Il était une fois au SAU… - Infectiologie · original article The new england journal of medicine 2016 n engl j med 364;21 nejm.org may 26, 2011 Bacterial Meningitis in the United

Méningite bactérienne

Bruno MourvillierRéanimation médicale et Infectieuse

GH Bichat Claude Bernard, [email protected]

DUCIV2 Février 2016

Il était une fois au SAU…

Plan

•Epidémiologie•Pronostic•Diagnostic•Séquence de prise en charge•Antibiothérapie•Lieu d’hospitalisation

Epidémiologie

original article

T h e n e w e ngl a nd j o u r na l o f m e dic i n e

n engl j med 364;21 nejm.org may 26, 20112016

Bacterial Meningitis in the United States, 1998–2007

Michael C. Thigpen, M.D., Cynthia G. Whitney, M.D., M.P.H., Nancy E. Messonnier, M.D., Elizabeth R. Zell, M.Stat., Ruth Lynfield, M.D.,

James L. Hadler, M.D., M.P.H., Lee H. Harrison, M.D., Monica M. Farley, M.D., Arthur Reingold, M.D., Nancy M. Bennett, M.D., Allen S. Craig, M.D.,

William Schaffner, M.D., Ann Thomas, M.D., Melissa M. Lewis, M.P.H., Elaine Scallan, Ph.D., and Anne Schuchat, M.D., for the Emerging Infections Programs Network

From the Centers for Disease Control and Prevention (M.C.T., C.G.W., N.E.M., E.R.Z., M.M.L., E.S., A.S.) and the Georgia De-partment of Human Resources (M.M.F.) — both in Atlanta; Minnesota Department of Health, Minneapolis (R.L.); Connecti-cut Department of Public Health, Hart-ford (J.L.H.); Johns Hopkins University Bloomberg School of Public Health, Bal-timore (L.H.H.); School of Public Health, University of California at Berkeley, Berkeley (A.R.); University of Rochester School of Medicine and Dentistry, Roch-ester, NY (N.M.B.); Vanderbilt University School of Medicine, Nashville (A.S.C., W.S.); and Oregon Public Health Division, Portland (A.T.). Address reprint requests to Dr. Thigpen at: 3150 Rampart Rd., Fort Collins, CO 80521, or at mthigpen@cdc .gov or [email protected].

N Engl J Med 2011;364:2016-25.Copyright © 2011 Massachusetts Medical Society.

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BackgroundThe rate of bacterial meningitis declined by 55% in the United States in the early 1990s, when the Haemophilus inf luenzae type b (Hib) conjugate vaccine for infants was introduced. More recent prevention measures such as the pneumococcal conjugate vaccine and universal screening of pregnant women for group B streptococcus (GBS) have further changed the epidemiology of bacterial meningitis.

MethodsWe analyzed data on cases of bacterial meningitis reported among residents in eight surveillance areas of the Emerging Infections Programs Network, consisting of ap-proximately 17.4 million persons, during 1998–2007. We defined bacterial meningitis as the presence of H. inf luenzae, Streptococcus pneumoniae, GBS, Listeria monocytogenes, or Neisseria meningitidis in cerebrospinal fluid or other normally sterile site in association with a clinical diagnosis of meningitis.

ResultsWe identified 3188 patients with bacterial meningitis; of 3155 patients for whom outcome data were available, 466 (14.8%) died. The incidence of meningitis changed by −31% (95% confidence interval [CI], −33 to −29) during the surveillance period, from 2.00 cases per 100,000 population (95% CI, 1.85 to 2.15) in 1998–1999 to 1.38 cases per 100,000 population (95% CI 1.27 to 1.50) in 2006–2007. The median age of patients increased from 30.3 years in 1998–1999 to 41.9 years in 2006–2007 (P<0.001 by the Wilcoxon rank-sum test). The case fatality rate did not change significantly: it was 15.7% in 1998–1999 and 14.3% in 2006–2007 (P = 0.50). Of the 1670 cases re-ported during 2003–2007, S. pneumoniae was the predominant infective species (58.0%), followed by GBS (18.1%), N. meningitidis (13.9%), H. inf luenzae (6.7%), and L. monocyto-genes (3.4%). An estimated 4100 cases and 500 deaths from bacterial meningitis occurred annually in the United States during 2003–2007.

ConclusionsThe rates of bacterial meningitis have decreased since 1998, but the disease still often results in death. With the success of pneumococcal and Hib conjugate vaccines in reducing the risk of meningitis among young children, the burden of bacterial men-ingitis is now borne more by older adults. (Funded by the Emerging Infections Pro-grams, Centers for Disease Control and Prevention.)

The New England Journal of Medicine Downloaded from nejm.org at Hinari Phase 1 sites -- comp on November 3, 2011. For personal use only. No other uses without permission.

Copyright © 2011 Massachusetts Medical Society. All rights reserved.

Charactéristiques 1998-1999 2006-2007 2006-2007vs 1998-1999

Nombre de cas pour 100 000 habitants (95%IC)Age

18-34 ans 0.99 (0.79-1.22 0.66 (0.50-0.86) -33 (-38 to -27)35-49 ans 1.23 (1.01-1.48) 0.95 (0.76-1.16) -23 (-29 to -17)50-64 ans 2.15 (1.75-2.57) 1.73 (1.44-2.06) -19 (-25 to -14)> 65 ans 2.64 (2.13-3.16) 1.92 (1.53-2.38) -27 (-32 to -22)Tous ages 2.00 (1.85-2.15) 1.38 (1.27-1.50) -31 (-33 to -29)

GermeS. pneumoniae 1.09 (0.98-1.20) 0.81 (0.72-0.90) -26 (-29 to -23)N. meningitidis 0.44 (0.37-0;51) 0.19 (0.14-0.24) -58 (-61 to -54)Streptocoque B 0.24 (0.20-0.30) 0.25 (0.21-0.31) 4 (-3 to 12)H. influenzae 0.12 (0.09-0.17) 0.08 (0.05-0.11) -35 (-42 to -27)L. monocytogenes 0.10 (0.08-0.16) 0.05 (0.03-0.08) -46 (-53 to -39)

Incidence Méningite Bactérienne chez l’AdulteEtats-Unis 1998-2007

original article









A BS TR AC T







original article









A BS TR AC T







Evolution des taux d’incidence des méningites bactériennesEpibac 2005-2011 – (redressés pour la couverture)

Isabelle Parent 2013

Epidémiologie

•0,7% des cas de tuberculose•Facteurs favorisant:

–Conditions socioéconomiques défavorisées–Alcoolisme–VIH

Lucas M J et al. Neurol Neuroimmunol Neuroinflammation 2014;1:e9

Marjolein J. Lucas, MDMatthijs C. Brouwer,

MD, PhDArie van der Ende, PhDDiederik van de Beek,

MD, PhD

Correspondence toDr. van de Beek:[email protected]

Supplemental dataat Neurology.org/nn

Outcome in patients with bacterialmeningitis presenting with a minimalGlasgow Coma Scale score

ABSTRACT

Objective: In bacterial meningitis, a decreased level of consciousness is predictive for unfavorableoutcome, but the clinical features and outcome in patients presenting with a minimal score on theGlasgow Coma Scale are unknown.

Methods: We assessed the incidence, clinical characteristics, and outcome of patients with bacterialmeningitis presenting with a minimal score on the Glasgow Coma Scale from a nationwide cohortstudy of adults with community-acquired bacterial meningitis in theNetherlands from2006 to 2012.

Results: Thirty of 1,083 patients (3%) presented with a score of 3 on the Glasgow Coma Scale. In22 of 30 patients (73%), the minimal Glasgow Coma Scale score could be explained by use ofsedative medication or complications resulting from meningitis such as seizures, cerebral edema,and hydrocephalus. Systemic (86%) and neurologic (47%) complications occurred frequently,leading to a high proportion of patients with unfavorable outcome (77%). However, 12 of 30 pa-tients (40%) survived and 7 patients (23%) had a good functional outcome, defined as a score of5 on the Glasgow Outcome Scale. Patients presenting with a minimal Glasgow Coma Scale scoreon admission and bilaterally absent pupillary light responses, bilaterally absent corneal reflexes,or signs of septic shock on admission all died.

Conclusions: Patients with community-acquired bacterial meningitis rarely present with a minimalscore on the Glasgow Coma Scale, but this condition is associated with high rates of morbidityand mortality. However, 1 out of 5 of these severely ill patients will make a full recovery, stressingthe continued need for aggressive supportive care in these patients. Neurol NeuroimmunolNeuroinflammation 2014;1:e9; doi: 10.1212/NXI.0000000000000009

GLOSSARYICP 5 intracranial pressure.

Bacterial meningitis is a serious and life-threatening disease.1 Streptococcus pneumoniae andNeisseria meningitidis are the predominant causative pathogens of this disease in adults,2 causing80%–85% of all cases, with high associated morbidity and mortality rates.3–5 Many patientswith bacterial meningitis present with an abnormal conscious state, and 15%–20% of patientsare comatose upon presentation.5 An abnormal conscious state, in most studies graded by theGlasgow Coma Scale, is a strong predictor for poor disease outcome in bacterial meningitis.5,6

The exact cause of an abnormal conscious state in bacterial meningitis remains unclear, but it islikely caused by a complex interaction between severe brain inflammation, raised intracranialpressure (ICP), and resulting complications such as hydrocephalus, cerebral (micro)infarctions,or epileptic seizures.7–9 The evaluation of patients with an abnormal conscious state in bacterialmeningitis might further be complicated by the use of antiepileptic or sedative medication.

