestoanincreasednumberof
microorganismsanddecreasedcapacitytoclearthemfromthebloodstream,
resultingintheirmigrationintoandeventualproliferationwithinascitesfluid.
Interestingly,adultswithSBPtypicallyhaveascites,butmostchildrenwithSBPdo
nothaveascites.Thereasonforandmechanismbehindthisisthesourceof
ongoinginvestigation.

Fibrinolysis
Alterationsinfibrinolysis(throughincreasedplasminogenactivatorinhibitoractivity)
andtheproductionoffibrinexudateshaveanimportantroleinperitonitis.The
productionoffibrinexudatesisanimportantpartofthehostdefense,butlarge
numbersofbacteriamaybesequesteredwithinthefibrinmatrix.Thismayretard

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systemicdisseminationofintraperitonealinfectionandmaydecreaseearlymortality
ratesfromsepsis,butitalsoisintegraltothedevelopmentofresidualinfectionand
abscessformation.Asthefibrinmatrixmatures,thebacteriawithinareprotected
fromhostclearancemechanisms.
Whetherfibrinultimatelyresultsincontainmentorpersistentinfectionmaydepend
onthedegreeofperitonealbacterialcontamination.Inanimalstudiesofmixed
bacterialperitonitisthatexaminedtheeffectsofsystemicdefibrinogenationand
thoseofabdominalfibrintherapy,heavyperitonealcontaminationuniformlyledto
severeperitonitiswithearlydeath(<48h)becauseofoverwhelmingsepsis.

Bacterialload
Bacterialloadandthenatureofthepathogenalsoplayimportantroles.Some
studiessuggestthatthenumberofbacteriapresentattheonsetofabdominal
infectionsismuchhigherthanoriginallybelieved(approximately2108CFU/mL,
muchhigherthanthe5105CFU/mLinocularoutinelyusedforinvitro
susceptibilitytesting).Thisbacterialloadmayoverwhelmthelocalhostdefense.

Bacterialvirulence
Bacterialvirulencefactors[3]thatinterferewithphagocytosisandwithneutrophil
mediatedbacterialkillingmediatethepersistenceofinfectionsandabscess
formation.Amongthesevirulencefactorsarecapsuleformation,facultative
anaerobicgrowth,adhesioncapabilities,andsuccinicacidproduction.Synergy
betweencertainbacterialandfungalorganismsmayalsoplayanimportantrolein
impairingthehost'sdefense.OnesuchsynergymayexistbetweenBacteroides
fragilisandgramnegativebacteria,particularlyEcoli(seetheimagebelow),where
coinoculationsignificantlyincreasesbacterialproliferationandabscessformation.

GramnegativeEscherichiacoli.

Enterococci
Enterococcimaybeimportantinenhancingtheseverityandpersistenceof
peritonealinfections.InanimalmodelsofperitonitiswithEcoliandBfragilis,the
systemicmanifestationsoftheperitonealinfectionandbacteremiarateswere
increased,aswerebacterialconcentrationsintheperitonealfluidandrateof
abscessformation.Nevertheless,theroleofEnterococcusorganismsin
uncomplicatedintraabdominalinfectionsremainsunclear.Antibioticsthatlack
specificactivityagainstEnterococcusareoftenusedsuccessfullyinthetherapyof
peritonitis,andtheorganismisnotoftenrecoveredasabloodbornepathogenin
intraabdominalsepsis.

Fungi
Theroleoffungiintheformationofintraabdominalabscessesisnotfully
understood.Someauthorssuggestthatbacteriaandfungiexistasnonsynergistic
parallelinfectionswithincompletecompetition,allowingthesurvivalofall
organisms.Inthissetting,treatmentofthebacterialinfectionalonemayleadtoan
overgrowthoffungi,whichmaycontributetoincreasedmorbidity.

