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MENINGITIS BAKTERIAL
Infeksi-infeksi system saraf pusat dapat dibagi kedalam dua kategori yang luas: primer yang meliputi meningen (meningitis) dan yang menyerang parenkim (encephalitis).2 Meningen adalah membran yang menutupi otak dan medula spinalis. Membran terdiri dari tiga lapisan: dura (lapisan luar yang kuat), arachnoid (lapisan tengah yang menyerupai jaring) dan ruang subarachnoid (lapisan lembut, lapisan dalam fibrous yang mengandung pembuluh darah yang memberi makan otak dan medula spinalis).1,2

Anatomi Infeksi-infeksi system saraf pusat dapat dibagi kedalam dua kategori yang luas: primer yang meliputi meningen (meningitis) dan yang menyerang parenkim (encephalitis).2 Meningen adalah membran yang menutupi otak dan medula spinalis. Membran terdiri dari tiga lapisan: dura (lapisan luar yang kuat), arachnoid (lapisan tengah yang menyerupai jaring) dan ruang subarachnoid (lapisan lembut, lapisan dalam fibrous yang mengandung pembuluh darah yang memberi makan otak dan medula spinalis).1,2 Meningitis secara anatomi dibagi kedalam inflamasi dura, kadang-kadang merujuk sebagai pachymeningitis, dimana ini jarang terjadi, serta leptomeningitis, yang paling sering terjadi dan didefinisikan sebagai inflamasi jaringan araknoid dan ruang subaraknoid.1 Berdasarkan pada temuan pus yang berlebihan, pachymeningitis paling sering terjadi dari infeksi bakterial (biasanya akibat organism staphilokokus dan streptokokkus) yang terletak dalam dura. Sumber-sumber organism sering menyebabkan kerusakan tengkorak (misalnya fraktur tengkorak), infeksi dari sinus paranasal, atau osteomyelitis kranial.2 Penyebab paling sering dari inflamasi meningeal adalah iritasi yang disebabkan oleh infeksi bakteri atau virus. Organisme yang bisanya masuk meningen terus ke dalam sirkulasi darah dari bagian lain tubuh. Kebanyakan kasus meningitis bakterial terletak pada dorsum atas dari otak; akan tetapi, pada kondisikondisi tertentu, meningitis dapat terjadi pada basis otak, seperti penyakit fungi dan tuberculosis (TB).1,2,3 Tergantung pada berat ringannya meningitis bakterial, proses inflamasi bakterial meningitis, proses inflamasi bisa tetap terjadi pada ruang subarachnoid. Pada bentuk yang kurang berat, barier pial tidak dipenetrasi, dan parenkim dasarnya tetap intak. Akan tetapi, pada bentuk yang lebih berat dari meningitis bakterial, barier pial mengalami kerusakan, dan parenkim dasarnya di invasi oleh proses inflamasi. Dengan demikian, meningitis bakterial dapat memicu penyebaran kortikal, khususnya bila tidak ditangani.2 Meningitis adalah syndroma klinik yang dikarakteristik oleh inflamasi meningen. Secara klinik, kondisi medis ini memunculkan manifestasi gejala-gejala meningeal seperti; sakit kepala, nuchal rigidity, photophobia dan peningkatan leukosit dalam cairan serebrospinal (pleositosis). Tergantung pada durasi gejala-gejala, meningitis dapat diklasifikasikan sebagai akut atau kronik. Meningitis akut menunjukkan evolusi dari gejala-gejala antara beberapa jam sampai hari, sedangkan meningitis kronik memiliki onset dan durasi dalam minggu sampai bulan. Durasi gejala-gejala dari meningitis kronik dikarakteristik sekurangnya 4 minggu.1,2,4,6 Terdapat sejumlah penyebab infeksi dan non infeksi dari meningitis. Contoh yang paling sering adalah penggunaan obat-obatan, misalnya obat antiinflamasi non streroid, antibiotik; dan carsinomatosis.1,4,5 Meningitis dapat juga diklasifikasikan sesuai dengan etiologinya. Meningitis bakterial akut menunjukkan penyebab bakteri syndrome ini. Meningitis bakterial dikarakteristik oleh onset akut gejala-gejala meningeal dan neutrophilic pleocytosis. Syndroma dinamai tergantung pada penyebab bakterial spesifik, misalnya, Streptococcus pneumoniae meningitis, meningococcal meningitis, atau Haemophilus influenzae

meningitis. Penyebab fungi dan parasit dari meningitis juga diberi nama sesuai dengan agent penyebabnya, seperti cryptococcal meningitis, Histoplasma meningitis, dan amebic meningoencephalitis.1,4,5,6 Patofisiologi Ada jalur utama dimana agent infeksi (bakteri, virus, fungi, parasit) dapat mencapai system saraf pusat (CNS) dan menyebabkan penyakit meningeal. Awalnya, agent infeksi berkolonisasi atau membentuk suatu fokal infeksi pada tuan rumah. Kolonisasi ini bisa berbentuk infeksi pada kulit, infeksi telinga, gigi, nasopharynx, traktus respiratorius, traktus gastrointestinal atau traktus urinarius. Kebanyakan pathogen meningeal ditransmisikan melewati rute respiratorik1,3,4 Dari area kolonisasi ini, organism menembus submucosa melawan pertahanan tuan rumah (misalnya, barier fisik, imunitas lokal, fagosit/makrofag) dan mencapai akses ke system saraf pusat melalui (1) invasi kedalam sirkulasi darah (bakteremia, viremia, fungemia, dan parasitemia) dan selanjutnya secara hematogenous dilepaskan ke system saraf pusat, dimana ini merupakan mode yang penyebaran yang paling sering untuk kebanyakan agent (misalnya, meningokokkus, cryptococcal, syphilitic, dan pneumococcal meningitis); (2) kerusakan neuronal (misalnya, nervus olfactory dan peripheral) dengan agent penyebab misalnya, Naegleria fowleri, Gnathostoma spinigerum; atau (3) kontak langsung (misalnya, sinusitis, otitis media, congenital malformations, trauma, inokulasi langsung selama manipulasi intrakranial).1,5,6 Sekali berada di dalam system saraf pusat, agent-agent infeksi ini akan dapat bertahan hidup oleh karena pertahanan tuan rumah (misalnya, immunoglobulin, neutrophil, komponen komplement) terbatas dalam kompartemen tubuh ini. Adanya agent dan replikasi yang dilakukan tidak terkontrol dan mendorong terjadinya suatu cascade inflamasi meningeal.1,2,3,5 Kunci patofisiologi dari meningitis termasuk peran penting dari cytokines (mis, tumor necrosis factoralpha [TNF-alpha], interleukin [IL]1), chemokines (IL-8), dan molekul proinflamasi lain dalam pathogenesis pleocytosis dan kerus akan neuronal selama bakterial meningitis. Peningkatan konsentrasi TNF-alpha, IL-1, IL-6, dan IL-8 dalam cairan serebrospinal adalah temuan khas pasien meningitis bakterial.2,5 Port de entry: kebanyakan masuk melewati rute respiratorik sehingga menyebabkan infeksi pada traktus respiratorik. Rute gastrointestinal atau traktus urinarius juga menjadi rute infeksi. Selanjutnya terjadi fokal infeksi. Dari fokal infeksi akan menembus submukosa dan mencapai susunan saraf pusat melalui: invasi kedalam sirkulasi darah, dari saraf yang rusak misalnya nervus olfactorius dan perifer. Port de entry yang lain adalah kontak langsung dari fokal infeksi sinusitis, otitis media, atau dari malformasi congenital, trauma, inokulasi langsung saat operasi kepala. 1,2,5 Frekuensi Amerika Serikat. Insiden meningitis bervariasi sesuai dengan agent etiologi spesifik. Meningitis bakterial masih merupakan penyebab signifikan morbiditas dan mortalitas di seluruh dunia. Angka serangan di Amerika Serikat pertahun dilaporkan 0.6-4 kasus per 100,000 populasi. Sebelumnya, 3 kasus yang paling pathogen dengan kasus mencapai 80 %, yaitu H influenzae type B (HIB), N meningitidis, dan S pneumoniae. Lebih dari dua decade lalu, epidemologi telah mengalami perubahan secara substansial oleh karena berbagai perkembangan.2,3,6 Internasional. Insiden meningitis diperkirakan lebih tinggi pada negara yang sedang berkembang oleh karena kurangnya akses pelayanan pencegahan seperti vaksinasi. Angka insdien 10 kali lipat lebih tinggi terjadi di negara sedang berkembang.2,3,6 Menurut data dari berbagai sumber, angka penderita meningoenscephalitis di Indonesia mencapai 18-40 % dengan angka kecacatan 40-50 %. Meningitis bacterial masih merupakan penyebab signifikan morbiditas dan mortalitas di seluruh dunia. Mortalitas dan morbiditas