The clinical features and outcome of the most severely ill patients, those who present with a scoreon the Glasgow Coma Scale of 3, are unknown. The time frame for concluding that neurologic

From the Departments of Neurology (M.J.L., M.C.B., D.v.d.B.) and Medical Microbiology (A.v.d.E.) and the Netherlands Reference Laboratoryfor Bacterial Meningitis (A.v.d.E.), Academic Medical Center, Center of Infection and Immunity Amsterdam (CINIMA), Amsterdam, theNetherlands.

Go to Neurology.org/nn for full disclosures. Funding information and disclosures deemed relevant by the authors, if any, are provided at the end ofthe article. The Article Processing Charge was paid by the authors.

This is an open access article distributed under the terms of the Creative Commons Attribution-Noncommercial No Derivative 3.0 License, whichpermits downloading and sharing the work provided it is properly cited. The work cannot be changed in any way or used commercially.

Neurology.org/nn © 2014 American Academy of Neurology 1

ª 2014 American Academy of Neurology. Unauthorized reproduction of this article is prohibited.

20%Fr

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Score de Glasgow

Etude COMBATEtude COMBATObservatoire national des mObservatoire national des mééningites bactningites bactéériennes de l'adulteriennes de l'adulte

EtatEtat--des des --lieuxlieux des inclusionsdes inclusions

Newsletter investigateurs n°6, Déc 2014

Chers collègues investigateurs,

Grâce à vous 430 patients ont été pré-inclus dans l’étude à ce jour et 345 d’entre eux sont inclus définitivement. Nous

nous rapprochons à grands pas des objectifs fixés pour la cohorte. Nous vous remercions vivement pour tous vos

efforts. Un grand merci en particulier pour vos réponses suite à notre dernière relance concernant les données

manquantes. Nous nous tenons à votre disposition pour répondre à vos questions et vous souhaitons d’excellentes

fêtes de fin d’année.

Courbe cumulative des inclusions au 2 dCourbe cumulative des inclusions au 2 dééc 2014c 2014

RRéépartition des micropartition des micro--organismesorganismes

1Klebsiella oxytoca

0,62Staphylococcus aureus

1Capnocytophaga cynodegmi

1Acinetobacter baumannii

15,453Non renseignés par les microbiologistes hospitaliers

1Non spécifiés2Pasteurella multocida7Klebsiella pneumoniae

1Enterococcus faecalis1Enterobacter cloacae

1Capnocytophaga canimorsus

4,616Autres microorganismes dont

1,24Escherichia coli4,114Listeria monocytogenes8,429Streptocoques non pneumocoque3,813Haemophilus influenzae

17,460Méningocoque44,6154Pneumocoque84,6292Identifiés par les microbiologistes hospitaliers

%nMicroorganismes

Informations renseignInformations renseignéées par les microbiologistes es par les microbiologistes hospitaliers chez les patients inclus dhospitaliers chez les patients inclus dééfinitivement (N=345)finitivement (N=345)

DonnDonnéées microbiologiqueses microbiologiques

Distribution mensuelle des inclusions au 2 dDistribution mensuelle des inclusions au 2 dééc 2014 c 2014

Informations renseignInformations renseignéées par les microbiologistes es par les microbiologistes hospitaliers des centres et des CNRhospitaliers des centres et des CNR

2529

17

28

18

1113 13 12

16

33

25

1517

10 1013

8 8 7 6

10 1 2 3 4 40 1 1

3 4

11

35 6 6

2 13

1 1

6

0

10

0

10

20

30

40

50

févr

-13

mar

s-1

3

avr-

13

mai

-13

juin

-13

juil-

13

aoû

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3

sep

t-1

3

oct

-13

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3

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3

jan

v-1

4

févr

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mar

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mai

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juin

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juil-

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aoû

t-1

4

sep

t-1

4

oct

-14

no

v-1

4

dé

c-1

4

Patients inclus

Patients pré-inclus uniquement

Nb de patients

0

75

150

225

300

375

450Nb de patients

Objectif Total patients Pré-inclus uniquement Inclus

févr-13

mars-13

avr-13

mai-13

juin-13

juil-13

août-13

sept-13

oct-13

nov-13

déc-13

janv-14

Févr-14

mars-14

avr-14

mai-14

juin-14

juil-14

août-14

sept-14

oct-14

nov-14

déc-14

Etude COMBATEtude COMBATObservatoire national des mObservatoire national des mééningites bactningites bactéériennes de l'adulteriennes de l'adulte

EtatEtat--des des --lieuxlieux des inclusionsdes inclusions

Newsletter investigateurs n°6, Déc 2014

Chers collègues investigateurs,

Grâce à vous 430 patients ont été pré-inclus dans l’étude à ce jour et 345 d’entre eux sont inclus définitivement. Nous

nous rapprochons à grands pas des objectifs fixés pour la cohorte. Nous vous remercions vivement pour tous vos

efforts. Un grand merci en particulier pour vos réponses suite à notre dernière relance concernant les données

manquantes. Nous nous tenons à votre disposition pour répondre à vos questions et vous souhaitons d’excellentes

fêtes de fin d’année.

Courbe cumulative des inclusions au 2 dCourbe cumulative des inclusions au 2 dééc 2014c 2014

RRéépartition des micropartition des micro--organismesorganismes

1Klebsiella oxytoca

0,62Staphylococcus aureus

1Capnocytophaga cynodegmi

1Acinetobacter baumannii

15,453Non renseignés par les microbiologistes hospitaliers

1Non spécifiés2Pasteurella multocida7Klebsiella pneumoniae

1Enterococcus faecalis1Enterobacter cloacae

1Capnocytophaga canimorsus

4,616Autres microorganismes dont

1,24Escherichia coli4,114Listeria monocytogenes8,429Streptocoques non pneumocoque3,813Haemophilus influenzae

17,460Méningocoque44,6154Pneumocoque84,6292Identifiés par les microbiologistes hospitaliers

%nMicroorganismes

Informations renseignInformations renseignéées par les microbiologistes es par les microbiologistes hospitaliers chez les patients inclus dhospitaliers chez les patients inclus dééfinitivement (N=345)finitivement (N=345)

DonnDonnéées microbiologiqueses microbiologiques

Distribution mensuelle des inclusions au 2 dDistribution mensuelle des inclusions au 2 dééc 2014 c 2014

Informations renseignInformations renseignéées par les microbiologistes es par les microbiologistes hospitaliers des centres et des CNRhospitaliers des centres et des CNR

2529

17

28

18

1113 13 12

16

33

25

1517

10 1013

8 8 7 6

10 1 2 3 4 40 1 1

3 4

11

35 6 6

2 13

1 1

6

0

10

0

10

20

30

40

50

févr

-13

mar

s-1

3

avr-

13

mai

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juin

-13

juil-

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aoû

t-1

3

sep

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3

oct

-13

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3

dé

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jan

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4

févr

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mar

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avr-

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mai

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aoû

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Patients pré-inclus uniquement

Nb de patients

0

75

150

225

300

375

450Nb de patients

Objectif Total patients Pré-inclus uniquement Inclus

févr-13

mars-13

avr-13

mai-13

juin-13

juil-13

août-13

sept-13

oct-13

nov-13

déc-13

janv-14

Févr-14

mars-14

avr-14

mai-14

juin-14

juil-14

août-14

sept-14

oct-14

nov-14

déc-14

345 patients inclus entre fev 2013 et nov 201475% des patients ont été admis en réanimation

Pronostic

En fonction du germe

En fonction âge

En fonction pays

Pronostic

D. Van de Beek, Nat Clin Pract Neurol. 2006 Sep;2(9):504-16.

Pneumocoque (%)

Méningocoque(%)

GOS1 (décès) 30 7

2 (état végétatif) 1 0

3 (handicap sévère) 5 2

4 (handicap modéré) 14 3

5 (handicap léger ou absent) 50 88

Séquelles neurologiquesSurdité 22 8

Déficit focal 7 1

Altération fonctions supérieures 25 4

Mortalité Listeria monocytogenes

27% Mylonakis et al. Medicine. 1998

17% Brouwer et al. CID.2006

29% Amaya-Villar et al.BMC InfectiousDiseases.2010

20% Thigpen et al. NEJM. 2011

Causes de décès

Weisfelt, Lancet Neurol. 2006 Apr;5(4):332-42.

Causes de décès (%)

Causes neurologiques 39-75%

Engagement cérébral 13-75%Complications cérébrovasculaires 14%

Causes systémiquesDéfaillance cardio-respiratoire 21-25%Sepsis 19%

Association complications systémiques et neurologiques

29-43%

Hearing Loss from Pneumococcal Meningitis • CID 2010:51 (15 October) • 917

M A J O R A R T I C L E

Factors Associated with the Occurrenceof Hearing Loss after Pneumococcal Meningitis

Lise Worsøe,1 Per Caye-Thomasen,1,5 Christian Thomas Brandt,3,4 Jens Thomsen,1,5 and Christian Østergaard,21Department of Oto-rhino-laryngology, Head and Neck Surgery, Copenhagen University Hospital Gentofte, Hellerup, 2Department of ClinicalMicrobiology, Copenhagen University Hospital Herlev, Herlev, 3Department of Infectious Diseases, Copenhagen University Hospital Hvidovre,Hvidovre, 4Copenhagen HIV Programme, Faculty of Health Sciences, University of Copenhagen, and 5Faculty of Health Sciences, Universityof Copenhagen, Copenhagen, Denmark

Background. On the basis of a nationwide registration during a 5-year period (1999–2003), the frequency andseverity of hearing loss was investigated retrospectively in 343 consecutive Danish patients who survived pneu-mococcal meningitis, to identify important risk factors (including the pneumococcal serotype) for developmentof hearing loss.