Abscessformation
Abscessformationoccurswhenthehostdefenseisunabletoeliminatethe
infectingagentandattemptstocontrolthespreadofthisagentby
compartmentalization.Thisprocessisaidedbyacombinationoffactorsthatshare
acommonfeature,ie,impairmentofphagocytotickilling.Mostanimalandhuman
studiessuggestthatabscessformationoccursonlyinthepresenceofabscess
potentiatingagents.Althoughthenatureandspectrumofthesefactorshavenot
beenstudiedexhaustively,certainfiberanalogues(eg,bran)andthecontentsof
autoclavedstoolhavebeenidentifiedasabscesspotentiatingagents.Inanimal
models,thesefactorsinhibitopsonizationandphagocytotickillingbyinterference
withcomplementactivation.

Cytokines
Theroleofcytokinesinthemediationofthebody'simmuneresponseandtheirrole
inthedevelopmentofthesystemicinflammatoryresponsesyndrome(SIRS)and
multipleorganfailure(MOF)havebeenamajorfocusofresearchoverthepast
decade.Comparativelyfewdataexistaboutthemagnitudeofthe
intraperitoneal/abscesscytokineresponseandimplicationsforthehost.Existing
datasuggestthatbacterialperitonitisisassociatedwithanimmenseintraperitoneal
compartmentalizedcytokineresponse.Higherlevelsofcertaincytokines(ie,tumor
necrosisfactoralpha[TNFalpha],interleukin[IL]6)havebeenassociatedwith
worseoutcomes,aswellassecondary(uncontrolled)activationofthesystemic
inflammatorycascade.

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Etiology
Theetiologyofdiseasedependsonthetype,aswellaslocation,ofperitonitis,as
follows:
Primaryperitonitis
Secondaryperitonitis
Tertiaryperitonitis
Chemicalperitonitis
Peritonealabscess
Primaryperitonitis
Spontaneousbacterialperitonitis(SBP)isanacutebacterialinfectionofascitic
fluid.Contaminationoftheperitonealcavityisthoughttoresultfromtranslocation
ofbacteriaacrossthegutwallormesentericlymphaticsand,lessfrequently,via
hematogenousseedinginthepresenceofbacteremia.
SBPcanoccurasacomplicationofanydiseasestatethatproducestheclinical
syndromeofascites,suchasheartfailureandBuddChiarisyndrome.Childrenwith
nephrosisorsystemiclupuserythematosuswhohaveasciteshaveahighriskof
developingSBP.ThehighestriskofSBP,howeverisinpatientswithcirrhosiswho
areinadecompensatedstate. [4]Inparticular,decreasedhepaticsyntheticfunction
withassociatedlowtotalproteinlevel,lowcomplementlevels,orprolonged
prothrombintime(PT)isassociatedwithmaximumrisk.Patientswithlowprotein
levelsinasciticfluid(<1g/dL)havea10foldhigherriskofdevelopingSBPthan
thosewithaproteinlevelgreaterthan1g/dL.Approximately1030%ofpatients
withcirrhosisandascitesdevelopSBP. [5]Theincidencerisestomorethan40%
withasciticfluidproteincontentsoflessthan1g/dL(whichoccurs15%ofpatients),
presumablybecauseofdecreasedasciticfluidopsonicactivity.
Morethan90%ofcasesofSBParecausedbyamonomicrobialinfection.The
mostcommonpathogensincludegramnegativeorganisms(eg,Ecoli[40%],K
pneumoniae[7%],Pseudomonasspecies,Proteusspecies,othergramnegative
species[20%])andgrampositiveorganisms(eg,Streptococcuspneumoniae[15%],
otherStreptococcusspecies[15%],andStaphylococcusspecies[3%])(seeTable
1).However,somedatasuggestthatthepercentageofgrampositiveinfections
maybeincreasing. [6,7]Onestudycitesa34.2%incidenceofstreptococci,ranking
insecondpositionafterEnterobacteriaceae. [7]Viridansgroupstreptococci(VBS)
accountedfor73.8%ofthesestreptococcalisolates.Asingleorganismisnotedin
92%ofcases,and8%ofcasesarepolymicrobial.
Anaerobicmicroorganismsarefoundinlessthan5%ofcases,andmultipleisolates
arefoundinlessthan10%.

