Infeksi Susunan Saraf Pusat

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BAGIAN NEUROLOGIBAGIAN NEUROLOGI FK UNDIP / RSUP DR KARIADI SEMARANGFK UNDIP / RSUP DR KARIADI SEMARANG DAFTAR MATA KULIAH DAN DOSEN DAFTAR MATA KULIAH DAN DOSEN PENGAMPUPENGAMPU

NO NO MATA KULIAHMATA KULIAH DOSEN PENGAMPU DOSEN PENGAMPU

11 Infeksi Susunan Saraf PusatInfeksi Susunan Saraf Pusat Dr Aris Catur Bintoro, SpsDr Aris Catur Bintoro, Sps

22 StrokeStroke Dr Dodik Tugasworo, SpS(K)Dr Dodik Tugasworo, SpS(K)

33 EpilepsiEpilepsi Dr Endang Kustiowati, SpS(K)Dr Endang Kustiowati, SpS(K)

44 Nyeri Kepala & VertigoNyeri Kepala & Vertigo Dr Herlina Suryawati, SpSDr Herlina Suryawati, SpS

55 Gangguan Gerak & Trauma Kepala Gangguan Gerak & Trauma Kepala Prof Dr Amin Husni, MSc, Prof Dr Amin Husni, MSc, SpS(K) SpS(K)

66 Nyeri muskuloskeletal & nyeri Nyeri muskuloskeletal & nyeri neuropatikneuropatik

Dr Dani Rahmawati, SpS(K)Dr Dani Rahmawati, SpS(K)

77 NeuropatiNeuropati Prof Dr Widiastuti, MSc, SpS(K)Prof Dr Widiastuti, MSc, SpS(K)

88 Neurogeriatri & tumor serebriNeurogeriatri & tumor serebri Dr Soetedjo, SpS(K)Dr Soetedjo, SpS(K)

99 Neurobehaviour & NeuropediatriNeurobehaviour & Neuropediatri Dr Hexanto Muhartomo, MKes, Dr Hexanto Muhartomo, MKes, SpSSpS

1010 NeuroemergensiNeuroemergensi Dr Retnoningsih, SpS, KIC Dr Retnoningsih, SpS, KIC

1111 Rehabilitasi MedikRehabilitasi Medik Dr Rudy Handoyo, SpRMDr Rudy Handoyo, SpRM

1212

INFEKSI SUSUNAN SARAF PUSAT

Dr Aris Catur Bintoro, SpS

BUKU ACUAN

• Gilroy : Basic neurology

• RT Johnson: Current therapy in neurologyc disease

• Adam & Victor : Principle of neurology

• Priguna Sidharta & Mahar Margono :

-Neurologi klinis dasar

-Neurologi dalam praktek umum

-Tatacara pemeriksaan neurologi

TUJUAN PENDIDIKAN

• TIU : Setelah menyelesaikan perkuliahan mahasiswa mampu mendiagnosis dan mengelola pasien infeksi SSP dengan

benar

• TIK : Mahasiswa mampuMenyebutkan etiologiMenjelaskan patologi / patogenesis Menjelaskan gejala & tandaMenegakkan diagnosisMelakukan terapi

INFEKSI SUSUNAN SARAF PUSAT

LOKASI

MeningitisEncephalitis Meningoencephalitis

CerebritisBrain abscess Cranial epidural abscessSubdural empyema

Myelitis transversa

KLASIFIKASI MENINGITIS

Penyebab (infeksi SSP) :Bakteri ProtozoaVirus Cacing Jamur

Cairan serebrospinal :-Piogenik-Non Piogenik (Aseptik)

Lapisan : Pakimeningitis (duramater)

Leptomeningitis (araknoid & piamater)

MENINGITIS MENINGITIS BAKTERIAL AKUTBAKTERIAL AKUT

DEFINISI

Infeksi cairan serebrospinal disertai

radang yang mengenai araknoid, piamater dan

derajat ringan bagian superfisial jaringan otak &

medulla spinalis

EPIDEMIOLOGI>> Negara berkembang, sosek tak mampu

Indonesia : data minimal

ETIOLOGI

Neonatus - 3 bl : E. coli (-), Strept group B (+), Listeria (+), Staph aureus (+)

3 bl – 6 th: H.Influenzae (-), N.Meningitidis (-), S.Pneumoniae (+)

6 – 20 th : N.Meningitidis, S.Pneumoniae, H. Influenzae

> 20 th : S.Pneumoniae, N.Meningitidis, Streptococcus, Staphylococcus

17%

6%

17%

5%2%3% 4%

25%

29%

Haemophilus

Neisseria

Strep Pn.

