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  • 1.Management of Neonates With Suspected or Proven Early-Onset Bacterial SepsisRichard A. Polin and the COMMITTEE ON FETUS AND NEWBORN Pediatrics 2012;129;1006; originally published online April 30, 2012;DOI: 10.1542/peds.2012-0541The online version of this article, along with updated information and services, is located on the World Wide Web at: PEDIATRICS is the official journal of the American Academy of Pediatrics. A monthly publication, it has been published continuously since 1948. PEDIATRICS is owned, published, and trademarked by the American Academy of Pediatrics, 141 Northwest Point Boulevard, Elk Grove Village, Illinois, 60007. Copyright 2012 by the American Academy of Pediatrics. All rights reserved. Print ISSN: 0031-4005. Online ISSN: 1098-4275. Downloaded from at Hacettepe University on May 9, 2012

2. Guidance for the Clinician inRendering Pediatric CareCLINICAL REPORTManagement of Neonates With Suspected or ProvenEarly-Onset Bacterial SepsisabstractRichard A. Polin, MD and the COMMITTEE ON FETUS ANDNEWBORNWith improved obstetrical management and evidence-based use ofKEY WORDSearly-onset sepsis, antimicrobial therapy, group B streptococcus,intrapartum antimicrobial therapy, early-onset neonatal sepsis is be- meningitis, gastric aspirate, tracheal aspirate, chorioamnionitis,coming less frequent. However, early-onset sepsis remains one of thesepsis screen, blood culture, lumbar puncture, urine culture,most common causes of neonatal morbidity and mortality in the pre-body surface cultures, white blood count, acute phase reactants,term population. The identication of neonates at risk for early-onsetprevention strategiessepsis is frequently based on a constellation of perinatal risk factors ABBREVIATIONSCFUcolony-forming unitsthat are neither sensitive nor specic. Furthermore, diagnostic tests CRPC-reactive proteinfor neonatal sepsis have a poor positive predictive accuracy. As a result,CSFcerebrospinal uidclinicians often treat well-appearing infants for extended periods of time, GBSgroup B streptococciI/Timmature to total neutrophil (ratio)even when bacterial cultures are negative. The optimal treatment of PMNpolymorphonuclear leukocyteinfants with suspected early-onset sepsis is broad-spectrum antimicro-PPROMpreterm premature rupture of membranesbial agents (ampicillin and an aminoglycoside). Once a pathogen is iden-This document is copyrighted and is property of the Americantied, antimicrobial therapy should be narrowed (unless synergism isAcademy of Pediatrics and its Board of Directors. All authorsneeded). Recent data suggest an association between prolonged empir-have led conict of interest statements with the AmericanAcademy of Pediatrics. Any conicts have been resolved throughical treatment of preterm infants (5 days) with broad-spectrum anti- a process approved by the Board of Directors. The Americanbiotics and higher risks of late onset sepsis, necrotizing enterocolitis, Academy of Pediatrics has neither solicited nor accepted anyand mortality. To reduce these risks, antimicrobial therapy should be commercial involvement in the development of the content ofthis publication.discontinued at 48 hours in clinical situations in which the probabilityof sepsis is low. The purpose of this clinical report is to provide a The guidance in this report does not indicate an exclusivecourse of treatment or serve as a standard of medical care.practical and, when possible, evidence-based approach to the manage-Variations, taking into account individual circumstances, may bement of infants with suspected or proven early-onset sepsis. Pediatrics appropriate.2012;129:10061015INTRODUCTIONSuspected sepsis is one of the most common diagnoses made in theNICU.1 However, the signs of sepsis are nonspecic, and inammatorysyndromes of noninfectious origin mimic those of neonatal sepsis. Mostinfants with suspected sepsis recover with supportive care (with orwithout initiation of antimicrobial therapy). The challenges for clinicians threefold: (1) identifying neonates with a high likelihood of sepsisdoi:10.1542/peds.2012-0541promptly and initiating antimicrobial therapy; (2) distinguishing high-All clinical reports from the American Academy of Pediatricsrisk healthy-appearing infants or infants with clinical signs who do not automatically expire 5 years after publication unless reafrmed,require treatment; and (3) discontinuing antimicrobial therapy once revised, or retired at or before that time.sepsis is deemed unlikely. The purpose of this clinical report is toPEDIATRICS (ISSN Numbers: Print, 0031-4005; Online, 1098-4275).provide a practical and, when possible, evidence-based approach to theCopyright 2012 by the American Academy of Pediatricsdiagnosis and management of early-onset sepsis, dened by the Na-tional Institute of Child Health and Human Development and VermontOxford Networks