infeksi tentir koas
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Anatomi Otak - Meningen
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Anatomi Sirkulasi LCS
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Lokalisasi Infeksi SSP
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Infeksi: masuknya material patogen ke dalam tubuh
5 TANDA KARDINAL INFLAMASI:5 TANDA KARDINAL INFLAMASI:Tumor, Rubor, Kalor, Dolor, Fungsio lesaTumor, Rubor, Kalor, Dolor, Fungsio lesa
Jenis material:Bakteri (spesifik, non spesifik)VirusJamurParasit/ protozoa
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Infeksi SSPMeningitis infeksi yang melibatkan selaput mening otak
terdiri dari :Meningitis Purulenta yang disebabkan oleh kuman
Bakteri a.l: Pneumokokus, stapilokokus, H. influenzae, sering pada orang dewasa sedangkan E. coli (sering menyerang anak-anak)
Meningitis Serosa yang disebabkan oleh Jamur, Virus, Protozoa, Parasit, M. Tuberculosa
Ensefalitis yaitu infeksi yang melibatkan jaringanotak.
Myelitis yaitu infeksi yang melibatkan sumsum tulang belakang
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Infeksi SSPMeningen
Meningitis Korteks Serebri
Serebritis, Ensefalitis Medula Spinalis
Spondilitis, Mielitis Abses
Abses otak, Abses paravertebra, Empyema subdural, Spinal epidural abses
Infeksi VirusInfeksi JamurInfeksi Parasit
Toksoplasma, cyctisercosisInfeksi Spirochaeta
Lyme disease, brucellosis, leptospirosisAIDS
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Sawar darah otak (blood brain barrier) merupakan “sekat” yg kuat
Material patogen bisa menembus sawar darah otak karena:Jumlah koloni kuman yg besarJumlah koloni kuman yg besarDaya tahan host menurunDaya tahan host menurunKemampuan penetrasi kuman yg kuatKemampuan penetrasi kuman yg kuat
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Menurut PenyebabInfeksi viral: enterovirus, Mumps, Herpes simplex,
CMV, Eipstein Barr, Varicella-zooster, HIV, Coxsackie virus
Infeksi Bakterial: Meningokokus, Penumokokus, H. influenza tipe B, N meningitidis, Streptokokus agalactiae, S pneumoniae
Infeksi Spiroketal: T pallidum (syphilis), B burgdorferi Infeksi Fungus: C neoformans, C immitis, B
dermatitidis, H capsulatum, candida spesies, S schenckii
Infeksi ProtozoaInfeksi Metasoa
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Changing Epidemiology of Acute Bacterial Meningitis in the US
Bacteria 1978-1981 1986 1995
H influenzae 48% 45% 7%
Listeria monocytogenes 2% 3% 8%
N meningitidis 20% 14% 25%
Streptococcus agalactiae 3% 6% 12%
S pneumoniae 13% 18% 47%
Bacteria 1978-1981 1986 1995
H influenzae 48% 45% 7%
Listeria monocytogenes 2% 3% 8%
N meningitidis 20% 14% 25%
Streptococcus agalactiae 3% 6% 12%
S pneumoniae 13% 18% 47%
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Chronic MeningitisCategory Agent
BacteriaBacteria M tuberculosis B burgdorferi T pallidum Brucella speciesFrancisella tularensis Nocardia speciesActinomyces species
FungiFungi C neoformans C immitis B dermatitidis H capsulatum Candida albicans Aspergillus speciesSporothrix schenckii
ParasitesParasites Acanthamoeba speciesN fowleri Angiostrongylus cantonensis G spinigerum B procyonis Schistosoma speciesS stercoralis Echinococcus granulosus
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MeningesMeninges
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Faktor Risiko meningitisUsia
Usia < 5 tahun, 15-24 tahun, lansiaLingkungan burukHamil
