Pendekatan diagnosis dan tatalaksana

infeksi SSP pada anak

Setyo Handryastuti
Divisi Neurologi
Departemen Ilmu Kesehatan Anak
FKUI-RSCM
 Pendahuluan

•  Meningitis bakterial akut ; subakut/kronik

(TB) ; ensefalitis virus akut
•  Tiga hal yang perlu dipahami :
–  Anatomi SSP
–  Etiologi dan patogenesis
–  Mekanisme terjadinya kegawatdaruratan
•  Pendekatan diagnosis dan tatalaksana
 Anatomi ensefalitis-meningitis
Vena   Sinus  sagitalis  superior  

Tulang  

Arachnoid   Dura  mater  

Ruang  
Ruang  SubDura    
subarachnoid  
Vili  arachnoid  
Piamater   granula8onis  

Trabekula  arakhnoid   Fissura  longitudinl    

Vena   Korteks  otak    

serebral  

Meningi&s  :  Tidak  selalu  ada  penurunan  kesadaran  

Ensefali&s    :  Penurunan  kesadaran  dan  kejang   Wikipedia.org  
Anatomi meningitis TBC

Paresis  saraf  kranial  

(II,III,IV,VI,VII)  serta  ggn  
serebelum  lebih  sering  

Sciencedirect.com  
Mengapa terjadi hidrosefalus ?
Aliran  Cairan  
serebrospinal  

 Ventrikel  
lateral  
Foramen  
Monroe  

Ventrikel  8ga  

Aquaductus  
Sylvii  
Ventrikel  
empat  
Foramen  
Luschka  &  
Magendie  
Ruang  
subarakhnoid    

•  Reabsorbsi  ke  
sinus  venosus  
via  granulasi  
arakhnoid  
Mengapa infeksi SSP terjadi penurunan kesadaran ?

Ascending  Re+cular  
Ac+va+ng  System  
(ARAS)  

Korteks  

Formasio  re8kularis  
Mengapa terjadi peningkatan tekanan intrakranial ?

Gangguan aliran CSS

Obstruksi, kelainan pleksus
koroid, ggn absorbsi CSS
Peningkatan volume otak
Edema otak difuse/fokal
Peningkatan volume darah
serebral
Obstruksi aliran vena, hipoksia/
hiperkarbia, hipertensi,
hipervolemia,kegagalan respons
autoregulasi.

Hukum
Monroe-Kellie
Mengapa terjadi peningkatan tekanan intrakranial ?
 Jenis edema otak

•  é permeabilitas kapiler : cairan

Edema intravaskular ke ruang ekstraselular
vasogenik •  Substansia alba

•  Ggn permeabilitas membran sel :

Edema penumpukan cairan, pembengkakan
sitotoksik neuron-glia-sel endotel.
•  Substansia grisea dan alba

•  Pemindahan cairan dari sistem

Edema ventrikel ke jaringan otak akibat é
interstisiel tekanan hidrostatik intraventrikel
karena ggn sirkulasi CSS.
 Penyebab edema otak dan terapi

Edema Edema Edema

vasogenik sitotoksik interstisiel
•  Tumor, abses, •  Hipoksia, •  Sumbatan aliran
infark, trauma, iskemia, infeksi CSS
perdarahan otak •  Cairan (Hidrosefalus),
•  Kortikosteroid hiperosmoler produksi CSS é
(NaCl 3%, (papiloma pleksus
Manitol 20%) koroid), absorbsi
CSS yang
berkurang
(ventrikulitis
•  Asetazolamid
 Penegakan diagnosis infeksi SSP

Manifestasi Pemeriksaan
Pencitraan
klinis CSS
•  Akut/kronik •  Paling penting •  Akut: tidak
•  Tanda infeksi •  Analisis rutin selalu
•  Kelainan •  Kultur, PCR membantu
neurologi diagnosis,
hanya melihat
•  Peningkatan
komplikasi
TIK
•  Subakut/
Kronik :
membantu
diagnosis
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 Prinsip tatalaksana infeksi SSP