Other Strep.

Listeria

Staph.

Mycobact

E. Coli

Others

PATOGENESIS

I)I) Kolonisasi Kuman nasofaringsKolonisasi Kuman nasofarings

Invasi lokal Invasi lokal (I : Mucosal invasion)(I : Mucosal invasion)

Bakteriemia Bakteriemia (II : intravascular survival)(II : intravascular survival)

Melekat pada endotel pleksus khoroid / endotel vaskular otakMelekat pada endotel pleksus khoroid / endotel vaskular otak

Kerusakan sel endotelKerusakan sel endotel

Invasi selaput otak Invasi selaput otak (III: crossing BBB)(III: crossing BBB)

Replikasi bakterial di LCS + inflamasi Replikasi bakterial di LCS + inflamasi (IV: Survival in CSF)(IV: Survival in CSF)

MeningitisMeningitis

1.1. Luka terbuka dikepalaLuka terbuka dikepala2.2. Penyebaran langsung dari :Penyebaran langsung dari :

a. Infeksi telinga bag. tengah (OM)a. Infeksi telinga bag. tengah (OM)b. Sinus paranasalisb. Sinus paranasalisc. Kulit kepala - mukac. Kulit kepala - mukad. Benda asing terinfeksi (shunting)d. Benda asing terinfeksi (shunting)

3.3. SepsisSepsis4.4. Thromboplebitis kortikalThromboplebitis kortikal5.5. Abses sub/ekstra dural Abses sub/ekstra dural 6.6. Lamina cribosa os ethmoidalis dan rhinorheaLamina cribosa os ethmoidalis dan rhinorhea7.7. Pungsi lumbalPungsi lumbal

Jalur Kuman mencapai Leptomening dan Subarachnoid Jalur Kuman mencapai Leptomening dan Subarachnoid

PATOLOGI

-Pneumokokus & H Influenza : eksudat di konveksitas-N.Meningitidis : eksudat di basal

-Lapisan Pia-Araknoid menebal dan adesi ganggu aliran LCS Hidrosefalus

-Reaksi inflamasi & fibrosis meningen dapat mencakup radix nn kranialis paresis n kranialis VII & disfungsi n VIII

PATOLOGI (Lanjutan)

-Inflamasi arteri & vena (vaskulitis) trombosis – infark hemiparesis, afasia, serebelar sign

-Kasus akut fulminan meninggal sebelum terjadi perubahan patologi di SSP

CLINICAL FEATURES

Early : -Fever-Irritability-Headache-Stiffneck

-Relative preservation of mental status-Lack of major focal neurological signs-No papil edema

CLINICAL FEATURES

Later SeizuresCranial nerve palsies (VII,VIII)Lethargy and stuporFocal neurological signs

CARACTERISTIC’S OF ETIOLOGYCARACTERISTIC’S OF ETIOLOGY

ETIOLOGY EPIDEMIOLOGY CLINICAL FEATURES

MORTALITY

S PneumoniaS Pneumonia Adult, head trauma, Adult, head trauma, anemia, alcoholicanemia, alcoholic

Cough, blood Cough, blood culture (+) 56% culture (+) 56%

20-60%20-60%

N Meningitidis

Youth, epidemics, spring /winter

Sore throat, petechiae, purpura

6-7 %

H InfluenzaeH Influenzae Child, winterChild, winter Earache, (+) blood Earache, (+) blood culture 79%culture 79%

7-8%7-8%

Streptococcus group B

Neonates, premature rupture of membrane

40-80%

E ColiE Coli Neonates, head Neonates, head trauma, neurosurgerytrauma, neurosurgery

Urinary tract Urinary tract infection 40%infection 40%

50%50%

Stap. aureus Neonates, elderly, head tr., neurosurgery

Listeria Listeria monocytogenmonocytogen..