Mortalitas meningitis bervarias tergantung agent spesifik. Angka mortalitas untuk meningitis virus (tanpa encephalitis) kurang dari 1 %. Pada pasien dengan defisiensi imunitas humoral (misalnya, agammaglobulinemia), enterovirus meningitis dapat memberikan hasil yang fatal. Meningitis bakterial umumnya fatal sebelum era antimicrobial. Dengan adanya terapi antimicrobial, keseluruhan angka mortalitas meningitis bakterial menurun tapi masih masih mengkuatirkan. Laju mortalitas diperkirakan 25%. Diantara penyebab yang sering dari acute bakterial meningitis, angka mortalitas tertinggi ditemukan pada pneumococcus. Angka mortalitas yang dilaporkan untuk tiap-tiap organism spesifik adalah 19-26% untuk S pneumoniae meningitis, 3-6% untuk H influenzae meningitis, 313% untuk N meningitidis meningitis, dan 15-29% untuk L monocytogenes meningitis.1,3,5 Ras dan jenis kelamin Semua ras tanpa terkecuali dapat terkena. Di Amerika Serikat, kulit hitam pria dilaporkan 3.3 kasus per 100,000 populasi dibandingkan dengan 2.6 wanita per 100,000 populasi. Angka serangan untuk meningitis bakterial dilaporkan 3.3 kasus pria per 100,000 populasi sedangkan wanita 2.6 kasus per 100,000 populasi.2,4 Gejala dan Tanda Gejala Presentasi klasik dari meningitis termasuk demam, sakit kepala, kekakuan pada leher, photophobia, nausea, vomiting, dan tanda-tanda disfungsi serebral (mis, lethargy, confusion, coma). Terdapat triad: demam, kekakuan pada leher, dan perubahan status mental ditemukan pada 2/3 pasien. Akan tetapi nilai prediktif negatif gejala-gejala ini tinggi (misalnya, jika demam, kekakuan leher, atau perubahan status mental tidak ada, akan mengeliminasi diagnosis meningitis pada 99-100% kasus). Presentasi klasik dari meningitis akut adalah onset gejala yang terjadi antara jam sampai beberapa hari, dibandingkan dengan meningitis kronis sampai minggu. Presentasi yang tidak khas dapat diobservasi pada kelompok tertentu. Orang tua, khususnya bagi mereka dengan adanya komorbiditas (mis, diabetes, renal dan liver disease), bisa muncul lethargi tanpa gejala meningeal. Pasien-pasien dengan neutropenia dapat muncul dengan gejala iritasi meningeal tersembunyi. Host dengan immunocompromised, termasuk resipien transplant organ dan jaringan serta pasien dengan HIV dan AIDS, dapat menunjukkan presentasi yang tidak khas. Tanda Tanda-tanda disfungsi serebral sering terjadi misalnya, confusion, irritability, delirium, dan koma. Ini biasanya bersamaan dengan demam dan photophobia. Tanda-tanda iritasi meningeal ditemukan hanya pada kira-kira 50% pasien meningitis bakterial, dan bila hal ini tidak ada tidak menyingkirkan meningitis. Palsy saraf cranial dapat ditemukan, terjadi akibat peningkatan tekanan intrakranial atau adanya eksudat yang membungkus nerve roots. Tanda neurologik fokal dapat terbentuk akibat iskemia yang berasal dari inflamasi vascular dan thrombosis. Kejang dapat terjadi pada kira-kira 30% pasien. Papilledema dan tanda-tanda peningkatan intrakranial lain dapat muncul.3,4,5,6

Etiologi
Meningitis bakterial akut Penggunaan vaksin HIB yang luas secara dramatikal merubah epidemiology bakterial meningitis dalam dekade terakhir (tabel 1). Meningitis yang paling sering kena pada seluruh kelompok umur, H influenzae meningitis secara dramatikal mengalami penurunan dari 48% sampai 7% dari seluruh kasus. Angka N meningitidis masih konstan pada 14-25%, dan organisme pada beberapa kasus terjadi antara umur 2-18 tahun. S pneumoniae menjadi penyebab paling sering pada seluruh kelompok umur (tabel 1).1,3

Resiko dan/atau faktor predisposisi Umur 0-4 minggu

Bateri pathogen S agalactiae (group B streptococci) E coli K1 L monocytogenes S agalactiae E coli H influenzae S pneumoniae N meningitidis N meningitidis S pneumoniae H influenzae S pneumoniae N meningitidis H influenzae S pneumoniae N meningitidis L monocytogenes Aerobic gram-negative bacilli S pneumoniae N meningitidis L monocytogenes Aerobic gram-negative bacilli

Umur 4-12 minggu

Umur 3 bulan sampai 18 tahun

Umur 18-50 tahun

Umur > 50 tahun

Immunocompromised state

Intrakranial manipulation, including neurosurgery Staphylococcus aureus Coagulase-negative staphylococci Aerobic gram-negative bacilli, including Pseudomonas aeruginosa Basilar skull fracture S pneumoniae H influenzae Group A streptococci Coagulase-negative staphylococci S aureus Aerobic gram-negative bacilli Propionibacterium acnes

