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    Hindawi Publishing CorporationEmergency Medicine InternationalVolume 2012, Article ID 320309,8pagesdoi:10.1155/2012/320309

    Review ArticleDiagnosis andManagement of BacterialMeningitis inthe Paediatric Population: A Review

    CatherineL. Tacon1 andOliver Flower2

    1 Sydney Childrens Hospital, Randwick, NSW, Australia2 Intensive Care Unit, Royal North Shore Hospital, St Leonards, NSW 2065, Australia

    Correspondence should be addressed to Catherine L. Tacon,[email protected]

    Received 3 March 2012; Accepted 3 August 2012

    Academic Editor: Chamisa Macindoe

    Copyright 2012 C. L. Tacon and O. Flower. This is an open access article distributed under the Creative Commons AttributionLicense, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properlycited.

    Paediatric bacterial meningitis is a neurological emergency which, despite advances in medical management, still has a significantmorbidity and mortality. Over recent decades new vaccines have led to a change in epidemiology of the disease; however, it remainsa condition that requires a high index of suspicion, prompt diagnosis, and early management in the emergency department. Newlaboratory techniques and clinical tools are aiding the diagnosis of bacterial meningitis, yet some controversies still exist in itsmanagement. This paper outlines the changing epidemiology of the disease, current diagnostic techniques as well as controversiesand advances in the management of bacterial meningitis in the paediatric population.

    1. Introduction

    Bacterial meningitis is a medical emergency characterised byinflammation of the meninges in response to bacterial infec-tion. Untreated, its mortality approaches 100%, and evenwith current antibiotics and advanced paediatric intensivecare, the mortality rate of the disease is approximately 510% [1]. Worldwide, the risk of neurological sequelae insurvivors following hospital discharge approaches 20% [2].Early diagnosis and appropriate management of the child

    with meningitis is therefore critical. The management andepidemiology of bacterial meningitis in the neonate differsfrom that of the infant and child; it will not be reviewed here.

    2. Epidemiology

    The incidence of bacterial meningitis is approximately 57per 100 000 population [1]. In developed countries,Neisseriameningitidis and Streptococcus pneumoniae are now thecommonest causes of acute bacterial meningitis in otherwisehealthy children [3] (seeTable 1). Previously, Haemophilusinfluenzae type B (Hib) accounted for up to 48% of allbacterial meningitis cases [4]; however, the introduction of

    the Hib vaccination program led to a dramatic reductionin the incidence of Hib meningitis. Hib now accountsfor only 7% of meningitis cases in the United States andis predominantly seen in unvaccinated adult patients [4].However, the burden of Hib in developing countries withoutadequate vaccination programs still remains significant; by2007 only 42% of children worldwide had access to the Hibimmunisation program [4].

    Streptococcus pneumoniae is now the commonest causeof bacterial meningitis in the United States and Europe

    [4]. Although seen in the healthy child, children witha basilar skull or cribriform fracture with a CSF leak,asplenism or HIV infection are at particular risk of devel-oping pneumococcal meningitis [3]. Furthermore, patientswith cochlear implants have a 30 times increased risk ofdeveloping pneumococcal meningitis [5]. The developmentof pneumococcal conjugate vaccines has led to a decline inthe incidence of pneumococcal meningitis in countries withan active immunisation program; however, concern exists asto the emergence of pneumococcal serotypes not covered bythe vaccines [4]. This, coupled by the increasing resistanceofStreptococcus pneumoniaeto conventional antibiotics, is ofgrowing concern [1].

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    Table1: Causative organisms.

    Organism Comment

    Streptococcus pneumoniae

    Commonest organismAffects healthy childrenAdditional risk factors: basilarskull or cribriform fracture,

    asplenism, HIV, and cochlearimplants

    Neisseria meningitidis Can cause epidemic, endemic, or

    sporadic infections

    Haemophilus influenzaetype B

    Reduced incidence afterintroduction of vaccinationprogram

    Group B streptococcus

    The less common pathogensGroup B streptococcus,E. ColiandL. monocytogenesmore commonin neonates

