Sepsis and the systemic inflammatory response syndrome Definitions epidemiology and prognosis.docx
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SepsisandthesystemicinflammatoryresponsesyndromeDefinitionsepidemiologyandprognosis
Sepsisandthesystemicinflammatoryresponsesyndrome:
Definitions,epidemiology,andprognosis
INTRODUCTION — Sepsisisaclinicalsyndromethatcomplicatessevereinfection.Itischaracterizedbythecardinalsignsofinflammation(vasodilation,leukocyteaccumulation,increasedmicrovascularpermeability)occurringintissuesthatareremotefromtheinfection.Systemicinflammatoryresponsesyndrome(SIRS)isanidenticalclinicalsyndromethatcomplicatesanoninfectiousinsult(eg,acutepancreatitis,pulmonarycontusion).CurrenttheoriesabouttheonsetandprogressionofsepsisandSIRSfocusondysregulationoftheinflammatoryresponse,includingthepossibilitythatamassiveanduncontrolledreleaseofproinflammatorymediatorsinitiatesachainofeventsthatleadtowidespreadtissueinjury.Thisresponsecanleadtomultipleorgandysfunctionsyndrome(MODS),whichisthecauseofthehighmortalityassociatedwiththesesyndromes.
Thedefinitions,epidemiology,riskfactors,andoutcomesofsepsisandSIRSarereviewedhere.Thepathophysiologyandtreatmentofsepsisarediscussedseparately.(See"Pathophysiologyofsepsis"and"Evaluationandmanagementofseveresepsisandsepticshockinadults".)
DEFINITIONS — Systemicinflammatoryresponsesyndrome(SIRS),sepsis,severesepsis,andsepticshockwereinitiallydefinedin1991byaconsensuspanelconvenedbytheAmericanCollegeofChestPhysicians(ACCP)andSocietyofCriticalCareMedicine(SCCM)[1].Thesedefinitionswerereconsideredin2001duringanInternationalSepsisDefinitionsConferencethatincludedrepresentativesfromtheACCP,SCCM,AmericanThoracicSociety(ATS),EuropeanSocietyofIntensiveCareMedicine(ESICM),andSurgicalInfectionSociety(SIS),andagainin2012bytheSCCMandESICM[2,3].Apracticalmodificationofthedefinitionshasbeenpublished,whichprovidesexacthemodynamicdefinitionsforsepsisandsepticshock[4].
SIRSisaclinicalsyndromethatisaformofdysregulatedinflammation.ThetermSIRShasroutinelybeenassociatedwithbothinfectiousprocesses(sepsis)andnoninfectiousinsults,suchasanautoimmunedisorder,pancreatitis,vasculitis,thromboembolism,burns,orsurgery.SIRSwaspreviouslydefinedastwoormoreabnormalitiesintemperature,heartrate,respiration,orwhitebloodcellcount[2].However,inpractice,itsclinicaldefinitionandpathophysiologyarenonequivocalsuchthatSIRSandearlysepsiscannotbereadilydistinguished.Thus,whenSIRSissuspecteditshouldpromptanevaluationforasepticfocus.
Thedefinitionsthatweprovidebelowarebasedupontheseresourcesandrepresentacontinuumofearlyinfectionthroughmultipleorgandysfunctionsyndrome(MODS).
Infection — Infectionistheinvasionofnormallysteriletissuebyorganisms.
Bacteremia — Bacteremiaisthepresenceofviablebacteriaintheblood.
Sepsis — Sepsisistheclinicalsyndromethatresultsfromadysregulatedinflammatoryresponsetoaninfection.Sepsisisdefinedasthepresence(probableordocumented)ofinfectiontogetherwithsystemicmanifestationsofinfection.Diagnosticcriteriaforsepsisincludeinfection(documentedorsuspected)andsomeofthefollowing[2,3]:
▪Generalvariables
∙Temperature>38.3or<36ºC
∙Heartrate>90beats/minormorethantwostandarddeviationsabovethenormalvalueforage
∙Tachypnea,respiratoryrate>20breaths/min
∙Alteredmentalstatus
∙Significantedemaorpositivefluidbalance(>20mL/kgover24hours)
∙Hyperglycemia(plasmaglucose>140mg/dLor7.7mmol/L)intheabsenceofdiabetes
▪Inflammatoryvariables
∙Leukocytosis(WBCcount>12,000microL–1)orleukopenia(WBCcount<4000microL–1)
∙NormalWBCcountwithgreaterthan10percentimmatureforms
∙PlasmaC-reactiveproteinmorethantwostandarddeviationsabovethenormalvalue
∙Plasmaprocalcitoninmorethantwostandarddeviationsabovethenormalvalue
▪Hemodynamicvariables
∙Arterialhypotension(systolicbloodpressureSBP<90mmHg,MAP<70mmHg,oranSBPdecrease>40mmHginadultsorlessthantwostandarddeviationsbelownormalforage)
▪Organdysfunctionvariables
∙Arterialhypoxemia(arterialoxygentension[PaO2]/fractionofinspiredoxygen[FiO2]<300)
∙Acuteoliguria(urineoutput<0.5mL/kg/hrforatleasttwohoursdespiteadequatefluidresuscitation)
∙Creatinineincrease>0.5mg/dLor44.2micromol/L
∙Coagulationabnormalities(internationalnormalizedratio[INR]>1.5oractivatedpartialthromboplastintime[aPTT]>60seconds)
∙Ileus(absentbowelsounds)
∙Thrombocytopenia(plateletcount<100,000microL–1)
∙Hyperbilirubinemia(plasmatotalbilirubin>4mg/dLor70micromol/L)
▪Tissueperfusionvariables
∙Hyperlactatemia(>1mmol/L)
∙Decreasedcapillaryrefillormottling
Severesepsis — Severesepsisreferstosepsis-inducedtissuehypoperfusionororgandysfunctionwithanyofthefollowingthoughttobeduetotheinfection[2,3]:
▪Sepsis-inducedhypotension
▪Lactateaboveupperlimitsoflaboratorynormal
▪Urineoutput<0.5mL/kg/hrformorethantwohoursdespiteadequatefluidresuscitation
▪AcutelunginjurywithPaO2/FIO2<250intheabsenceofpneumoniaasinfectionsource
▪AcutelunginjurywithPaO2/FIO2<200inthepresenceofpneumoniaasinfectionsource
▪Creatinine>2mg/dL(176.8micromol/L)
▪Bilirubin>2mg/dL(34.2micromol/L)
▪Plateletcount<100,000microL–1
▪Coagulopathy(INR>1.5)
Sepsis-inducedhypotensionisdefinedasasystolicbloodpressure(SBP)<90mmHgormeanarterialpressure(MAP)<70mmHgoraSBPdecrease>40mmHgorlessthantwostandarddeviationsbelownormalforageintheabsenceofothercausesofhypotension.