as sepsis with onset at 3 days of age.1006FROM THE AMERICAN ACADEMY OF PEDIATRICS Downloaded from at Hacettepe University on May 9, 2012 3. FROM THE AMERICAN ACADEMY OF PEDIATRICSPATHOGENESIS ANDmost of these women with histologicThe major risk factors for early-onsetEPIDEMIOLOGY OF EARLY-ONSET chorioamnionitis do not have a positiveneonatal sepsis are preterm birth,SEPSISplacental culture.3 The incidence of clin- maternal colonization with GBS, ruptureical chorioamnionitis varies inversely of membranes >18 hours, and mater-Before birth, the fetus optimally iswith gestational age. In the Nationalnal signs or symptoms of intra-amnioticmaintained in a sterile environment.Institute of Child Health and Humaninfection.1416 Other variables includeOrganisms causing early-onset sepsisDevelopment Neonatal Research Net- ethnicity (ie, black women are at higherascend from the birth canal eitherwork, 14% to 28% of women delivering risk of being colonized with GBS), lowwhen the amniotic membranes rupturepreterm infants at 22 through 28 weekssocioeconomic status, male sex, andor leak before or during the course ofgestation exhibited signs compatible low Apgar scores. Preterm birth/lowlabor, resulting in intra-amniotic infec-with chorioamnionitis.4 The major risk birth weight is the risk factor mosttion.2 Commonly referred to as cho-factors for chorioamnionitis include closely associated with early-onset sep-rioamnionitis, intra-amniotic infectionlow parity, spontaneous labor, longersis.17 Infant birth weight is inverselyindicates infection of the amniotic uid,length of labor and membrane rupture,related to risk of early-onset sepsis.membranes, placenta, and/or decidua.multiple digital vaginal examinationsThe increased risk of early-onset sep-Group B streptococci (GBS) can alsosis in preterm infants is also related to(especially with ruptured membranes),enter the amniotic uid through occult complications of labor and deliverymeconium-stained amniotic uid, internaltears. Chorioamnionitis is a major riskand immaturity of innate and adaptivefetal or uterine monitoring, and pres-factor for neonatal sepsis. Sepsis can immunity.18begin in utero when the fetus inhales ence of genital tract microorganismsor swallows infected amniotic uid. (eg, Mycoplasma hominis).5The neonate can also develop sepsis inAt term gestation, less than 1% of DIAGNOSTIC TESTING FOR SEPSISthe hours or days after birth whenwomen with intact membranes will The clinical diagnosis of sepsis in thecolonized skin or mucosal surfaces arehave organisms cultured from amni- neonate is difcult, because many ofcompromised. The essential criterionotic uid.6 The rate can be higher ifthe signs of sepsis are nonspecic andfor the clinical diagnosis of chorio- the integrity of the amniotic cavity isare observed with other noninfectiousamnionitis is maternal fever. Other compromised by procedures before conditions. Although a normal physicalcriteria are relatively insensitive. When birth (eg, placement of a cerclage orexamination is evidence that sepsis isdening intra-amniotic infection (cho-amniocentesis).6 In women with pre-not present,19,20 bacteremia can occurrioamnionitis) for clinical researchterm labor and intact membranes, the in the absence of clinical signs.21 Avail-studies, the diagnosis is typically based rate of microbial invasion of the amni-able diagnostic testing is not helpful inon the presence of maternal fever ofotic cavity is 32%, and if there is pre- deciding which neonate requires em-greater than 38C (100.4F) and at leastterm premature rupture of membranespirical antimicrobial therapy but cantwo of the following criteria: maternal (PPROM), the rate may be as high asassist with the decision to discontinueleukocytosis (greater than 15 000 cells/75%.7 Many of the pathogens recoveredtreatment.22mm3), maternal tachycardia (greater from amniotic uid in women with pre-than 100 beats/minute), fetal tachycar- term labor or PPROM (eg, UreaplasmaBlood Culturedia (greater than 160 beats/minute),species or Mycoplasma species) doA single blood culture in a sufcientuterine tenderness, and/or foul odor of not cause early-onset sepsis.810 How- volume is required for all neonatesthe amniotic uid. These thresholds are ever, both Ureaplasma and Myco-with suspected sepsis. Data suggestassociated with higher rates of neo-plasma organisms can be recoveredthat 1.0 mL of blood should be thenatal and maternal morbidity. from the bloodstream of infants whoseminimum volume drawn for cultureNonetheless, the diagnosis of cho-birth weight is less than 1500 g.11 When when a single pediatric blood culturerioamnionitis must be considered even a pathogen (eg, GBS) is recovered from bottle is used. Dividing the specimen inwhen maternal fever is the sole abnor-amniotic uid, the attack rate of neo- half and inoculating aerobic and an-mal nding. Although fever is commonnatal sepsis can be as high as 20%.12aerobic bo