Renal transplant, Renal transplant, Neonates, Neonates,

Absence of nuchal Absence of nuchal rigidity rigidity

DIAGNOSIS

Pemeriksaan LCS -Tekanan : > 180 mmH2O

-Warna : keruh – purulen-Sel : PMN, 200 – 10.000-Protein : > 75 mg/100 ml-Gula : < 40%-Pengecatan -Jumlah kuman -Kultur-Antigen : RIA, EIA, Latex

CAIRAN SEREBROSPINAL NORCAIRAN SEREBROSPINAL NORMALMAL

Warna : jernih

Tekanan : 70 – 180 mm H20

Sel : 0 – 5 / mm3 , MN

Glukosa : 45 – 80 mg%

Protein : 15 – 45 mg%

PUNGSI LUMBALPUNGSI LUMBAL INDIKASI Konfirmasi diagnosis (infeksi, perdarahan,blok subaraknoid) Identifikasi organisme Memasukkan zat kontras (myelografi) Pengobatan (injeksi intra thecal)

KONTRA INDIKASI Infeksi pada daerah suntikan Adanya TIK meningkat Abses / tumor fossa posterior

KOMPLIKASI Nyeri kepala Herniasi otak Perdarahan spinal subdural/epidural/subaraknoid Lain2 : iritasi radikuler, infeksi

DIAGNOSIS

• Pemeriksan darah tepi • Cel reactive protein • Kultur dan sensitivitas sumber infeksi• X foto • CT scan kepala (+kontras) • EEG

TERAPI

UMUM

• Prinsip 5B• Cairan, infus dalam jumlah cukup• Panas, diturunkan• Kejang, diatasi dengan inj. Diazepam iv• TIK meningkat, diturunkan : inj.

Kortikosteroid, drip manitol 20% • Hidrosefalus, dilakukan shunting• Fisioterapi pasiv - aktiv

KHUSUS

Prinsip antibiotika :Bersifat bakterisidKonsentrasi tinggi di LCSObati infeksi parameningealJenis AB tergantung : kultur, kepekaan,

usia

Antibiotika dosis tinggi IV : Antibiotika dosis tinggi IV :

Kadar bakterisidal dalam LCS 10 - 20 x konsentrasi bakterisidal minimal organisme

Sifat antibiotika ideal :Sifat antibiotika ideal :Larut dalam lemak menembus BBBAktif dalam LCS purulen dan asam

Antibiotika tepat : Antibiotika tepat :

• LCS steril dalam 24 - 36 jam

Lama pemberian :Lama pemberian :• Pneumokok : 10 - 14 hari• H. Influenza : 10 hari• Meningokok : 7 hari• Gram ( - ) : 21 hari• Umumnya hingga bebas panas 7 hari

Empiric Antibiotic therapy of Bacterial MeningitisEmpiric Antibiotic therapy of Bacterial Meningitis

Patient GroupPatient Group AntibioticAntibiotic

NeonatesAmpicillin + Aminoglycoside or Ampicillin + Cefotaxime

Infants (1-3 mo) Ampicillin + Cefotaxime

Children (3 mo - 6 yr) Ampicillin + CefotaximeOlder Children, adults (no

spesific risk factors)Penicillin G or third generation cephalosporin

Immunocompromised patient

Third generation cephalosporin + Ampicillin (+Aminoglycoside)

Neurosurgery, head trauma patients

Third generation cephalosporin + Nafcillin (+ Aminoglycoside)

Chronic CSF fistulaThird generation cephalosporin + Nafcillin

Bacterial Pathogens

OrganismOrganism Antibiotic*Antibiotic*

H. InfluenzaeH. InfluenzaeThird generation cephalosporin, Ampicillin (if sensitive), Chloramphenicol

S. pneumoniaeS. pneumoniaePenicillin G, third generation cephalosporin, Chloramphenicol

Reduced penicillin Reduced penicillin sensitivesensitive

Third generation cephalosporin

Penicillin resistantPenicillin resistantThird generation cephalosporin or Vancomycin

N. meningitidisN. meningitidis Penicillin G, Chloramphenicol

S. agalactiaeS. agalactiae Penicillin or ampicillin

OrganismOrganism Antibiotic*Antibiotic*

L. monocytogenesL. monocytogenesAmpicillin (plus aminoglycoside) or

trimethoprim-sulfamethoxazole

EnterobacteriaceaeEnterobacteriaceaeThird generation cephalosporin with or

without aminoglycoside

P. aeraginosaP. aeraginosaCeftazidime + aminoglycoside or

fluroquinolone (eg. Ciprofloxacin)

S. aureusS. aureus Nafcillin

* Third generation cephalosporins : Third generation cephalosporins : Cefotaxime ; Ceftriaxone; CeftizoximeCefotaxime ; Ceftriaxone; Ceftizoxime For penicillin allergic patientFor penicillin allergic patient

