2. INTRODUCTION
MENINGITIS is inflammation
of the protective membrane
covering the brain and spinal
cord known as meninges,
in particular the arachnoid and
the pia mater.
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4. Bacterial Meningitis
Streptococcus pneumoniae (50%), Neisseria meningitidis
(25%), group B streptococci (15%), Listeria monocytogenes
(10%) and Haemophilus influenzae type b (<10% ).
Risk factors include coexisting acute or chronic
pneumococcal sinusitis or otitis media, alcoholism,
diabetes, splenectomy, hypogammaglobulinemia,
complement deficiency, and head trauma with basilar skull
fracture and CSF rhinorrhea.
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6. Clinical features -
The classic clinical triad of meningitis is fever, headache,
and nuchal rigidity, but the classic triad may not be present.
Altered sensorium, vomiting, photophobia, seizures.
Cranial nerve palsy( 3rd,4th,6th,7th,8th)
Papilloedema.
Kernig’s and Brudzinski’s signs are classic signs
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9. Treatment -
IV Ceftriaxone - 2gm, 12hourly for 7-14 days
IV Meropenem - 2gm, 8hourly for 7-14 days
IV Vancomycin 1-2gm, 12hourly for 7-14 days
Inj dexamethasone 10mg iv 6 hourly, started 20 min
before antibiotics, for 4 weeks with tapering dose, it
inhibits TNF-a production.
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11. TUBERCULOUS MENINGITIS
Tuberculous meningitis results from the hematogenous
spread of primary or postprimary pulmonary TB or from the
rupture of a subependymal tubercle into the subarachnoid
space.
The disease often presents subtly as headache and slight
mental changes after a prodrome of weeks of low-grade
fever, malaise, anorexia and irritability.
Typically, the disease evolves over 1–2 weeks, a course
longer than that of bacterial meningitis.
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12. complication
Because meningeal involvement is pronounced at the base
of the brain, paresis of cranial nerves (ocular nerves in
particular) is a frequent finding and the involvement of
cerebral arteries may produce focal ischemia. The ultimate
evolution is toward coma, with hydrocephalus and
intracranial hypertension.
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13. Diagnosis
CSF study.
Culture of CSF is diagnostic in up to 80% of cases and
remains the gold standard.
Real time automated nucleic acid amplification (the Xpert
TB/RIF assay) has a sensitivity of up to 80% and is the
preferred initial diagnostic option.
Imaging studies (CT and MRI) may show hydrocephalus
and abnormal enhancement of basal cisterns or ependyma,
enchanced ring lesion called tuberculoma.
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16. Treatment
AntiTuberculosis drug - HRZE( isoniazid (300 mg/d),
rifampin (10 mg/kg per day), pyrazinamide (30 mg/kg per
day in
divided doses), ethambutol (15–25 mg/kg per day) for 2
months f/by HR for 10 month.
Inj dexamethasone 0.4 mg/kg per day given IV with
tapering by 0.1 mg/kg per week until the fourth week.
In special case, HIV patient should given antiTuberculosis
drugs and later ART after 8 weeks, to avoid IRIS( immune
resconstitution inflammatory syndrome )
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17. VIRAL MENINGITIS
Clinical features are same
in all meningitis.
Diagnosis-
serology- PCR for specific
virus.
CSF study
MRI brain.
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19. Treatment
IV acyclovir - 15-30 mg/kg/day in 3 divided dose for
14 days.
Tab famciclovir - 500 mg, 8 hourly
Tab valacyclovir -1000mg, 8 hourly
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20. FUNGAL MENINGITIS
Fungal meningitis is rare; the most common cause is
Cryptococcus, Histoplasma, Blastomyces, Coccidioides,
candida, aspergellus.
The fungi are usually inhaled (bird dropping) and then
spread by the blood to the central nervous system.
Risk factors - immunocompromised conditions (HIV),
Steroids use, organ transplantation, malignancy.
The most common complication of fungal meningitis is
hydrocephalus.
Investigation- CSF study, serology, india ink stain, imaging
study.
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22. Treatment
Inj amphotericin iv 3mg/kg/day for 14days.
Tab flucytosine 100mg/kg/day for 14 days.
Tab fluconazole 200mg od for 14 days .
In cryptococcal meningitis - treatment is continued
for
1 year.
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23. PARASTIC MENINGITIS
Angiostrongylus cantonensis (neurologic
angiostrongyliasis), Baylisascaris procyonis
(baylisascariasis; neural larva migrans), Gnathostoma
spinigerum (neurognathostomiasis), Naegleria
fowleri(amebic meningitis).
These parasites normally infect animals not people. People
get infected primarily by eating infected animals or
contaminated foods.
Investigation- csf study, serology, MRI brain.
Treatment - no specific treatment.
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25. SPINAL MENINGITIS
Injury may occur to motor and sensory nerve roots as they
traverse the subarachnoid space and penetrate the meninges.
These cases present as multiple radiculopathies with
combinations of radicular pain, sensory loss, motor weakness,
and urinary or fecal incontinence.
Meningeal inflammation can encircle and damage the cord,
resulting in a myelopathy.
Electrophysiologic testing (electromyography, nerve conduction
studies, and evoked response testing) may be helpful in
determining whether there is involvement of cranial and spinal
nerve roots.
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26. Chronic meningitis
Chronic meningitis is suspected when a characteristic
neurologic syndrome exists for >4 weeks and is associated
with a persistent inflammatory response in the
cerebrospinal fluid (CSF).
Five categories of disease account for most cases of
chronic meningitis:
(1) meningeal infections
(2) malignancy
(3) autoimmune inflammatory disorders
(4) chemical meningitis
(5) parameningeal infections.
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27. Causes - Mycobacterium tuberculosis, Borrelia burgdorferi,
Syphilis, Actinomyces, Nocardia, Brucella, Tropheryma
whipplei, Leptospirosis, virus, fungus, parasite, malingancy,
SLE, sarcoidosis, wegeners.
Persistent headache, hydrocephalus, cranial neuropathies,
radiculopathies, and cognitive or personality changes are
the cardinal features.
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