Methods. Results of blood and cerebrospinal fluid (CSF) biochemistry, bacterial serotyping, follow-up au-diological examinations, and medical records were collected, and disease-related risk factors for hearing loss wereidentified. The mean pure-tone hearing threshold levels were compared with normative data.

Results. Of 240 patients examined by use of audiometry, 129 (54%) had a hearing deficit, and 50 (39%) ofthese 129 patients were not suspected of hearing loss at discharge from hospital. Of the 240 patients, 16 (7%)had profound unilateral hearing loss, and another 16 (7%) had bilateral profound hearing loss. Significant riskfactors for hearing loss were advanced age, the presence of comorbidity, severity of meningitis, a low CSF glucoselevel, a high CSF protein level, and a certain pneumococcal serotype ( ). By applying multivariate logisticP ! .05regression analysis, we found that advanced age, female sex, and a certain serotype were significant risk factors,because fewer patients with serotype 6B had hearing loss than did patients with serotype 12F ( ), whichP p .03was the most commonly occurring serotype.

Conclusion. Hearing loss is common after pneumococcal meningitis, and audiometry should be performedon all those who survive pneumococcal meningitis. Important risk factors for hearing loss are advanced age, femalesex, severity of meningitis, and bacterial serotype.

Streptococcus pneumoniae remains the most common

cause of bacterial meningitis and is associated with a

high risk of an unfavorable outcome, with hearing loss

as the most common complication [1]. Studies on the

incidence and severity of hearing loss in adults are

scarce. Most investigations have dealt with children,

were rather small in size, and were often part of larger

series on meningitis of various etiologies. The reported

Received 16 February 2010; accepted 13 July 2010; electronically published 3September 2010.

Reprints or correspondence: Dr Lise Worsøe, Dept of Oto-rhino-laryngology, Headand Neck Surgery, Copenhagen University Hospital Gentofte, DK-2900 Hellerup,Copenhagen, Denmark ([email protected]).

Clinical Infectious Diseases 2010; 51(8):917–924! 2010 by the Infectious Diseases Society of America. All rights reserved.1058-4838/2010/5108-0007$15.00DOI: 10.1086/656409

incidence of hearing impairment as sequela of pneu-

mococcal meningitis ranges from 7% to 36% of sur-

vivors [2–5]. It has been suggested that the higher figure

may be closer to the actual incidence, considering the

difficulties in detecting hearing loss, even severe cases,

in retrospective studies. Moreover, little is known about

risk factors for hearing loss.

The incidence and serotype pattern of pneumococcal

meningitis vary by geographic location [6–8], and case-

fatality rates differ according to occurring serotype [9,

10]. However, to our knowledge, the correlation be-

tween serotype and postmeningitis hearing loss has not

been addressed previously and may be of interest in

relation to future treatment and vaccination strategies.

This study represents a nationwide investigation of the

frequency and severity of postmeningitis hearing loss

in consecutive Danish patients with pneumococcal

meningitis during a 5-year period (1999–2003).

at HINARI Ivory Coast Administrative Account on November 3, 2011http://cid.oxfordjournals.org/

Downloaded from

Hearing Loss from Pneumococcal Meningitis • CID 2010:51 (15 October) • 919

Figure 1. Mean pure-tone thresholds after pneumococcal meningitis in Denmark from 1999 to 2003 and the reference values individually matched forbetter and worse ear, age, and sex (normative data). A, Data obtained from the better ear ( ), compared with matched references. B, Data obtainedn p 240from the worse ear ( ), compared with matched references. C, Data obtained from both ears ( ), compared with matched references (panelsn p 240 n p 480A and B combined). Data represent patients with no, mild, severe, or profound hearing loss (HL). The bars indicate the 95% confidence interval. Thenumbers in parentheses indicate sample size of ears tested at the individual frequencies. A mean HL distributed evenly across the frequency spectrumis apparent.

Figure 2. Age distribution, survival, and hearing outcome for meningitis due to Streptococcus pneumoniae in Denmark from 1999 to 2003 ( ).N p 505The hearing loss was determined by audiometric testing. Adult patients had a higher mortality and a higher occurrence of hearing loss, compared withpediatric patients ( ).P ! .001

sion, whereas the majority of audiometric assessments (87%)were performed 2 months or more after hospital admission.

Comparison of bedside hearing evaluation and audiometrictesting. The incidence of hearing loss was significantly higher

for patients tested by use of audiometry than for patients withhearing data obtained from medical records (54% [129/240]vs 27% [81/305]; ). For 192 patients, hearing data ex-P ! .001isted both from medical records and from audiometry proper.

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Table 1. Risk Factors for Hearing Loss after Streptococcus pneumoniae Meningitis in Denmark from 1999 to 2003

Risk factor

Patients withno hearing loss

(np111)

Patients withhearing lossa

(np127)

Univariate analysis Multivariate analysis

ORb (95% CI) P ORb (95% CI) P

Female sex 63/111 (57) 59/127 (47) 0.66 (0.40–1.10) .12 0.46 (0.23–0.93) .03Age 12 years 52/111 (47) 100/127 (79) 4.20 (2.39–7.40) !.001 6.39 (3.03–13.5) !.001Predisposing condition 7/97 (7) 9/102 (9) 1.24 (0.44–3.48) .68 …Ear focus 43/103 (42) 57/117 (49) 1.33 (0.78–2.26) .30 …Lung focus 16/103 (16) 19/118 (16) 1.04 (0.51–2.16) .91 …Presence of comorbidityc 12/97 (12) 24/102 (24) 2.18 (1.02–4.65) .044 0.88 (0.34–2.28) .80Fever 92/95 (97) 102/104 (98) 1.66 (0.27–10,2) .58 …Back rigidity 50/81 (62) 60/92 (65) 1.16 (0.63–2.16) .63 …Decreased consciousness 80/89 (90) 107/114 (94) 1.72 (0.61–4.81) .30 …Convulsion 23/97 (24) 31/110 (28) 1.26 (0.68–2.36) .47 …Receipt of mechanical ventilation 26/98 (27) 59/115 (51) 2.92 (1.64–5.20) !.001 1.91 (0.92–3.95) .08Receipt of steroid therapy 24/95 (25) 19/105 (18) 0.65 (0.33–1.29) .22 …CSF WBC count, cells/mL 1608 (533–3517) 1979 (530–5383) 1.23 (0.89–1.70) .20 …

Proportion of patients 94/111 104/127 … …CSF protein level, g/L 1.8 (1.0–3.2) 3.1 (1.9–5.0) 1.28 (1.12–1.47) !.001 …

Proportion of patients 85/111 96/127 … …CSF glucose level, mmol/L 1.6 (0.4–3.2) 0.7 (0.3–2.0) 0.73 (0.60–0.90) .003 …

Proportion of patients 83/111 91/127 … …CSF/blood glucose ratio 0.22 (0.05–0.50) 0.10 (0.04–0.26) 0.11 (0.02–0.63) .01 …

Proportion of patients 56/111 60/127 … …Blood WBC count, 109 cells/L 21.5 (13.9–26.7) 18.9 (11.5–26.3) 0.99 (0.96–1.02) .41 …

Proportion of patients 94/111 104/127 … …Serum sodium level, mmol/L 133 (130–136) 136 (133–139) 1.16 (1.07–1.27) .001 …

Proportion of patients 56/111 63/127 … …

NOTE. Data are proportion (%) of patients or median values (interquartile range), unless otherwise indicated. Hearing loss was determined by use of audiometry.CI, confidence interval; CSF, cerebrospinal fluid; OR, odds ratio; WBC, white blood cell.

a Two patients were excluded from the analysis because they had 11 episode of meningitis.b Calculated per additional units for continuous data, except for CSF WBC count, which was log10 cells/mL.c Underlying disease was defined as previous splenectomy, presence of immunodeficiency, cancer, diabetes mellitus, alcoholism, and/or chronic obstructive

lung disease/asthma, or the use of immunosuppressive drugs.

Fifty patients were evaluated as having no hearing loss at hos-pital discharge; however, an abnormal audiometric test resultwas demonstrated subsequently. In addition, audiometric test-ing could not confirm the suspicion of hearing loss for 8 adultpatients. Six of these 8 patients had an ear focus and weredischarged after a median of 12 days (range, 10–27 day), sothe initial hearing loss could potentially be of conductive causesand may have improved before audiometric testing. The sen-sitivity, specificity, and positive and negative predictive valuesof medical records regarding hearing loss were respectively 51%,91%, 87%, and 62% for all patients (38%, 100%, 100%, and81% for children and 54%, 77%, 85%, and 42% for adults).Therefore, all hearing data are from audiometric testing only.

Occurrence and severity of hearing loss. A significantlyhigher proportion of patients with posthospitalization audio-metric data had hearing loss, compared with patients examinedafter receiving the mailed request in relation to this study (102/171 [60%] vs 27/69 [39%]; ). Of the 240 patients testedP p .004

by use of audiometry, 105 (44%) had hearing loss in the betterear. Of these patients, 81 (77%) were classified as having mildhearing loss, 8 (8%) were classified as having severe hearingloss, and 16 (15%) were classified as having profound hearingloss. Of the 123 patients (51%) with hearing loss in the worseear, 69 (56%) were classified as having mild hearing loss, 22(18%) were classified as having severe hearing loss, and 32(26%) were classified as having profound hearing loss. Of the240 patients tested by use of audiometry, 109 (54%) were foundto have at least unilateral mild hearing loss, whereas there were56 patients (23%) who had severe to profound hearing loss inat least 1 ear, 32 patients (13%) who had profound hearingloss unilaterally or bilaterally, and 16 patients (7%) who hadprofound hearing loss bilaterally.

