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
Encephalitis

H. influenzae

N. meningitis

0 1 12 5 10 20 40 60 or >

MONTHS YEARS
AGE
 0-2 mo : Streptococcus gr B, E. Coli
 2 mo – 5 yo : Streptococcus pneumonia,
Neisseria meningitis, Haemophilus influenzae.
 > 5 yo : Streptococcus pneumoniae, Neisseria
meningitis.
 irritability  arching back
 fever  cries when picked up
 sleeping more than or being held
usual  inconsolable crying
 poor feeding  bulging fontanelle (soft
 high-pitched cry spot on an infant's
head)
 noticeably different
temperament
 neck and/or back pain  refusing to eat
 headache  decreased level of
 sleepiness consciousness
 confusion  seizures
 irritability  photophobia
 fever (sensitivity to 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
 Secara makroskopis hasil LP sedikit memberikan gambaran akan infeksi..
Liquor yang keruh menunjukkan infeksi bakteri,sedangkan jernih karena virus.

Liquor Bakteri Virus

Leukosit(sel darah putih) 1000 – 5000 sel/ul 25 – 500 sel/ul
Protein 100 – 500 mg/dl 20 – 80 mg/dl
Glukosa < 40 mg/dl > 40 mg/dl
Laktat > 35 mg/dl 10 – 20 mg/dl
 White blood cell (WBC) counts over 1000/mm3
usually are caused by bacterial infections. (pmn)
 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%, 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
 Usia 1-3 bulan
 Ampicillin 200-400 mg/kgBB/hari IV dalam 4 dosis +
cefotaxime 200-300 mg/kg BB/hari dalam 4 dosis atau
 Ceftriaxone 100 mg/kgBB/hari iv dalam 2 dosis
 Usia > 3 bulan
 Cefotaxime 200-300 mg/kg/hari dalam 3-4 dosis
 Ceftriaxone 100 mg/kg/hari dalam 2 dosis
 Ampicillin 200-400 mg/kg/hari IV dalam 4 dosis +
Chloramfenikol 100 mg/kgbb/ hari dalam 4 dosis
 Dexametason 0,6 mg/kgBB/hari Iv dalam 4 dosis selama 4
hari.
 Lama pengobatan : 10-14 hari.
 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 :
Pernafasan ireguler
Koma Peningkatan suhu tubuh
Pupil terfiksasi  Hidrosefalus
Spasme kronik
 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.