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MENINGITIS

dr. Pertiwi Febriana Chandrawati


MSc,SpA

Meningitis is an infection of the sheaths that cover the brain


and spinal cord.
Meningitis is usually caused by an infection with a virus, with a
bacterium or even with fungi.

1. acute pyogenic (bacterial) meningitis


2.acute aseptic (viral) meningitis
3.acute focal suppurative infection (brain

abscess,subdural and extradural empyema)


4.chronic bacterial infection (tuberculosis).

To

develop bacterial meningitis, the


invading organism must gain access to the
subarachnoid space. This is usually via
hematogenous spread from the upper
respiratory tract where the initial
colonization has occurred.
Less frequently, there is direct spread from
a contiguous focus (eg, sinusitis,
mastoiditis, otitis media) or through an
injury, such as a skull fracture. ( direct
implantation )

The

cell walls of both gram-positive


and gram-negative bacteria contain
potent triggers of the inflammatory
response. In the gram-positive
bacteria, teichoic acid is considered
the major pathogenic component. In
gram-negative bacteria,
lipopolysaccharide or endotoxin is
the major pathogenic component.

The mediators of the inflammatory response


include cytokines (tumor necrosis factor,
interleukin 1, 6, 8, 10), platelet activating factor,
nitric oxide, prostaglandins, and leukotrienes.

These mediators cause disruption of the blood


brain barrier, vasodilation, neuronal toxicity,
meningeal inflammation, platelet aggregation,
and activation of leukocytes. The capillary
endothelial cell is the main site of injury in
bacterial meningitis

For

both meningitis and encephalitis,


the greatest occurrence is in children
younger than 4 years with a peak
incidence in those aged 3-8 months.

Risk

factors for bacterial meningitis

Age
Low family income
Attendance at day care
Head trauma
Splenectomy
Chronic disease
Children with facial cellulitis, periorbital
cellulitis, sinusitis, and septic arthritis
have an increased risk of meningitis.
Maternal infection and pyrexia at the
time of delivery are associated with
neonatal meningitis.

E. coli
S. pneumoniae
H. influenzae
N. meningitis
0

12

MONTHS

10

YEARS
AGE

20

40

60 or >

irritability
fever
sleeping more
than usual
poor feeding
high-pitched cry

arching back
cries when picked
up or being held
inconsolable crying
bulging fontanelle
(soft spot on an
infant's head)
noticeably
different
temperament

neck and/or back


pain
headache
sleepiness
confusion
irritability
fever

refusing to eat
decreased level of
consciousness
seizures
photophobia
(sensitivity to
light)
nausea and
vomiting
neck stiffness

1.
2.

1.
2.

Do not rely on these signs due to low


efficacy in pediatrics
Kernig's Sign and Brudzinski's Sign
Test Sensitivity: 5%
Test Specificity: 95%
Nuchal and spinal rigidity
Test Sensitivity: 30%
Test Specificity: 68%
So a high degree of clinical suspicion is
required

White blood cell (WBC) counts over 1000/mm3


usually are caused by bacterial infections.
Gram stain may aid in diagnosis, but the
diagnosis may be missed in up to 30% of
cases of culture-proven disease.
The protein concentration usually is elevated
in bacterial meningitis
Normal CSF glucose should be greater than
two-thirds that of the serum glucose. Levels
less than 50% of serum are suggestive of
bacterial meningitis.

The WBC count in viral meningitis is

usually below 500/mm3, with greater


than 50% lymphocytes.
The protein may be elevated.
The glucose level may be normal or low.
Gram stain results are negative.

Hearing loss is the most encountered


sequelae; it occurs
* in 30% cases of S. pneumoniae
meningitis,
* in 20% of H. influenzae meningitis,
* in 10% of N. meningitidis meningitis.
Mental retardation, seizures, delay in
language acquisition, visual impairment,
behavioural problems and
hydrocephalus.

Other serious
complications can
include:

1.

Brain damage

1.

Epilepsy

2.

Changes in eye
sight

Encephalitis

is a similar disease of
the central nervous system. This
disease is an inflammation of brain
parenchyma. Often, a viral agent is
responsible. Viral entry occurs
through hematogenous or neuronal
routes.

HSV

type 1 and 2 (almost


exclusively in neonates), VZV,
EBV, measles virus (PIE and SSPE),
mumps, and rubella are spread
through person-to-person contact.
Mycoplasma species
Rickettsia
Toxoplasmosis

Severe headache
Sudden fever
Drowsiness
Vomiting
Confusion
Seizures

CSF

analysis shows pleocytosis


(predominantly mononuclear cells)
and high levels of protein. A small
percentage (3-5%) of samples have
normal CSF. Identification of viral
antigen or nucleic acid may provide
some diagnostic help.

Bacterial meningitis can be treated with a number


of effective antibiotics. It is important, however,
that treatment be started early in the course of the
disease. Appropriate antibiotic treatment of most
common types of bacterial meningitis should
reduce the risk of dying from meningitis to below
15%,
15% although the risk is higher among the elderly.