Rentan infeksi listeriaKontak dengan binatang Immunocompromised
AIDS, DM, obat imunosupresanSplenektomi
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Infeksi mencapai SSP Melalui luka terbuka di kepala Penyebaran infeksi langsung dari otitis media,sinus- sinus paranasal, kulit kepala dan wajah Penyebaran melalui darah (septisemia/bakteriemia) Abses otak Infeksi Retrograde sepanjang saraf Infeksi langsung pada CSF akibat trauma/ LP yang tak steril
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Penyebaran Mikroorganisme predominan
LangsungKraniotomi & fraktur kraniumMelalui sinus paranasalisDefek ektodermal kongenitalVP shunting
Neural (melalui akson)
Olfactory
Hematogen
Staphylococcus aureus & gol. Enterobakter
Staphylococcus epidermidis
Tetanus, rabies, vorus herpes
HSV, Naegleria fowleri
H. influenzae, a. pneumoniae, N. meningitidis, TBCFungi (kriptokokus, coccidioides)Riketsia Enterovirus, arbovirus, mumps, HIV, virus khoriomeningits limfositikPlasmodium falciparum, tripanosoma, cacing pita
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Gejala & TandaMeningeal SignKaku Kuduk (Nuchal Rigidity)Brudzinski I-IVKernig
Gejala klinis:DemamKaku kudukKelemahan umumMual/ muntahFotofobiaKejang ( 2 atau lebih gejala klinis di atas → curiga meningitis)
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Meningeal sign
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Meningeal sign
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MeningitisRadang meningen (otak, med. Spinalis, LCS)Gejala & tanda: nyeri kepala, meningeal sign
(+), fotofobia, febris
EnsefalitisRadang ensefalonGejala & tanda: disfungsi kognitif, gangguan
perilaku, gangguan bicara, gangguan kesadaran, defisit neurologis fokal (kejang, hemiparesis )
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Pemeriksaan Penunjang Infeksi SSPLCS (pungsi lumbal)PCR (polymerase chain reaction)MRI (magnetic resonance imaging)Kultur jaringanLab. DarahRö thoraxEEG (elektroensefalografi)CT Scan (computerized tomography scan)
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Herniasi
A
B
C
Gejala & Tanda:
•Kesadaran menurun
•Anisokori pupil
•Muntah proyektil
•Paresis N. VI
•Hipertensi
•Bradikardi
Cushing’s Syndrome
A: herniasi Sub Falcial;
B: herniasi Uncal; C: herniasi tonsilar
A: herniasi Sub Falcial;
B: herniasi Uncal; C: herniasi tonsilar
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Infeksi VirusJumlah virus & virulensinyaDaya tahan tubuh yang rendah seperti :
Penyakit kronikGangguan imunologikReaksi alergiDemam, obat-obatanRadioterapi
Adanya kerusakan ginjal, paru, hepar, jantung & susunan eritropoetik
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Bisa sembuh dalam < 10 hari, paling banyak disebabkan oleh enterovirus
Gejala & tanda:Dewasa:
Febris, nyeri kepala, mual, muntah, fotofobia, mengantuk, kaku kuduk, nyeri tulang/ sendi, nyeri tenggorokan, rash
Bayi & anak: Inaktif, demam tinggi, iritabel, muntah, nafsu
makan turun, lemahPenatalaksanaan:
Terapi suportifAntiinflamasiAntiviral Antibiotika
MeningitisMeningitisVIRUSVIRUS
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EtiologiHerpes Virus
Herper simplex, varicella-zoster, epstein Barr, CMVMyxo/ paramyxo Virus
Influenza/ parainfluenza, Mumps, measles, adenovirus,LCM, rabies, HIV
EnterovirusPoliovirus, coxsackievirus, echovirus, toga virus
West Nile/ Japanese Encephalitis VirusEastern equine, western equine, venezuelan equine, St.