Secondaryperitonitis
Commonetiologicentitiesofsecondaryperitonitis(SP)includeperforated
appendicitisperforatedgastricorduodenalulcerperforated(sigmoid)coloncaused
bydiverticulitis,volvulus,orcancerandstrangulationofthesmallbowel(seeTable
1).Necrotizingpancreatitiscanalsobeassociatedwithperitonitisinthecaseof
infectionofthenecrotictissue.
ThepathogensinvolvedinSPdifferintheproximalanddistalGItract.Gram
positiveorganismspredominateintheupperGItract,withashifttowardgram
negativeorganismsintheupperGItractinpatientsonlongtermgastricacid
suppressivetherapy.Contaminationfromadistalsmallbowelorcolonsource
initiallymayresultinthereleaseofseveralhundredbacterialspecies(andfungi)
hostdefensesquicklyeliminatemostoftheseorganisms.Theresultingperitonitisis
almostalwayspolymicrobial,containingamixtureofaerobicandanaerobicbacteria
withapredominanceofgramnegativeorganisms(seeTable1).
Asmanyas15%ofpatientswhohavecirrhosiswithasciteswhowereinitially
presumedtohaveSBPhaveSP.Inmanyofthesepatients,clinicalsignsand
symptomsalonearenotsensitiveorspecificenoughtoreliablydifferentiate
betweenthe2entities.Athoroughhistory,evaluationoftheperitonealfluid,and
additionaldiagnostictestsareneededtodosoahighindexofsuspicionis
required.
Table1.CommonCausesofSecondaryPeritonitis(OpenTableinanewwindow)
SourceRegions

Causes
Boerhaavesyndrome

Malignancy

Esophagus

Trauma(mostlypenetrating)

Iatrogenic*

Pepticulcerperforation

Malignancy(eg,adenocarcinoma,lymphoma,gastrointestinal
stromaltumor)

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Stomach
Trauma(mostlypenetrating)

Iatrogenic*

Pepticulcerperforation

Trauma(bluntandpenetrating)
Duodenum
Iatrogenic*

Cholecystitis

Stoneperforationfromgallbladder(ie,gallstoneileus)or
commonduct

Malignancy
Biliarytract
Choledochalcyst(rare)

Trauma(mostlypenetrating)

Iatrogenic*

Pancreatitis(eg,alcohol,drugs,gallstones)

Trauma(bluntandpenetrating)
Pancreas
Iatrogenic*

Ischemicbowel

Incarceratedhernia(internalandexternal)

Closedloopobstruction

Crohndisease
Smallbowel
Malignancy(rare)

Meckeldiverticulum

Trauma(mostlypenetrating)

Ischemicbowel

Diverticulitis

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Malignancy

UlcerativecolitisandCrohndisease
Largeboweland
appendix

Appendicitis

Colonicvolvulus

Trauma(mostlypenetrating)

Iatrogenic

Pelvicinflammatorydisease(eg,salpingooophoritis,tubo
ovarianabscess,ovariancyst)

Malignancy(rare)

Uterus,salpinx,
andovaries

Trauma(uncommon)

*IatrogenictraumatotheupperGItract,includingthepancreasandbiliarytract
andcolon,oftenresultsfromendoscopicproceduresanastomoticdehiscenceand
inadvertentbowelinjury(eg,mechanical,thermal)arecommoncausesofleakin
thepostoperativeperiod.
CommonorganismsculturedinsecondaryperitonitisarepresentedinTable2,
below. [8]
Table2.MicrobialFloraofSecondaryPeritonitis(OpenTableinanewwindow)
Type