The mean pure-tone thresholds for the better ear, the worseear, and both ears are shown in Figure 1. Patients with mildto profound hearing loss were found to have an average hearingloss (DPTA) of 27.5 dB (95% confidence interval [CI], 22.4–

at HIN

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Worsoe, CID 2010

Stratification Clinique MortalitéI GCS 15

signes focaux : 013%

II GCS 11-14ou

GCS 15 + signes focaux

31%

III GCS < 11 71%

Critères PronostiquesBritish Medical Research Council (1948)

Quelques éléments de clinique

Clinique

Country Netherlands France Spain Iceland Denmark

Observation periodNumber of patients

98-02696

01-0460

96-10295

75-94119

89-10172

Headache 87% 87% - - 58%

Nausea/vomiting 74% - 45% - -

Neck stiffness 83% - 69% 82% 65%

Rash 26% - 20% 52% -

Fever (>38.0°) 77% 93% 95% 97% 87%

Altered mental status 69% 30% 54% 66% 68%

Coma 14% - 7% 13% 16%

Focal neurologic deficits 34% 23% 15% - 21%

Triadoffever,neckstiffnessandalteredmentalstatus

44% - 41% 51% 45%

La clinique

Signe clinique Fréquence (%)

Fièvre 59 – 100

Confusion 56 – 96

Céphalées 21 – 81

Raideur de nuque 57 - 92

Choi, CID 2001; 33:1380–5

Méningites à pneumocoques: facteurs de risque

q Ages « extrêmes »: < 2 ans, > 50 ans

q Splénectomie, asplénisme

q VIH et autres immunodépressions

q Drépanocytose

q Dénutrition, alcoolisme, diabète

q Hypogammaglobulinémie liée à l’X et

autres déficits en Ig

q Syndrome de Wiscott-Aldrich

q Déficit en complément

q Brêche dure mère avec fuite de LCRq Implants cochléaires (enfants)

Lésions muqueuse ORL: sinusite, otite avec ou sans co-infection virale

En réanimation

•Age moyen: 56 + 17 (18-90 ans)•Triade classique (94/163, 55%)•SAPS II: 46 + 23•GCS: 9 + 3 ( 10 + 3 admission hôpital)•Plus de 50% des patients ont un FDR identifié(Idp dont HIV, diabète, brèche méningée, infection ORL)•71% sous VM et 24% en choc septique• Convulsions: 18 à 34%

Auburtin, Crit care med 2006Garcia-Cabrera E, ESICM 2008Lucas, Neurol Neuroimmunol 2014

Listeria: Facteurs favorisants

§ Cas sporadiques mais épidémies par contamination alimentaire possibles (charcuteries…).

§ Pas de terrain particulier: 30% des cas

§ Facteurs favorisants ou immunodépression: 70%

- Cancers, hémopathies malignes

- Corticoïdes au long cours

- Diabète

- Grossesse

En faveur de ListeriaCaractéristiques Commentaires

Age > 50 ans Age: 65+18*70% > 60 ans**

Immunosuppression 66%*Pas de terrain à risque: 25%**

Rhombencephalite 20 à 50%

Atteinte paires crâniennes 7%*

Examen direct négatifLCR « panaché »

60%*Le plus souvent PN

* Brouwer MC et al Clin Infect Dis 2006, **BEH 2008 (France)

Tuberculose neuromeningée

•Signes d’atteinte basilaire: paralysie nerfs craniens, troubles neurovégétatifs, rétention aiguë d’urine•Localisations extra-neurologiques•Hyponatrémie•LCR: lymphocytaire peu cellulaire, hypoglycorachique, hyperprotéinorachie mais pas toujours aussi typique•TDM: hydrocéphalie, prise de contraste des méninges de la base, infarctus

LactateSerum Procalcitonin

2011;15:R136254 patients

35 :BM

181: viral meningitis

CSF: 3.8 mmol/L:

Se: 94%, Sp: 92%

NPV: 99%, PPV:82%

0.28 ng/mlSe: 95%, Sp: 100%

NPV: 100%, PPV: 97%%

Les examens suivants sont optionnels

• Test immunochromatographique (binax NOW streptococcus pneumoniae® test)

• PCR sur le LCR • PCR méningocoque sur le sang• Biopsie cutanée en présence de purpura (PCR

méningocoque, ED et culture)• Dosage du lactate dans le LCR• Dosage de la procalcitonine sérique• Règles d’aide à la décision clinique aidant à différencier

méningite bactérienne et virale (règle de Hoen chez l’adulte et l’enfant, le Bacterial Meningitis Score ou le Meningitest® chez l’enfant)

Diagnostic microbiologique

• Examen direct LCR : 60-90%– 25%si < 103 ; 60%:103-105; 97%> 105)– pneumocoque (90%) > autres– antibiothérapie préalable

• Culture LCR: 85%• Hémocultures: environ 2/3 des cas • Examen direct et cultures de lésions

purpuriques (N. meningitidis)

Culture + Cultures – RT-PCR+

S. pneumoniae 50 26

N. meningitidis 91 107

2011

C-/RT-PCR+

•Recherche de BAAR dans le LCR +++ (A II)– Volume à analyser > 5 ml (A II)– Analyses répétées– Examen direct + jusqu’à 80% des malades– Négativation rapide après début ttt anti BK

•PCR BK (B II):– Sensibilité 56% (IC 95: 46-66%)– Spécificité 98% (IC 95: 97-99%)– ADN reste détectable longtemps après début ttt anti BK

•Adénosine déaminase (ADA): non recommandé en routine

Thwaites, J Infection 2009

Urgence à l’antibiothérapie

OR IC 95% P

Délai ATB 1.09/h 1.01-1.19 0.035

Facteurs de risque 1.55 0.997-2.21 0.052

Coma 1.58 0.88-2.86 0.13

Absence corticoides 1.52 0.82-2.79 0.18

Autre que meningocoque 2.07 0.69-6.18 0.19

Age 1.02/an 0.99-1.48 0.19

Køster-Rasmussen, J Infection (2008) 57, 449-54

Mortalité délai ATB

Proulx et al. QJM 2005

Amaya-Villar, ESICM 2008

Délai médian série espagnole:5h34min

La quadrature du cercle

•Confirmer le diagnostic•Débuter précocement l’antibiothérapie•Prendre en charge les défaillances d’organe

Physiopathologie

Bactérie

Colonisation

Pénétration muqueuses

Bactériémie Infection contigüe du SNC

Pénétration SNC

Multiplication dans espace sous-arachnoïdien

Libération substances inflammatoires et toxiques

Leucocytes

Vascularite

Ischémie

Œdèmecytotoxique

Agression neuronale

↑ Perméabilité BHE

Œdèmevasogénique

RésistanceÉlimination

LCR

Œdèmeinterstitiel

Stimulationet toxicité gliale

Antibiothérapie

Modalités de Prise en Charge

Rifampicine 600mgX2 pendant 48h

Mortalité délai ATB

Proulx et al. QJM 2005

Amaya-Villar, ESICM 2008

Délai médian série espagnole:5h34min

Mortalité et délaiprise en charge

h

%

ATB/TDM/PL

TDM/ATB/PL

TDM/PL/ATB%

Proulx et al., QJM 2005

%

Hémocultures

Patients Hc positives (%)

87 Méningites à pneumocoque (1) 64,5%

352 Méningites à pneumocoque (2) 74%

696 Méningites bactériennes 66%

156 Méningites à pneumocoque en réa 67%

(1) Kastenbauer, Brain 2003,126, 1015-25(2) (2)(3) DVDB, Nejm2004, 351;18, 1849(4) Auburtin, Crit Care Med 2006,34;11:2758

Scanner ou PL?

Hasbun, N Engl J Med 2001

Présence caractéristique clinique à l’admission*

TDM normale TDM anormale Total

Non 93 (97) 3 (3) 96 (100)

Oui 86 (62) 53 (38) 139 (100)

Total 179 (76) 56 (24) 235 (100)

*60 ans, immunodéprimé, maladie du système nerveux central, convulsion la semaine précédente, et anomalies suivantes: trouble de conscience, incapacité à répondre à 2 questions consécutives correctement, incapacité à exécuter 2 ordres successifs, paralysie oculomotrice, anomalies du champ visuel, paralysie faciale, monoparésie, anomalies du langage.

Scanner ou PL ?

Caractéristiques cliniques Anomalies sur TDM p

OUI NON

Signe de localisationOuiNon

12/20 (60)17/55 (31)

8/20 (40)38/55 (69)

0,03

Convulsion – 24hOuiNon

9/14 (64)20/61 (33)

5/14 (36)41/61 (67)

0,04

GCS < 12OuiNon

26/50 (52)3/25 (12)

24/50 (48)22/25 (88)

0,001

Kastenbauer, Nejm 2002

Convulsions et TDM

Convulsions Sans convulsion

P

TDM anormale 57 (53) 158(40) 0.01Sinusite/Otite 20 42 0.02Infarctus 21 43 0.02Œdème 15 42 0.32Hydrocéphalie 3 15 0.78Empyème 9 17 0.09Autre 8 22 0.17

Zoons E, Neurology 2008

together with the first dose of antibiotics and a restrictive ap-proach to early LP with CT before LP in patients presentingwith “red flags” were adopted. The necessity to start antibioticsbefore CT in suspected ABM was emphasized. At follow-up,median duration to antibiotic treatment was found to exceed2 hours, which was longer than that reported in 1994–2004[16]. Even if this duration was in agreement with that reportedby others [2, 4, 7, 21, 22, 24, 25, 27], the risk with delayed treat-ment had to be balanced against potential risks associated withLP. The documentation for LP-induced herniation in uncon-scious adults with elevated ICP alone was found to be limited,with available data showing that LP could be performed withoutserious consequences [3]. Also taking into account that in-creased ICP cannot be ruled out by a CT investigation, it wasconcluded that CT before LP added little to the managementof ABM in adults without focal neurological signs or signs ofimminent herniation.