Louis Powasson, miscellaneous California
MeningitisMeningitisVIRUSVIRUS
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Meningitis ViralBersifat benigne , gejalanya kadang sangat
ringanPada keadaan berat memberikan gejala:
Sakit kepalaKaku kudukLP : Pleiositosis limfositer . liquor jernihPenyebab : paling sering dari kelompok enterovirus :
– V. poliomyelitis– V. coxsakie– V. ECHO (Entero Cytophatic Human Orphan)– Penetrasi melalui lintasan oral fecal / droplet spray
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Meningitis VirusMeningitis VirusGejala & tandaDemam <7 hariNyeri kepalaMualDefisit sensorikKejangRigiditasKaku kudukFotofobia Mengantuk
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Ensefalitis ViralSering berupa meningoensephalitisGambaran klinis :
– Konvulsi merupakan gejala utama– Gangguan kesadaran (acut organic brain
syndrome)– Gejala serebellar– Nyeri serta kaku kuduk
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Ensefalitis Viral Ensephalitis virus terbagi atas 3 kelompok :
Ensephalitis primer berasal dari :– Virus kelompok herpes simpleks– Virus influenza– Virus ECHO, Coxsackhie– Arbo virus
Ensephalitis primer yang belum diketahui penyebabnya Ensephalitis Parainfeksiosa akibat komplikasi penyakit virus
(misalnya : rubeola, varisela, herpes zoster, parotitis epidemika, mononucleosis infeksiosa, vaksinasi)
(54% menyerang anak anak , 31 % disebabkan oleh Virus herpes simpleks, 17 % virus ECHO)
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Meningitis BakterialMeningitis BakterialMenurut lapisan:
Pachymeningitis (duramater)Leptomeningitis (arakhnoid, piamater)
Menurut etiologi:Bakteri, virus, ricketsia, jamur, cacing,
protozoaMenurut LCS:
PurulentaSerosa (TB, virus)
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KOLONISASI KUMAN
Invasi Lokal (I. Muccosal invasion)
Bakteriemia (II: Intravascular Survival)
Melekat pada Pleksus Choroideus/ Endotil Vaskuler Otak
Kerusakan endotil
Invasi Selaput Otak (III: Crossing Blood Brain Barier)
Replikasi bakteri di LCS + Inflamasi LCS (IV: Survival in CSF)
MENINGITIS
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Mikroorganisme mencapai leptomening & subarakhnoid melalui
Luka terbuka di kepalaPenyebaran langsung dari:
Infeksi telinga bag. Tengah (otitis media)Sinus paranasalKulit kepala-mukaBenda asing yg terinfeksi (mis: VP shunting)
SepsisTromboflebitis kortikalAbses sub/ ekstradural ke otakLamina kribrosa os ethmoidalis & rhinorheaPungsi lumbalNeurotoksin dari fokus yg jauh
MeningitisMeningitisBAKTERIALBAKTERIAL
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Penatalaksanaan Penatalaksanaan umum
Bed rest, cegah dekubitus (alih baring tiap 4-6 jam) Terapi cairan adekuat 5B (blood, brain, breathing, bowel, bladder) Terapi simtomatik
Penatalaksanaan spesifik Antibiotika: dosis adekuat, larut dalam lemak,
menembus sawar darah otak, aktif dalam LCS yg bersifat asam, pemberian intravena
Antibiotika mempengaruhi bakteri dgn cara:- Merintangi replikasi dari informasi genetik- Mengganggu translasi genetik sintesis protein- Mengubah struktur fungsi dinding sel- Membatasi fungsi membran sel
MeningitisMeningitisBAKTERIALBAKTERIAL
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Antibiotika Antibiotika selama 14 hariSifat antibiotika ideal:
Larut dalam lemak → menembus sawar darah otak (beberapa antibiotika β-laktamase/ penisilin & sefalosporin II/ III sulit menembus sawar darah otak)
Aktif dalam LCS purulen & asam Jika antibiotika sensitif, LCS bisa steril dalam 24-36
jam
MeningitisMeningitisBAKTERIALBAKTERIAL
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Anak/ kgBBAnak/ kgBB DewasaDewasa