Dosage of Antibiotics Commonly Used in the Dosage of Antibiotics Commonly Used in the Therapy of Bacterial MeningitisTherapy of Bacterial Meningitis

AntibioticAntibiotic Children (>1 mo)Children (>1 mo) AdultsAdults

NafcillinNafcillin 50 mg/kg q6h50 mg/kg q6h 1.5 g q4h1.5 g q4h

GentamycinGentamycin 11--2 mg/kg iv q8h2 mg/kg iv q8h

Penicillin GPenicillin G 50.000 U/kg q4h50.000 U/kg q4h 3 3 -- 4 MU q4h4 MU q4h

Dose and dosing intervalDose and dosing interval

AmpicillinAmpicillin 100 mg/kg q8h100 mg/kg q8h 2 g q4h2 g q4h

CefotaximeCefotaxime 50 mg/kg q6h50 mg/kg q6h 22--3 g q6h3 g q6h

CeftriaxoneCeftriaxone 50 mg/kg q12h50 mg/kg q12h 2 g q12h2 g q12h

CeftazidimeCeftazidime 50 mg/kg q6h 2 g q8h50 mg/kg q6h 2 g q8h

ChloramphenicolChloramphenicol 25 mg/kg q6h25 mg/kg q6h 1.5 g q6h1.5 g q6h

VancomycinVancomycin 10 mg/kg q6h10 mg/kg q6h 0.5 g q6h0.5 g q6h

COMPLICATIONS

Common SeizuresPersistent FeverHearing lossFocal neurological signsIncreased intracranial pressureSIADH : Na < 130 mEq/L (serum)

Na & osmolality (urin)Subdural effusion

COMPLICATIONS

Less common ShockDICComaHydrocephalusSubdural empyemaBrain abscess

PENCEGAHAN

Anak 1-12 th: Rifampisin 10 mg/kgBB/12 jamDiatas 12 th : “ 600 mg, 1xH Influenzae, pemberian 4 hariN Meningitidis, pemberian 2 hari

VaksinasiH Influenzae type B infants efektifMeningococcus. S Pneumonia belum terbukti

PROGNOSIS

Tergantung : -Umur -Virulensi-Kedinian pengobatan-Jenis & dosis AB

A.A. Non kontrast CT scan menunjukkan adanya edema cerebri ( E ).Non kontrast CT scan menunjukkan adanya edema cerebri ( E ).

B.B. CECT menunjukkan adanya penyerapan kontrast pada girus.CECT menunjukkan adanya penyerapan kontrast pada girus.

C.C. NCMRI T1W pada penderita yang sama, tak jelas menunjukkan adanya kelainan.NCMRI T1W pada penderita yang sama, tak jelas menunjukkan adanya kelainan.

Meningitis supurativa dengan edema atau infark kortex

D. T2W menunjukkan adanya edema multiple pada daerah gyrus cortex cerebri. ( panah terbuka )

E. Dengan pemberian kontrast, tampak adanya penyerapan kontrast pada meningen.

Meningitis supurativa dengan edema atau infark kortex

MENINGITIS TUBERKULOSA

PATOGENESIS -Aktivasi infeksi laten mycobacterium TB-Aktivasi infeksi laten mycobacterium TB

-Kuman di respiratory tract -Kuman di respiratory tract via via hematogen hematogen

ke mening & permukaan otak ke mening & permukaan otak Tuberkel, Tuberkel,

pecah, masuk ke subaraknoid pecah, masuk ke subaraknoid Meningitis Meningitis TBTB

PATOLOGI-Eksudat di basal sisterna, >>MN-Hidrosefalus obstruktif-Arteritis, infark serebri

GAMBARAN KLINIK

Stadium I : sadar, rangsang meningeal, demam Stadium II: kesadaran, ggn. neurologik fokal Stadium III: stupor – koma

Bayi : rewel, fontanella menonjol Orang tua : demam (-), kesadaran, timbul kaku kuduk secara perlahan Kelainan neurologik fokal :

Paresis n VI, oftalmoplegi, hemiparesis

DIAGNOSIS

Pemeriksaan LCSwarna jernih/ santokromtekanan sel 50-500, >>MN, pada awalnya PMNprotein > 100mg/dlglukosa < 20 mg/dlpengecatan, biakan kuman

Tes antigen : darah & LCSPemeriksaan darah tepi; LEDPCRX foto torakCT scan kepala