In 2009, Swedish recommendations for ABMmanagement inadults were revised. Deletion of moderately to severely impairedconsciousness and new onset seizures as contraindications toimmediate LP constituted the major change. The reasons forthis change have been discussed in detail elsewhere [16, 17].In addition to being issued on the Swedish Society for InfectiousDiseases home page (www.infektion.net), the new recommen-dations were presented in a national medical journal in 2008[28, 29] and at the annual Swedish Medical Conference in 2009.

The present results demonstrate that after the change in theguidelines, adults with ABM were treated, on average, morethan 1 hour earlier. This finding held after confounding factors

were considered. Optimally, in ABM, use of antibiotics and cor-ticosteroids should be initiated within 0.5–1 hour from admis-sion [18–20].During 2010–2012, treatment starts were achievedwithin 1 hour in 35% of the cases and within 2 hours in 60%.Although far from the recommended time frames, these figuresare higher than those for 2005–2009 as well as most findingsfrom other countries that had treatment starts a median of2–4 hours after arrival [2, 4, 7, 21, 22, 24, 25, 27]. In line withprevious findings, old age and nonmeningococcal etiologywere associated with delayed treatment, and severely impairedmental status was associated with earlier treatment [2, 7, 12, 13].

The decrease in door-to-antibiotic time in 2010–2012 thatoccurred following the guideline revision was associated witha concomitant decrease in mortality. This decrease did not re-sult in a compensatory increased risk for neurological or hear-ing deficits; on the contrary, the rate of sequelae also decreasedsignificantly (Figure 2). Whereas the significance remained forsequelae after adjusting for confounding factors, this was notthe case for mortality. Mortality, however, was significantly as-sociated with delayed antibiotic treatment, which is consistentwith findings by others [2, 4, 7, 25]. In the current study, therewas a relative increase in mortality of about 13% for each hourof delay. Thus, the shorter door-to-antibiotic time likely con-tributed to the improved outcome observed in 2010–2012.

During 2008–2012, cerebral CT scan was performed in 83%of the patients. CT preceded LP in more than half of all casesand antibiotic treatment was not administered before CT in39% of all cases. As in other studies [7, 21, 22, 25], the sequenceof neuroimaging before LP resulted in a delay in adequate

Table 3. Main Outcomes and Main Confounders Related to Different Sequences of Lumbar Puncture and Computerized Tomography ofthe Brain

Outcome and Confounders LP Without Prior CT LP After CT P Value

Number of patients (%): n = 414 178 (43.0) 236 (57.0)Outcomes:Treatment <1 h: n/n available data (%): n = 343 60/154 (39.0) 47/189 (24.9) <.01Treatment <2 h: n/n available data (%): n = 343 95/154 (61.7) 91/189 (48.1) <.05

Mortality: 6/178 (3.4) 27/236 (11.4) <.01Sequelaea in survivors: n/n available data (%): n = 334 32/151 (21.2) 65/183 (35.5) <.01Favorable outcomeb: n/n available data (%): n = 367 119/157 (75.8) 92/210 (43.8) <.001

ConfoundersAge >60 y 86/178 (48.3) 102/236 (43.2) NSRLS ≥3/GCS ≤11 on admission: n/n available data (%) 55/160 (34.4) 75/221 (33.9) NSPneumococcal etiology: 68/178 (38.2) 129/236 (54.7) <.01Meningococcal etiology: 38/178 (21.3) 21/236 (8.9) <.01

Main outcomes were time from admission to adequate antibiotic treatment, mortality, and sequelae and main confounders were age, mental status on admission,and etiology. Two-tailed Fisher exact test was used for P values.Abbreviations: CT, computerized tomography; GCS, Glasgow coma scale; LP, lumbar puncture; NS, not statistically significant; RLS, reaction level scale.a Neurological and/or hearing deficits at follow-up 2–6 months after discharge (proportions of survivors with available data).b Recovery to normal activity without neurological or hearing deficits at follow-up 2–6 months after discharge (proportions of all patients with available data).

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together with the first dose of antibiotics and a restrictive ap-proach to early LP with CT before LP in patients presentingwith “red flags” were adopted. The necessity to start antibioticsbefore CT in suspected ABM was emphasized. At follow-up,median duration to antibiotic treatment was found to exceed2 hours, which was longer than that reported in 1994–2004[16]. Even if this duration was in agreement with that reportedby others [2, 4, 7, 21, 22, 24, 25, 27], the risk with delayed treat-ment had to be balanced against potential risks associated withLP. The documentation for LP-induced herniation in uncon-scious adults with elevated ICP alone was found to be limited,with available data showing that LP could be performed withoutserious consequences [3]. Also taking into account that in-creased ICP cannot be ruled out by a CT investigation, it wasconcluded that CT before LP added little to the managementof ABM in adults without focal neurological signs or signs ofimminent herniation.

In 2009, Swedish recommendations for ABMmanagement inadults were revised. Deletion of moderately to severely impairedconsciousness and new onset seizures as contraindications toimmediate LP constituted the major change. The reasons forthis change have been discussed in detail elsewhere [16, 17].In addition to being issued on the Swedish Society for InfectiousDiseases home page (www.infektion.net), the new recommen-dations were presented in a national medical journal in 2008[28, 29] and at the annual Swedish Medical Conference in 2009.

The present results demonstrate that after the change in theguidelines, adults with ABM were treated, on average, morethan 1 hour earlier. This finding held after confounding factors

were considered. Optimally, in ABM, use of antibiotics and cor-ticosteroids should be initiated within 0.5–1 hour from admis-sion [18–20].During 2010–2012, treatment starts were achievedwithin 1 hour in 35% of the cases and within 2 hours in 60%.Although far from the recommended time frames, these figuresare higher than those for 2005–2009 as well as most findingsfrom other countries that had treatment starts a median of2–4 hours after arrival [2, 4, 7, 21, 22, 24, 25, 27]. In line withprevious findings, old age and nonmeningococcal etiologywere associated with delayed treatment, and severely impairedmental status was associated with earlier treatment [2, 7, 12, 13].

The decrease in door-to-antibiotic time in 2010–2012 thatoccurred following the guideline revision was associated witha concomitant decrease in mortality. This decrease did not re-sult in a compensatory increased risk for neurological or hear-ing deficits; on the contrary, the rate of sequelae also decreasedsignificantly (Figure 2). Whereas the significance remained forsequelae after adjusting for confounding factors, this was notthe case for mortality. Mortality, however, was significantly as-sociated with delayed antibiotic treatment, which is consistentwith findings by others [2, 4, 7, 25]. In the current study, therewas a relative increase in mortality of about 13% for each hourof delay. Thus, the shorter door-to-antibiotic time likely con-tributed to the improved outcome observed in 2010–2012.

During 2008–2012, cerebral CT scan was performed in 83%of the patients. CT preceded LP in more than half of all casesand antibiotic treatment was not administered before CT in39% of all cases. As in other studies [7, 21, 22, 25], the sequenceof neuroimaging before LP resulted in a delay in adequate

Table 3. Main Outcomes and Main Confounders Related to Different Sequences of Lumbar Puncture and Computerized Tomography ofthe Brain

Outcome and Confounders LP Without Prior CT LP After CT P Value

Number of patients (%): n = 414 178 (43.0) 236 (57.0)Outcomes:Treatment <1 h: n/n available data (%): n = 343 60/154 (39.0) 47/189 (24.9) <.01Treatment <2 h: n/n available data (%): n = 343 95/154 (61.7) 91/189 (48.1) <.05

Mortality: 6/178 (3.4) 27/236 (11.4) <.01Sequelaea in survivors: n/n available data (%): n = 334 32/151 (21.2) 65/183 (35.5) <.01Favorable outcomeb: n/n available data (%): n = 367 119/157 (75.8) 92/210 (43.8) <.001

ConfoundersAge >60 y 86/178 (48.3) 102/236 (43.2) NSRLS ≥3/GCS ≤11 on admission: n/n available data (%) 55/160 (34.4) 75/221 (33.9) NSPneumococcal etiology: 68/178 (38.2) 129/236 (54.7) <.01Meningococcal etiology: 38/178 (21.3) 21/236 (8.9) <.01

Main outcomes were time from admission to adequate antibiotic treatment, mortality, and sequelae and main confounders were age, mental status on admission,and etiology. Two-tailed Fisher exact test was used for P values.Abbreviations: CT, computerized tomography; GCS, Glasgow coma scale; LP, lumbar puncture; NS, not statistically significant; RLS, reaction level scale.a Neurological and/or hearing deficits at follow-up 2–6 months after discharge (proportions of survivors with available data).b Recovery to normal activity without neurological or hearing deficits at follow-up 2–6 months after discharge (proportions of all patients with available data).