Simtomatik dan suportif

•  Nutrisi, cairan, antipiretik, anti konvulsan
Etiologi
•  Anti virus, antibiotika, OAT
Peningkatan tekanan intrakranial
•  Cairan hiperosmoler : NaCl 3% atau Manitol
20%, terapi lain : furosemid
Penanganan komplikasi
•  Tindakan bedah, medikamentosa
(kortikosteroid), pemantauan perkembangan/
fungsi penglihatan/pendengaran
 Diagnosis diferensial infeksi SSP
Klinis/Lab. Ensefalitis akut MB akut MB subskut/kronik
(TB)
Awitan Akut Akut Kronik
Demam < 7 hari < 7 hari > 7 hari
Kejang Umum/fokal Umum/fokal Umum/fokal

Penurunan Somnolen- CM-Apatis Variasi, apatis - sopor

kesadaran sopor
Paresis ++ +/- ++
ekstremitas
Paresis saraf - +/- ++
kranial
Perbaikan Lambat Cepat Lambat
kesadaran
Etiologi Tidak semua +/- TBC/riw. kontak
dpt
diidentifikasi
Terapi Simpt/antiviral Antibiotik OAT
Meningitis bakterialis akut
 Epidemiologi

•  Mortalitas : 18-40%, morbiditas : 30-50%

•  Peradangan pada selaput otak :
–  Peningkatan jumlah sel PMN dalam CSS
–  Bakteri penyebab infeksi dalam CSS
•  Laki-laki > perempuan
•  80% : anak
–  70% diantaranya berusia 1-5 tahun
Supurasi meningen
 Etiologi

•  Streptococcus B haemolyticus,
Neonatus Escherichia coli, Listeria monocytogenes,
enterobacter

•  E. coli, L. monocytogenes, Neisseria

Bayi dan meningitides, S. agalactiae, S.
balita pneumoniae, Haemophyllus influenzae
type B

•  N.meningitidis, S.pneumoniae, H.
> 5 tahun influenzae type B

Swaimanns Pediatric Neurology Principle and Practices 2018

Mann K, Jackson MA.Pediatr rev 2008
 Patogenesis
•  Kolonisasi kuman di saluran napas atas
Hematogen •  Pneumonia, sepsis
•  Bayi, balita

•  Penyebaran infeksi secara langsung

Perkontinuitatum •  Sinusitis/mastoiditis kronis,OMSK, caries dentis
•  Usia sekolah

Implantasi •  Trauma kepala terbuka, implantasi koklea

langsung •  Tindakan bedah saraf, Pungsi lumbal

•  Aspirasi cairan amnion pada amnionitis/flora kuman

Transplasenta normal
•  Neonatus

Swaimanns Pediatric Neurology Principle and Practices 2018

Chavez-Bueno S, Mc Cracken JH. Pediatr Clin N Am 2005
 Batuk,pilek,demam  

HEMATOGENIK  

Tanda  rangsang  
meningeal  

Defisit  neurologi  
dan  penurunan  
kesadaran    

Chavez-Bueno S, Mc Cracken JH. Pediatr Clin N Am 2005

 Manifestasi klinis ≈ Patogenesis

¡  Sangat bervariatif tergantung :

¡  Umur, cepat/lambat diagnosis ditegakkan, respons
tubuh terhadap infeksi.
¡  Neonatus-3 bulan :
§  Risiko tinggi:prematur, infeksi intrapartum,KPD
§  Tidak khas
§  Gejala sepsis disertai defisit neurologi (kesadaran
menurun, UUB membonjol,kejang.

Schwaimann. Pediatric Neurology 2018

JJ Volpe. Neurology of the newborn 2017
 Manifestasi klinis ≈ Patogenesis

•  Usia 3 bulan-2 tahun

–  Demam, muntah, iritabel, gelisah, kejang, high
pitched cry, UUB membonjol, tanda rangsang
meningeal sulit dievaluasi,
–  Pikirkan pada setiap kejang demam kompleks
•  Usia > 2 tahun
–  Gambaran klasik
–  Demam, muntah, nyeri kepala, kejang, dapat terjadi
penurunan kesadaran, tanda rangsang meningeal
(kaku kuduk, Bruzinski, Kernig) jelas
–  Paresis saraf kranial (N.III, N,IV, N.VI, N.VII)