Diagnosis berdasar: -Klinis & laboratorium-Ditemukan kuman TB dari LCS

DIAGNOSIS BANDING

Meningitis ok. Sifilis , jamurMeningitis bakterial dg pengobatan tak sempurna

TERAPI Daya tembus OATB pada meningen berbeda

OBAT INFLAMASI NON INFLMS

STREPTOMISINSTREPTOMISIN Baik Buruk

INH Baik Baik

RIFAMPISINRIFAMPISIN Baik Buruk

PIRAZINAMID Baik Baik

ETAMBUTOLETAMBUTOL Baik Buruk

Kombinasi : 4 macam obat2 bulan I : R + I + P + E (+S)7 bulan II : R + I

OBATOBAT DEWASADEWASA ANAKANAK

INH 400 mg/hari 10-20 mg/kg/hari

RIFAMPISIN 600 mg/hari 15-25 mg/kg/hari

PIRASINAMID 1500 mg/hari 20-35 mg/kg/hari

ETAMBUTOLSTREPTOMISIN

500 mg/hari750 mg, im 20 mg/kg/hari

KORTIKOSTEROID

Indikasi :

Kesadaran makin memburuk

gejala fokal progresifgejala gangguan batang otak, MS,

radik

Dosis : inj. Deksametason 4x 1-2 amp 1 minggu tappering of hingga 3 minggu.

Meningitis Tuberculosa

A. CT Scan tanpa kontras.B. CT Scan dengan kontras menunjukkan adanya

penyerapan kontras pada daerah tentorium dan spatium subarachnoid.

C. CT Scan dengan kontras.D. Hari ke 3 setelah CT Scan A-C; tampak

terjadinya infark cerebri.

Pre C Post C Post C

Meningoencephalitis TB dengan multiple tuberculoma dan kalsifikasi. Untuk melihat adanya kalsifikasi CT lebih baik

daripada MRI

Encephalitis dan Ventrikulitis, kesan : TBC

MRI Nn. D.I.S. 16 th .

ABSES OTAK

PATOGENESIS

Penyebaran kuman langsungPenyebaran kuman langsung

- telinga, sinus, mastoid, gigi- telinga, sinus, mastoid, gigi

- trauma kepala, tindakan bedah- trauma kepala, tindakan bedah

Penyebaran kuman hematogenPenyebaran kuman hematogen

- paru, saluran cerna, jantung- paru, saluran cerna, jantung

Lokasi : -substansia alba Lokasi : -substansia alba

-substansia alba – grisea junction-substansia alba – grisea junction

Perkembangan absesPerkembangan abses : :

Early cerebritisEarly cerebritis (hari 1-3)(hari 1-3)

Late cerebritisLate cerebritis (hari 4-9)(hari 4-9)

Early capsulated formation (hari 10-Early capsulated formation (hari 10-14)14)

Late capsulated formationLate capsulated formation (> 14 (> 14 hari)hari)

ETIOLOGY

Chronic ear inf.Chronic ear inf. Aerob and anaerob streptococci,Aerob and anaerob streptococci, Temporal lobe or 15 % Temporal lobe or 15 %B Fragilis, EnterobacteriaceaeB Fragilis, Enterobacteriaceae cerebellar hem. cerebellar hem.

Frontal or Frontal or Staphylococcus aureus, streptococci, Frontal lobe 20%Staphylococcus aureus, streptococci, Frontal lobe 20%Ethmoid sinusitisEthmoid sinusitis B fragilis, haemophilusB fragilis, haemophilus

Periodontal inf.Periodontal inf. Mixed flora, streptococciMixed flora, streptococci Frontal lobe Frontal lobe 15% 15%

Pulmonary inf.Pulmonary inf. Mixed flora, B fragilis,Mixed flora, B fragilis, parietal and other 15% parietal and other 15%Streptococci, nocardiaStreptococci, nocardia lobes (often multiple) lobes (often multiple)

EndocarditisEndocarditisMixed flora, S aureusMixed flora, S aureus multiple, small multiple, small

Cranial truma orCranial truma or Staphylococcus pyrogens/aureusStaphylococcus pyrogens/aureus adjacent to site of 5% adjacent to site of 5%SurgerySurgery Streptococci, enterobacterStreptococci, enterobacter injury injury

GAMBARAN KLINIS

Tergantung dari letak lesi dan akibat Tergantung dari letak lesi dan akibat kenaikan TIKkenaikan TIK