Organism

Percentage

Aerobic

Gramnegative Escherichiacoli

60%

Enterobacter/Klebsiella 26%

Proteus

22%

Pseudomonas

8%

Grampositive Streptococci

28%

Enterococci

17%

Staphylococci

7%

Anaerobic

Bacteroides

72%

Eubacteria

24%

Clostridia

17%

Peptostreptococci

14%

Peptococci

11%

Fungi

Candida

2%

Otherrare,nonsurgicalcausesofintraabdominalsepsisincludethefollowing:
Chlamydiaperitonitis
Tuberculosisperitonitis
Acquiredimmunodeficiencysyndrome(AIDS)associatedperitonitis
Themostcommoncauseofpostoperativeperitonitisisanastomoticleak,with
symptomsgenerallyappearingaroundpostoperativedays57.Afterelective
abdominaloperationsfornoninfectiousetiologies,theincidenceofSP(causedby
anastomoticdisruption,breakdownofenterotomyclosures,orinadvertentbowel
injury)shouldbelessthan2%.Operationsforinflammatorydisease(ie,
appendicitis,diverticulitis,cholecystitis)withoutperforationcarryariskoflessthan
10%forthedevelopmentofSPandperitonealabscess.Thisriskmayriseto
greaterthan50%ingangrenousboweldiseaseandvisceralperforation.
Afteroperationsforpenetratingabdominaltrauma,SPandabscessformationare
observedinasmallnumberofpatients.Duodenalandpancreaticinvolvement,as
wellascolonperforation,grossperitonealcontamination,perioperativeshock,and
massivetransfusion,arefactorsthatincreasetheriskofinfectioninthesecases.
Peritonitisisalsoafrequentcomplicationandsignificantlimitationofperitoneal

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dialysis. [3]Peritonitisleadstoincreasedhospitalizationandmortalityrates.

Tertiaryperitonitis
Tertiaryperitonitis(seeTable3,below)developsmorefrequentlyin
immunocompromisedpatientsandinpersonswithsignificantpreexistingcomorbid
conditions.Althoughrarelyobservedinuncomplicatedperitonealinfections,the
incidenceoftertiaryperitonitisinpatientsrequiringICUadmissionforsevere
abdominalinfectionsmaybeashighas5074%.
Tuberculousperitonitis(TP)israreintheUnitedStates(<2%ofallcausesof
peritonitis),butitcontinuestobeasignificantproblemindevelopingcountriesand
amongpatientswithhumanimmunodeficiencyvirus(HIV)infection.Thepresenting
symptomsareoftennonspecificandinsidiousinonset(eg,lowgradefever,
anorexia,weightloss).ManypatientswithTPhaveunderlyingcirrhosis.Morethan
95%ofpatientswithTPhaveevidenceofascitesonimagingstudies,andmore
thanhalfofthesepatientshaveclinicallyapparentascites.
Inmostcases,chestradiographicfindingsinpatientswithTPperitonitisare
abnormalactivepulmonarydiseaseisuncommon(<30%).ResultsonGramstain
ofasciticfluidarerarelypositive,andcultureresultsmaybefalselynegativeinup
to80%ofpatients.Aperitonealfluidproteinlevelgreaterthan2.5g/dL,alactate
dehydrogenase(LDH)levelgreaterthan90U/mL,orapredominantlymononuclear
cellcountofgreaterthan500cells/LshouldraisesuspicionofTPbuthavelimited
specificityforthediagnosis.Laparoscopyandvisualizationofgranulomason
peritonealbiopsyspecimens,aswellascultures(requires46wk),maybeneeded
forthedefinitivediagnosishowever,empirictherapyshouldbeginimmediately.
Table3.MicrobiologyofPrimary,Secondary,andTertiaryPeritonitis(OpenTablein
anewwindow)
Peritonitis

AntibioticTherapy
EtiologicOrganisms

(Type)