Penicilin GPenicilin G 50.000 U/ 4 jam50.000 U/ 4 jam 3-4 M / 4 jam3-4 M / 4 jam
Ampicilin Ampicilin 75-100 mg/ 6 jam75-100 mg/ 6 jam 2 g/ 4 jam2 g/ 4 jam
Cefotaxime Cefotaxime 50 mg/ 6 jam50 mg/ 6 jam 2-3 g/ 6 jam2-3 g/ 6 jam
Ceftriaxone Ceftriaxone 50 mg/ 12 jam50 mg/ 12 jam 2-3 g/ 24 jam2-3 g/ 24 jam
CefizoximeCefizoxime 50 mg/ 6 jam50 mg/ 6 jam 4 g/ 8 jam4 g/ 8 jam
NafcillinNafcillin 50 mg/ 6 jam50 mg/ 6 jam 1,5 g/ 4 jam1,5 g/ 4 jam
Chloramphenicol Chloramphenicol 25 mg/ 6 jam25 mg/ 6 jam 1,5 g/ 6 jam1,5 g/ 6 jam
Vancomycin Vancomycin 10 mg/ 6 jam10 mg/ 6 jam 0,5 g/ 6 jam0,5 g/ 6 jam
Trimetoprim-Trimetoprim-SulfamethoxazoleSulfamethoxazole
25 mg/ 6 jam25 mg/ 6 jam 25 mg/ 6 jam25 mg/ 6 jam
MeningitisMeningitisBAKTERIALBAKTERIAL
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MeningitisMeningitisBAKTERIALBAKTERIAL
< 1 bln Etiologi: β atau δ streptokokus, enterobacteriaceae, listeria
AB: ampicilin/ amoxicilin + gentamisin, ampicilin + cefotaxime
1-3 bln Etiologi: H. influenzae, pneumokokus, meningokokus,
AB: ampicilin + cefotaxime/ ceftiaxone, ampicilin/ amoxicilin + gentamisin
>3 bln, <7 thn
Etiologi: H. influenzae, pneumokokus, meningokokus
AB: ceftriaxone, cefotaxime, ampicilin + chloramphenicol/ cefuroxime
>7 thn, dewasa
Umum: N. meningitidis, S. pneumoniae, L. monocytogenes (AB: ceftriaxone/ cefotaxime, chloramphenicol)
Alkoholik/ > 60 thn: Enterobactericeae, pseudomonas, H. influenzae (AB: penicilin G, ampicilin/ amoxicilin + cefotaxime/ ceftriaxone, chloramphenicol
Post kraniotomi/ trauma neurospinal: pseudomonas, S. aureus, pneumokokus, enterobactericeae (AB: vancomycin + ceftazidime)
Fistula LCS: streptokokus.
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Antiinflamasi KortikosteroidMenghambat reaksi inflamasi dalam cav.
SubarakhnoidDosis (deksametason): 0,15 mg/kgBB/kali tiap
6 jam → tapp off tiap 5 hari → 3 mingguMencegah toksin bakteri masuk ke dalam LCS →
mencegah trombosis SSPIndikasi deksametason:
Status mental sangat tergangguEdema otak/ TIK ↑: edema vasogenik, sitotoksik, interstisial
MeningitisMeningitisBAKTERIALBAKTERIAL
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Penatalaksanaan TIK ↑Head up 30˚Obat hiperosmolar:
Mannitol 20% Gliserol
Hiperventilasi → pCO2 20-30 mmHgBarbiturat: menurunkan metabolismeMempertahankan MAP > 50 mmHg
MeningitisMeningitisBAKTERIALBAKTERIAL
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Major causes of acute meningitis (all ages, worldwide). "Other" viruses include herpes simplex virus type 2, arthropod-borne viruses, Epstein-Barr virus, influenza virus, and measles virus, as well as infections caused by Mycoplasma pneumoniae, M tuberculosis, Leptospira, fungi and rickettsiae that may be difficult to differentiate from viral meningitis.
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Streptokkokus pneumoniae (paru, telinga, sinus)
Neisseria meningitidis (sal. napas bagian atas)
Haemophilus influenzae (sal. napas bagian atas, telinga, sinus)
Listeria monocytogenes (tanah, debu, makanan terkontaminasi)
MeningitisMeningitisBAKTERIALBAKTERIAL
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KomplikasiHidroseflus Infark otakSeizureParesis (Pan arteritis hemiplegia )Paralisis Nn. Craniales (Oftalmoplegia )Arachnoiditis → mortalitas + 50%
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Meningitis TBMeningitis TBPatogenesis
Anak: TB miliar → hematogen → plexus choroideus → meningitis
Dewasa: reaktivasi infeksi TB laten → kuman TB masuk jar. Otak → tuberkel → daya tahan tubuh ↓ → tuberkel pecah (patognomonis: TB paru, alkoholik, iimmunocompromise, daerah endemis TB)
Fokus primer: paru-paru, infeksi TB di os mastoid, spondilitis TB