-Nyeri kepala -Nyeri kepala 65%65%

-Mual, muntah-Mual, muntah 50%50%

-Kejang fokal / umum -Kejang fokal / umum 65%65%

-Gangguan kesadaran -Gangguan kesadaran 50%50%

bersifat progresifbersifat progresif

-Bila di serebelum :-Bila di serebelum : -ataksia-ataksia

-nistagmus-nistagmus

-edema papil-edema papil

LABORATORIUM

-Darah :-Darah : lekosit 40% normallekosit 40% normal

LED LED 75% meningkat75% meningkat

-LCS : -LCS : tak memberi informasi, bahayatak memberi informasi, bahaya

-CT scan (+kontras) : “ring enhancement”-CT scan (+kontras) : “ring enhancement”

-MRI-MRI

-EEG-EEG

DIAGNOSISBerdasar temuan klinis dan laboratorium (CT Berdasar temuan klinis dan laboratorium (CT scan)scan)

TERAPI

-Terbaik kombinasi antibiotika dan -Terbaik kombinasi antibiotika dan kraniotomikraniotomi

-Antibiotika yang menembus BBB-Antibiotika yang menembus BBB

-Kuman -Kuman AerobAerob : -Penicillin G, Ampicillin, : -Penicillin G, Ampicillin,

Chloramfenicol, Cefotaxim, Chloramfenicol, Cefotaxim, CeftriaxoneCeftriaxone

-Kuman -Kuman AnaerobAnaerob : : MetronidazoleMetronidazole

-Kortikosteroid-Kortikosteroid ::

(+) kurangi edema(+) kurangi edema

(-) efek resistensi kuman >> (-) efek resistensi kuman >>

Antibiotic IV Dosage **Penicillin G 3 milliion units, q4hNafcillin 2g, q4hVancomycin 1g, q8hMetronidazole 500 mg, q6hChloramphenicol 1.5 g, q6hCeftriaxone 2 g, q12hCeftazidime 2g, q8hCefotaxime 2g, q6hGentamycine 1.5 mg/kg, q8h

For suspected Toxoplasmosis Gondii abcess :Sulfadiazine 4 g, q6hPyrimethamine 75 mg, q8h ***

*Dosing for infants, children, and adults who weigh less than 60 kg must be done on a per kilogram basis according to published guidelines. Adjustments in doses must also be made if renal functions is impaired

** Standard i.v adult dosage *** Folinic acid must be administered concurrently, 10 mg per day

Antibiotics Dosing Schedules Useful in theTreatment of Brain Abcess and Parameningeal Infections of Adults*

PROGONOSIS

-Antibiotika + kraniotomi -Antibiotika + kraniotomi mortalitas mortalitas 8%8%

-Penyebab kematian :-Penyebab kematian :

Kenaikan TIKKenaikan TIK

Abses pecahAbses pecah

Diagnosis terlambatDiagnosis terlambat

Cerebritis dan Abses cerebri

CT Scan kepala dengan kontrast menunjukkan adanya sinusitis frontalis (panah tertutup), cerebritis (Ce) dan abses lobus frontalis (panah terbuka).

Cerebritis dengan AbsesCT Scan an. D. 8 th.

Tanpa kontrast Dengan kontrast

INFEKSI VIRUS

PATOLOGI

Virus menyebar ke sistem saraf via Virus menyebar ke sistem saraf via hematogen hematogen menembus sel menembus sel endotel & pleksus koroideus endotel & pleksus koroideus

Infiltrasi limfosit perivaskular dan Infiltrasi limfosit perivaskular dan proliferasi mikroglia daerah proliferasi mikroglia daerah subkorteksubkortek

GAMBARAN KLINIK

Awal : demam, nausea, nyeri kepala

Lanjut : - gangguan kesadaran- kejang fokal / umum- defisit neurologis- rangsang meningeal

(Meningoensefalitis)

Lokasi Predileksi

Eneterovirus : sel meningeal

Mumps virus : sel ependym nyeri kepala, kaku kuduk

Polio virus: motor neuron paralisis flaksid Rabies : sistim Limbik hiperaktif, agresif

LABORATORIUM

Pemeriksaan LCS; -Tekanan : N / -Sel limfosit : < 1000, MN-Protein : N / -Glukosa : N /