CSF shunts

Meningitis kronik
Meningitis kronis adalah kumpulan gejala dan tanda iritasi meningeal dengan CSF pleocytosis yang menetap untuk lebih dari 4 minggu. Agent-agent yang bertanggung jawab terhadap meningitis kronis pada tabel 3.2,4 Tabel 3. Bakteri Penyebab meningitis kronis

Category Agent Bakteri M tuberculosis

B burgdorferi T pallidum Brucella species Francisella tularensis Nocardia species Actinomyces species

Penanganan
Penanganan prehospital 1,5

Evaluasi dan penanganan pasien shock atau hipotensi dengan infuse kristaloid sampai terjadi euvolemik. Penanganan kejang sesuai protokol Proteksi jalan nafas pasien yang mengalami penurunan kesadaran. Untuk pasien sadar dengan kondisi stabil denga n tanda vital normal, berikan oksigen, akses intravena dan kirim cepat ke bagian emergensy. Penanganan gawat darurat 1,2,5

Meningitis akut: sesuai keadaan pasien, pemeriksaan cairan serebrospinal dalam mengindentifikasi meningitis akut untuk identifikasi organism spesifik dan kerentanan. Meningitis sub akut: pada pasien ini, pemeriksaan cairan cerebrospinal merupakan langkah penting untuk mendokumentasikan ada atau tidaknya infeksi saraf pusat dan tipe organisme penyebab infeksi. Pemberian antibiotika untuk memperlambat replikasi infeksi. Kondisi pasien dan perawatan bagian darurat selanjutnya dengan observasi 8-12 jam, kemudian periksa ulang cairan cerebrospinal (segera dilakukan bila kondisi pasien memburuk). Jika terjadi perubahan granulositosis awal terhadapmononuclear predominance, glukosa cairan cerebrospinal, dan pasien terlihat baik, infeksi pasien mungkin nonbakterial. Pada pasien akut, lakukan lumbal punksi dan berikan dosis pertama antibiotic dengan atau tanpa steroid antara 30 menit. Lakukan CT scan bila terjadi defisit neurologis. Penanganan komplikasi sistemik meningitis bacterial akut: hipotensi dan/atau shock, hipoksemia, hiponatremia, aritmia jantung dan iskemia, cardiovaskuler disease (CVD), dan eksaserbasi penyakit kronik. Perhatikan tanda hidrosephalus dan peningkatan tekanan intrakranial. Tangani demam dan nyeri, kontrol ketegangan dan batuk, hindari kejang, dan hindari hipotensi sistemik. Sebaliknya pada pasien stabil, penanganan cukup dengan elevasi kepala dan monitoring status neurologik. Beberapa center menganjurkan penggunaan dieresis awal (misalnya, furosemide 20 mg IV, mannitol 1 g/kg IV), untuk memproteksi volume sirkulasi. Hiperventilasi pada pasien yang diintubasi, dengan sasaran PaCO2 25-30 mm Hg, dapat menurunkan tekanan intracranial dengan singkat; hiperventilasi dengan PaCO2 <25 mm Hg

dapat menurunkan cerebral blod flow yang tidak sebanding dan memicu iskemia system saraf pusat. Pertimbangan pemasangan monitor ICP pada pasien koma atau mereka dengan tanda peningkatan tekanan intracranial. Dengan peningkatan tekanan intrakranial, ambil cairan serebrospinal sampai tekanan menurun 50 % dan pertahankan pada tekanan kurang dari 300 mm air, hanya dilakukan pada kasus-kasus tertentu.2,5 Pencegahan kejang: lorazepam 0.1 mg/kg IV dan IV load dengan phenytoin 15 mg/kg atau phenobarbital 5-10 mg/kg. Kontroversi seputar pemberian dexamethasone, yang diberikan dengan atau sebelum antibiotika.2 Dexamethasone dapat mengganggu cytokine-mediated neurotoxic effects dari bacteriolysis. Efek maksimum pada hari pertama penggunaan antibiotik. Meta-analysis 10 tahun pada percobaan klinik, dexamethasone menurunkan morbiditas, khususnya insiden dan severeitas dari neurosensory hearing loss, untuk meningitis H influenzae dan diduga keuntungan yang diperoleh untuk meningitis S pneumoniae sebanding pada pemakaian anak-anak. Tidak ada studi yang adekuat pada orang dewasa mengenai penggunaan dexametazone, meskipun secara patofisiologi mungkin sama. Meta-analysis menduga bahwa batas terapi dexamethasone sampai 2 hari, diduga sudah optimal. Studi terbaru dari Eropa terus mendukung penggunaan dexametasone di negara-negara yang sedang berkembang (bila dibandingkan dengan negara maju), barangkali berhubungan dengan insiden relatif meningitis TB. Secara teori, efek anti-inflamasi menurunkan permeabilitas blood-brain barrier dan menghalangi penetrasi antibiotik kedalam cairan serebrospinal. Menurunkan level vankomisin dalam cairan cerebrospinal telah dikonfirmasi pada hewan yang ditangani dengan steroid, pada manusia belum dilakukan. Beberapa center percaya bahwa seluruh antibiotika mencapai konsentrasi inhibisi minimal dalam cairan serebrospinal tanpa mempertimbangkan penggunaan streroid. Dexamethasone tidak mengganggu vankomisin secara klinik. Di negara yang sedang berkembang, penggunaan gliserol oral (dexamethasone) telah dipelajari sebagai terapi adjunctive untuk penanganan meningitis bacterial pada anak-anak. Dalam studi yang terbatas, penggunaannya terlihat menurunkan insiden neurologic sequelae dengan efek samping yang kecil.2 Terapi antibiotika idealnya didasarkan pada identifikasi organisme dengan pewarnaan gram. Neonati umur 1 bulan, mikroorganisme yang sering, streptokokus group B atau D, Enterobacteriaceae (mis, E coli), dan L monocytogenes. Penanganan primer adalah kombinasi ampicillin (umur 0-7 hari: 50 mg/kg IV q8h; umur 8-30 hari: 50-100 mg/kg IV q6h) plus cefotaxime 50 mg/kg IV q6h (sampai 12 g/d). Penanganan alternatif ampicillin (umur 0-7 hari: 50 mg/kg IV q8h; umur 8-30 hari: 50-100 mg/kg IV q6h) plus gentamicin (umur 0-7 hari: 2.5 mg/kg IV atau IM q12h; umur 8-30 hari: 2.5 mg/kg IV atau IM q8h). Beberapa center merekomendasikan penambahan acyclovir 10 mg/kg IV q8h untuk herpes simplex encephalitis.2,5 Pada bayi (1-3 bulan).

