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MENINGITIS

INTRODUCTION: Meningitis, encephilitis and brain abcess are
the most common inflammatory condition of the brain and
spinal cord. Inflammatory can be caused by bacteria, virus,
fungi and chemical. CNS infectoin may occur via bloodstream
by primary site or along cranial and spinal nerves. The
mortality rate is approximately 15% in the general population,
with higher rates in elderly patient. Up to 15% of those who
recover have long term neurologic defect.

DEFINITION: Menigitis is acute inflammation of the piamater
and arachnoid memebrane surrounding the brain and spinal
cord.therefore infection is always cerebrospinal infection .

ETIOLOGY OF MENINGITIS: Meningitis is usually occur in the
fall, winters, early spring and is often secondary to viral
respiratory infection. Older adults and person who are
delibitated are more common affected than general population.

– Acute respiratory tract infection : Reccurent respiratory
infection can lead to meningitis.
– Direct spread : This may occur as a result of fracture of
skull, either in case of penetrating injury of cranial vault.
– Infection through blood stream : In such case meningiti
follow bacteremia eg; pneumonia, empyema,
osteomyelitis, typoid

Epidemiology
Although meningitis is a notifiable disease in many countries,
the exact incidence rate is unknown.[9] Bacterial meningitis
occurs in about 3 people per 100,000 annually in Western
countries. Population-wide studies have shown that viral
meningitis is more common, at 10.9 per 100,000, and occurs
more often in the summer. In Brazil, the rate of bacterial
meningitis is higher, at 45.8 per 100,000 annually. In sub-
Saharan Africa, large epidemics of meningococcal meningitis
occur in the dry season, leading to it being labeled the
"meningitis belt"; annual rates of 500 cases per 100,000 are
encountered in this area, which is poorly served by medical
care. These cases are predominantly caused by
meningococci.]The most recent epidemic, affecting Nigeria,
Niger, Mali and Burkina Faso, started in January 2009 and is
ongoing.
Meningococcal disease occurs in epidemics in areas where
many people live together for the first time, such as army
barracks during mobilization, college campuse and the annual
Hajj pilgrimage.
There are significant differences in the local distribution of
causes for bacterial meningitis. For instance, N. meningitides
groups B and C cause most disease episodes in Europe, while
group A meningococci are more common in China and amongst
Hajj pilgrims. In the "meningitis belt" of Africa, group A and C
meningococci cause most of the outbreaks. Group W135
meningococci have caused several recent epidemics in Africa
and during the Hajji . These differences are expected to change
further as vaccines against common strains are introduced
TYPES OF MENINGITIS ON THE BASIS OF ETIOGY :
– Meningococcal infection: Nesseria meningitis
– Hemophilus meningitis : Hemophilus influenza
– Pneumococcal meningitis : Streptococcal pneumoniae
– Tubercular meningitis : Mycobcterium tuberculosis
– Virul meningitis : Enterovirus, Herpes simplex, HIV virus

PATHOPHYSIOLOGY OF MENINGITIS :
There are different types of etiological factors that ae
responsible for causing meningitis . It can be transmitted
direcly or indirectly.

Meningeal infection occur in two ways

Respiratory After cranial
raumatic injury to facial
bones

caustive agent entres in blood stream

cross blood brain barrier

cause inflammatory infection in meninges

inlammatory infection reaction in meninges

inflammatory of subarachnoid space and piamater

since there is little room for expansion within cranial vault

cause increase ICP

due to leukocytosis incrase thickness of CSF

it interfers with circulation and reabsorbtion

external and internal hydrocehlaus

Complicated stage: in acute fumligant stage there may be
Disseminated intravascular cogulopathy

CLINICAL MANIFESTATION OF MENINGITIS :
Clinical manifestations of meningitis are as follow

• Headache and fever: headache and fever occur in
the course of meningitis. Fever is due to infection and
headache is due to increase intracranial pressure.
• Nuccal rigidity : Nuccal rigidity is because of incrase
intracranial pressure. Patient can not able to flex his
neck, forceful flexion of neck can lead to pain.
• Positive kernig’s sign: When patient is lying down
with the thigh flexed on abdomen , the leg can not be
completely extended.
• Positive brudzinski’s sign: When patient is flexed,
flexion of kness and leg is produced.
• Photophobia: Patient suffering from extreme
sensitivity to light.
• Behaviral manifestations
• Seizures
• Diplopia
• Dysphagia
• Disorientation
• Retention of urine
• Rigidity of back
• In case of disseminated intravascular coagulopathy:
rashe and bleeding disorders