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Meningitis TB tidak selalu disertai TB miliar, TB miliar tidak selalu disertai meningitis TB
Meningitis TB terjadi jika kuman TB masuk ke ruang subarakhnoid
Penyebaran hematogen tidak segera disertai penyebaran ke SSP, stlh beberapa bln/ thn jika sistem imun terganggu → tuberkel pecah → LCS → cav. Subarakhnoid → ventrikel → meningitis
MeningitisMeningitisTBTB
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Stadium (British Med. Council)
Stadium Meningitis TB (British Med. Council )Stadium IGejala TB umum, meningeal sign +/ -, hidrosefalusKematian <7%, sebagian besar sembuh, sekuele(-)Stadium IIKesadaran ↓, defisit neurologis (+) (inflamasi & fibrosis
daerah basal ≈ meningitis basilaris)Kematian ≈ 25%, sembuh, sekuele (+)Stadium IIIKejang (+), reflex patela (-), reflex achiles (+)Kematian >50%, jika sembuh sekuele (+) beratStadium IVKoma, syok
MeningitisMeningitisTBTB
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Pemeriksaan Penunjang
LCStekanan↑, jernih (xantokrom), pellicle (+)
(dibiarkan selama 1 malam)Sel ↑ (50-5.000/ mm³ (MN), protein ↑ (100-500 mg
%), glukosa↓ 6-40mg% (≈ < 40% nilai GDS)CT Scan
(+) kontras: enhancement daerah sisterna basalhidrosefalus
Rö thoraxTest tuberkulin (PPD 5 TU)ICT TBMycotec TBPCR (polymerase chain reaction)
MeningitisMeningitisTBTB
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Diagnosis
Gejala klinis: panas (subfebris), sefalgia, kaku kuduk (+) >14 hari)
Pemeriksaan penunjang: 1. LCS: lekosit >20/ mm³, protein >100 mg/ dl,
glukosa <45 mg/ dl (< 40% nilai GDS)2. CT Scan: eksudat sisterna basalis, hidrosefalus,
defisit neurologis fokal3. TB di luar SSP atau PPD 5 TU (+)4. Hiponatremi atau LED ↑
Suspek TB: gejala klinis + > 1 laboratorium di atas Highly Probable: gejala klinis + 3-4 lab. Probable: gejala klinis + 2 lab. Possible: gejala klinis + 1 lab.
MeningitisMeningitisTBTB
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Enhancement sisterna basalis ≈ meningitis basilaris
MeningitisMeningitisTBTB
Tuberkel
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Medikamentosa
SimtomatisEtiologis → OAT: toksisitas↑, resistensi↑
1st Line Drugs Isoniazid (INH) Rifampicin Pyrazinamid Ethambutol
2nd line Drugs Streptomycin Ciprofloxacin Etionamid
MeningitisMeningitisTBTB
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INH + Vit. B6INH + Vit. B6
Pilihan utama: 12-18 bulanDewasa 400-600 mg/hari, Anak 10-20 mg/kg
BB/hariTerbaik:
Molekul kecil → toksisitas rendahMurahMenembus sawar darah otakPengobatan 2 thn: bakterisida kurangResistensi sedikit (mencegah resistensi:
streptomisin + ethambuthol)ESO: neuropati perifer (+ Vit. B6. piridoksin 25-50
mg/hari), hepatotoksik, euforia, mania
MeningitisMeningitisTBTB
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StreptomisinStreptomisin
Dewasa 750-1000 mg/hari, Anak 20 mg/kg BB/ hari
Molekul besarKuman yg masuk LCS (terapi 8 minggu→ LCS
bersih)Resistensi ↑ESO: vertigo, ototoksik, gangguan fungsi
ginjal
MeningitisMeningitisTBTB
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RifampisinRifampisinDewasa 450-600 mg/hari, Anak 15-25
mg/kgBB/hari+ 60% kadar obat masuk LCSESO: hepatotoksik (jika SGPT/ ALT > 5x
normal→ STOP!!), trombositopenia (jarang)
Dosis 15 mg/kgBB/hari Dapat menembus sawar darah otak, masuk
LCS Diberikan pd penderita usia >13 thn (ESO:
buta → tes visual, tes buta warna)
EthambutolEthambutol
MeningitisMeningitisTBTB
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Pyrazinamid Pyrazinamid Dosis 20-25 mg/kgBB/hariESO: hepatotoksik, presipitasi GOUT,
eksaserbasi DM