Penanganan primer adalah cefotaxime (50 mg/kg IV q6h, sampai 12 g/d) atau ceftriaxone (dosis awal: 75 mg/kg, 50 mg/kg q12h sampai 4 g/day) plus ampicillin (50-100 mg/kg IV q6h). Penanganan alternative adalah chloramphenicol (25 mg/kg PO atau IV q12h) plus gentamicin (2.5 mg/kg IV atau IM q8h). Jika yang ada cephalosporin-resistant S pneumoniae (DRSP), >2%, tambahan vancomycin (15 mg/kg IV q8h). Sangat perlu dexamethasone (0.4 mg/kg IV q12h untuk 2 hari atau 0.15 mg/kg IV q6h untuk 4 hari) mulai 15-20 menit sebelum dosis awal antibiotik. Pada bayi yang lebih tua atau anak-anak (3 bulan- 7 tahun), mikroorganisme yang sering adalah S pneumoniae, N meningitidis, dan H influenzae. Penanganan primer, cefotaxime (50 mg/kg IV q6h sampai 12 g/hari) atau ceftriaxone (dosis awal: 75 mg/kg, kemudian 50 mg/kg q12h sampai 4 g/hari). Jika DRSP >2%, tambah vancomycin (15 mg/kg IV q8h). Negara-negara dengan prevalensi DRSP rendah, pertimbangkan penicillin G (250,000 U/kg/d IM/IV dalam 3-4 dosis terbagi). Bila penyebab DRSP, penicillin G. Penanganan alternatif (atau jika alergi penisilin berat) adalah chloramphenicol (25 mg/kg PO/IV q12h) plus vancomycin (15 mg/kg IV q8h). Pertimbangkan dexamethasone (0.4 mg/kg IV q12h dalam 2 hari atau 0.15 mg/kg IV q6h untuk 4 hari) mulai 15-20 menit sebelum dosis pertama antibiotika.1,2,5 Umur 7-50 tahun, mikroorganisme yang sering S pneumoniae, N meningitidis, dan L monocytogenes. Area DRSP (drug resistant S pneumonia) >2%, cefotaxime (dosis pediatri: 50 mg/kg IV q6h sampai 12 g/d; dewasa: 2 g IV q4h) atau ceftriaxone (pediatri: initial dose: 75 mg/kg, kemudian 50 mg/kg q12h sampai 4 g/hari; dosis dewasa: 2 g IV q12h) plus vancomycin (pediatri: 15 mg/kg IV q8h; dewasa: 750-1000 mg IV q12h atau 10-15 mg/kg IV q12h). Beberap center menambahkan rifampin (pediatrik: 20 mg/kg/d IV; dewasa: 600 mg PO qd). Jika spesies Listeria species, tambahkan ampicillin (50 mg/kg IV q6h). Alternatif (atau jika alergi penisilin) yaitu chloramphenicol (12.5 mg/kg IV q6h: tidak bactericidal) atau clindamycin (dosis pediatri: 40 mg/kg/hari IV dalam 3-4 dosis; dewasa: 900 mg IV q8h: aktif in vitro tapi tidak ada data klinik) atau meropenem (pediatri: 20-40 mg/kg IV q8h; dewasa: 1 g IV q8h: aktif in vitro tapi sedikit data klinik; hindari imipenem). Area prevalensi DRSP rendah, gunakan cefotaxime (dosis pediatri: 50 mg/kg IV q6h sampai 12 g/d; dewasa: 2 g IV q4h) atau ceftriaxone (pediatri: 75 mg/kg dosis initial kemudian 50 mg/kg q12h sampai 4 g/d; dewasa: 2 g IV q12h) plus ampicillin (50 mg/kg IV q6h). Penanganan alternatif (atau jika alergi penicilin) adalah chloramphenicol (12.5 mg/kg IV q6h) plus trimethoprim/sulfamethoxazole (TMP/SMX; TMP 5 mg/kg IV q6h) atau meropenem (pediatri: 20-40 mg/kg IV q8h; dewasa: 1 g IV q8h). Data terbatas pada penggunaan dexamethasone pada orang dewasa. Pemberian dosis pertama dexamethasone (0.4 mg/kg q12h IV selama 2 hari atau 0.15 mg/kg q6h untuk 4 hari) 15-20 menit sebelum dosis pertama antibiotika.2,5 Lebih dari 50 tahun atau dewasa dengan penyakit keterbatasan atau alkoholisme, mikroorganisme sering S pneumoniae, coliforms, H influenzae, Listeria species, Pseudomonas aeruginosa, dan N meningitidis.

Penanganan primer dengan prevalensi DRSP >2% apakah dengan cefotaxime (2 g IV q4h) atau ceftriaxone (2 g IV q12h) plus vancomycin (750-1000 mg IV q12h atau 10-15 mg/kg IV q12h). Jika pewarnaan gram CSF memperlihatkan basil gram negative, gunakan ceftazidime (2 g IV g8h). Pada area prevalensi DRSP, gunakan cefotaxime (2 g IV q4h) atau ceftriaxone (2 g IV q12h) plus ampicillin (50 mg/kg IV q6h). Pilihan penanganan lain termasuk meropenem, TMP/SMX, dan doxycycline. Data terbatasu untuk penggunaan deksametason, di negara berkembang bila diduga S pneumoniae dan untuk dugaan TB atau fungi. Dosis awal dexamethasone (0.4 mg/kg q12h IV untuk 2 hari atau 0.15 mg/kg q6h untuk 4 hari) 15-20 menit sebelum dosis antibiotik pertama.1,2,5 Pasien trauma trauma atau neurosurgery microorganism S pneumoniae, Staphylococcus aureus, coliforms, dan P aeruginosa. Penanganan primer vancomycin (1 g IV q12h) plus ceftazidime (2 g IV q8h). Alternatif meropenem (1 g IV q8h). Profilaksis pasien dengan dugaan N meningitidis Rifampin (pediatri: anak <1 mo - 5 mg/kg q12h; anak >1 mo - 10 mg/kg q12h; dewasa: 600 mg PO bid) for 4 doses Alternatif- Ciprofloxacin (dewasa) 500 mg PO dosis tunggal atau ceftriaxone (<15 y: 125 mg; >15 y: 250 mg) IM dosis tunggal.2 Prognosis 2 Pasien-pasien dengan meningitis virus biasanya prognosisnya baik untuk pemulihan Prognosis buruk pada pasien dengan umur ekstrim (yaitu, <2 tahun, >60 tahun) dan mereka dengan komorbiditas signifikan dan imunodefisiensi. Pasien yang menunjukkan gangguan level kesadaran, meningkatkan resiko perkembangan neurologic sequelae atau kematian. Kejang selama episode meningitis juga menjadi faktor resiko mortalitas atau neurologic sequelae. Meningitis bacterial akut adalah kondisi medis darurat dan keterlambatan memulai terapi antimikroba yang efektif meningkatkan morbiditas dan mortalitas. Adanya peositas level rendah (<20 cells) pada pasien meningitis bacterial diduga memberikan hasil buruk. Meningitis yang disebabkan oleh S pneumoniae, L monocytogenes, dan basil gram negatif memiliki tingkat fatalitas lebih tinggi dibandingkan dengan meningitis yang disebabkan oelh bakteri lain. Prognosis meningitis yang disebabkan oleh pathogen oportunistik, tergantung pada pathogen oportunistik, juga tergantung pada fungsi imun yang mendasari tuan rumah.