(Suggested)
Class

TypeofOrganism
Ecoli(40%)

Kpneumoniae(7%)

Pseudomonas
species(5%)

Proteusspecies(5%)
Primary

Gram
negative

Thirdgenerationcephalosporin
Streptococcus
species(15%)

Staphylococcus
species(3%)

Anaerobicspecies(<
5%)

Ecoli

Enterobacterspecies
Gram
negative

Klebsiellaspecies

Proteusspecies

Streptococcus
species
Gram
positive

Secondgenerationcephalosporin

Thirdgenerationcephalosporin

Penicillinswithanaerobicactivity
Enterococcus

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species

Secondary

Quinoloneswithanaerobicactivity
Bacteroidesfragilis
Quinoloneandmetronidazole
OtherBacteroides
species

Aminoglycosideandmetronidazole

Eubacteriumspecies
Anaerobic
Clostridiumspecies

Anaerobic
Streptococcus
species

Secondgenerationcephalosporin

Thirdgenerationcephalosporin

Enterobacterspecies Penicillinswithanaerobicactivity

Pseudomonas
species
Gram
negative

Quinoloneswithanaerobicactivity

Quinoloneandmetronidazole
Enterococcus
species

Tertiary

Aminoglycosideandmetronidazole

Carbapenems

Triazolesoramphotericin
(consideredinfungaletiology)
Gram
positive

Staphylococcus
species

Fungal

Candidaspecies

(Altertherapybasedonculture
results.)

Chemicalperitonitis
Chemical(sterile)peritonitismaybecausedbyirritantssuchasbile,blood,barium,
orothersubstancesorbytransmuralinflammationofvisceralorgans(eg,Crohn
disease)withoutbacterialinoculationoftheperitonealcavity.Clinicalsignsand
symptomsareindistinguishablefromthoseofSPorperitonealabscess,andthe
diagnosticandtherapeuticapproachshouldbethesame. [9]
Peritonealabscess
Peritonealabscessdescribestheformationofaninfectedfluidcollection
encapsulatedbyfibrinousexudate,omentum,and/oradjacentvisceralorgans.The
overwhelmingmajorityofabscessesoccursubsequenttoSP.Abscessformation
maybeacomplicationofsurgery.Theincidenceofabscessformationafter
abdominalsurgeryislessthan12%,evenwhentheoperationisperformedforan
acuteinflammatoryprocess.Theriskofabscessincreasesto1030%incasesof
preoperativeperforationofthehollowviscus,significantfecalcontaminationofthe
peritonealcavity,bowelischemia,delayeddiagnosisandtherapyoftheinitial
peritonitis,andtheneedforreoperation,aswellasinthesettingof
immunosuppression.Abscessformationistheleadingcauseofpersistentinfection
anddevelopmentoftertiaryperitonitis.

Epidemiology
Theoverallincidenceofperitonealinfectionandabscessisdifficulttoestablishand
varieswiththeunderlyingabdominaldiseaseprocesses.SBPoccursinboth
childrenandadultsandisawellknownandominouscomplicationofcirrhosis. [5]Of
patientswithcirrhosiswhohaveSBP,70%areChildPughclassC.Inthese

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patientswithcirrhosiswhohaveSBP,70%areChildPughclassC.Inthese
patients,thedevelopmentofSBPisassociatedwithapoorlongtermprognosis.
Oncethoughttooccuronlyinthoseindividualswithalcoholiccirrhosis,SBPisnow
knowntoaffectpatientswithcirrhosisfromanycause.Inpatientswithascites,the
prevalencemaybeashighas18%.Thisnumberhasgrownfrom8%overthepast
2decades,mostlikelysecondarytoanincreasedawarenessofSBPand
heightenedthresholdtoperformdiagnosticparacentesis.
Althoughtheetiologyandincidenceofhepaticfailuredifferbetweenchildrenand
adults,inthoseindividualswithascites,theincidenceofSBPisroughlyequal.Two
peakagesforSBParecharacteristicinchildren:oneintheneonatalperiodandthe
otheratage5years.