ASSESSMENT AND DIAGNOSTIC FINDING
– History taking and physical examinations : history of
previous illness, fever, head injury, medications, upper
respiratory tract infections.
– Physical examination: it include head to toe examination
and assessment nuccal rigidity, kerning sign, brudzinski’s
sign.
– Blood culture : culture of the causative organism.
– CSF examination: by lumbar puncture.

LUMBAR PUNCTURE :
Lumbar puncture is the insertion of needle into lumbar
region of spinal cord in such a way that the needle enters
the lumbar subarachoid space of spinal cord below the
level of spinal canal.
In the adult the spinal cord ends at the
lower level of
first lumbar vertebrae; but in new infant it ends slighty at
lower level
Of the vertebrae.

PURPOSE :
– CSF examination
– To determine causative agent
– To determine csf pressure
– To determine presence or absence of blood in csf
– To administer spinal anaesthesia.
.

PREPRATIONS OF ARTICLES:

1. LP needle – 2 size with their stillete
2. Sponge holding forceps
3. Small bowel to take cleaning lotion syrings
4. Specimen bottles
5. Cotton bolls, gauze piece
6. Gloves, gown, mask
7. Three way adapter, monometer and tubing to measure the
pressure of CSF

Any unsterile tray containing:

1. Mackintosh and towel
2. Kidney tray
3. Spirit , iodine, tr . benzoid, paper bag
4. Lignocaine 5%
5. Sterile normal saline fill monometer
6. Adhesive tray
7. Tr. Benzoid or helix spray

Proprocedure :
– Determine whether written consent has taken.
– Explaine the procedure to the patient and describe
sensations that are likely during the procedure.
– Determine whether patient has any question and
misconceptions about the procedure, reassure the
patient that the needle will not enter the spinal cord.
– Instruct the patient to void before procedure.

Procedure :

– Patient is positioned correctly (knee chest positioned). The
patient is positioned on one side at the edge of bed.
– Skin is prepared as for a surgical procedure, cleanse the
puncture site.
– Numb the site and then a spinal needle is inserted into the
subarachnoid space through the third and fourth lumbar
interspace.
– A specimen of CSF is collected in three bottles , labelled in
order of collection. A pressure reading may be obtained .
the needle is withdrawn.
– A small dressing is applied to puncture site.
– The tubes of CSF are sent to the labortory immediately.

POSTPROCEDURE

– Instruct the patient to lie prone for 2 to 3 hrs to reduce the
risk of leakage of CSF.
– Monitor the patient for complocations of lumbar puncture.

PHYSICAL FINDINGS
– Normally CSF is crystal clean.
– Turbulence indicate infection
– Blood indicates hemmorrhage

FEATURE NORMAL BACTERIA VIRAL TUBERCUL
S MENINGITI MENINGITI AR
S S MENINGITI
S
Naked eye 70-200 mm Cloudy Sligtly turbid Sligtly turbid
of H2O

CSF 0-4 mm of Above 200 Above280 Above 300
pressure H2O mm of H20

Cells 0-4 1000 – 100-1000 100-1000
Lymphocytes/ 10000 mononuclear mononuclear
ul neutrophils/ / ul / ul