REFERENSI 1. Swartz, M. N. Meningitis: bakterial, viral, and other. Bakterial meningitis. Goldman: cecil medicine, 23rd ed 2007.Chapter 437

2. Razonable RR. Meningitis. Mayo Clinic College of Medicine. Updated: Aug 26, 2009 available athttp://emedicine.medscape.com/article/232915. 3. Tolan RW. Amebic meningoencephalitis. Saint Peters University hospital.update Jan 21, 2009. Available at.http://emedicine.medscape.com/article/996227. 4. Lazoff M. meningitis. Editor-in-Chief, Medical Computing Review. Update Feb 2, 2010. Available at.http://emedicine.medscape.com/article/784389. 5. Incesu L. Meningitis, Bakterial. Ondokuz Mayis University School of Medicine; Department of Radiology, Ondokuz Mayis University Hospital, Turkey Updated: Mar 13, 2009. Available at.http://emedicine.medscape.com/article/341971. 6. Gonzlez-Scarano. Central Nervous System Diseases Due to Slow Viruses and Prions. .Department of Neurology, University of Pennsylvania School of Medicine. Chapter XVII. June 2005. ACP Medicine, 2007 Edition. 7. Nath A., Berger JR. Acute Viral Encephalitis. Goldman: Cecil Medicine, 23rd ed. Copyright 2007 Sauders, an imprint of Elsevier. Chapter 439. 8. Tidy C. Encephalitis and Meningoencephalitis. at. http://www.patient.co.uk Update Oct. 30, 2010. Available

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cute bacterial meningitis is rapidly progressive bacterial infection of the meninges and subarachnoid space. Findings typically include headache, fever, and nuchal rigidity. Diagnosis is by CSF analysis. Treatment is with antibiotics and corticosteroids given as soon as possible. For neonatal meningitis, see Neonatal Bacterial Meningitis

Pathophysiology
Most commonly, bacteria reach the subarachnoid space and meninges via hematogenous spread. Bacteria may also reach the meninges from nearby infected structures (eg, sinuses, the middle ear) or through a congenital or acquired defect in the skull or spine (eg, a penetrating head wound, a neural tube defect, an opening made during neurosurgery). Because WBCs, immunoglobulins, and complement are normally sparse or absent from CSF, bacteria initially multiply without causing inflammation. Later, bacteria release endotoxins, teichoic acid, and other substances that trigger an inflammatory response with mediators such as WBCs and TNF. Typically in CSF, levels of protein increase, and because bacteria consume glucose and because less glucose is transported into the CSF, glucose levels decrease. Inflammation in the subarachnoid space is accompanied by cortical encephalitis and ventriculitis. Complications are common and may include Hydrocephalus (in some patients) Arterial or venous infarcts due to inflammation and thrombosis of arteries and veins in superficial and sometimes deep areas of brain Abducens palsy due to inflammation of the 6th cranial nerve Deafness due to inflammation of the 8th cranial nerve or structures in the middle ear Subdural empyema Increased intracranial pressure (ICP) due to cerebral edema Brain herniation (the most common cause of death during the acute stages) Systemic complications (which are sometimes fatal), such as septic shock, disseminated intravascular coagulation (DIC), or hyponatremia due to syndrome of inappropriate antidiuretic hormone secretion (SIADH)

Etiology
Likely causes depend on Patient age Route of entry Immune status of the patient

Age: In children and young adults, the most common causes are

Neisseria meningitidis Streptococcus pneumoniae

N. meningitidis meningitis occasionally causes death within hours. Sepsis caused by N. meningitidissometimes results in bilateral adrenal hemorrhagic infarction (Waterhouse-Friderichsen syndrome). Haemophilus influenzae type B, previously the most common cause of meningitis in children < 6 yr and overall, is now a rare cause in the US and Western Europe, where the H. influenzae vaccine is widely used. However, in areas where it is not widely used, H. influenzae is a common cause, particularly in children aged 2 mo to 6 yr. In middle-aged adults and in the elderly, the most common cause of meningitis is S. pneumoniae

Less commonly, N. meningitidis causes meningitis in middle-aged and older adults. As host defenses decline with age, patients may develop meningitis due to L. monocytogenes or gram-negative bacteria.

Table 2
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Causes of Bacterial Meningitis by Patient Age


Age Group
Children and young adults

Bacteria
Neisseria meningitidis Streptococcus pneumoniae S. aureus* Haemophilus influenzae (rare in developed countries but still seen in countries where the H. influenzae type B vaccine is not widely used)

Middle-aged adults

S. pneumoniae S. aureus* N. meningitidis (less common in this age group)

The elderly

S. pneumoniae S. aureus* Listeria monocytogenes Gram-negative bacteria

*S. aureus occasionally causes severe meningitis in patients of all ages, It is the most common cause of

meningitis that develops after a penetrating head wound.

Route: Routes of entry include the following:

By hematogenous spread (the most common route) From infected structures in or around the head (eg, sinuses, middle ear, mastoid process), sometimes associated with a CSF leak Through a penetrating wound After a neurosurgical procedure (eg, if a ventricular shunt becomes infected) Through congenital or acquired defects in the skull or spine

Having any of the above conditions increases the risk of acquiring meningitis.

Table 3
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Causes of Bacterial Meningitis by Route


Route Infection in or around the head (eg, sinusitis, otitis, mastoiditis), sometimes with a CSF leak Bacteria Streptococcus pneumoniae Haemophilus influenzae Anaerobic and microaerophilic streptococci Bacteroides sp Staphylococcus aureus Penetrating head wound Damaged skin (eg, skin infections, abscesses, pressure ulcers, large burns) An infected shunt A neurosurgical procedure S. epidermidis Gram-negative bacteria (eg, Klebsiella pneumoniae,Acinetobacter calcoaceticus, Escherichia coli) S. aureus S. aureus

Immune status: Overall, the most common causes in immunocompromised patients are

S. pneumoniae L. monocytogenes Pseudomonas aeruginosa Mycobacterium tuberculosis N. meningitidis Gram-negative bacteria

But the most likely bacteria depend on the type of immune deficiency: Defects in cell-mediated immunity (eg, in AIDS, Hodgkin lymphoma, or drug-induced immunosuppression): L. monocytogenes or mycobacteria Defects in humoral immunity or splenectomy: S. pneumoniae or, less frequently, N. meningitidis (both can cause fulminant meningitis) Neutropenia: P. aeruginosa or gram-negative enteric bacteria

In very young infants (particularly premature infants) and the elderly, T-cell immunity may be weak; thus, these age groups are at risk of meningitis due to L monocytogenes.