Schwaimann. Pediatric Neurology 2018

 Penegakan diagnosis

•  Manifestasi klinis
•  Pemeriksaan cairan serebrospinal
–  Makroskopis : keruh, purulen
–  Peningkatan ∑ sel sampai ribuan (> 1000 sel/mm3,
hitung jenis predominan PMN.
–  Fase awal : ∑ sel normal sampai ratusan, hitung
jenis limfositer
–  Protein meningkat dan penurunan glukosa
(< 60% kadar glukosa darah)
–  Pewarnaan gram, kultur dan uji resistensi
–  PCR (Sensitifitas 86% dan spesifisitas 97%)
 m ee/ /e m ee/ /
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t p s s : tp ss :
hh Tatalaksana antibiotikahh tp
t t t p t t
Bacterial Infections of the Nervous System 887

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TABLE 114-3 Antimicrobial Therapy of Bacterial Meningitis

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Part A. Empirical Therapy Pending Culture and Susceptibility Data
Age Likely Pathogens

b o o
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0–1 mo
/ e
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Streptococcus agalactiae, Escherichia coli, Listeria monocytogenes

ee ee e
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1–3 mo

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S. agalactiae, L. monocytogenes, Streptococcus pneumoniae,

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Neisseria meningitidis, Haemophilus influenzae b

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Ampicillin + (cefotaxime or ceftriaxone) plus vancomycin
(see text)
3 mo–21 yr

t p s
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Pathogen
t
hh t t Therapy hh tp
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Part B. Specific Therapy

Streptococcus agalactiae Ampicillin or penicillin G for 14–21 days; first 3 days, add gentamicin; cefotaxime also acceptable
Listeria monocytogenes Ampicillin for 14–21 days; first 3 days, add gentamicin

rs
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Streptococcus pneumoniae

ee eers
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Penicillin MIC < 0.1 μg/ml and ceftriaxone or cefotaxime MIC ≤ 0.5 μg/ml: penicillin G or ampicillin for 10–14

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days
b o o
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Penicillin MIC ≥ 0.1 μg/ml and ceftriaxone or cefotaxime MIC ≤ 0.5 μg/ml: ceftriaxone or cefotaxime for 10–14

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for 10–14 days
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Neisseria meningitidis

t p s
p s :/ t p ss :/
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t
hh
Haemophilus influenzae b
t t hh tp
t t
Ceftriaxone or cefotaxime for 10 days; alternative: ampicillin if isolate is susceptible
Part C. Antimicrobial Dosage

Schwaimann.
Dose (mg/kg Per Day) Pediatric Neurology 2018
Agent Age 0–7 Days Age 8–28 Days Infants and Children
 Listeria monocytogenes Ampicillin for 14–21 days; first 3 days, add gentamicin

kkeers
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Streptococcus pneumoniae

k e r
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Penicillin MIC < 0.1 μg/ml and ceftriaxone or cefotaxime
days; ceftriaxone or cefotaxime also acceptable
MIC ≤ 0.5 μg/ml: penicillin G or ampicillin for 10–14

o
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b o o
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Penicillin MIC ≥ 0.1 μg/ml and ceftriaxone or cefotaxime MIC ≤ 0.5 μg/ml: ceftriaxone or cefotaxime for 10–14

Tatalaksana ee/ e
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for 10–14 daysb antibiotika ee/ e
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/ e MIC 1.0 μg/ml: (ceftriaxone or cefotaxime) + vancomycin

: / / t
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t m
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vancomycin ± rifampin for 10–14 days

: / /t/.tm.m
Penicillin MIC ≥ 0.1 μg/ml and ceftriaxone or cefotaxime MIC ≥ 2.0 μg/ml: (ceftriaxone or cefotaxime) +

Neisseria meningitidis
p ss : / p ss : /
Penicillin G for 7 days; alternatives: ampicillin, ceftriaxone, cefotaxime

hhttttp
Haemophilus influenzae b
hhttttp
Ceftriaxone or cefotaxime for 10 days; alternative: ampicillin if isolate is susceptible
Part C. Antimicrobial Dosage
Dose (mg/kg Per Day)
Agent Age 0–7 Days Age 8–28 Days Infants and Children

k e r
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Ampicillin 150–200 divided every 8 hr

k e r
e s
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o
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b o o
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Ceftriaxone
Gentamicin
Not recommended

e /e/
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e e b 80–100 divided every 12–24 hr

e / e
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7.5 divided every 8 hr

e
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7.5 divided every 8 hr
Penicillin G

