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DR Bambang Ensefalitis

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ENSEFALITIS

Bambang Mulyawan
fk-umm
Ensefalitis

Infeksi jaringan otak oleh berbagai macam


mikro organisme
Encephalitis

 An inflammation of the brain


parenchyma, presents as diffuse and/or
focal neuropsychological dysfunction
 Most commonly a viral infection with
parenchymal damage varying from mild
to profound

Encephalitis, Emedicine.com
Encephalitis

 Primary encephalitis
 Post - infectious or Para - infectious
encephalitis

A text book of Infectious disease I, ้ ง


สมาคมโรคติดเชือแห่
 Meningitis – inflammation
of the meninges
 Encephalitis – infection
of the brain parenchyma
 Meningoencephalitis –
inflammation of brain +
meninges
 Aseptic meningitis –
inflammation of meninges
with sterile CSF
Etiologi

I. Infeksi – virus

II. Infeksi non virus

III.Para-infeksi-post-infeksi, alergi

IV. Penyakit “Slow-virus”

V. Penyebab tidak diketahui (50%)


Etiology of Encephalitis
Viruses are the most common cause of
encephalitis.
 Arbovirus

 Rabies Virus

 Herpes Simplex virus-1

 AIDS

Viruses also can play a role in causing


encephalitis as an after effect of systemic
diseases:
 Influenza

 Measles
Etiology of Encephalitis
Systemic diseases continued:
 Chicken Pox

 German Measles

Other organisms involved:


 Candida

 Aspergillus

 Cryptococcus

 Toxoplasma gondii
Etiologi
Klasifikasi Steigman, 1981
I. Infeksi langsung
A. Antar manusia
1. Virus RNA
Mumps, Morbili, Rubella, Enterovirus
2. Virus DNA
Herpes virus, Varisella-zooster, CMV, Virus EP
B. Melalui serangga
1. Arbovirus
2. Flafivirus
C. Melalui mamalia
Rabies, Virus B Limpositik, Kloriomeningitis
II. Para-infeksius – post infeksius, alergi

A. Penyakit morbilli, rubela, mump, varisella zoster,

influensa

B. Vaksinasi : Rabies, morbili, influenza, vaksinia

III. “Slow virus”

A. SSPE

B. Progresif multifokal lekoensepalopati


Herpes simplex 1 encephalitis

 Symptoms
 Depressed level of consciousness
 Blood tinged CSF

 Temporal lobe focus on CT scan or


EEG
 + PCR

 Neonates typically will have


cutaneous vessicles
 Treatment - IV acyclovir
Pathophysiology (1)

 Primary infection with HSV-1 usually


occurs in the oropharyngeal mucosa
and is typically asymptomatic.
 Symptomatic disease is characterized
by fever, pain, and an inability to
swallow caused by lesions on the
buccal and the gingival mucosa. The
duration of illness is 2 to 3 weeks.

12
Pathophysiology (2)
 After primary infection, HSV-1 is
spread by retrograde transport via a
division of the trigeminal nerve

 The virus then establishes latency in


the trigeminal ganglion.
Reactivation of latent ganglionic
infection with replication of virus
leads to viral encephalitis

13
Pathophysiology (3)

 HSV-1 encephalitis may also be the


result of primary infection from
either intranasal inoculation of virus
with direct invasion of the olfactory
bulb and tract leading to  infection
in the temporal cortex and limbic
system structures.

14
HSV-1 encephalitis showing extensive destruction
of inferior frontal and anterior temporal lobes.
(seizures, personality change, and neurologic
deficits)

15
Japanese Encephalitis
 Most important cause of
arboviral encephalitis
worldwide, with over
45,000 cases reported
annually
 Transmitted by culex
mosquito, which breeds in
rice fields
› Mosquitoes become
infected by feeding on
domestic pigs and wild
birds infected with
Japanese encephalitis
virus
› Infected mosquitoes
transmit virus to humans
and animals during the
feeding process
History of Japanese Encephalitis

 1800s – recognized in Japan


 1924 – Japan epidemic. 6125 cases, 3797
deaths
 1935 – virus isolated in brain of Japanese patient
who died of encephalitis
 1938 – virus isolated from Culex mosquitoes in
Japan
 1948 – Japan outbreak
 1949 – Korea outbreak
 1966 – China outbreak
 Today – extremely prevalent in South East Asia
30,000-50,000 cases reported each year
Distribution of Japanese
Encephalitis in Asia, 1970-1998
Patogenesis

Virus  tubuh  susunan limfatik berkembang biak

 darah  susunan saraf pusat  kelainan neurologis

Antigen virus (virusnya sendiri sudah tidak ada di otak)

Reaksi jaringan saraf  demielinisasi, kerusakan

vaskuler & perivaskuler


PATOGENESIS ARBOVIRUS
(Gigitan serangga)

Inokulasi
(Subkuta
n)