Titer antibodiPCRCT scan / MRIEEG

DIAGNOSISDIAGNOSISPemeriksaan fisik & hasil laboratorium

TERAPI

Simtomatik : - kebutuhan cairanSimtomatik : - kebutuhan cairan

- turunkan demam- turunkan demam

- atasi kejang- atasi kejang

- kurangi edema otak- kurangi edema otak

Antivirus :Antivirus :

-Acyclovir : 10 mg/kg,q8h,iv 14d (H -Acyclovir : 10 mg/kg,q8h,iv 14d (H simplex)simplex)

5 mg/kg,q8h,iv, 5 d (H 5 mg/kg,q8h,iv, 5 d (H zooster)zooster)

SIGN OF TESTSIGN OF TEST BACTERIAL M.BACTERIAL M. VIRAL M. VIRAL M.

Clinical FeaturesClinical Features SeveritySeverity Often severeOften severe Often mild Often mild High Fever High Fever CommonCommon UncommonUncommon Shaking chillsShaking chills CommonCommon UncommonUncommon CourseCourse Untreated course worsens Untreated course worsens Seldom worsens Seldom worsens

after after first day first day

Systemic signsSystemic signs May have upper respiratorMay have upper respiratory y May have May have parotitis, or parotitis, or tract infection or otitis mediatract infection or otitis media diarrheadiarrhea

Previous healthPrevious health May be poor or have May be poor or have Often healthy Often healthyimmunodeficienciesimmunodeficiencies

CSF examinationCSF examination CellsCells Predominantly neutrophilsPredominantly neutrophils Pred. Pred.

lymphocyteslymphocytes GlucoseGlucose usually lowusually low Usually normal Usually normal ProteinProtein ElevatedElevated N or N or

slightly elevatedslightly elevated Gram stainGram stain Often bacteria seenOften bacteria seen No bacteria seen No bacteria seen Bacterial antigensBacterial antigens Often detectedOften detected Absent Absent

Blood TestBlood Test White blood cell countWhite blood cell count usually elevatedusually elevated Often Often

normalnormal Blood cultureBlood culture Positive greater than 60%Positive greater than 60% Sterile Sterile

INFEKSI HIV-AIDS

ETIOLOGY

Human immunodeficiency virus type 1 (HIV-1)

Characterized : Opportunistic infections Malignant neoplasms Variety of neurologic disturbances

Transmission : Sexual activity Contaminated blood or blood products

Classification of HIV Infection

LABORATORY category

1. CD4 lymphocyte count > 500 cell/mm3

2. CD4 “ “ 200 – 499 cell/mm3

3. CD4 “ “ < 200 cell/mm3

CLINICAL Category

HIV and the brain

o Meningitis• HIV itself• TB • Cryptococcal• Syphilitic

o Space occupying lesions• Toxoplasmosis• Tuberculomas• Lymphoma

HIV and the brain

o EncephalitisEncephalitis– HIV dementiaHIV dementia– Progressive multifocal leukoencephalopathy Progressive multifocal leukoencephalopathy

(PML)(PML)– CMV, HSV, HZV encephalitisCMV, HSV, HZV encephalitis– ToxoplasmosisToxoplasmosis

o Strokes and intracerebral haemorrhageStrokes and intracerebral haemorrhage

HIV and the spinal cord

o Vacuolar myelopathyVacuolar myelopathyo SyphilisSyphiliso HZV, HSV, CMV, HTLV-1HZV, HSV, CMV, HTLV-1o TBTBo LymphomaLymphoma

Usually subacute over weeks

Headache 50%Fever 45%Behaviour changes 40%Confusion 15-52%Focal signsSeizures 24-29%

TOXOPLASMOSIS, Clinical features

Reactivation of latent infectionReactivation of latent infectionToxo seroprevalence 12-46% Toxo seroprevalence 12-46%

LaboratoryLaboratory : CD4 > 200 virtually excludes Toxo : CD4 > 200 virtually excludes Toxo Over 80% have CD4 < 100Over 80% have CD4 < 100

CT/MRICT/MRI : Typically multiple ring enhancing lesions : Typically multiple ring enhancing lesions

TreatmentTreatment : :- Sulphadiazine and Pyrimethamine is first - Sulphadiazine and Pyrimethamine is first choicechoice- Co-trimoxazole (80/400mg) 4 tablets BD x - Co-trimoxazole (80/400mg) 4 tablets BD x 4/52,4/52, then 2 tablets BD x 8/52then 2 tablets BD x 8/52

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