Knowing whether meningitis is caused by a virus or


a bacterium is important because of differences in
the seriousness of the illness and the treatment
needed.

1.
2.
3.
4.
5.

6.
7.

Antibiotika harus sesuai (2 fase)


Mempertahankan metabolisme otak
Pengawasan thd kenaikan tek.
Intrakranial
Atasi kejang
Pengelolaan cairan normovolemia
Hipervolemia
Dehidrasi
Atasi hiperpireksia
Perawatan meningitis

DIET

CAIR

LUNAK

1.
2.

PERAWATAN MENINGITIS
PENGOBATAN
a. Homeostasis cairan iv
b. Konvulsi / st. konvulsius
Berantas kejang secepatnya
Oksigenasi yang adekuat
c. Kortikosteroid
d. Antibiotik

I. BELUM ADA HASIL BIAKAN & UJI SENSITIVITAS EMPIRIK


KUMAN
KOMBINASI

OBAT
Ampisilin 200 400 mg/kg BB
Kloramfenikol 100 mg/lg BB

atau

Ampisilin 200 400 mg/kg BB


Sefurokxim 100 200 mg/kg BB

PD. NEONATUS

Ampisilin 200 400 mg/kg BB


Gentamycin 6 mg/kg BB

KUMAN
N. Influensa
S. Pneumonia

N. Meningitis
Gram Negatif

Staphylococus

OBAT
- Kloramfenikol, ampisilin
- Seftriakson, Sefotaksim
- Penisilin, Kloramfenikol
- Sefuroksim, Seftriakson
- Vankomisin
- Penisilin, Kloramfenikol
- Sefuroksim, Seftriakson
- Sebutaksim, Septazidin
- Seftriakson, Amikasin
- Gentamysin, netilmisin
- Nafsilin, Vankomisin
- Rifampisin

Arachnoid membrane
Choroid plexus epithelium
Endothelial cells dari serebral
microvasculature
Memisahkan
Intravascular compartment dari otak & cairan
serebro spinal

Akibat pemisahan / peregangan


intercellular tight junctions
1. Pada sel endothelial dari
cerebral microvasculatur
2. Pada endothel choroid plexus

1.

2.
3.

4.

Penghambatan sintesis dinding sel


Penisilin, Sefalosporin, Vankumisin, Basitrasin, Sikloserin,
Ristosetin
Penghambatan fungsi membran sel
Amfoterisin B, Kolistin, Polimiksin, Imadazol dll
Penghambatan sintesis protein
Kloram fenikol, Entromisin, Limkomisin, Tetrasiklin,
Aminoglikosid, Amikasin, Neo Strepto, Tobra, Netilmisin
Penghambatan sintesis asam nukleat
Asam Nalidiksat, Novobiosin, Rifampin, Sulfonamid,
Trimetopirin

a.

Pemilihan AB yang tepat

b.

Cara pemberian & dosis


Absorbsi, metabolisme,
ekskresi

a.

Monitoring & efek samping


OUT COME

TERGANTUNG
1. Umur
2. Jenis kelamin
3. Berat ringan infeksi
4. Lama sakit seb. Pengobatan
5. Kepekaan bakteri thd AB
6. Status gizi
SUPORTIF
PERAWATAN

Radang

selaput otak yang


disebabkan oleh Mycobacterium
tuberculosis.
Usia 3 bulan sampai 5 tahun
Mortalitas : 10-20 %

Anamnesis : demam kronis atau akut, penurunan BB,


kejang, imunisasi BCG, kontak dengan pasien dewasa.
PD :
Stadium I :
gejala gastrointestinal, tanpa kelainan neurologi.
apatis, iritabel,nyeri kepala intermiten.
Stadium II :
mengantuk,disorientasi
Rangsang meningeal,refleks tendon meningkat,
abdomen hilang, klonus patela dan pergelangan kaki.
N. kranialis VII, IV,VI,III terlibat.
Stadium III :
Koma
Pernafasan ireguler
Pupil terfiksasi
Peningkatan suhu
Spasme kronik
tubuh
Hidrosefalus

CBC
LP : -

CSF jernih atau xantokrom


- sel meningkat 500 sel/mm dom limfosit
- Glukosa : menurun

PCR
ELISA
Latex Particle Agglutination
CT Scan atau MRI : lesi parenkim dasar otak,
infark, tuberkuloma
Ro foto : TB paru.

INH 5-10 mg/kgBB/hari max 300mg/hr


Rif 10-20 mg/kgBB/hari max 600 mg/hr
PZA 20-40 mg/kgBB/hari max 2000

mg/hr
Etambutol 15-25 mg/kgBB/hari max
2500mg/hr
Prednison 1-2 mg/kgBB/hari, selama 23 mgg, dilanjutkan dg tapp-off.