: / / t
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100,000–150,000 Units divided

: t .m.m
150,000–200,000 Units divided

/ / / t
300,000–400,000 Units divided

t p s
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every 12 hr

t p ss : /
every 6 hr every 4–6 hr

hh tp
Rifampin 10 divided every 12 hr 20 divided every 12 hr 20 divided every 12 hr
Vancomycin t
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MIC, Minimum inhibitory concentration.
t t 30 divided every 8 hr 40–60 divided every 6 hr

(From Weinberg GA, Buchanan AM. Meningitis. In: McInerny TK, Adam HM, Cambell DE, Kamat DM, Kelleher KJ (eds). American Academy of
Pediatrics Textbook of Pediatric Care, 2nd Edition. Elk Grove Village, IL: American Academy of Pediatrics; 2017. p. 2295–309).

ee r s
r s
kk Lama  terapi  pada  anak  10-­‐14   k e e rs
rs
o
o o b o o
o ho k
ari,   neonatus  21  hari  
monitoring for changes in level of consciousness, develop- imaging studies to exclude mass lesions and other pathologies

e /e/ e b
ment of seizures, changes in vital signs, and development of
SIADH. If high intracranial pressure is a major clinical concern
e e e
needs to be adapted to the individual patient. The sicker the
/ / e
patient and the more rapidly progressive the disease, the more
e
: / / t
/ .
t m
and treatment has been initiated or is anticipated, then a

. m
neurosurgeon should be consulted and placement of an intra-
: / / t
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tm
urgent is the start of antibiotic therapy. Antibiotic therapy

.m
should not be delayed by more than approximately 15 minutes

s : / Schwaimann.
cranial pressure monitoring device considered.

p s Pediatric
p s
Neurology
s : / 2018
in critically ill patients for an attempt to obtain CSF or blood.

Antibiotics ttttp ttttp The choice of empiric antibiotics depends on the pathogens
suspected to be causative, which in turn depends in part on
 Tatalaksana lain

•  Suportif : IVFD, nutrisi, antipiretik, antikonvulsan.

•  Peningkatan TIK karena edema sitotoksik
–  Manitol 20% 0,25-1 gram/kgBB tiap 6-8 jam
–  NaCl 3% 1-3 ml/kgBB tiap
6-8 jam
•  Deksametason untuk menekan sitokin inflamasi :
–  Etiologi Haemophillus influenzae type B
–  0,6-1 mg/kgBB/hari dibagi 3-4 dosis, pemberian sebelum
(15-30 menit)/bersamaan dengan AB IV, selama 2-4 hari.
–  Mengurangi komplikasi gangguan pendengaran, menurunkan
angka kematian dan kecacatan

Chavez-Bueno S, Mc Cracken JH. Pediatr Clin N Am 2005

Mann K, jackson MA. Pediatr Rev 2008
Van de Beek D, De Gans J, Mc Intyre P, Prasad K. Cochrane
Database review 2008
 Patogenesis komplikasi

Hidrosefalus  dan  ventrikuli8s  

Fig. 1. Coronal view illustrating meningeal layers and common sites of central nervous system
infections. (Reproduced from Lewin JJ, LaPointe M, Ziai WC. Central nervous system infections
in the critically ill. Journal of Pharmacy Practice 2005;18(1):25–41; with permission.)
 Abses  otak  
Hidrosefalus  &  
Ventrikuli8s  

Meningi8s  &  Empiema  

subdural  
Meningitis bakterialis
subakut/kronik (TB)
 Epidemiologi

•  Meningoensefalitis
•  Bentuk TBC kronik yang terbanyak di negara berkembang
•  Mortalitas dan morbiditas yang tinggi.
•  Menyerang semua umur
•  Insiden tertinggi : 6 bulan-6 tahun
•  Infeksi campak,pertusis dan trauma kepala sering
mendahului timbulnya meningitis TB
•  Satu dari 300 kasus infeksi TB yang tidak diobati.