Symptoms and Signs


In most cases, bacterial meningitis begins with 3 to 5 days of insidiously progressive nonspecific symptoms including malaise, fever, irritability, and vomiting. However, meningitis may be more rapid in onset and can be fulminant, making bacterial meningitis one of the few disorders in which a previously healthy young person may go to sleep with mild symptoms and never awaken. Typical meningeal symptoms and signs include fever, tachycardia, headache, photophobia, changes in mental status (eg, lethargy, obtundation), nuchal rigidity (although not all patients report it), and sometimes, when Staphylococcus aureus is the cause, back pain. Seizures occur early in up to 40% of children with acute bacterial meningitis and may occur in adults. Up to 12% of patients present in coma. Severe meningitis may cause papilledema, but papilledema may be absent early, even when ICP is increased. Accompanying systemic infection by the organism may cause rashes, petechiae, or purpura (which suggest meningococcemia); pulmonary consolidation (often in meningitis due to S. pneumoniae); or heart murmurs (which suggest endocarditiseg, often caused by S. aureus or S. pneumoniae). Atypical presentations in adults : Fever and nuchal rigidity may be absent or mild in immunocompromised or elderly patients and in alcoholics. Often, in the elderly, the only sign is confusion in those who were previously alert or

altered responsiveness in those who have dementia. In such patients, starting appropriate antibiotics before head CT or MRI may be prudent.

If bacterial meningitis develops after a neurosurgical procedure, symptoms often take days to develop.

Diagnosis
CSF analysis As soon as acute bacterial meningitis is suspected, blood cultures and lumbar puncture for CSF analysis (unless contraindicated) are done. If the patient is very ill, antibiotics are given immediately. The need for confirmation should not delay treatment. Clinicians should suspect bacterial meningitis in patients with typical symptoms and signs, usually fever, changes in mental status, and nuchal rigidity. However, clinicians must be aware that symptoms and signs are different in neonates and infants and may be absent or initially mild in the elderly, alcoholics, and immunocompromised patients. Diagnosis can be challenging in patients who have had a neurosurgical procedure (because such procedures can also cause changes in mental status and neck stiffness) and in the elderly and alcoholics (because changes in mental status may be due to falls and subdural hematomas). Focal seizures or focal neurologic deficits may indicate a focal lesion such as a brain abscess. Because untreated bacterial meningitis is lethal, tests should be done if there is even a small chance of meningitis. Testing is particularly helpful in infants, the elderly, alcoholics, immunocompromised patients, and patients who had neurosurgical procedure because symptoms may be atypical.

Sidebar 1

Pearls & Pitfalls


Do a lumbar puncture even if findings are not specific for meningitis, particularly in infants, the elderly, alcoholics, immunocompromised patients, and patients who have had neurosurgery.

If findings suggest acute bacterial meningitis, routine tests include CSF analysis CBC and differential Metabolic panel

Blood cultures plus PCR (if available)

Lumbar puncture: Unless contraindicated, lumbar puncture is done immediately to obtain CSF for analysis, the mainstay of diagnosis.

Contraindications to immediate lumbar puncture are signs suggesting markedly increased ICP or a mass; typically, these signs include focal deficits, papilledema, deterioration in consciousness, and seizures. In such cases, lumbar puncture may cause brain herniation and thus is deferred until neuroimaging (typically contrast-enhanced CT or MRI) is done to check for increased ICP or a mass. When lumbar puncture is deferred, treatment is best begun immediately (after blood sampling for culture and before neuroimaging). After ICP, if increased, has been lowered or if no mass is detected, lumbar puncture can be done. CSF should be sent for analysis: cell count, protein, glucose, Gram staining, culture, PCR (if available), and other tests as indicated clinically. Simultaneously, a blood sample should be drawn and sent to have the CSF:blood glucose ratio determined. CSF cell count should be determined as soon as possible because WBCs may adhere to the walls of the collecting tube, resulting in a falsely low cell count; in extremely purulent CSF, WBCs may lyse. Typical CSF findings in bacterial meningitis include increased pressure, fluid that is often turbid, a high WBC count (consisting predominantly of PMNs), elevated protein, and a low CSF:blood glucose ratio. A CSF glucose level of 18 mg/dL or a CSF:blood glucose ratio of < 0.23 strongly suggests bacterial meningitis. However, changes in CSF glucose may lag 30 to 120 min behind changes in blood glucose. In acute bacterial meningitis, an elevated protein level (usually 100 to 500 mg/dL) indicates blood-brain barrier injury. CSF cell count and protein and glucose levels in patients with acute bacterial meningitis are not always typical. Atypical CSF findings may include Normal in early stages except for the presence of bacteria Predominance of lymphocytes in about 14% of patients, particularly in neonates with gramnegative meningitis, patients with meningitis due to L. monocytogenes, and some patients with partially treated bacterial meningitis Normal glucose in about 9% of patients Normal WBC counts in severely immunosuppressed patients

Table 4
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CSF Findings in Meningitis


Condition Predominant Cell Type* Protein* Glucose* Specific Tests

Normal CSF

All lymphocytes (05 cells/L)

< 40 mg/dL

> 50 % of blood glucose

None

Bacterial meningitis

Leukocytes (usually PMNs), often greatly increased

Elevated

< 50% of blood glucose (may be extremely low)

Gram staining (yield is high if 10 colonyforming units of bacteria/ mL are present) Bacterial culture PCR if available PCR (to check for enteroviruses or herpes simplex, herpes zoster, or West Nile virus) IgM (to check for West Nile virus or other arboviruses)

Viral meningitis Lymphocytes (may be mixed; PMNs and lymphocytes during the first 2448 h)

Elevated

Usually normal

Tuberculous meningitis

PMNs and lymphocytes (usually pleocytosis)

Elevated

< 50% of blood glucose (may be extremely low)

Acid-fast staining PCR Mycobacterial culture (ideally using a CSF sample of 30 mL)

Interferon- tests of serum and (if available) CSF Fungal meningitis Usually lymphocytes Elevated < 50% of blood glucose (may be extremely low) Cryptococcal antigen test Serologic tests forCoccidioides immitis orHistoplasma sp antigen, especially if patients have recently spent time in an endemic area Fungal culture (ideally using a CSF sample of 30 mL) India ink (forCryptococcus sp)
*Changes in cell count, glucose, and protein may be minimal in severely immunocompromised patients.

In tuberculous meningitis, CSF acid-fast staining can be insensitive, sensitivity of PCR is only about 50%, and culture requires up to 8 wk. Positive CSF interferon- tests indicate tuberculous meningitis, but serum interferon- tests may only indicate prior infection. Thus, confirming a diagnosis of tuberculous meningitis is difficult, and if it is strongly suspected, even if not confirmed, it is treated presumptively.