    Escherichia coli

    Non typeableH. influenzae

    Other gram-negative bacilli

    Listeria monocytogenes

    Group A streptococci

    Staphylococcal species Penetrating head trauma and

    neurosurgery

    Streptococci

    Aerobic gram-negativebacilli

    There are six serogroups ofNeisseria menigitidiswith theability to cause severe meningitis: A, B, C, X, Y and W-135 [6]. Infection with Neisseria meningitidis can be eitherepidemic or endemic [3], and although the majority of casesin the United States are sporadic [4], N. meningitidis is theonly bacteria that can cause epidemics of meningitis [6].Throughout America and Europe serogroups B, C, and Yaccount for the majority of meningococcal meningitis cases[4], with serogroup B being the leading cause of endemicmeningitis in developed countries overall [6,7]. SerogroupA N. meningitidisis also a significant problem, particularlyin the sub-Saharan meningitis-belt, where it is responsiblefor a number of large-scale epidemics [6]. While a conjugatemeningococcal vaccine for serogroups A, C, Y, and W-135has shown reductions in meningococcal disease in somepopulations [3], development of an effective vaccine against

    serogroup B has been difficult. Recent trials have shownpromise in the use of a new multicomponent serogroup Bvaccine [7, 8], but currently the lack of a widely available,effective vaccination against N. meningitidis B, as well asthe lack of access to vaccinations in populations at riskof epidemics, such as in sub-Saharan Africa, means thatN. meningitidis still remains a significant cause of bacterialmeningitis [6].

    In developed countries less than 20% of bacterialmeningitis in the paediatric population aged 3 monthsand over is caused by organisms other than S. pneumoniaeor N. meningitidis. The less-common causative organismsinclude Group BStreptococcus,Escherichia coli, nontypeable

    H. influenzae, other gram-negative bacilli,Listeria monocyto-genes, and group A streptococci [4]. In addition patients whohave had penetrating head trauma or neurosurgery are alsoat risk of developing meningitis from staphylococcal species,streptococci, and aerobic gram-negative bacilli [3, 9], andthis should be considered in such a child presenting with

    possible bacterial meningitis.

    3. Diagnosis

    Early diagnosis and treatment of bacterial meningitis iscritical, and a high index of clinical suspicion is essential.Diagnosis involves both clinical assessment and the use oflaboratory investigations.

    3.1. Clinical. The clinical symptoms and signs of bacterialmeningitis in children vary depending on the age of the childand duration of disease. Nonspecific signs include abnormalvital signs such as tachycardia and fever, poor feeding,

    irritability, lethargy, and vomiting [4]. Signs of fulminantsepsis such as shock, disseminated intravascular coagulation(DIC), purpuric rash, and coma may be present and aremore common in meningococcal meningitis [1]. These signshowever are more likely to develop later in the course of theillness (median time between 13 and 22 hours) [10] whereasnonspecific, often overlooked symptoms, such as leg pain,may be present within 8 hours in more than 70% of childrenwith meningococcal meningitis and should prompt furtherimmediate evaluation [10,11]. Classical signs of meningitissuch as nuchal rigidity, bulging fontanelle, photophobia, anda positive Kernigs or Brudzinskis sign (more common inchildren older than 12 to 18 months) may also be present

    [3]. A recent systematic review found that the presence ofmeningeal signs increased the likelihood of the diagnosisof meningitis, and conversely their absence decreased thelikelihood [12]; however, other studies have shown thatno classical symptoms and signs of meningitis are able todistinguish accurately between children with or withoutmeningitis [13], and so these signs should be interpretedwith caution.

    Seizures may be present in 2030% of children withbacterial meningitis, more commonly with S. pneumoniaeand Hib infections than with N. meningitidis [3]. A recentstudy has suggested that the presence of complex seizuresmore than doubles the risk of meningitis [12]. Focal

    neurological signs may also be found, as may a reduced levelof consciousness. Coma on presentation is associated with aworse prognosis than a child presenting with irritability orlethargy alone [3].

    3.2. Laboratory Investigations

    3.2.1. Lumbar Puncture. Whilst a lumbar puncture (LP) isnecessary for the definitive diagnosis of bacterial menin-gitis and should be performed where a clinical suspicionfor meningitis exists, contraindications often preclude thisinvestigation. These contraindications (seeTable 2) includesigns of raised intracranial pressure, such as an alteration

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    Table2: Contraindications to lumbar puncture [9].