Prognosis
Overthepastdecade,thecombinationofbetterantibiotictherapy,moreaggressive
intensivecare,andearlierdiagnosisandtherapywithacombinationofoperative
andpercutaneoustechniqueshaveledtoasignificantreductioninmorbidityand
mortalityrelatedtointraabdominalsepsis.
Spontaneousbacterialperitonitis
ThemortalityrateinSBPmaybeaslowas5%inpatientswhoreceiveprompt
diagnosisandtreatment.However,inhospitalizedpatients,1yearmortalityrates
mayrangefrom5070%. [10]Thisisusuallysecondarytothedevelopmentof
complications,suchasgastrointestinalbleeding,renaldysfunction,andworsening
liverfailure. [11]Patientswithconcurrentrenalinsufficiencyhavebeenshowntobe
atahigherriskofmortalityfromSBPthanthosewithoutconcurrentrenal
insufficiency.
MortalityfromSBPmaybedecreasingamongallsubgroupsofpatientsbecauseof
advancesinitsdiagnosisandtreatment.Theoverallmortalityrateinpatientswith
SBPmayexceed30%ifthediagnosisandtreatmentaredelayed,butthemortality
rateislessthan10%infairlywellcompensatedpatientswithearlytherapy.As
manyas70%ofpatientswhosurviveanepisodeofSBPhavearecurrentepisode
within1year,andinthesepatients,themortalityrateapproaches50%.Some
studiessuggestthattherecurrencerateofSBPmaybedecreasedtolessthan
20%withlongtermantibioticprophylaxis(eg,quinolones,trimethoprim
sulfamethoxazole)however,whetherthisimproveslongtermsurvivalwithoutliver
transplantationisunclear.

Secondaryperitonitisandperitonealabscess
UncomplicatedSPandsimpleabscessescarryamortalityrateoflessthan5%,but
thisratemayincreasetogreaterthan3050%insevereinfections.Theoverall
mortalityraterelatedtointraabdominalabscessformationislessthan1020%.
Factorsthatindependentlypredictworseoutcomesincludeadvancedage,
malnutrition,presenceofcancer,ahighAPACHEIIscoreonpresentation,
preoperativeorgandysfunction,thepresenceofcomplexabscesses,andfailureto
improveinlessthan2472hoursafteradequatetherapy.
Insevereintraabdominalinfectionsandperitonitis,themortalityratemayincrease
togreaterthan3050%.Theconcurrentdevelopmentofsepsis,SIRS,andMOF
canincreasethemortalityratetogreaterthan70%,and,inthesepatients,more
than80%ofdeathsoccurwithanactiveinfectionpresent.
SorianoetalfoundthatcirrhoticpatientswithSPwhounderwentsurgicaltreatment
tendedtohavealowermortalityratethandidthosewhoreceivedmedicaltherapy
only(53.8%vs81.8%,respectively). [12]Amongthesurgicallytreatedpatientswith
SP,thesurvivalratewasgreaterinthosewiththeshortesttimebetweendiagnostic
paracentesisandsurgery.Theseresearchersconcludedthattheprognosisof
cirrhoticpatientswithSPcouldbeimprovedviaalowthresholdofsuspiciononthe
basisofRunyon'scriteriaandmicrobiologicdata,promptuseofabdominalCT
scanning,andearlysurgicalevaluation.

Tertiaryperitonitis
Incomparisonwithpatientswithotherformsofperitonitis,patientswhodevelop
tertiaryperitonitishavesignificantlylongerICUandhospitalstays,higherorgan
dysfunctionscores,andhighermortalityrates(5070%).