Protien 15-45 mg/dl Incresed Increased Increased

Glucose 50-80 mg / dl Decreased Normal Decreased

Bacteriolog sterile Causative Sometimes Tuberculus
y agent sterile bacili

– Skull x-ray studies
– CT scan
– Ventriculostmy

MANAGEMENT
PREVENTION- For some causes of meningitis, prophylaxis
can be provided in the long term with vaccine, or in the short
term with antibiotics.
Since the 1980s, many countries have included immunization
against Haemophilus influenzae type B in their routine
childhood vaccination schemes. This has practically eliminated
this pathogen as a cause of meningitis in young children in
those countries. In the countries where the disease burden is
highest, however, the vaccine is still too expensive. Similarly,
immunization against mumps has led to a sharp fall in the
number of cases of mumps meningitis, which prior to
vaccination occurred in 15% of all cases of mumps.
Meningococcus vaccines exist against groups A, C, W135 and
Y.In countries where the vaccine for meningococcus group C
was introduced, cases caused by this pathogen have decreased
substantially. A quadrivalent vaccine now exists, which
combines all four vaccines. Immunization with the ACW135Y
vaccine against four strains is now a visa requirement for
taking part in the Hajj. Development of a vaccine against group
B meningococci has proved much more difficult, as its surface
proteins (which would normally be used to make a vaccine)
only elicit a weak response from the immune system, or cross-
react with normal human proteins. Still, some countries (New
Zealand, Cuba, Norway and Chile) have developed vaccines
against local strains of group B meningococci; some have
shown good results and are used in local immunization
schedules.]
Routine vaccination against Streptococcus pneumoniae with
the pneumococcal conjugate vaccine (PCV), which is active
against seven common serotypes of this pathogen, significantly
reduces the incidence of pneumococcal meningitis. The
pneumococcal polysaccharide vaccine, which covers 23 strains,
is only administered in certain groups (e.g. those who have had
a splenectomy, the surgical removal of the spleen); it does not
elicit a significant immune response in all recipients, e.g. small
children.
Childhood vaccination with Bacillus Calmette-Guérin has been
reported to significantly reduce the rate of tuberculous
meningitis, but its waning effectiveness in adulthood has
prompted a search for a better vaccine.
Short-term antibiotic prophylaxis is also a method of
prevention, particularly of meningococcal meningitis. In cases
of meningococcal meningitis, prophylactic treatment of close
contacts with antibiotics (e.g. rifampicin, ciprofloxacin or
ceftriaxone) can reduce their risk of contracting the condition,
but does not protect against future infections.
Antibiotics
Empiric antibiotics (treatment without exact diagnosis) must be
started immediately, even before the results of the lumbar
puncture and CSF analysis are known. The choice of initial
treatment depends largely on the kind of bacteria that cause
meningitis in a particular place. For instance, in the United
Kingdom empirical treatment consists of a third-generation
cefalosporin such as cefotaxime or ceftriaxone.[17][19] In the USA,
where resistance to cefalosporins is increasingly found in
streptococci, addition of vancomycin to the initial treatment is
recommended.[3][4][17] Empirical therapy may be chosen on the
basis of the age of the patient, whether the infection was
preceded by head injury, whether the patient has undergone
neurosurgery and whether or not a cerebral shunt is present.
For instance, in young children and those over 50 years of age,
as well as those who are immunocompromised, addition of
ampicillin is recommended to cover Listeria monocytogenes.
Once the Gram stain results become available, and the broad
type of bacterial cause is known, it may be possible to change
the antibiotics to those likely to deal with the presumed group
of pathogens.

The results of the CSF culture generally take longer to become
available (24–48 hours). Once they do, empiric therapy may be
switched to specific antibiotic therapy targeted to the specific
causative organism and its sensitivities to antibiotics.For an
antibiotic to be effective in meningitis, it must not only be
active against the pathogenic bacterium, but also reach the
meninges in adequate quantities; some antibiotics have
inadequate penetrance and therefore have little use in
meningitis. Most of the antibiotics used in meningitis have not
been tested directly on meningitis patients in clinical trials.
Rather, the relevant knowledge has mostly derived from
laboratory studies in rabbits.
Tuberculous meningitis requires prolonged treatment with
antibiotics. While tuberculosis of the lungs is typically treated
for six months, those with tuberculous meningitis are typically
treated for a year or longer. In tuberculous meningitis there is a
strong evidence base for treatment with corticosteroids,
although this evidence is restricted to those without AIDS.
Steroids
Adjuvant treatment with corticosteroids (usually
dexamethasone) reduces rates of mortality, severe hearing loss
and neurological damage in adolescents and adults from high
income countries which have low rates of HIV. The likely
mechanism is suppression of overactive inflammation.
Professional guidelines therefore recommend the
commencement of dexamethasone or a similar corticosteroid
just before the first dose of antibiotics is given, and continued
for four days. Given that most of the benefit of the treatment is
confined to those with pneumococcal meningitis, some
guidelines suggest that dexamethasone be discontinued if
another cause for meningitis is identified.
Adjuvant corticosteroids have a different role in children than in
adults. Though the benefit of corticosteroids has been
demonstrated in adults as well as in children from high-income
countries, their use in children from low-income countries is not
supported by evidence; the reason for this discrepancy is not
clear. Even in high-income countries, the benefit of
corticosteroids is only seen when they are given prior to the
first dose of antibiotics, and is greatest in cases of H. influenzae
meningitis, the incidence of which has decreased dramatically
since the introduction of the Hib vaccine. Thus, corticosteroids
are recommended in the treatment of pediatric meningitis if
the cause is H. influenzae and only if given prior to the first
dose of antibiotics, whereas other uses are controversial.
Viral and fungal meningitis
Viral meningitis typically requires supportive therapy only; most
viruses responsible for causing meningitis are not amenable to
specific treatment. Viral meningitis tends to run a more benign
course than bacterial meningitis. Herpes simplex virus and
varicella zoster virus may respond to treatment with antiviral
drugs such as aciclovir, but there are no clinical trials that have
specifically addressed whether this treatment is effective. Mild
cases of viral meningitis can be treated at home with
conservative measures such as fluid, bedrest, and analgesics.
Fungal meningitis, such as cryptococcal meningitis, is treated
with long courses of highly dosed antifungals, such as
amphotericin B and flucytosine.