    Contraindication Comment

    Raised intracranial pressure:

    Alteration in level ofconsciousness

    Papilloedema

    Focal neurological signs Excluding an isolated cranial

    nerve VI or VII palsy

    Prolonged seizuresDelay lumbar puncture for 30minutes in simple, short seizuresonly

    History of selected CNSdisease

    CSF shunts, hydrocephalus,trauma, post neurosurgery, orknown space-occupying lesion

    ImmunocompromiseHIV/AIDS, onimmunosuppressive therapy,post-transplantation

    Coagulation disorders

    Cardiorespiratoryinsufficiency

    Localised infection at site ofneedle insertion

    in level of consciousness, papilloedema, prolonged seizures,or focal neurological signs, as well as coagulation disorders,cardiorespiratory instability, a history of immunosuppres-sion, certain central nervous syndrome (CNS) conditions,or localised infection at the site of insertion of the lumbarpuncture needle [1]. LP may be delayed until these con-traindications no longer exist; however, administration ofantibiotics and appropriate therapy should not be delayed ifthe LP cannot be performed immediately.

    Initial analysis of the CSF should include microscopywith gram stain, culture and measurement of protein, andglucose levels. CSF findings suggestive of bacterial meningitisare outlined inTable 3. Typically the CSF white cell count(wcc) is >1000 cells/mm3 although it may not be elevatedin the early phase of the infection [3], and the majority ofwhite cells are polymorphonuclear (PMNs). CSF protein istypically elevated (100200 mg/dL) and glucose low (CSFto serum ratio

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    Table3: Lumbar puncture findings1 [3,9].

    CSF finding Normal2 Viral Bacterial Partially treated bacterial

    White cell count (cells/mm3) 1000

    PMNs 0 2040% >8590% >80%

    Protein (mg/dL)

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    Suspected

    bacterial

    meningitis

    No

    Immediate blood

    cultures andlumbar puncture

    Dexamethasone

    and empirical

    antibiotic therapy

    Yes

    Immediate

    blood

    cultures

    Dexamethasone

    and empirical

    antibiotic therapy

    CT scan of headshows no evidence

    of raised ICP

    Lumbarpuncture

    Contraindication tolumbar puncture or delay

    in performance of lumbar

    puncture?

    Figure1: Management of suspected bacterial meningitis [9].

    design. This, in addition to a recent trial which failed toshow any benefit of glycerol in adult meningitis patients [37],means that further well-designed prospective studies shouldbe performed before glycerol is recommended as routine

    therapy.

    4.2. Supportive Care. Any child with a diagnosis of bacterialmeningitis will need supportive therapy, which may includecardiorespiratory support in a paediatric intensive careunit and directed management of complications, such asseizures, cerebral oedema, SIADH, DIC, or shock. Early,protocolized, aggressive care by a consultant supervisedpaediatric team improves survival and outcomes [38]. Earlyintubation and ventilation should be considered for any childwith evidence of respiratory compromise, threatened airway,ongoing shock, retractable seizures, or elevated intracranialpressure [30]. A recent Cochrane meta-analysis found some

    evidence to support the use of maintenance, rather thanrestrictive fluids in the first 48 hours [39]. This meta-analysis found an improvement in the rate of early spasticityand seizures and in later overall neurological sequelae inchildren receiving maintenance fluids [39]. These findingswere however based on studies where late presentation and

    high mortality rates were common. In areas where earlypresentation is more common there are currently insufficientstudies to definitively guide fluid management [39].

    4.3. Chemoprophylaxis. Close contacts of all children withmeningococcal meningitis should receive chemoprophylaxis(ceftriaxone, rifampicin, or ciprofloxacin), and contacts ofthose with Hib should receive ceftriaxone or rifampicin[3,27]. Unvaccinated children less than 5 years of age shouldalso be vaccinated against H. influenzaeas soon as possible[27]. Patients should be kept in respiratory isolation for atleast the first 24 hours after commencing antibiotic therapy[1].

    5. Conclusion

    Paediatric bacterial meningitis is a medical emergency whichrequires a high index of clinical suspicion, prompt diag-nosis, and early, aggressive protocolized management. Newvaccination programs have led to a change in epidemiologyof the disease; however, it remains prevalent worldwide.Advances in clinical and investigation techniques are aidingthe diagnosis of bacterial meningitis, and a combination oftechniques is useful to confirm or exclude the diagnosis.While antibiotics, steroids, and supportive therapy remainthe mainstay of treatment, further research should be

    performed into the roles of adjuvant therapy.

    Conflict of Interests

    The authors declare they have no conflict of interest.

    Acknowledgment

    The authors would like to thank Dr. Francis Lockie for hisinsightful comments about this paper.

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