Schwaimann. Pediatric Neurology Principles and Practices.2018

Ramachandran TS. Tuberculous meningitis.http://www.emedicine 2007
 Manifestasi klinis ≈ Patogenesis
¡  Stadium 1 (prodroma)
§  Demam, mual, apatis, iritabel, defisit neurologi (-)
¡  Stadium 2 (transisi/meningitis)
§  Penurunan kesadaran sampai sopor, tanda rangsang
meningeal jelas, tetraparesis/hemiparesis, paresis nervus
kranial (III,IV,VI,VII), klonus, tuberkel di koroid,
funduskopi : edema papil/atrofi papil.
§  Paresis N. VI lebih sering terjadi dari n.kranial lain
¡  Stadium 3 (terminal)
§  Koma, pupil tidak bereaksi, hipertermia, pernapasan tidak
teatur.
§  Terjadi jika pengobatan terlambat/tidak adekuat

Ramachandran TS. Tuberculous meningitis.http://www.emedicine 2007

Patogenesis
Tahap pertama

Pertusis,  campak,  trauma   Tahap kedua

kepala,  HIV,  gizi  buruk  

Ramachandran TS. Tuberculous meningitis.http://www.emedicine 2007

Supurasi dan inflamasi meningen basal,
hidrosefalus
Stroke akibat proses vaskulitis
Tuberkuloma
Pengobatan
•  Terapi suportif : IVFD, nutrisi, antipiretik,
antikonvulsan.
•  é tekanan intrakranial : manitol 20%/NaCl 0.9%
•  Kortikosteroid untuk menekan reaksi inflamasi
selama 2-3 minggu kemudian diturunkan bertahap
selama 1 minggu.
•  INH 5-10 mg/kgBB/hari selama 9-12 bulan
•  Rifampisin 10-20 mg/kgBB/hari selama 9-12 bulan
•  Pirazinamid 20-40 mg/kgBB/hari selama 2 bulan
•  Etambutol 15-25 mg/kgBB/hari selama 2 bulan
 Komplikasi

•  Hidrosefalus
•  Palsi serebral
•  Disabilitas intelektual
•  Epilepsi
•  Gangguan koordinasi motorik, ataksia
•  Gangguan sensoris
•  Gangguan pendengaran dan penglihatan
Ensefalitis virus
 : /
: / t
/ .
t m
. m
t t p
t s
p
hhEtiologis
896 PART XIV Infections of the Nervous System

kke rs
rs
BOX 115-1

e
Selected Viruses Associated with Neurologic
and
me

ooo
b o
Disease in Pediatric Populations

e b o
b o
tati
ham

/ e
DNA VIRUSES

/
pat
Adenoviruses
Adenovirus—several types

/ t t . me
Herpesviruses

. m e
Herpes simplex viruses types 1
for
ma

t p s
p :
s /
: /
and 2
Cytomegalovirus
clin
sid

t
hh t Varicella zoster virus
Epstein-Barr virus
Human herpesviruses 6 and 7
giti
ent
ing
RNA VIRUSES
eva
Arenaviruses Picornaviruses

s
foo

ok e
k r
e rs
Lymphocytic
choriomeningitis virus
Polioviruses types 1-3
Nonpolio enteroviruses
exa
dis

o o o
Parechoviruses nop

bo Bunyaviruses Reoviruses

e /e/ b
e b o (EB
cie

e
La Crosse encephalitis Colorado tick fever virus
virus
California encephalitis virus

: /
: / / .
Rotavirus

t t m
. m En
Flaviviruses

t
hh t
Japanese encephalitis virus
p
t
St. Louis encephalitis virus
Rabies virus
s
p sRetroviruses
Human immunodeficiency viruses
types 1 and 2
Human T-cell lymphotropic virus
In
tur
tom
neu
Tick-borne encephalitis type 1 som
viruses cal
West Nile virus

k e r s
rs
Dengue virus

k e
Zika virus
liti
enc

o
booo Orthomyxoviruses Rhabdoviruses

e b o
b o
or
sug

/ e
Influenza virus Rabies virus tive
Paramyxoviruses

m
Togaviruses

t . . mee / The
alit
Mumps virus
Measles virus

p s :
s /
: / t
Eastern equine encephalitis virus

/
Western equine encephalitis virus
dif
as
Nipah virus

t
hh t t p
Venezuelan equine encephalitis
virus
Chikungunya virus
Rubella virus
ate
unc

Oth
Schwaimann. Pediatric Neurology Principles and Practices 2018 Gu
(Fig. 115-2). La Crosse encephalitis, a common arthropod- ebe
borne disorder in the United States, typically affects children neu
 Patogenesis

•  Langsung menginvasi jaringan otak Penurunan  kesadaran    

lebih  cepat/gejala  
•  Hematogen (viremia) utama    

–  Arbovirus à Sistem retikuloendotelial à SSP.