Dewasa 3-4 gr/hari, Anak 200 mg/kgBB/hari TIDAK MASUK LCS ESO: anoreksia, nausea, vomitus
PAS PAS
MeningitisMeningitisTBTB
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EtionamidEtionamidDosis: 0,5-1 gr/ hari, 2-4 x/ hariPenetrasi di LCS baikESO: hipotensi postural, depresi, tremor,
drowsiness, gangguan penghiduToksisitas: GI, hepar, SSP
MeningitisMeningitisTBTB
Ciprofloxacin Ciprofloxacin
Dosis: 750 mg, 2x/ hari ESO: psikosis, tremor Kontraindikasi: anak, wanita hamil
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KombinasiKombinasi
INH + streptomisin + ethambutol → bakterisida kurang
Meningkatkan bakterisida:INH + streptomisin + rifampicinINH + ethambutol + rifampicinPirazinamid + INH + rifampicin tiap hari
selama 2 bln dilanjutkan: INH + rifampicin tiap hari selama 10 bln, atau INH 900 mg + rifampicin 600 mg 2x/ minggu
MeningitisMeningitisTBTB
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KortikosteroidKortikosteroidDexamethason 5mg i.v/ 6 jam selama 3 minggu
→ tapp off tiap 5 hari, atau methylprednisolonDiberikan pada stadium II, III, IV (allergic
reaction thd tuberculo protein)TIDAK MENGHAMBAT: rifampicin, streptomisin,
ethambutolMenurunkan eksudat & ↑ reabsorbsi cav. Subarakhnoid
→ mencegah hidrosefalusmencegah hidrosefalus mencegah arakhnoiditismencegah arakhnoiditis menurunkan edema serebri & blok spinalmenurunkan edema serebri & blok spinal menurunkan gangguan Nn. kraniales & radiksmenurunkan gangguan Nn. kraniales & radiks
Menurunkan kemungkinan vaskulitis → mencegah infark
MeningitisMeningitisTBTB
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Penyulit/ komplikasi Hidrosefalus, lesi Nn. Kranialis (optalmoplegi), iskemik/
infark otak, epilepsi, SIADH, atrofi N. II, retardasi mental
Medikamentosa INH: dewasa 400-600 mg/hari, anak 10-20
mg/kgBB/hari, lama terapi: 12-18 bulan, ESO: neuropati perifer (+ B 6), hepatitis. Jika resisten: streptomycin + ethambuthol
Streptomycin: dewasa 750-1000 mg/hari i.m, anak 20 mg/kgBB/hari i.m, lama terapi: 8 minggu, ESO: vertigo, ototoksik, gangguan ginjal
Rifampicin: dewasa 450-600 mg/hari, anak 15-25 mg/kgBB/hari, ESO: hepatotoksik
Ethambuthol: 15 mg/kgBB/hari (usia >13 thn), ESO: buta
Pirazinamid: 20-25 mg/kgBB/hari, ESO: hepatotoksik
MeningitisMeningitisTBTB
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Untuk meningkatkan efek bakterisidal INH + Strep + Rifampicin INH + Ethambuthol + Rifampicin Pirazinamid + INH + Rifampicin: tiap hari (2 bln) → INH
+ Rifampicin tiap hari (10 bln) atau INH 900 mg + Rifampicin 600 mg 2x/ minggu
Kortikosteroid Diberikan pada stadium II-IV Preventif: arachnoiditis, hidrosefalus, vaskulitis Dosis 5 mg i.v/ 6 jam, selama 3 minggu, tapp off tiap 5
hari Menurunkan edema serebri Tidak menghambat: Rifampicin, Streptomycin,
Ethambuthol Menurunkan eksudat & meningkatkan reabsorbsi
dalam sub arakhnoid
MeningitisMeningitisTBTB
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Komplikasi MeningitisKomplikasi MeningitisEdema serebriSIADHSubdural effusionHemi/ kuadriparesisKejangParalisis Nn. KranialisGangguan vestibulerHidrosefalusRetardasi mentalKomplikasi akut: syok sepsis, edema serebri, DIC,
hiponatremia, miokarditis
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Ensefalitis Peradangan ensefalonGejala & tanda
SefalgiaDefisit neurologis fokalKejang
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Ensefalitis
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Abses OtakAbses OtakAbses ≈ massa yg terbentuk dari kumpulan
material mikroorganisme hidup & mati (piogenik) → penumpukan di dalam/ di antara parenkim otak
Etiologi:Bakteri (tersering): staph. aureus, strep. anaerob,
