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Chorioamnionitis Clinical Presentation Author: Michael P Sherman, MD, FAAP; Chief Editor: Ted Rosenkrantz, MD more... Updated: Apr 2, 2014 History The timehonored clinical signs and symptoms of chorioamnionitis include the following: Fever (an intrapartum temperature >100.4ºF or >37.8ºC) Significant maternal tachycardia (>120 beats per minute [bpm]) Fetal tachycardia (>160180 bpm) Purulent or foulsmelling amniotic fluid or vaginal discharge Uterine tenderness Maternal leukocytosis (total blood leukocyte count >15,00018,000 cells/μL) Of these criteria, intrapartum maternal fever appears to be the most frequent. [1] When at least 2 of the aforementioned criteria are present, the risk of neonatal sepsis is increased. Each clinical sign and symptom of chorioamnionitis, however, is by itself of low predictive value. The signs and symptoms of maternal chorioamnionitis or amniotic fluid infection are so subjective that some experts have recommended the following: If a physician is trying to decide about an evaluation and treatment of an infant, ask the obstetrician if he or she believes chorioamnionitis is present. Moreover, silent chorioamnionitis is prominent, [2] and thus signs and symptoms in the infected newborn infant take on added significance. An increasing or decreasing total leukocyte count may be more important than a single determination. Abnormalities in either umbilical vein interleukin (IL)6 levels or an increasing neonatal immaturetototal neutrophil ratio, along with clinical criteria associated with chorioamnionitis, improve the sensitivity and predictive accuracy of identifying the septic neonate. Risk of neonatal infection increases as the duration of ruptured membranes lengthens. [82] Chorioamnionitis may initiate uteroplacental bleeding or a placental abruption. [83] Intrauterine infection is increased in placenta previa and manifests with vaginal bleeding. [84] Labor and delivery may be rapid in the presence of chorioamnionitis. Alternatively, infection may cause uterine atony, requiring labor to be augmented with oxytocin. Ultimately, a poor labor pattern may require an instrumented delivery or a cesarean delivery. Each of these antepartum and intrapartum factors must be considered when evaluating the newborn for the presence of bacterial infection. Although many cytokines and inflammatory markers have been proposed as diagnostic tests for early onset sepsis (EOS), none has been of sufficient predictive value to gain wide acceptance. [85, 86] Some cytokines are only secreted over a limited time frame during the start of infection, and inflammatory markers may be more sustained in their presence. Creactive proteins are useful to exclude infection and stop antibiotics. Investigations suggest that procalcitonin and IL6 used together may enhance laboratory diagnosis of EOS. [85] Physical The physical examination of the pregnant women with chorioamnionitis may reveal no signs or symptoms of infection. [2] Conversely, a pregnant woman with chorioamnionitis may appear ill, even toxic. Physical symptoms may include the following: Fever Tachycardia (>120 bpm) Hypotension Diaphoresis Cool or clammy skin Uterine tenderness Foulsmelling or abnormal vaginal discharge The fetus may also have tachycardia (>160180 bpm). Although heart rate characteristics used to diagnose EOS are under investigation, [87] this type of analysis has not been applied to the fetal heart rate when chorioamnionitis is evident. A biophysical profile (BPP) performed on the fetus using ultrasonography may reveal a lower than normal score, but ultrasonic biophysical profile assessment has not been predictive of clinical chorioamnionitis. [88] Lack of fetal breathing has been associated with fetal infection. [89, 90] Intrauterine ultrasonography has identified "sludge" at the amniotic fluid interface with the cervix that is also associated with hyperechogenic, freefloating material in the amniotic fluid. [7] This finding was seen in asymptomatic women at risk for preterm delivery. Aseptic aspiration of the "sludge" showed the material had a low glucose content, many neutrophils, and grampositive cocci. Furthermore, electronic fetal monitoring lacks precision to identify the fetal inflammatory response syndrome and subsequent neonatal sepsis. [91] Clinical signs and symptoms of chorioamnionitis are not always associated with placental evidence of inflammation. [3] This is particularly true if maternal fever is the sole criterion for the diagnosis. Epidural anesthesia during the intrapartum period has been associated with fever in the mother and the neonate [92, 93] ; however, the pathophysiology of the fever and its adverse effects on the mother, fetus, or infant remains controversial. [94, 95, 96, 97]

Chorioamnionitis Clinical Presentation

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  • 4/19/2015 ChorioamnionitisClinicalPresentation

    http://emedicine.medscape.com/article/973237clinical#showall 1/13

    ChorioamnionitisClinicalPresentationAuthor:MichaelPSherman,MD,FAAPChiefEditor:TedRosenkrantz,MDmore...