–  Akut
•  Neuronal
–  Herpes simpleks, rabies, polio à transport
retrograde di neuron.
–  Akut/kronik (reaktifasi)

Lewis P, Glaser CA.Pediatr Rev 2005

 Manifestasi klinis

•  Tanda-tanda infeksi akut/Prodroma

–  Demam, diare, nyeri tenggorokan,ruam kulit, batuk-
pilek
•  Defisit neurologi (global/fokal)
–  Kejang, perubahan perilaku, afasia, hemiparesis,
paresis saraf kranial, diplopia, ataksia, disartria
•  Peningkatan tekanan intrakranial
–  Nyeri kepala, muntah, penurunan kesadaran

Lewis P, Glaser CA.Pediatr Rev 2005

Schwaimann.Pediatric Neurology 2018
Ziai WC,Lewin JJ. Neurol Clin 2008
 Manifestasi klinis ≈ predileksi

¡  Rabies/JE : brain-stem encephalitis

¡  Disartria, diplopia, ataksia
¡  Arbovirus :Gejala global
§  Demam,muntah,penurunan kesadaran
¡  Herpes simpleks :Gejala fokal
§  Hemiparesis, kejang fokal, paresis nervus
kranial,afasia,anosmia

Lewis P, Glaser CA.Pediatr Rev 2005

Schwaimann.Pediatric Neurology 2017
Ziai WC,Lewin JJ. Neurol Clin 2008
 Diagnosis
•  Identifikasi virus : PCR/kultur CSS
•  Manifestasi klinis, gambaran CSS
•  CSS : Jernih, jumlah sel 50-200/mm3 sampai
1000/mm3 , limfositer, protein normal/sedikit
meningkat, glukosa normal
•  EEG : perlambatan umum/fokal
•  CT-Scan/MRI : edema otak difus, fokal pada
HSE EEG  dan  CT-­‐Scan/MRI  
8dak  khas  kecuali  pada  
HSV    

Lewis P, Glaser CA.Pediatr Rev 2005

Menkes . Textbook of Clinical Neurology 2006
Ziai WC,Lewin JJ. Neurol Clin 2008
 Tatalaksana
•  Perawatan ideal : ICU
•  Terapi sebagian besar suportif
–  Airway, Breathing,Circulation
–  Nutrisi, keseimbangan cairan dan elektrolit
–  Antikonvulsan dan antipiretik
•  Terapi etiologi virus :
–  HSV dan varisela : Aciclovir
–  Adenovirus : cidofovir/ribafirin
–  Enterovirus : pleconaril
•  Hipertermia à surface cooling
•  Deksametason tidak lagi digunakan
Lewis P, Glaser CA.Pediatr Rev 2005
Schwaimann.Pediatric Neurology 2017
 Komplikasi

•  Tergantung etiologi dan usia pasien

•  Palsi serebral
•  Disabilitas intelektual
•  Epilepsi, pada ensefalitis HSV : epilepsi fokal
•  Gangguan perilaku

Schwaimann.Pediatric Neurology 2017

 Ensefalitis HSV

•  Dapat diobati dengan hasil yang baik

•  Defisit neurologis fokal : kejang fokal,
hemiparesis, gangguan perilaku/memori
•  EEG : perlambatan di daerah temporal, PLEDS
(periodic lateralizing epileptiform discharge)
•  CT-Scan/MRI kepala : Edema fokal,
perdarahan/nekrosis di daerah temporal.
•  Terapi : Asilklovir 20 mg/kgBB/kali IV, tiap 8
jam selama 14-21 hari.
Bayi perempuan, 11 bulan dengan demam, letargi, kejang fokal motor kiri, 3 hari tidak mau
makan-minum

Leonard, J. R. et al. Am. J. Roentgenol. 2000;174:1651-1655

PLED

Sphelman. Atlas of EEG.