Bacterial Meningitis and Early LP • CID 2015:60 (15 April) • 1167

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M A J O R A R T I C L E

Adult Bacterial Meningitis: Earlier Treatmentand Improved Outcome Following GuidelineRevision Promoting Prompt Lumbar Puncture

Martin Glimåker,1 Bibi Johansson,1 Örjan Grindborg,1 Matteo Bottai,2 Lars Lindquist,1 and Jan Sjölin31Unit for Infectious Diseases, Department of Medicine, Karolinska Institutet and Karolinska University Hospital, 2Unit of Biostatistics, Institute ofEnvironmental Medicine, Karolinska Institutet, Stockholm, and 3Section of Infectious Diseases, Department of Medical Sciences, Uppsala University,Sweden

Background. In suspected acute bacterial meningitis (ABM), cerebral computerized tomography (CT) is recom-mended before lumbar puncture (LP) if mental impairment. Despite guideline emphasis on early treatment, per-forming CT prior to LP implies a risk of delayed treatment and unfavorable outcome. Therefore, Swedishguidelines were revised in 2009, deleting impaired mental status as a contraindication for LP without prior CTscan. The aim of the present study was to evaluate the guideline revision.

Methods. The Swedish quality registry for community-acquired ABM was analyzed retrospectively. Door-to-an-tibiotic time and outcome were compared among patients treated 2005–2009 (n = 394) and 2010–2012 (n = 318).The effect of different LP–CT sequences was analyzed during 2008–2012.

Results. Adequate treatment was started 1.2 hours earlier, and significantly more patients were treated <2 hoursfrom admission 2010–2012 than 2005–2009. Compared with CT before LP, immediate LP resulted in 1.6 hoursearlier treatment, significant increase in door-to-antibiotic times of <1 and <2 hours, and a favorable outcome.In 2010–2012, mortality was lower (6.9% vs 11.7%) and the risk of sequelae at follow-up decreased (38% vs 49%)in comparison with 2005–2009. Treatment delay resulted in a significantly increased risk for fatal outcome, with arelative increase in mortality of 12.6% per hour of delay.

Conclusions. The deletion of impaired mental status as contraindication for prompt LP and LP without priorCT scan are associated with significantly earlier treatment and a favorable outcome. A revision of current interna-tional guidelines should be considered.

Keywords. bacterial meningitis; lumbar puncture; guidelines; time to treatment; outcome.

Acute bacterial meningitis (ABM) is a rare but potenti-ally life-threatening disease. Despite modern antibiotictreatment, use of corticosteroids, and advanced inten-sive care, ABM is still associated with a mortality ofabout 10%–30% and a high risk of neurological deficits[1–8]. ABM leads to cerebral edema and increasedintracranial pressure (ICP) that may result in brain

herniation, which is a major cause of morbidity andmortality [5, 9–13]. Lumbar puncture (LP) is the main-stay in the diagnosis of ABM; however, a long-standingcontroversy exists regarding the potential risk of LP-induced brain herniation [10, 11, 14–17]. Current inter-national guidelines use the “red flags” of papilledema,focal neurological signs, moderate to severe impairmentof mental status, immunocompromised state, and newonset seizures to identify patients with an increased riskof a cerebral mass lesion and elevated ICP and, thus,with contraindications to immediate LP. In these pa-tients, cerebral computed tomography (CT) before LP isrecommended [18–20]. Similar guidelines were intro-duced in Sweden in 2004. However, as in other interna-tional reports, CT was performed too often andadherence to the recommendations to start antibiotics

Received 23 September 2014; accepted 24 December 2014; electronically pub-lished 5 February 2015.

Correspondence: Martin Glimåker, MD, PhD, Department of Infectious Diseases,Karolinska University Hospital, 171 76 Stockholm, Sweden ([email protected]).

Clinical Infectious Diseases® 2015;60(8):1162–9© The Author 2015. Published by Oxford University Press on behalf of the InfectiousDiseases Society of America. All rights reserved. For Permissions, please e-mail:[email protected]: 10.1093/cid/civ011

1162 • CID 2015:60 (15 April) • Glimåker et al

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Clin Infect Dis. (2015) 60 (8): 1162-1169.

Indication TDM avant PL

•Survenue de convulsions récentes•Trouble de la conscience (GCS<11)•Déficit neurologique focalisé (item 2 à 11 score NIHSS)

–Commandes (ouverture des yeux, ouverture du poing)–Oculomotricité–Champ visuel–Paralysie faciale–Motricité membre supérieur–Motricité membre inférieur–Ataxie–Sensibilité–Langage–Dysarthrie–Extinction, négligence

CC Méningites, SPILF 2009

Rationnel

•Diminution de la réponse inflammatoire et permettre ainsi de diminuer le risque de dommages cérébraux•Plusieurs études expérimentales chez l’animal ont conclu à un effet positif sur les produits de l’inflammation

D’après Mustafa M, J Infect Dis 1989

0"

5"

10"

15"

20"

25"

H0" H6" H8" H10" H12" H20"

Méningite"(MB)"MB+CTX"H6"MB+CTX+DXM"H6"MB+CTX"H6+DXM"H7"

TNFα (ng/ml)

Dexamethasone (1)

Dexamethasone (2)

DXM n’est pas l’arme absolue…

De Gans, N Engl J Med 2002; 347:1549-56

DXM dans le temps

1998-2002 2006-2008 p

DXM 10mgX4 11 (3%) 217 (79%) <0.001

Décès 107 (30%) 61 (22%) 0.018

Evolution défavorable

177 (50%) 109 (39%) 0.016

Surdité 55 (22%) 25 (11%) 0.005

Complications systémiques

134 (38%) 117 (42%) NS

DVDB, Neurology 2010

Corticothérapie adjuvante

•Oui en particulier si méningite à pneumocoque•Forte dose: DXM 10mg IV x 4 pdt 4j•Avant la 1ere dose d’antibiotique voire en même temps•Inutile à posteriori ?•Si état de choc: HSHC 50mg x 4

En pratiqueTDM avant PL2 HémoculturesDXM 10mg IVD

Cefotaxime 2g IVDTDMPL

PL d’emblée2 Hémocultures

PLSi trouble:

DXM 10mg IVD, cefotaxime 2g IVD

En fonction examen direct:+DXM

Antibiothérapie adaptée

Suspicion Méningite/méningoencéphalite

Indication TDM?

Si TDM, DXM/Antibiothérapie

Ponction Lombaire

Normale Nbreux élémentsG basse, P élevée

Nbreux élémentsG Nle, P peu élevée

Nbreux élémentsGR

G Nle, P élevée

MéningiteBactérienne

MéningiteVirale

MéningiteHerpétique

Pression LCR

N=216 Pression LCR < 40 cmH2O

Pression LCR > 40 cmH2O

N 131 (61%) dont 38 (18%) P nle

85 (39%)

Coma 14 (11%) 20 (24%) P=0,01

Evolution défavorable

30% 35%

DVDB, N Engl J Med 351;18:1849-59

Stratification Clinique MortalitéI GCS 15

signes focaux : 013%

II GCS 11-14ou


31%

III GCS < 11 71%

Critères PronostiquesBritish Medical Research Council (1948)

Corticothérapie adjuvanteCritères modifiés duBMRC

Clinique Protocole thérapeutique

I GCS 15signes focaux : 0

TTT IV 2 SEMAINESDXM 0.3 mg/kg semaine 1

0.2mg/kg semaine 2Puis TTT PO 4 semaines

II GCS 11-14ou


TTT IV 4 SEMAINESDXM 0.4mg/kg/j semaine 1

0.3mg/kg/j semaine 20.2mg/kg/j semaine 30.1mg/kg/j semaine 4

Puis TTT PO 4 SEMAINESDXM 4 mg / jDécroissance 1mg/j par semaine

III GCS < 11

Germe évoqué Antibiotique Dosage *Suspicion de pneumocoque(cocci Gram +)

CéfotaximeOuceftriaxone

300 mg/kg/j i.v., soit en 4 perfusions, soit en administration continue avecdose de charge de 50 mg/kg sur 1 heure**100 mg/kg/j i.v., en 1 ou 2 perfusions

Suspicion de méningocoque(cocci Gram –)

CéfotaximeOuceftriaxone

200 mg/kg/j i.v., soit en 4 perfusions, soit en administration continue avecdose de charge de 50 mg/kg sur 1 heure**75 mg/kg/j i.v., en 1 ou 2 perfusions

Suspicion de listériose(Bacille Gram +)

Amoxicilline+gentamicine

200 mg/kg/j i.v., soit en 4 perfusions, soit en administration continue3 à 5 mg/kg/j i.v., en 1 perfusion unique journalière

64

Méningites à pneumocoque de l’adulte : évolution de la résistance aux β-lactamines

E. Varon données CNR pour 2010

Sensibilité N. meningitidis (données CNR)

Antibiotiques 2010 (n=3083)

Pénicilline G 20,7% de sensibilité réduite*

Céfotaxime** 100% sensible

Ceftriaxone 100% sensible

Ciprofloxacine 5 souches résistantes

Rifampicine 3 souches résistantes

*Pénicilline G : CMI ≥0,125 mg/L** Cefotaxime: CMI ≤ 0,25mg/L

Durée de traitementMicro-organismes Durée recommandée

S. pneumoniae 10-14 j

N. meningitidis 7 j

H. influenzae 7-10j

L. monocytogenes 21 j

Recommandations internationales

Délai médian réalisation PL: 5h51 (1h09-26h20)

Délai médian antibiothérapie: 6h31 (1h04-17h48)

Delaire, ECCMID 2014

Prise en charge méningite bactérienne SAU

95 patients suspects de méningite (2010-2011)

Delaire, ECCMID 2014

42%

58%

Antibiothérapie(type/dose)

Appropriée (n=15)Inappropriée (n=21)