    Updated:Apr2,2014

    HistoryThetimehonoredclinicalsignsandsymptomsofchorioamnionitisincludethefollowing:

    Fever(anintrapartumtemperature>100.4For>37.8C)Significantmaternaltachycardia(>120beatsperminute[bpm])Fetaltachycardia(>160180bpm)PurulentorfoulsmellingamnioticfluidorvaginaldischargeUterinetendernessMaternalleukocytosis(totalbloodleukocytecount>15,00018,000cells/L)

    Ofthesecriteria,intrapartummaternalfeverappearstobethemostfrequent.[1]

    Whenatleast2oftheaforementionedcriteriaarepresent,theriskofneonatalsepsisisincreased.Eachclinicalsignandsymptomofchorioamnionitis,however,isbyitselfoflowpredictivevalue.Thesignsandsymptomsofmaternalchorioamnionitisoramnioticfluidinfectionaresosubjectivethatsomeexpertshaverecommendedthefollowing:Ifaphysicianistryingtodecideaboutanevaluationandtreatmentofaninfant,asktheobstetricianifheorshebelieveschorioamnionitisispresent.Moreover,silentchorioamnionitisisprominent,[2]andthussignsandsymptomsintheinfectednewborninfanttakeonaddedsignificance.

    Anincreasingordecreasingtotalleukocytecountmaybemoreimportantthanasingledetermination.Abnormalitiesineitherumbilicalveininterleukin(IL)6levelsoranincreasingneonatalimmaturetototalneutrophilratio,alongwithclinicalcriteriaassociatedwithchorioamnionitis,improvethesensitivityandpredictiveaccuracyofidentifyingthesepticneonate.

    Riskofneonatalinfectionincreasesasthedurationofrupturedmembraneslengthens.[82]Chorioamnionitismayinitiateuteroplacentalbleedingoraplacentalabruption.[83]Intrauterineinfectionisincreasedinplacentapreviaandmanifestswithvaginalbleeding.[84]Laboranddeliverymayberapidinthepresenceofchorioamnionitis.Alternatively,infectionmaycauseuterineatony,requiringlabortobeaugmentedwithoxytocin.Ultimately,apoorlaborpatternmayrequireaninstrumenteddeliveryoracesareandelivery.Eachoftheseantepartumandintrapartumfactorsmustbeconsideredwhenevaluatingthenewbornforthepresenceofbacterialinfection.

    Althoughmanycytokinesandinflammatorymarkershavebeenproposedasdiagnostictestsforearlyonsetsepsis(EOS),nonehasbeenofsufficientpredictivevaluetogainwideacceptance.[85,86]Somecytokinesareonlysecretedoveralimitedtimeframeduringthestartofinfection,andinflammatorymarkersmaybemoresustainedintheirpresence.Creactiveproteinsareusefultoexcludeinfectionandstopantibiotics.InvestigationssuggestthatprocalcitoninandIL6usedtogethermayenhancelaboratorydiagnosisofEOS.[85]

    PhysicalThephysicalexaminationofthepregnantwomenwithchorioamnionitismayrevealnosignsorsymptomsofinfection.[2]Conversely,apregnantwomanwithchorioamnionitismayappearill,eventoxic.

    Physicalsymptomsmayincludethefollowing:

    FeverTachycardia(>120bpm)HypotensionDiaphoresisCoolorclammyskinUterinetendernessFoulsmellingorabnormalvaginaldischarge

    Thefetusmayalsohavetachycardia(>160180bpm).AlthoughheartratecharacteristicsusedtodiagnoseEOSareunderinvestigation,[87]thistypeofanalysishasnotbeenappliedtothefetalheartratewhenchorioamnionitisisevident.Abiophysicalprofile(BPP)performedonthefetususingultrasonographymayrevealalowerthannormalscore,butultrasonicbiophysicalprofileassessmenthasnotbeenpredictiveofclinicalchorioamnionitis.[88]

    Lackoffetalbreathinghasbeenassociatedwithfetalinfection.[89,90]Intrauterineultrasonographyhasidentified"sludge"attheamnioticfluidinterfacewiththecervixthatisalsoassociatedwithhyperechogenic,freefloatingmaterialintheamnioticfluid.[7]Thisfindingwasseeninasymptomaticwomenatriskforpretermdelivery.Asepticaspirationofthe"sludge"showedthematerialhadalowglucosecontent,manyneutrophils,andgrampositivecocci.Furthermore,electronicfetalmonitoringlacksprecisiontoidentifythefetalinflammatoryresponsesyndromeandsubsequentneonatalsepsis.[91]

    Clinicalsignsandsymptomsofchorioamnionitisarenotalwaysassociatedwithplacentalevidenceofinflammation.[3]Thisisparticularlytrueifmaternalfeveristhesolecriterionforthediagnosis.