Sepsis-inducedtissuehypoperfusionisdefinedasinfection-inducedhypotension,elevatedlactate,oroliguria.
Septicshock — Septicshockisdefinedassepsis-inducedhypotensionpersistingdespiteadequatefluidresuscitation,whichmaybedefinedasinfusionof30mL/kgofcrystalloids(aportionofthismaybealbuminequivalent).Septicshockisatypeofvasodilatoryordistributiveshock[2,3].Inotherwords,itresultsfromamarkedreductioninsystemicvascularresistance,oftenassociatedwithanincreaseincardiacoutput.(See"Shockinadults:
Types,presentation,anddiagnosticapproach".)
Multipleorgandysfunctionsyndrome — Multipleorgandysfunctionsyndrome(MODS)referstoprogressiveorgandysfunctioninanacutelyillpatient,suchthathomeostasiscannotbemaintainedwithoutintervention.ItisatthesevereendoftheseverityofillnessspectrumofbothSIRSandsepsis.MODScanbeclassifiedasprimaryorsecondary:
▪PrimaryMODSistheresultofawell-definedinsultinwhichorgandysfunctionoccursearlyandcanbedirectlyattributabletotheinsultitself(eg,renalfailureduetorhabdomyolysis)
▪SecondaryMODSisorganfailurethatisnotindirectresponsetotheinsultitself,butisaconsequenceofthehost’sresponse(eg,acuterespiratorydistresssyndromeinpatientswithpancreatitis)
TherearenouniversallyacceptedcriteriaforindividualorgandysfunctioninMODS.However,progressiveabnormalitiesofthefollowingorgan-specificparametersarecommonlyusedtodiagnoseMODSandscoringsystemsareusedtopredictICUmortality[5]:
▪PaO2/FiO2ratio
▪Plateletcount
▪Serumbilirubin
▪Serumcreatinine(orurineoutput)
▪Glasgowcomascore
▪Hypotension
RISKFACTORS — Thepopulationatriskofdevelopingsepsisislarge.Atanygivenmoment,approximately50percentofICUpatientshaveanosocomialinfectionand,therefore,areathighriskforsepsis[6].Otherriskfactorsincludethefollowing[7-11]:
▪Bacteremia–Patientswithbacteremiaoftendevelopsystemicconsequencesofinfection.Inastudyof270bloodcultures,95percentofpositivebloodcultureswereassociatedwithsepsis,severesepsis,orsepticshock[12].
▪Advancedage(≥65years)–Theincidenceofsepsisisdisproportionatelyincreasedinolderadultpatientsandageisanindependentpredictorofmortalityduetosepsis.Moreover,olderadultnon-survivorstendtodieearlierduringhospitalizationandolderadultsurvivorsmorefrequentlyrequireskillednursingorrehabilitationafterhospitalization[13].
▪Immunosuppression–Comorbiditiesthatdepresshost-defense(eg,neoplasms,renalfailure,hepaticfailure,AIDS)andimmunosuppressantmedicationsarecommonamongpatientswithsepsis,severesepsis,orsepticshock.
▪Diabetesandcancer–Diabetesandsomecancersmayaltertheimmunesystem,resultinanelevatedriskfordevelopingsepsis,andincreasetheriskofnosocomialsepsis.
▪Communityacquiredpneumonia–Severesepsisandsepticshockdevelopinapproximately48and5percent,respectively,ofpatientswithcommunity-acquiredpneumonia[14].
▪Geneticfactors–Bothexperimentalandclinicalstudieshaveconfirmedthatgeneticfactorscanincreasetheriskofinfection.Infewcases,monogenicdefectsunderlievulnerabilitytospecificinfection,butgeneticfactorsaretypicallygeneticpolymorphisms.Geneticstudiesofsusceptibilitytoinfectionhaveinitiallyfocusedondefectsofantibodyproduction,oralackofTcells,phagocytes,naturalkillercells,orcomplement.Recently,geneticdefectshavebeenidentifiedthatimpairrecognitionofpathogensbytheinnateimmunesystem,increasingsusceptibilitytospecificclassesofmicroorganisms[15].
EPIDEMIOLOGY
Incidence — Inthelate1970s,itwasestimatedthat164,000casesofsepsisoccurredintheUnitedStateseachyear[16-18].Thishasdramaticallyincreased,withmorerecentestimatesindicatingthatmorethan1,665,000casesofsepsisarediagnosedintheUnitedStatesannually(figure1)[
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