A small number of cells may be present normally in neonates or after a seizure.

PCR = polymerase chain reaction; PMNs = polymorphonuclear neutrophils.

Identification of the causative bacteria involves Gram staining, culture, and, when available, PCR. Gram staining provides information rapidly, but the information is limited. For bacteria to be reliably

detected with Gram stain, about 10 bacteria/mm must be present. Results may be falsely negative if CSF is handled carelessly, if bacteria are not adequately resuspended after CSF has been allowed to settle, or if errors in decolorization or reading of the slide occur. Diagnosis of the specific bacteria and determination of antibiotic sensitivity requires bacterial culture. If clinicians suspect an anaerobic infection or other unusual bacteria, they should tell the laboratory before samples are plated for cultures. Prior antibiotic therapy can reduce the yield from Gram staining and culture. PCR, if available, may be a useful adjunctive test, especially in patients who have already received antibiotics. Until the cause of meningitis is confirmed, other tests using samples of cerebrospinal fluid or blood may be done to check for other causes of meningitis, such as viruses (particularly herpes simplex), fungi, and cancer cells. Samples from other sites suspected of being infected (eg, urinary or respiratory tract) are also cultured .

Prognosis
For children < 19 yr, the mortality rate may be as low as 3% but is often higher; survivors may be deaf and neuropsychologically impaired. The mortality rate is about 17% for adults < 60 yr but up to 37% in those > 60. Community-acquired meningitis due to S. aureus has a mortality rate of 43%. In general, mortality rate correlates with depth of obtundation or coma. Factors associated with a poor prognosis include Age > 60 yr Coexisting debilitating disorders A low Glasgow coma score at admission Focal neurologic deficits A low CSF cell count Increased CSF pressure (particularly)

Seizures and a low CSF:serum glucose ratio may also indicate a poor prognosis.

Treatment
Antibiotics Corticosteroids to decrease cerebral inflammation and edema

Antibiotics are the mainstay of therapy. In addition to antibiotics, treatment includes measures to decrease brain and cranial nerve inflammation and increased ICP. Most patients are admitted to an ICU. Antibiotics: Antibiotics must be bactericidal for the causative bacteria and must be able to penetrate the bloodbrain barrier.

If patients appear ill and findings suggest meningitis, antibiotics (see Table 5: Initial Antibiotics for Acute
Bacterial Meningitis

) are started as soon as blood cultures are drawn. If lumbar puncture is delayed

pending neuroimaging results, treatment begins before neuroimaging. If patients do not appear very ill or have atypical symptoms and the diagnosis is less certain, antibiotics can wait until CSF results are known.

Sidebar 2

Pearls & Pitfalls


If patients appear ill and acute meningitis is suspected, treat them with antibiotics and corticosteroids as soon as blood for cultures is drawn.

Appropriate empiric antibiotics depend on the patient's age and immune status and route of infection (see Table 5: Initial Antibiotics for Acute Bacterial Meningitis ). In general, clinicians should use antibiotics that are effective against S. pneumoniae, N. meningitidis, and S. aureus. Sometimes (eg, in neonates and some immunosuppressed patients), herpes simplex encephalitis cannot be excluded; thus, acyclovir

is added. Antibiotic therapy may need to be modified based on results of culture and sensitivity testing. Commonly used antibiotics include 3rd-generation cephalosporins for S. pneumoniae and N. meningitidis, ampicillin

for L monocytogenes, and vancomycin

for penicillin-resistant strains of S. pneumoniae and for S. aureus.

Table 5
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Initial Antibiotics for Acute Bacterial Meningitis


Patient Group Suspected Bacteria Provisional Antibiotics

Age < 3 mo Streptococcus agalactiae Escherichia coli or other gramnegative bacteria Listeria monocytogenes Staphylococcus aureus* plus Ceftriaxone Ampicillin

or cefotaxime

3 mo18 yr

Neisseria meningitidis S. pneumoniae S. aureus* Haemophilus influenzae

Cefotaxime

or ceftriaxone

plus Vancomycin

1850 yr

S. pneumoniae N. meningitidis S. aureus*

Ceftriaxone

or cefotaxime

plus Vancomycin

> 50 yr

S. pneumoniae L. monocytogenes S. aureus Gram-negative bacteria N. meningitidis(unusual in this age group)

Ceftriaxone

or cefotaxime

plus Ampicillin

plus Vancomycin

Route Sinusitis, otitis, CSF leaks S. pneumoniae H. influenzae Gram-negative bacteria includingPseudomonas aeruginosa Anaerobic or microaerophilic streptococci Bacteroides fragilis S. aureus* or meropenem plus Ceftazidime

Vancomycin

plus Metronidazole

Penetrating head wounds, neurosurgical procedures, shunt infections

S. aureus S. epidermidis Gram-negative bacteria includingP. aeruginosa S. pneumoniae

Vancomycin

plus Ceftazidime

Immune status AIDS, other conditions that impair cell-mediated immunity S. pneumoniae L. monocytogenes Gram-negative bacteria includingP. aeruginosa S. aureus* plus Ceftazidime Ampicillin

plus Vancomycin

*S. aureus is an uncommon cause of meningitis except when the route is a penetrating head wound or a neurosurgical procedure. However, it can cause meningitis in all patient groups. Thus, vancomycin or other antistaphylococcal antibiotics should be given if clinicians think that this bacteria is a possible, even if unlikely, cause.

S. pneumoniae is the most common causative bacteria in patients with a CSF leak or acute otitis. Such patients may be treated with vancomycin and ceftriaxone or cefotaxime

. However, when meningitis is accompanied by subdural empyema or develops after a neurosurgical procedure, other bacteria, including P. aeruginosa, are more likely to be present; in such cases, initial treatment should include vancomycin plus ceftazidime

plusmetronidazole .

H. influenzae should be considered in children < 5 yr with no record of H. influenzae type b conjugate vaccination.

Table 6
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Specific Antibiotics for Acute Bacterial Meningitis


Bacteria Age Group
Children and adults

Antibiotics* Comments
Vancomycin

Gram-positive bacteria (unidentified)

plus Ceftriaxone

(cefotaxime

) andampicillin

Gram-negative bacilli (unidentified)

Children and adults

Cefotaxime

(or ceftriaxone

,meropenem

, or ceftazidime

) plus Gentamicin

, tobramycin

, oramikacin

if systemic infection is

suspected Haemophilus influenzae type b Children and adults (cefotaxime Ceftriaxone

) Neisseria meningitidis Children and adults (cefotaxime Ceftriaxone Penicillin G

is used for susceptible ) Streptococcus pneumoniae Children and adults Vancomycin Penicillin G

after sensitivities are k

and ceftriaxone

may be used for susc (cefotaxime known.

strains after sensitivitie

) Staphylococcus aureus and S. epidermidis Children and adults with or without rifampin Vancomycin Vancomycin

is used for methicillinstrains, or nafcillin

oroxacillin

may be used after sen are known. Rifampin

is added if no improve

occurs with vancomyc

ornafcillin

. Listeria sp Children and adults Ampicillin Penicillin G

(penicillin G

is used for susceptible

after sensitivities are k Trimethoprim

) or Trimethoprim

/sulfamethoxazole is u penicillin.

patients who are allerg

/sulfamethoxazole Enteric gram-negative bacteria (eg,Escherichia coli, Klebsiella sp,Proteus sp) (cefotaxime Children and adults Ceftriaxone

) plus Gentamicin

, tobramycin

, oramikacin

if systemic infection is

suspected Pseudomonas sp Children and adults (ceftazidime Meropenem

orcefepime

), usually alone but sometimes with an aminoglycoside or Aztreonam

*Alternative antibiotics are in parentheses.