staph. α / β hemolitikus, E. coli, bacteroidesJamur: neiseria asteroides, candida, aspergilusParasit (jarang): E. histolitika, cystecircosis,
schistosomiasis
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Gejala & Tanda:Defisit neurologis fokal (mass effect progresif)Nyeri kepalaGangguan mentalTanda-tanda infeksiMeningeal sign
Diagnosis banding:Tumor otak, SDH kronik, meningitis kronik, viral
encephalitis
AbsesAbsesOtakOtak
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Patogenesis Fokus infeksi:
Langsung: otitis atau mastoiditis (≈lobus temporal, serebelum), sinusitis (≈lobus frontal), meningitis (jarang), osteomielitis, selulitis orbita
Hematogen: peny. Jantung bawaan, fistula arteriovenosa, infeksi paru, infeksi ekstrakranial
Trauma: trauma kepala tembus, kraniotomiKriptogenik (+20%)
Mikroorganisme: Streptokokus (paling banyak)Anaerob/ mikrofili (33-50%)
AbsesAbsesOtakOtak
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Lokasi: Hematogen; tersering di daerah subst. alba & griseaPerkontinuitatum; daerah dekat permukaan otakSerebrum 80% (paling sering di lobus frontal atau
parietal, jarang di lobus temporal), serebelum 20-30%Sifat:
Soliter atau multipel 5-20% (fokus dari tempat lain: endokarditis, pulmoner
Prognosis:Mortalitas 45%
Tanpa operasi 100% Dengan operasi 20%
Morbiditas 50%
AbsesAbsesOtakOtak
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Awal: peradangan difus jar. otak (infiltrat lekosit, edema, perlunakan, kongesti), kadang disertai petekiae
Hari-minggu: nekrosis & pencairan pusat lesi → rongga abses → astroglia, fibroblas, makrofag mengelilingi jar. nekrotik → abses tak berbatas tegas
Lanjut: fibrosis yg progresif → kapsul berdinding konsentris
AbsesAbsesOtakOtak
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Stadium Abses OtakStadium 1 (Early Cerebritis)
• Infeksi & inflamasi fase awal, hari ke-1-3• Batas abses belum tegas• Infiltrat perivaskuler
Stadium 2 (Late Cerebritis)• Mulai terbentuk pusat nekrotik, hari ke-4-9
Stadium 3 (Early Capsule)• Neovaskularisasi, hari ke-10-13• Pusat nekrotik
Stadium 4 (Late Capsule)• Terbentuk kapsul kolagen, > hari ke-14• Pusat nekrotik• Gliosis di sekitar kapsul
AbsesAbsesOtakOtak
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Serebritis Serebritis
FIG 1. Images acquired on hospital day 5 during the early stage of left orbitofrontal cerebritis.A. Shows hyperintense subcortical white matter of left frontal lobe (arrow).B. Postcontrast T1-weighted image shows no contrast enhancement around an ill-defined hypointense area (arrow). Note mucosal enhancement in left frontal sinus (white arrow).
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AbsesAbsesOtakOtak
CT Scan: Tanpa kontras ≈ area
hipodens (LCS) (+) kontras ≈ ring
enhancement Edema periabses
EEG Gel. Lambat 3x/ det
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AbsesAbsesOtakOtak
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Medikamentosa:• Keberhasilan terapi:
Sedini mungkin (serebritis, kapsul belum terbentuk) Lesi kecil Gejala muncul < 2 minggu Perbaikan klinis dalam minggu I terapi
• Antibiotika (mikroorganisme belum jelas): Vancomycin; dws: 1 g/12jam, anak: 15 mg/kgBB/8jam →
DIKOMBINASI: Sefalosporin III/ IV → DIKOMBINASI (salah satu):
Metronidazol; dws: 30 mg/kgBB/hari, anak: 10 mg/kgBB/8jam
Chloramphenicol; dws: 1 g/6jam, anak: 15-25 mg/kgBB/6jam
Rifampicin (p.o); 9 mg/kgBB/hari dosis tunggal, POST TRAUMA
• Antibiotika (mikroorganisme jelas): Streptokokus → Penisilin G; dws: 5 juta unit/6jam, anak:
50-750 ribu unit/kgBB/6jam Toksoplasma gondii → Clindamycin 4x300 mg p.o +
fansidar 2x1
AbsesAbsesOtakOtak
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Penatalaksanaan LCS:
