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GEETANJALI COLLEGE OF NURSING
 SEMINAR ON :
MENINGITIS
GANPAT DAS VAISHNAV
M.Sc (N) FINAL YEAR
GCN , UDAIPUR
MENINGITIS
INTRODUCTION:-
Although meningitis is a notifiable disease, the exact
incidence rate is unknown.
 In 2010 – 420, 000 deaths
In 2013 - 303,000 deaths.
It can occur as a complication of other disease and 50% is
an opportunistic infection.
DEFINITION
Meningitis (from Greek méninx, "membrane”)
is an acute inflammation of the meninges.
Caused by either bacteria or virus.
INCIDENCE
Newborns 20–30% may die from bacterial meningitis.
Common in 1 month to 5 years of children but more
common in boy.
This risk is lower in older children.
Rises again in adulthood.
 In adults, 66% of all cases emerge without disability. The
main problems are deafness (14%) and cognitive
impairment (10%)
RISK FACTORS
Systemic infections
 Viral RTIs
Tobacco use
Impaired Immune system
Over crowding
Vaccinations
Seasonal:
 Winter
 Spring
TYPES
Bacterial Meningitis
Also known as septic meningitis.
Extremely serious that requires immediate care.
Can lead to permanent damage of brain or
disability and death.
Spreads by:-coughing or sneezing
Treatment available : antibiotics as per causative
organism.
Causative Agents:
Streptococcus Pneumonia 30-80 %
Neisseria meningitis 15- 40 %
Hemophilus Influenza 2-7 %
2. TUBERCULAR MENINGITIS
TB meningitis is caused by Mycobacterium
tuberculi.
Infection with this bacterium begins usually in the
lungs
1 – 2% of cases the bacteria travel via the
bloodstream.
Unlike other types of meningitis its progresses
very slowly and symptoms are vague
3. VIRAL MENINGITIS
Also known as aseptic meningitis.
More common than bacterial form and usually less
serious.
Less likely to have permanent brain damage after
the infection resolves.
Treatment: No specific treatment available.
Most patients recover completely on their own
Causative agents:
Enterovirus
Adenovirus
Measles virus
Herpes simplex virus
Varicella
4. FUNGAL MENINGITIS
It is much less common than the other two
infections.
It is rare in healthy people but it is more likely in
persons who have impaired immune system
PATHOPHYSIOLOGY
Bacteria enters blood stream/ trauma
Enters the mucosal surface/ cavity
Breakdown of normal barriers
Crosses the blood brain barrier
Proliferates in the CSF
Inflammation of the meninges
Increase in ICP
CLINICAL MANIFISTATION
KERNIG’S SIGN
 Severe stiffness of the hamstrings causes an
inability to straighten the
leg when the hip
is flexed to 90 degrees.
BRUDZINKI’SIGN
Severe neck stiffness causes a patient's hips and
knees to flex
when the neck is
flexed
NUCHAL RIGIDITY
Nuchal rigidity is a reduced
Ability to flex the neck forward
Due to stiffness of the neck
Muscles.
ASSESSMENT AND DIAGNOSIS
History taking
Physical assessment
CT and MRI
Blood culture and sensitivity
Lumbar Puncture
MEDICAL MANAGEMENT
BACTERIAL MENINGITIS:
Third-generation cefalosporin such as cefotaxime
or ceftriaxone
Vancomycin is added in the regime in case of
resistance.
Dexamethasone
Dehydration and shock can be treated with fluid
therapy.
Phenytoin for seizure management.
TUBERCULAR MENINGITIS
ATT medications are started:
Isoniazid; rifampacin; pyrazinamide and
streptomycin.
Second line drugs:
Aminoglycosides; Fluroquinolones
Conventional therapy is given for 6-9 months
VIRAL MENINGITIS:
Treatment is mostly supportive and no medicines
are prescribed.
Seizure prophylaxis:
Lorazepam or phenytoin or barbiturate.
Increased ICP:
Inj. Mannitol 1g/kg followed by 0.25-0.5g/kg Q6H
or/and dexamethasone Rest is advised
Rest is advised
In case hydrocephalus is present VP or LP shunt is
required.
Adequate hydration is to be maintained
Antipyretics
Anti emetics
COMPLICATIONS
Sensori-neural hearing loss
Epilepsy/ seizures
Memory loss
Paralysis
Learning difficulty
Behavioural difficulty
Decreased intelligence
Septicaemia
Death
GCNS Meningitis Seminar

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GCNS Meningitis Seminar