36 patients sur 95 avec antibiothérapie pour méningite

Prise en charge méningite bactérienne SAU

Nom

bre

de c

as

21 6

2

3

7

24

5

34

Délai entre 1ere dose atb et PL<2 2-3,9 4-5,9 6-7,9 >80

10

5

20

15

25

30

35

40

Culture NégativeCulture positivePourcentage de positivité

0

10

20

30

40

50

60

70

80Pourcentage culture positive

N. meningitidis 2 5 3 2 0S. pneumoniae 0 1 0 2 0L. monocytogenes 0 0 0 1 0

Effect of delayed lumbar punctures on the diagnosis of acute bacterial meningitis in adultsB. Michael, April 1, 2010

Etude rétrospective sur 92 patients vus aux urgences pour méningite

84 patients analysables:- aucun n’a la PL avant le scanner

- 67% des malades ont une PL retardée du fait du scanner

- seulement 20 patients avaient une CI à la PL

Traitementsadjuvants

•Osmothérapie:–Glycerol:pasd’effetdansuneétudeEuropéenne,surmortalitédanscertainesétudes–Autres(SSH,mannitol):pasdedata

•Paracetamol:pasd’effetetpastesterseul•Hypothermiemodérée:–1RCTarrêtéepoursurmortalité,2étudesdecohortes

•PIC:étudesdecohorte

Traitementsadjuvants

•Osmothérapie,paracetamol,anti-épileptiquesnonrecommandés.GlyceroletHypothermiecontre-indiqué(gradeD)•Pressionintra-craniennepeutêtreutileaucasparcasmaispasrecommandéeenroutine(gradeC)•Ig,Héparine,Pcanonrecommandées(gradeD)

Induced Hypothermia in Severe Bacterial MeningitisA Randomized Clinical TrialBruno Mourvillier, MD; Florence Tubach, MD, PhD; Diederik van de Beek, MD, PhD; Denis Garot, MD; Nicolas Pichon, MD; Hugues Georges, MD;Laurent Martin Lefevre, MD; Pierre-Edouard Bollaert, MD; Thierry Boulain, MD; David Luis, MD; Alain Cariou, MD; Patrick Girardie, MD; Riad Chelha, MD;Bruno Megarbane, MD, PhD; Arnaud Delahaye, MD; Ludivine Chalumeau-Lemoine, MD; Stéphane Legriel, MD; Pascal Beuret, MD; François Brivet, MD;Cédric Bruel, MD; Fabrice Camou, MD; Delphine Chatellier, MD; Patrick Chillet, MD; Bernard Clair, MD; Jean-Michel Constantin, MD; Alexandre Duguet, MD;Richard Galliot, MD; Frédérique Bayle, MD; Hervé Hyvernat, MD; Kader Ouchenir, MD; Gaetan Plantefeve, MD; Jean-Pierre Quenot, MD;Jack Richecoeur, MD; Carole Schwebel, MD; Michel Sirodot, MD; Marina Esposito-Farèse, PhD; Yves Le Tulzo, MD, PhD; Michel Wolff, MD

IMPORTANCE Despite advances in care, mortality and morbidity remain high in adults withacute bacterial meningitis, particularly when due to Streptococcus pneumoniae. Inducedhypothermia is beneficial in other conditions with global cerebral hypoxia.

OBJECTIVE To test the hypothesis that induced hypothermia improves outcome in patientswith severe bacterial meningitis.

DESIGN, SETTING, AND PATIENTS An open-label, multicenter, randomized clinical trial in 49intensive care units in France, February 2009–November 2011. In total, 130 patients wereassessed for eligibility and 98 comatose adults (Glasgow Coma Scale [GCS] score of !8 for<12 hours) with community-acquired bacterial meningitis were randomized.

INTERVENTIONS Hypothermia group received a loading dose of 4°C cold saline and werecooled to 32°C to 34°C for 48 hours. The rewarming phase was passive. Controls receivedstandard care.

MAIN OUTCOMES AND MEASURES Primary outcome measure was the Glasgow Outcome Scalescore at 3 months (a score of 5 [favorable outcome] vs a score of 1-4 [unfavorable outcome]).All patients received appropriate antimicrobial therapy and vital support. Analyses wereperformed on an intention-to-treat basis. The data and safety monitoring board (DSMB)reviewed severe adverse events and mortality rate every 50 enrolled patients.

RESULTS After inclusion of 98 comatose patients, the trial was stopped early at the request ofthe DSMB because of concerns over excess mortality in the hypothermia group (25 of 49patients [51%]) vs the control group (15 of 49 patients [31%]; relative risk [RR], 1.99; 95% CI,1.05-3.77; P = .04). Pneumococcal meningitis was diagnosed in 77% of patients. Mean (SD)temperatures achieved 24 hours after randomization were 33.3°C (0.9°C) and 37.0°C (0.9°C)in the hypothermia and control group, respectively. At 3 months, 86% in the hypothermiagroup compared with 74% of controls had an unfavorable outcome (RR, 2.17; 95% CI,0.78-6.01; P = .13). After adjustment for age, score on GCS at inclusion, and the presence ofseptic shock at inclusion, mortality remained higher, although not significantly, in thehypothermia group (hazard ratio, 1.76; 95% CI, 0.89-3.45; P = .10). Subgroup analysis onpatients with pneumococcal meningitis showed similar results. Post hoc analysis showed alow probability to reach statistically significant difference in favor of hypothermia at the endof the 3 planned sequential analyses (probability to conclude in favor of futility, 0.977).

CONCLUSIONS AND RELEVANCE Moderate hypothermia did not improve outcome in patientswith severe bacterial meningitis and may even be harmful. Careful evaluation of safety issuesin future trials on hypothermia are needed and may have important implications in patientspresenting with septic shock or stroke.

TRIAL REGISTRATION clinicaltrials.gov Identifier: NCT00774631

JAMA. doi:10.1001/jama.2013.280506Published online October 8, 2013.

Supplemental content atjama.com

Author Affiliations: Authoraffiliations are listed at the end of thisarticle.

Corresponding Author: BrunoMourvillier, MD, RéanimationMédicale et Infectieuse, AssistancePublique-Hôpitaux de Paris, GroupeHospitalier Bichat-Claude Bernard46, Rue Henri Huchard, 75018 Paris,France ([email protected]).

Research

Original Investigation | CARING FOR THE CRITICALLY ILL PATIENT

E1

Downloaded From: http://jama.jamanetwork.com/ on 11/07/2013

Therapeutic hypothermia for adult community-acquired bacterialmeningitis—Historical control study

Marko Kutleša a,*, Dragan Lepur b, Bruno Barši!c a

aUniversity of Zagreb, School of Medicine, University Hospital for Infectious Diseases “Dr. Fran Mihaljevi!c”, Department of Intensive Care Medicine andNeuroinfectology, Zagreb, CroatiabUniversity of Zagreb, School of Dental Medicine, Department of Intensive Care Medicine and Neuroinfectology, University Hospital for Infectious Diseases“Dr. Fran Mihaljevi!c”, Zagreb, Croatia

A R T I C L E I N F O

Article history:Received 4 April 2014Received in revised form 3 May 2014Accepted 22 May 2014Available online 2 June 2014

Keywords:Therapeutic hypothermiaBacterial meningitisClinical outcome

A B S T R A C T

Objective: Despite advances in antibiotic therapy and critical care, community-acquired bacterialmeningitis (CABM) continues to have poor outcome in a significant portion of patients. This study wasdesigned to assess the efficacy of therapeutic hypothermia (TH) in the treatment of CABM.Material and methods: In a period from January 2009 to January 2013, 41 enrolled patients with CABMwere treated with TH. Their outcome was compared to 90 patients in the historical control group thatwere recruited from the existing database and included patients in a period between 1994 and 2008 withGlasgow coma scale score (GCS) !9 and respiratory failure. TH was indicated in patients with GCS !9,respiratory failure, and breath holding index !0.835 (measured with transcranial Doppler). If theacoustic window was absent, GCS !9 plus optic nerve sheath diameter of "6 mm plus respiratory failurewere indications for TH.Results: Outcome variables were mortality and neurologic recovery measured with the Glasgow outcomescale (GOS). The incidence of hospital mortality (19.5% vs 48.9%, p = 0.002) and adverse neurologicaloutcome (GOS 1–3) (43.9% vs 65.6%, p = 0.023) were significantly lower in patients treated with TH.Multivariate analysis confirmed the positive effect of TH on hospital mortality (OR = 0.059, 95% CI 0.017–0.211) and risk of adverse neurological outcome (OR = 0.209, 95% CI 0.082–0.534) after an adjustment forother risk factors of unfavorable patients' outcome.Conclusions: The new therapeutic concept based on hypothermia significantly improves the outcome inadult patients with severe CABM.

ã 2014 Elsevier B.V. All rights reserved.

1. Introduction

Despite advances in antibiotic therapy and critical care,community-acquired bacterial meningitis (CABM) continues toimpose high rates of morbidity and mortality [1–4]. Given thatbacterial meningitis is frequently associated with poor outcomes,new treatment strategies are needed.

The ominous nature of intracranial hypertension (ICH) andcerebrovascular dysregulation due to vascular inflammation iscrucial for adverse outcome in patients with CABM. Since theadjuvant treatment of CABM has not substantially evolved in

recent years, mortality rates of CABM have mostly remainedunaffected. Current treatment options are known to be ofhumble efficacy and might even be harmful in patients withreduced carbon dioxide vasoreactivity (CO2R) [5,6]. In themajority (76%) of patients with severe CABM (GCS !9), thecerebral blood flow (CBF) chemoregulation is significantlyimpaired or completely lost with subsequent hypoperfusionor “luxury” perfusion [7]. In addition, the reduced CO2R wasconfirmed as an accurate predictor of adverse outcome inpatients with CABM [7]. Furthermore, the effect of dexametha-sone on mortality in adult patients with pneumococcalmeningitis has remained controversial [8,9].