Otherfactorsaffectingprognosis
Severalscoringsystems(eg,APACHEII,SIRS,multipleorgandysfunction
syndrome[MODS],Mannheimperitonitisindex)havebeendevelopedtoassessthe
clinicalprognosisofpatientswithperitonitis.Mostofthesescoresrelyoncertain
hostcriteria,systemicsignsofsepsis,andcomplicationsrelatedtoorganfailure.
Althoughvaluableforcomparingpatientcohortsandinstitutions,thesescoreshave
limitedvalueinthespecificdaytodayclinicaldecisionmakingprocessforany
givenpatient.Ingeneral,themortalityrateislessthan5%withanAPACHEIIof
lessthan15andrisestogreaterthan40%withscoresabove15.RisingAPACHEII
scoresondays3and7areassociatedwithanincreaseofmortalityratestogreater
than90%,whereasfallingscorespredictmortalityratesoflessthan20%.
Themortalityratewithoutorganfailuregenerallyislessthan5%butmayriseto
greaterthan90%withquadrupleorganfailure.Adelayofmorethan24daysin
institutingeithermedicaltherapyorsurgicaltherapyhasbeenclearlyassociated
withincreasedcomplicationrates,thedevelopmentoftertiaryperitonitis,theneed
forreoperation,multipleorgansystemdysfunction,anddeath.
Outcomesareworseinpatientsrequiringemergentreoperationsforpersistentor
recurrentinfections(3050%increaseinthemortalityrate)however,patients
undergoingearlyplannedsecondlookoperationsdonotdemonstratethistrend.

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Persistentinfection,recoveryofenterococci,andmultidrugresistantgramnegative
organisms,aswellasfungalinfection,arerelatedtoworseoutcomesandrecurrent
complications.
Patientsolderthan65yearshaveathreefoldincreasedriskofdeveloping
generalizedperitonitisandsepsisfromgangrenousorperforatedappendicitisand
perforateddiverticulitisthanyoungerpatientsandare3timesmorelikelytodie
fromthesediseaseprocesses.Olderpatientswithperforateddiverticulitisare3
timesmorelikelythanyoungerpatientstohavegeneralizedratherthanlocalized
(ie,pericolic,pelvic)peritonitis.Thesefindingsareconsistentwiththehypothesis
thatthebiologicfeaturesofperitonitisdifferinelderlypersons,whoaremorelikely
topresentwithanadvancedormoresevereprocessthanyoungerpatientswith
peritonitis.
Overall,studiessuggestthathostrelatedfactorsaremoresignificantthanthetype
andsourceofinfectionwithregardtotheprognosisinintraabdominalinfections. [13]

PatientEducation
Forpatienteducationresources,DigestiveDisordersCenteraswellasAbdominal
PaininAdults,Appendicitis,DiverticulosisandDiverticulitis,Cirrhosis,andSepsis
(BloodInfection).
ClinicalPresentation