Tekanan ↑Pleiositosis PMN (25-300), jika kronis: limfosit dominanProtein ↑, Cl & Glukosa normal
Operatif:Mass effectLokasi dekat ventrikel (risiko ruptur → intraventrikel)TIK meningkatDefisit neurologis progresif
Antiedema:Manitol 20% 1,0-1,5 g/kgBB (250 cc) dalam 20-30
menitSteroid dosis tinggi: deksametason 16-24 mg/hari, 4-
6x/ hari → tapp off tiap 5 hari
AbsesAbsesOtakOtak
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Menghilangkan fokus infeksi & efek massaMedikamentosa:
Sefalosporin gen. III/ IV: cefotaksim 1-2gr/ 12 jam, ceftriakson 1-2gr/ 24 jam, ceftazidim, cefizoksim, cefepime
Ampisilin 2gr/ 6 jam i.v (200-400 mg/kgBB/hari selama 2 minggu)
Kloramfenikol 1gr/ 6 jam i.v selama 2 minggu Metronidazol 500mg/ 8 jam i.v selama 2 minggu Antiedema: manitol, deksametason, metilprednisolon Operatif: jika tindakan konservatif gagal atau Ø
abses 2cm Penyulit: herniasi, hidrosefalus obstruktif, koma
AbsesAbsesOtakOtak
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Spondilitis TBSpondilitis TB≈ Pott’s disease2% TB atau 40-50% TB muskuloskeletalGejala & tanda
Gejala umum TB, nyeri punggungDiagnosis
Rö vertebra, CT scan, MRIDiagnosis banding
Osteitis purulenta, tumor med. Spinalis
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Spondilitis TB
Baji/ gibbusBaji/ gibbus
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Hidrosefalus
Hidrosefalus: akumulasi LCS krn sistem drainase yg tergangguKomunikan: jika blok pada sistem ventrikel
(foramen)Non komunikan: jika blok di luar sistem
ventrikelAkut → CITO operatif→ herniasi → kematianKronik → konservatif → kompensasi
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Etiologi Hidrosefalus
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Pungsi Lumbal
Indikasi LPFebrile unknown origin (FUO)Suspek infeksi SSPMencari etiologi/ mikroorganisme
Kontraindikasi LPTIK ↑ (dioptri >3)Sedang kejangLuka daerah LP
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Pungsi Lumbal
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Komplikasi Infeksi SSP
TIK meningkatKejangHidrosefalusSubdural effusionSubdural empyemaDefisit neurologisSIADHSyok sepsis
Sindr. Waterhouse-Friderichsen Hemorrhagic infarction kelj. Adrenal Severe purpura
Disseminated Intravascular Coagulation (DIC) >8% penderita, sering terjadi pada minggu I sakit
Adult Respiratory Distress Syndrome (ARDS) + 3,5% penderita, mortalitas 100%
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Tetanus ≈ 7 Days DiseaseNeurotoksin kuman gram (+) c. tetani
(tetanospasmin)→ paralitik spastik3 jenis :
Localited tetanusCephalic tetanusGeneralized tetanus
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Stadium TetanusStadium 1 (mild): lock jaw, spasme
terbatas, disfagia, opistotonusStadium 2 (moderate): spasme ringan-
sedang, takipneu, rigiditas jelasStadium 3 (severe): trismus berat,
spastisitas umum, spasme spontan, disfagia, takipneu, takikardia, disotonomi
Stadium 4: ≈ stadium 3, autonomic storm
TetanusTetanus
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Gejala KlinisMasa inkubasi 5-14 hariKejangTrismus, lock jawOpistotonusKaku kudukRisus sardonicusDisfagia Obstruksi laring akibat
aspirasiRiwayat luka
Pemeriksaan penunjangLab. Darah: SGOT↑, CPK ↑,
myoglobinuria, kultur C. tetani
TetanusTetanus
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Komplikasi Miokarditis: demam, rash, eosinofilia
primer, biomarker nekrosis ↑, EKG ≈ infark miokard (ST elevasi)
Disotonomi: tek. darah instabil, cardiac arrest, vasokonstriksi, hipersalivasi, pireksia, ileus, diare, gagal ginjal, disritmik jantung
BronkopneumoniaSepsisGangguan traktus GIGagal napas
TetanusTetanus