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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
 Forboth 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 1 12 5 10 20 40 60 or >

MONTHS YEARS
AGE
 irritability  arching back
 fever  cries when picked
 sleeping more up or being held
than usual  inconsolable crying
 poor feeding  bulging fontanelle
 high-pitched cry (soft spot on an
infant's head)
 noticeably
different
temperament
 neck and/or back  refusing to eat
pain  decreased level of
 headache consciousness
 sleepiness  seizures
 confusion  photophobia
 irritability (sensitivity to
 fever light)
 nausea and
vomiting
 neck stiffness
 Do not rely on these signs due to low
efficacy in pediatrics
 Kernig's Sign and Brudzinski's Sign
1. Test Sensitivity: 5%
2. Test Specificity: 95%
 Nuchal and spinal rigidity
1. Test Sensitivity: 30%
2. 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
 Encephalitisis 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
 CSFanalysis 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. Antibiotika harus sesuai (2 fase)
2. Mempertahankan metabolisme otak
3. Pengawasan thd kenaikan tek.
Intrakranial
4. Atasi kejang
5. Pengelolaan cairan  normovolemia
 Hipervolemia
 Dehidrasi
6. Atasi hiperpireksia
7. Perawatan meningitis

DIET CAIR LUNAK


1. PERAWATAN MENINGITIS
2. 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 OBAT
KOMBINASI 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 OBAT
N. Influensa - Kloramfenikol, ampisilin
- Seftriakson, Sefotaksim
S. Pneumonia - Penisilin, Kloramfenikol
- Sefuroksim, Seftriakson
- Vankomisin
N. Meningitis - Penisilin, Kloramfenikol
- Sefuroksim, Seftriakson
Gram Negatif - Sebutaksim, Septazidin
- Seftriakson, Amikasin
- Gentamysin, netilmisin
Staphylococus - 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. Penghambatan sintesis dinding sel
Penisilin, Sefalosporin, Vankumisin, Basitrasin, Sikloserin,
Ristosetin
2. Penghambatan fungsi membran sel
Amfoterisin B, Kolistin, Polimiksin, Imadazol dll
3. Penghambatan sintesis protein
Kloram fenikol, Entromisin, Limkomisin, Tetrasiklin,
Aminoglikosid, Amikasin, Neo Strepto, Tobra, Netilmisin
4. 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/mm³ 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 2-
3 mgg, dilanjutkan dg tapp-off.