    Epiduralanesthesiaduringtheintrapartumperiodhasbeenassociatedwithfeverinthemotherandtheneonate[92,93]however,thepathophysiologyofthefeveranditsadverseeffectsonthemother,fetus,orinfantremainscontroversial.[94,95,96,97]

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  • 4/19/2015 ChorioamnionitisClinicalPresentation

    http://emedicine.medscape.com/article/973237clinical#showall 2/13

    Epiduralanesthesiaandmaternaland/orneonatalfeversresultinmoreevaluationsforsepsisandantibiotictreatmentinneonates,althoughtheincidenceofsepsiscomparedwiththatinaneonatalpopulationwhosemothersdidnotreceiveepiduralanesthesiaduringlaborisunknown.Epiduralanesthesiaduringlaborisassociatedwithothertypesofneonatalmorbidity,suchasseizures,thatarealsoriskfactorsforsepsis.

    Althoughtheexactmechanismsfor"epiduralfever"duringlaborremainunclear,nulliparity,dysfunctionallabor,prolongedlabor,maternalexhaustion,dehydration,and/orprolongedruptureofmembranesmaybeoperativeinpathogenesis.[98]

    Inthesettingofepiduralanesthesiaduringlabor,thefollowingclinicalcoursehasbeenobserved.Thefetususuallyhastachycardiawhenthemotherisfebrileduringlabor.Atbirth,thenewbornmayalsohaveafever(temperature>37.8C).Iftheneonateisnotseptic,thetemperatureelevationdissipatesrapidlyfollowingbirth,andthenewbornsubsequentlyexhibitsnormalbehavior.Usuallyatemperatureelevationintheneonatehasreturnedtonormalwithin3060minutesafterbirth.Furthermore,thesenoninfected,febrileneonateshavenormalApgarscoresandappearremarkablywellfollowingbirth.Suchnewbornscanbeobservedforillnessratherthanundergoingasepticworkupandantibiotictherapy.However,judgmentmustbebasedonmanyfactors,includingtheintrapartumadministrationofbroadspectrumantibioticstothemother.

    Maternalchorioamnionitisincreasesthepotentialthatthefollowingclinicalpresentationsmaybeevidentintheneonate.Signsandsymptomsofneonatalsepsisareoftennonspecificandsubtle.Theneonatemaydemonstratebehavioralabnormalitiessuchaslethargy,hypotonia,weakcry,andpoorsuck.

    Tachypnea,respiratorydistress(eg,expiratorygrunt,retractions),cyanosis,pulmonaryhemorrhage,and/orapnea(ie,pulmonarymanifestationsofpneumonia,sepsis,orboth),mustbeimmediatelyappreciatedbycaregivers.Nurserypersonnelmustbeawarethataneonatewhoisbornwithoutrespiratorydistressbutwhodevelopssignsandsymptomsofpulmonarydiseaseinthefirst612hoursoflifehasaheightenedriskforcongenital(infectious)pneumonia.

    Tachycardia,hypotension,prolongedcapillaryrefilltime,coolandclammyskin,paleormottledappearance,oliguria(ie,cardiovascularmanifestationsofsepsis),oracombinationofthesemaybeobserved.ManyofthesesignsoccurlateinthecourseofEOS.Caregiversmustalsoconsiderotherexplanationsforthesephysicalfindings,suchasdevelopmentaldefectsinthecardiovascularsystem(ie,cardiovascularmalformationswithabnormalitiesofaorticbloodflow)orinbornerrorsofmetabolism.

    Abdominaldistension,vomiting,diarrhea,bloodystools,oracombinationofthesemaybeobserved.GIsymptomsmaybenonspecificinpatientswithEOS.

    Thermalregulatoryabnormalities(ie,hypothermiaorhyperthermia),behavioralabnormalities,apnea,seizures(ie,CNSmanifestations),oracombinationmaybeseen.Abulgingfontanelornuchalrigidityisnotareliablesignofmeningitisinaneonate.

    Pallor,petechiaeorpurpura,andovertbleeding(ie,hematopoieticinvolvement,liverinvolvement,orboth)maybeseenandrequiresimmediatediagnosticandtherapeuticattention.