Adjuvant treatment with therapeutic hypothermia (TH) forpatients with severe CABM is of particular interest because it haswell documented neuroprotective effects. Amongst others, it isvery effective in reducing ICH and improving cerebral perfusionpressure [10,11]. Our previously reported results indicate afavorable effect of TH in patients with CABM [12]. Recently

* Corresponding author at: Department of Intensive Care Medicine andNeuroinfectology, University Hospital for Infectious Diseases “Dr. Fran Mihaljevi!c”,Mirogojska 8, Zagreb 10000, Croatia. Tel.: +385 1 2826 253; fax: +385 1 2826 255.

E-mail addresses: [email protected] (M. Kutleša), [email protected] (D. Lepur),[email protected] (B. Barši!c).

http://dx.doi.org/10.1016/j.clineuro.2014.05.0180303-8467/ã 2014 Elsevier B.V. All rights reserved.

Clinical Neurology and Neurosurgery 123 (2014) 181–186

Contents lists available at ScienceDirect

Clinical Neurology and Neurosurgery

journal homepage: www.else vie r .com/locate /c l ine uro

Therapeutic hypothermia for adult community-acquired bacterialmeningitis—Historical control study

Marko Kutleša a,*, Dragan Lepur b, Bruno Barši!c a

aUniversity of Zagreb, School of Medicine, University Hospital for Infectious Diseases “Dr. Fran Mihaljevi!c”, Department of Intensive Care Medicine andNeuroinfectology, Zagreb, CroatiabUniversity of Zagreb, School of Dental Medicine, Department of Intensive Care Medicine and Neuroinfectology, University Hospital for Infectious Diseases“Dr. Fran Mihaljevi!c”, Zagreb, Croatia

A R T I C L E I N F O

Article history:Received 4 April 2014Received in revised form 3 May 2014Accepted 22 May 2014Available online 2 June 2014

Keywords:Therapeutic hypothermiaBacterial meningitisClinical outcome

A B S T R A C T

Objective: Despite advances in antibiotic therapy and critical care, community-acquired bacterialmeningitis (CABM) continues to have poor outcome in a significant portion of patients. This study wasdesigned to assess the efficacy of therapeutic hypothermia (TH) in the treatment of CABM.Material and methods: In a period from January 2009 to January 2013, 41 enrolled patients with CABMwere treated with TH. Their outcome was compared to 90 patients in the historical control group thatwere recruited from the existing database and included patients in a period between 1994 and 2008 withGlasgow coma scale score (GCS) !9 and respiratory failure. TH was indicated in patients with GCS !9,respiratory failure, and breath holding index !0.835 (measured with transcranial Doppler). If theacoustic window was absent, GCS !9 plus optic nerve sheath diameter of "6 mm plus respiratory failurewere indications for TH.Results: Outcome variables were mortality and neurologic recovery measured with the Glasgow outcomescale (GOS). The incidence of hospital mortality (19.5% vs 48.9%, p = 0.002) and adverse neurologicaloutcome (GOS 1–3) (43.9% vs 65.6%, p = 0.023) were significantly lower in patients treated with TH.Multivariate analysis confirmed the positive effect of TH on hospital mortality (OR = 0.059, 95% CI 0.017–0.211) and risk of adverse neurological outcome (OR = 0.209, 95% CI 0.082–0.534) after an adjustment forother risk factors of unfavorable patients' outcome.Conclusions: The new therapeutic concept based on hypothermia significantly improves the outcome inadult patients with severe CABM.

ã 2014 Elsevier B.V. All rights reserved.

1. Introduction

Despite advances in antibiotic therapy and critical care,community-acquired bacterial meningitis (CABM) continues toimpose high rates of morbidity and mortality [1–4]. Given thatbacterial meningitis is frequently associated with poor outcomes,new treatment strategies are needed.

The ominous nature of intracranial hypertension (ICH) andcerebrovascular dysregulation due to vascular inflammation iscrucial for adverse outcome in patients with CABM. Since theadjuvant treatment of CABM has not substantially evolved in

recent years, mortality rates of CABM have mostly remainedunaffected. Current treatment options are known to be ofhumble efficacy and might even be harmful in patients withreduced carbon dioxide vasoreactivity (CO2R) [5,6]. In themajority (76%) of patients with severe CABM (GCS !9), thecerebral blood flow (CBF) chemoregulation is significantlyimpaired or completely lost with subsequent hypoperfusionor “luxury” perfusion [7]. In addition, the reduced CO2R wasconfirmed as an accurate predictor of adverse outcome inpatients with CABM [7]. Furthermore, the effect of dexametha-sone on mortality in adult patients with pneumococcalmeningitis has remained controversial [8,9].

Adjuvant treatment with therapeutic hypothermia (TH) forpatients with severe CABM is of particular interest because it haswell documented neuroprotective effects. Amongst others, it isvery effective in reducing ICH and improving cerebral perfusionpressure [10,11]. Our previously reported results indicate afavorable effect of TH in patients with CABM [12]. Recently

* Corresponding author at: Department of Intensive Care Medicine andNeuroinfectology, University Hospital for Infectious Diseases “Dr. Fran Mihaljevi!c”,Mirogojska 8, Zagreb 10000, Croatia. Tel.: +385 1 2826 253; fax: +385 1 2826 255.

E-mail addresses: [email protected] (M. Kutleša), [email protected] (D. Lepur),[email protected] (B. Barši!c).

http://dx.doi.org/10.1016/j.clineuro.2014.05.0180303-8467/ã 2014 Elsevier B.V. All rights reserved.

Clinical Neurology and Neurosurgery 123 (2014) 181–186

Contents lists available at ScienceDirect

Clinical Neurology and Neurosurgery

journal homepage: www.else vie r .com/locate /c l ine uro

RCT Multicentrique Méthodologie Cohorte historique monocentrique

GCS<9 Inclusion GCS<9 et CO2R diminuée ou ONSD > 6mm

45/45 Effectifs 41/90

48h Hypothermie 1 à 5j selon CO2R

76% Pneumocoque 66%

88% DXM 0%

GOS<5 à 90j Critère de jugement Décès ou GOS 1-3

SurmortalitéHR 1.76

Résultat Réduction MortalitéHR 0,367 décès J28

Clin Neurol Neurosurg 2014Mourvillier, JAMA 2013

Où hospitaliser ?

•Discussion au cas par cas avec équipe de réanimation, en fonction:–Clinique initiale–Facteurs mauvais pronostic–Comorbidités associées

FDR évolution défavorableFlores-Cordero

N=64 APACHE II 8.74 (1.7-44.77)

Auburtin N=80 Thrombopénie < 100pH > 7.47Ventilation mécanique

32.7 ( 3.2-332.5)33.1 (3.4-319.7)48.8 (2.6-901.5)

Auburtin N=156 SAPS II (par point)PSDPATB > 3HEléments > 1000G/L

1.12 (1.072-1.153)6.83 (2.94-20.08)14.12 (3.93–50.9)0.30 (0.10-0.944)

Garcia-Cabrera

N=163 Alcoolisme chroniqueAge > 65 ansVentilation mécaniqueMannitol

6.983.2411.00.36

Van de Beek N=696 Age avancé, otite ou sinusite, GCS bas, tachycardie, Hc+, VS augmentée, thrombopénie, peu d ’éléments dans LCR

PL de contrôle ?• Si évolution défavorable (?) ou PSDP (IDSA)• Pratique peu étayée dans la littérature

PL n°1 (n=45) PLC ( n=45) pJ 4 ± 2

T° 39 37,4Glycorachie ( mmol/l) 1,2 ± 2 3 ± 2 0.001

Proteinorachie ( g/l) 6 ± 4 3 ± 2 0.001

Eléments 2196 ± 2599 3306 ± 5482 0.73PN 2089 ± 2565 3015 ± 5087 0.78

Direct + 92 % ( n=41) 45 % ( n=20)

Culture + 92 % ( n=41) 0% ( n=0)

Denneman L et al. J Infect 2013

• Stérilisationassuréedans100%descas:aucunéchecmicrobiologique

• Dosagedurapport[Antibio]/CMI

Recherche d’un intérêt thérapeutique

< 5 CMI11%

Entre 5 et 10 CMI21%

> 10 x CMI68%

Aucun échec microbiologiqueAucune modification de dose ou de traitement

Complication Fréquence Examenscomplémentaires Traitement

Convulsions 17% TDMouIRMEEG(infracliniques)

Tttanti-épileptique

Hydrocéphalie 3-5% TDMouIRM DVEsiindiquée

AVCischémique 14-25% TDMouIRM NA

AVChémorragique 3% TDMouIRM Neurochirurgie?

Empyème 3% TDMouIRM Neurochirurgie?

Abcèscérébral 2% TDMouIRM Neurochirurgie?

Thrombophlébitecérébrale

1% TDMouIRM Pasdepreuve

Sepsissévère 15% Selonorgane Cfautresreco

Surdité 17-22% Audiogramme Implantcochléaire?

Evaluationneuropsy 13-40% Testsspécifiques ?

Décembre 2012

11 patients/1032 (1%) sous DXM

Conclusions

•Identification des patients

•Corticothérapie et Antibiothérapie précoces

•La TDM cérébrale si indiquée ne doit pas

retarder la prise en charge

•Lieu d’hospitalisation concerté

DXM

DXM avant ATB

Castelblanco RL et al. Lancet Infect Dis 2014

Documents

Il était une fois au SAU… - Infectiologie · original article The new england journal of medicine 2016 n engl j med 364;21 nejm.org may 26, 2011 Bacterial Meningitis in the United