Replikasi virus
(Jaringan lokal)

Viremia
Seluruh
Kapiler Jaringan tubuh Infeksi
serebral
Sel endotel
vaskuler
Otak
Jonson RT 1987 Parenkim otak
Inokulasi (Intra nasal)

Replikasi Replikasi
(paru) (Nasofaring)

Dara Neural
h
Olfaktorius

Organ Serebrum Batang

Ota Serebrum
k

Kern.E.R 1985
PERJALANAN PENYAKIT
Bergantung dari :

1. Virus

2. Lokalisasi lesi

3. Luas lesi

4. Faktor imunitas

5. Faktor umur

6. Gangguan metabolik

7. Penyakit penyerta
GEJALA KLINIS

 Gejala umum

 Panas mendadak

Hiperpireksia

 Sakit kepala

 Mual

 Muntah
Clinical Presentation

 Any degree of altered consciousness,


ranging from mild lethargy to deep
coma.
 Personality changes, hallucinations,
agitations and other behavior disorders.
 Focal or generalization seizures may
occur.
 Neurological disturbances

24
GEJALA NEUROLOGIK
 Kesadaran : Apatis, somnolen, sopor, koma

 Kejang : Twitching

Focal/umum, lama

 Saraf otak : Ptosis, diplopia, strabismus, nistagmus

Piramidal : Hemiparesis

 Ekstrapiramidal : Khorea, Athetosis, Rigiditas


LABORATORIUM

 Cairan serebrospinal kadang-kadang normal /

peninggian sel / glukosa sedikit

 Virologik dan serologik

 Autopsi post mortem


DIAGNOSIS

1. Gejala klinis – anamnesis

2. Biakan darah / CSF

3. Serologik, serum / CSF

4. Biopsi otak

5. Patologi anatomi
Imaging
DIAGNOSIS BANDING
1. Ensefalitis Non-virus

2. Penyakit metabolik, hipoglikemia, uremia ensefalopati

3. Intoksikasi – Reye sindrom

4. Tumor / Abses otak

5. Perdarahan subaraknoid

6. Multipel sklerosis akut

7. Status epileptikus
PENGOBATAN
Simptomatik
1. Membrantas kejang
Valium I.V Dosis : 0,3 – 0,5 mg/kgbb
Rekatl Dosis : 5 – 10 mg
Penobarbital
Awal 8-10 mg/kgbb/hari
Maintenance 4-5 mg/kgbb/hari
2. Hiperpireksia
 Surface cooling
 Khlorpromazine 2-4 mg/kgbb/hari
 Prometazine 4-6 mg/kgbb/hari
3. Edema otak
 Deksametason 0,5 mg/kgbb/hari
4. Keseimbangan air dan elektrolit

 Glukosa 5-10 % + NaCl Fisiologis 3 : 1

 KCl dan “Base Corrector”

5. Tekanan intrakranial

 Manitol

 Gliserol

6. Infeksi sekunder

 Antibiotik
PENGOBATAN ETIOLOGIK

1. Adenosin Arabinoside (ARA-A)

 Dosis 15 mg/kgbb/hari I.V. – 10 hari

2. Acyclovir (ACV)

 Dosis 10 mg/kgbb tiap 8 jam I.V dalam

infus, perlahan, 10 hari


PENGOBATAN ETIOLOGIK

1. Adenosin Arabinoside (ARA-A)

 Dosis 15 mg/kgbb/hari I.V. – 10 hari

2. Acyclovir (ACV)

 Dosis 10 mg/kgbb tiap 8 jam I.V dalam

infus, perlahan, 10 hari


PROGNOSIS

 Angka kematian 35% - 50%

 Gejala sisa 20% - 40% yang hidup berupa :

 Paresis / paralisis

 Epilepsi

 Retardasi mental

 Gangguan tingkah laku

 Gerakan khoreo athetoid

 Gangguan penglihatan

 Gangguan pendengaran
PENCEGAHAN

 Vaksinasi : - morbili

- mump

- rubella

 Pembasmian vektor serangga


The Brain
 By the end of the lesson you should be
able to
 Describe the structure and function of
the brain
 State the function and location of
cerebrum, cerebellum, medulla and
hypothalamus
 State the location of sensory and motor
strip
The Brain
 weighs 1300 - 1400 g

 made up of about 100


billion neurons

 “the most complex living


structure on the
universe” Society for Neuroscience

 makes us who we are


The Brain

Phineas gage
Brain structure
Cerebrum

cerebellum
hypothalamus

Pituitary gland
brain functions
medulla
Parts of the cerebrum

alcohol and the brain


Sensory and motor strips
Sensory homunculus
Motor strip and
Motor strip
homunculus
The Brain
Can you
 Describe the structure and function of
the brain
 State the function and location of
cerebrum, cerebellum, medulla and
hypothalamus
 State the location of sensory and motor
strip
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