ContributorInformationandDisclosures
Author
BrianJDaley,MD,MBA,FACS,FCCP,CNSCProfessorandProgramDirector,DepartmentofSurgery,Chief,
DivisionofTraumaandCriticalCare,UniversityofTennesseeHealthScienceCenterCollegeofMedicine
BrianJDaley,MD,MBA,FACS,FCCP,CNSCisamemberofthefollowingmedicalsocieties:American
AssociationfortheSurgeryofTrauma,EasternAssociationfortheSurgeryofTrauma,SouthernSurgical
Association,AmericanCollegeofChestPhysicians,AmericanCollegeofSurgeons,AmericanMedical
Association,AssociationforAcademicSurgery,AssociationforSurgicalEducation,ShockSociety,Societyof
CriticalCareMedicine,SoutheasternSurgicalCongress,TennesseeMedicalAssociation
Disclosure:Nothingtodisclose.
SpecialtyEditorBoard
BSAnand,MDProfessor,DepartmentofInternalMedicine,DivisionofGastroenterology,BaylorCollegeof
Medicine
BSAnand,MDisamemberofthefollowingmedicalsocieties:AmericanAssociationfortheStudyofLiver
Diseases,AmericanCollegeofGastroenterology,AmericanGastroenterologicalAssociation,AmericanSociety
forGastrointestinalEndoscopy
Disclosure:Nothingtodisclose.
ChiefEditor
JulianKatz,MDClinicalProfessorofMedicine,DrexelUniversityCollegeofMedicine
JulianKatz,MDisamemberofthefollowingmedicalsocieties:AmericanCollegeofGastroenterology,
AmericanCollegeofPhysicians,AmericanGastroenterologicalAssociation,AmericanGeriatricsSociety,
AmericanMedicalAssociation,AmericanSocietyforGastrointestinalEndoscopy,AmericanSocietyofLaw,
Medicine&Ethics,AmericanTraumaSociety,AssociationofAmericanMedicalColleges,PhysiciansforSocial
Responsibility
Disclosure:Nothingtodisclose.
Acknowledgements
BSAnand,MDProfessor,DepartmentofInternalMedicine,DivisionofGastroenterology,BaylorCollegeof
Medicine
BSAnand,MDisamemberofthefollowingmedicalsocieties:AmericanAssociationfortheStudyofLiver
Diseases,AmericanCollegeofGastroenterology,AmericanGastroenterologicalAssociation,andAmerican
SocietyforGastrointestinalEndoscopy
Disclosure:Nothingtodisclose.
AlexJacocks,MDProgramDirector,Professor,DepartmentofSurgery,UniversityofOklahomaSchoolof
Medicine
Disclosure:Nothingtodisclose.
ChandlerLong,MDResidentPhysician,DepartmentofSurgery,UniversityofTennesseeMedicalCenter
Knoxville
Disclosure:Nothingtodisclose.
KetulRPatel,MDResident,DepartmentofInternalMedicine,ProvidenceHospital
KetulRPatel,MDisamemberofthefollowingmedicalsocieties:AmericanCollegeofGastroenterology,
AmericanCollegeofPhysicians,andAmericanMedicalAssociation
Disclosure:Nothingtodisclose.
MichaelHPiper,MD,FACG,FACPClinicalAssistantProfessor,DepartmentofInternalMedicine,Divisionof
Gastroenterology,WayneStateUniversitySchoolofMedicineConsultingStaff,DigestiveHealthAssociates
PLC
MichaelHPiper,MD,FACG,FACPisamemberofthefollowingmedicalsocieties:AlphaOmegaAlpha,
AmericanCollegeofGastroenterology,AmericanCollegeofPhysicians,andMichiganStateMedicalSociety
Disclosure:Nothingtodisclose.
KennethLReed,DOFellowinGastroenterology,ProvidenceHospital,Michigan

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PeritonitisandAbdominalSepsis:Background,Anatomy,Pathophysiology

KennethLReed,DOisamemberofthefollowingmedicalsocieties:AmericanCollegeofGastroenterology,
AmericanCollegeofOsteopathicInternists,AmericanGastroenterologicalAssociation,AmericanOsteopathic
Association,AmericanSocietyforGastrointestinalEndoscopy,andCrohnsandColitisFoundationofAmerica
Disclosure:Nothingtodisclose.
FranciscoTalavera,PharmD,PhDAdjunctAssistantProfessor,UniversityofNebraskaMedicalCenterCollege
ofPharmacyEditorinChief,MedscapeDrugReference
Disclosure:MedscapeSalaryEmployment
BradleyJWarren,DO,FACG,FACOIConsultingStaff,DigestiveHealthAssociates,PLC
BradleyJWarren,DO,FACG,FACOIisamemberofthefollowingmedicalsocieties:AmericanCollegeof
Gastroenterology,AmericanOsteopathicAssociation,andAmericanSocietyforGastrointestinalEndoscopy
Disclosure:Nothingtodisclose.

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