Prognosis
Untreated, bacterial meningitis is almost always fatal. Viral
meningitis, in contrast, tends to resolve spontaneously and is
rarely fatal. With treatment, mortality (risk of death) from
bacterial meningitis depends on the age of the patient and the
underlying cause. Of the newborn patients, 20–30% may die
from an episode of bacterial meningitis. This risk is much lower
in older children, whose mortality is about 2%, but rises again
to about 19–37% in adults. Risk of death is predicted by various
factors apart from age, such as the pathogen and the time it
takes for the pathogen to be cleared from the cerebrospinal
fluid,the severity of the generalized illness, decreased level of
consciousness or abnormally low count of white blood cells in
the CSF.Meningitis caused by H. influenza and meningococci
has a better prognosis compared to cases caused by group B
streptococci, coliforms and S. pneumoniae.In adults, too,
meningococcal meningitis has a lower mortality (3–7%) than
pneumococcal disease.
In children there are several potential disabilities which result
from damage to the nervous system. Sensorineural hearing
loss, epilepsy, learning and behavioral difficulties, as well as
decreased intelligence, occur in about 15% of survivors. Some
of the hearing loss may be reversible.[37] In adults, 66% of all
cases emerge without disability. The main problems are
deafness (in 14%) and cognitive impairment (in 10%).
NURSING MANAGEMENT
NURSING ASSESSMENT
Subjective assessment ; Important health information –
previous respiratory , tuberculosis or any other infection. Any
history of head injury. Asking patient for various signs eg,
headache, neckpain, weakness.
Objective assessment: Assessment of signs of the signs eg.
Weakness, brudzinski sign.
NURSING DIAGNOSIS
 Ineffective cerebral tissue perfusion related to effects of
increased ICP.
 Altered body temperature related to infection
 High risk to infection related to decreased immune
response
 Impaired skin integrity relatd to perlonged bed rest and
diaphoresis
 Altered nutritional pattern related to dysphagia.
 Anxiety related to disease condition.
NURSING INTERVENTIONS
 Optimizing the cerebral tissue perfusion
– Elevation of head at 30 to 60 degree to promote venous
drainage.
– Oxygen administration to prevent hypoventilation.
– Administration of mannitol.
– Extreme rotation and felextion of neck are avoided.
– Emotional stress and frequent arousal from sleep are
avoided.
 To maintain body temperature
– Assess the temperature every hourly
– Complete bed rest
– Care should be taken not to reduce temperature too
rapidly because shivering may be result
– Topoid sponge bath with water may be effective in
lowering the temperature
– Acetaminophine may be used to reduce the temperature.
 To prevent fraom risk of infection to other part
– Maintain strict asepsis is like handwashing and using
sterile articles
– Patient ‘s bed should be leane, dry and warm
– Patient is sponged daily
– Routine examination of CSF and blood culture
– Antibiotics should be given