    Asonephysiologicsystemmayaffectanother,signsandsymptomsmayoriginatefrommorethanonedysfunctionalorgan.However,manyneonatalconditionsresembleneonatalsepsisthus,physiciancaregiversmusthaveanopenmindregardingotherclinicalconditionsthatmayinvolvesignsandsymptomsresemblingthoseofneonatalsepsis.Thoseconditionsinclude,butarenotlimitedto,thefollowing:

    Cardiovascularmalformations,especiallyleftsidedobstructivelesionscausingpoorsystemiccardiacoutputEndocrinedisordersthatmayalsocauseshocklikestates,suchasdifferenttypesofcongenitaladrenalinsufficiencyorhypoglycemiaassociatedwithhyperinsulinemiaSeriousCNStraumaordysfunctionfromanycauseandsubtleseizureswithsystemicmanifestationsAnemiacausedbyunrecognizedisoimmunizationorbloodlossfromconditionssuchasfetomaternaltransfusionsyndrome

    CausesMaternalchorioamnionitisoccurswhenprotectivemechanismsoftheurogenitaltractand/oruterusfailduringpregnancyorwhenincreasednumbersofmicrobialfloraorhighlypathogenicmicroorganismsareintroducedintotheurogenitalenvironment.[38,99,100,101,102,103]

    Ascendinginfectionintothevagina,thenthecervix,andfinallyintotheuterinecavity,fetalmembranes,andplacentaistheconsequenceofmanyfactors(ie,innatehostdefenses,healthybacterialflora,pathologicbacterialload,bacterialvirulencefactorsandtoxinproduction).Ashortcervixhasbeenrecognizedaseitherariskfactororasurrogateformicrobialinvasionoftheamnioticfluid.[6,104]

    Urogenitalhygieneisobviouslyimportantinestablishinghealthybacterialflora.Healthybacteria(ie,lactobacilli)[105]andnaturalpeptideantibioticsinthevaginaandcervixmayhavearoleinpreventinginfectionsduringpregnancy.[106]Mucus,phagocytes,andnaturalantibioticproteins(ie,lactoferrin,lysozyme,betadefensins)inthecervicovaginalsecretionsattempttomaintainanormalbacterialflora.[100]Bacterialinterference,mainlyproducedvialactobacillilivinginanacidicvaginalenvironmentandproducingbacteriocins,alsohelpstokeeppathogenicbacteriafromgainingafootholdinthecervicovaginalsecretions.[107,108]Thesemechanismsofhostprotectionmaybealteredinasignificantnumberofpregnantwomenwhodevelopchorioamnionitis.

    Oralhygienemayinfluencerectalandurogenitalbacterialfloraduringpregnancy.Althoughthetheoryiscontroversial,intenseinteresthasfocusedonaconnectionamongperiodontitis,abnormalrectalcolonization,andpretermdelivery.[109,110]

    Rectalbacterialfloraisbelievedtobeimportantinestablishingabnormalurogenitalcolonizationduringpregnancy.[111,112,113]Alterationsinvaginalandcervicalhostdefensemechanismsduringpregnancycausevaginitis,[114]bacterialvaginosis,urinaryinfections,andotherurogenitalinfections.Orogenitalcontactmayalsoaltereithercolonicorurogenitalmicrobialfloraandultimatelycauseascendinginfectionandchorioamnionitis.[115,116]

    Similarly,coitushasbeenlinkedwithchorioamnionitis.[117,118]

    Currently,researchersaretryingtounderstandhowhostdefensemechanismspreventurogenitalinfectionduringpregnancy.Theconceptofbacterialcommunitiesmaybeimportantinthepathogenesisofchorioamnionitisbecause

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  • 4/19/2015 ChorioamnionitisClinicalPresentation

    http://emedicine.medscape.com/article/973237clinical#showall 3/13

    certainmicrobesprovidesupporttoothers.Theprevalenceanddiversityofbacterialspeciesinfetalmembranesduringpretermlaboremphasizesfurtherresearchonthistopicisneeded.[119]Metagenomicsusesnonculture,molecularmethodstodelineateallmicrobesinhabitinganenvironment.Thus,theintestinalmicrobiomeisunderintensescrutinytounderstandnecrotizingenterocolitisorinflammatoryboweldisease.Initialreportsusingmolecularmethodstounderstandintrauterineinfection,fetalinflammation,andpretermdeliveryhavebeenpublished.[119,120]

    Clinicaleventsassociatedwithchorioamnionitisincludethefollowing:

    Historyofprematurebirth(withincreasingriskatearliergestationalage)PresenceofprematurelaborPrematurelyrupturedfetalmembranes(beforelaborhasitsonset)Prolongedruptureofthefetalmembranes

    Inareportofpatientswithclinicalsignsandsymptomsofchorioamnionitis,38%showednohistologicevidenceofplacentalinflammation.Thus,othercausesofsignsandsymptomsthatresemblematernalchorioamnionitismustbesought.