If gram-positive bacteria are pleomorphic, ampicillin

is included to cover Listeria sp.

Amikacin

is used in areas where gentamicin

resistance is common. Because aminoglycosides have poor CSF penetration, they are infrequently used for treatment of meningitis. Whe they may have to be given intrathecally or via an Ommaya reservoir, especially in patients with Pseudomonas meningitis. When aminogly used, renal function should be monitored.

Table 7
Open table in new window

Common IV Antibiotic Dosages for Acute Bacterial Meningitis*


Antibiotic Dosage Children > 1 mo
Ceftriaxone 50 mg/kg q 12 h 2 g q 12 h

Adults

Cefotaxime

50 mg/kg q 6 h

2 g q 46 h

Ceftazidime

50 mg/kg q 8 h

2gq8h

Cefepime

2 g q 12 h

2 g q 812 h

Ampicillin

75 mg/kg q 6 h

23 g q 4 h

Penicillin G

4 million units q 4 h

4 million units q 4 h

Nafcillin

50 mg/kg q 6 h

2gq4h

andoxacillin

Vancomycin

15 mg/kg q 6 h

1015 mg/kg q 8 h

Meropenem

40 mg/kg q 8 h

2gq8h

Gentamicin

2.5 mg/kg q 8 h

2 mg/kg q 8 h

andtobramycin

Amikacin

10 mg/kg q 8 h

7.5 mg/kg q 12 h

Rifampin

6.7 mg/kg q 8 h

600 mg q 24 h

Chloramphenicol

25 mg/kg q 6 h

1gq6h

*For neonatal dosages, see Table 1: Recommended Dosages of Selected Parenteral Antibiotics for Neonates .

Renal function should be monitored.

Corticosteroids: Dexamethasone

is used to decrease cerebral and cranial nerve inflammation and edema; it should be given when therapy is started. Adults are given 10 mg IV; children are given 0.15 mg/kg IV. Dexamethasone

is given immediately before or with the initial dose of antibiotics and q 6 h for 4 days.

Other measures: The effectiveness of other measures is less well-proved. Patients presenting with papilledema or signs of impending brain herniation are treated for increased ICP: elevation of the head of the bed to 30, hyperventilation to a PCO2 of 27 to 30 mm Hg to cause intracranial vasoconstriction, and osmotic diuresis with IV mannitol

. Usually, adults are given mannitol

1 g/kg IV bolus over 30 min, repeated prn q 3 to 4 h or 0.25 g/kg q 2 to 3 h, and children are given 0.5 to 2.0 g/kg over 30 min, repeated prn.

Supportive measures can include IV fluids, anticonvulsants, treatment of concomitant infections, and treatment of specific complications (eg, corticosteroids for Waterhouse-Friderichsen syndrome, surgical drainage for subdural empyema).

Prevention
Use of vaccines for H. influenzae type B and, to a lesser extent, for N. meningitidis and S. pneumoniaehas reduced the incidence of bacterial meningitis. Physical measures: Keeping patients in respiratory isolation (using droplet precautions) for the first 24 h of therapy can help prevent meningitis from spreading. Gloves, masks, and gowns are used.

Vaccination: Vaccination can prevent certain types of bacterial meningitis.

A conjugated pneumococcal vaccine effective against 7 serotypes, including > 80% of organisms that cause meningitis, is recommended for all children (see Pneumococcal Disease and Table 2:Recommended Immunization Schedule for Ages 06 yr ).

Routine vaccination against H. influenzae type b is highly effective and begins at age 2 mo. A quadrivalent meningococcal vaccine is given to Children who are 2 to 10 yr if they have an immunodeficiency or functional asplenia All children at age 11 to 12 yr Older children, college students living in dormitories, and military recruits who have not had the vaccine previously Travelers to endemic areas Laboratory personnel who routinely handle meningococcal specimens

During an epidemic, the population at risk (eg, college students, a small town) must be identified, and its size must be determined before proceeding to mass vaccination. The effort is expensive and requires public education and support, but it saves lives and reduces morbidity. The meningococcal vaccine does not protect against serotype B meningococcal meningitis; this information should kept in mind when a vaccinated patient presents with symptoms of meningitis. Chemoprophylaxis: Anyone who has prolonged face-to-face contact with a patient who has meningitis (eg, household or day care contacts, medical personnel and other people who are exposed to the patient's oral secretions) should be given postexposure chemoprophylaxis.

For meningococcal meningitis, chemoprophylaxis consists of one of the following: Rifampin

600 mg (for children > 1 mo, 10 mg/kg; for children < 1 mo, 5 mg/kg) po q 12 h for 4 doses Ceftriaxone 250 mg (for children < 15 yr, 125 mg) IM for 1 dose For adults, a fluoroquinolone (ciprofloxacin

or levofloxacin

500 mg or ofloxacin 400 mg) po for 1 dose Chemoprophylaxis against H. influenzae type b is rifampin

20 mg/kg po once/day (maximum: 600 mg/day) for 4 days. There is no consensus on whether children < 2 yr require prophylaxis for exposure at day care. Chemoprophylaxis is not usually needed for contacts of patients with other types of bacterial meningitis.

Key Points
Common causes include N. meningitidis and S. pneumoniae in children and adults and Listeria sp in infants and the elderly; S. aureus occasionally causes meningitis in people of all ages. Typical features may be absent or subtle in infants, alcoholics, the elderly, immunocompromised patients, and patients who develop meningitis after a neurosurgical procedure. If patients have focal neurologic deficits, obtundation, seizures, or papilledema (suggesting increased ICP or a mass), lumbar puncture is deferred pending results of neuroimaging. Acute bacterial meningitis, unless atypical or mild, is treated as soon as possible, before the diagnosis is confirmed. Common empirically chosen antibiotic regimens often include 3rd-generation cephalosporins (for S. pneumoniae and N. meningitidis), ampicillin

(for L. monocytogenes), and vancomycin (for penicillin-resistant strains of S. pneumoniae and for S. aureus). Routine vaccination for S. pneumoniae and N. meningitidis and chemoprophylaxis against N. meningitidishelps prevent meningitis.