    Epiduralanesthesiaduringlabormaybeassociatedwithmaternalfeverandfetaltachycardia(seeSpecialConcerns).Otherconditions,suchasdehydrationormaternalexhaustionduringlabor,mayresultinmaternalfeverandmustbeconsideredascausesofthefebrilestate.

    ContributorInformationandDisclosuresAuthorMichaelPSherman,MD,FAAPProfessor,DepartmentofChildHealth,UniversityofMissouriColumbiaSchoolofMedicineNeonatologist,Women'sandChildren'sHospitalProfessorEmeritus,DepartmentofPediatrics,UniversityofCalifornia,Davis,SchoolofMedicine

    MichaelPSherman,MD,FAAPisamemberofthefollowingmedicalsocieties:AmericanAcademyofPediatrics,AmericanAssociationfortheAdvancementofScience,AmericanAssociationofImmunologists,AmericanPediatricSociety,AmericanSocietyforMicrobiology,AmericanThoracicSociety,EuropeanSocietyforPaediatricResearch,PediatricInfectiousDiseasesSociety,PerinatalResearchSociety,SocietyforPediatricResearch,andWesternSocietyforPediatricResearch

    Disclosure:Nothingtodisclose.

    Coauthor(s)NaomiFLauriello,MDAssistantProfessorofNeonatology,UniversityofMissouriWomen'sandChildren'sHospital

    NaomiFLauriello,MDisamemberofthefollowingmedicalsocieties:AmericanAcademyofPediatrics

    Disclosure:MedIQHonorariaSpeakingandteaching

    KatsufumiOtsuki,MD,PhDAssociateProfessor,Chief,DepartmentofObstetricsandGynecology,ShowaUniversityKotoToyosuHospital,Japan

    Disclosure:Nothingtodisclose.

    SpecialtyEditorBoardTedRosenkrantz,MDProfessor,DepartmentsofPediatricsandObstetrics/Gynecology,DivisionofNeonatalPerinatalMedicine,UniversityofConnecticutSchoolofMedicine

    TedRosenkrantz,MDisamemberofthefollowingmedicalsocieties:AmericanAcademyofPediatrics,AmericanMedicalAssociation,AmericanPediatricSociety,ConnecticutStateMedicalSociety,EasternSocietyforPediatricResearch,andSocietyforPediatricResearch

    Disclosure:Nothingtodisclose.

    MaryLWindle,PharmDAdjunctAssociateProfessor,UniversityofNebraskaMedicalCenterCollegeofPharmacyEditorinChief,MedscapeDrugReference

    Disclosure:Nothingtodisclose.

    ArunKPramanik,MD,MBBSProfessorofPediatrics,LouisianaStateUniversityHealthSciencesCenter

    ArunKPramanik,MD,MBBSisamemberofthefollowingmedicalsocieties:AmericanAcademyofPediatrics,AmericanThoracicSociety,NationalPerinatalAssociation,andSouthernSocietyforPediatricResearch

    Disclosure:Nothingtodisclose.

    CarolLWagner,MDProfessorofPediatrics,MedicalUniversityofSouthCarolina

    CarolLWagner,MDisamemberofthefollowingmedicalsocieties:AmericanAcademyofPediatrics,AmericanChemicalSociety,AmericanMedicalWomen'sAssociation,AmericanPublicHealthAssociation,AmericanSocietyforBoneandMineralResearch,AmericanSocietyforClinicalNutrition,MassachusettsMedicalSociety,NationalPerinatalAssociation,andSocietyforPediatricResearch

    Disclosure:Nothingtodisclose.

    ChiefEditorTedRosenkrantz,MDProfessor,DepartmentsofPediatricsandObstetrics/Gynecology,DivisionofNeonatalPerinatalMedicine,UniversityofConnecticutSchoolofMedicine

    TedRosenkrantz,MDisamemberofthefollowingmedicalsocieties:AmericanAcademyofPediatrics,AmericanMedicalAssociation,AmericanPediatricSociety,ConnecticutStateMedicalSociety,EasternSocietyforPediatricResearch,andSocietyforPediatricResearch

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    Disclosure:Nothingtodisclose.

    AdditionalContributorsResearchbytheauthor,MichaelSherman,issupportedbyNIHgrantR44HD057744andagrantfromtheGerberFoundation.TheauthorappreciatesthereviewofthemanuscriptundertakenbyJanSherman,RN,NNP,PhD,andherhelpfulrecommendationsforimprovement.

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