Vous êtes sur la page 1sur 60

MENINGITIS

Dr.Rakesh TP
Sr. Lecturer in Medicine
Terms
Meningitis

Encephalitis

Cerebritis

Abscess
Classical signs
Neck rigidity
Kernig’s sign
Brudzinski’s sign

May be absent in
Extremes of age
coma
Immunosuppressed
ACUTE BACTERIAL MENINGITIS
Acute Bacterial Meningitis
Acute purulent infection within the
subarachnoid space

Most common form of suppurative CNS


infection

H influenzae decreasing  <10%

Common organisms are


Streptococcus pneumoniae50%
N. meningitidis25%
Group B streptococci 15 %
Listeria monocytogenes 10%
S. pneumoniae

Predisposing conditions
• Pneumococcal pneumonia
• Sinusitis or otitis media
• Alcoholism
• Diaetes
• Splenectomy, Hypogammaglobulinemia
• Complement deficiency
• Head trauma with basilar skull fracture
and CSF rhinorrhea

Mortality  20% despite antibiotic


therapy
N. meningitidis
25% of all cases of bacterial meningitis

60% of cases in children and young adults

Petechial or purpuric skin lesions

Nasopharyngeal colonization

Complement deficiency increased


meningococcal infections.
Enteric gram-negative bacilli

Chronic and debilitating diseases such as


Diabetes
Cirrhosis
Alcoholism
Chronic urinary tract infections

Also complicate neurosurgical


procedures, particularly craniotomy.
Group B streptococcus (S. agalactiae)
Neonates
Now increasing frequency in individuals >50
years of age

L. monocytogenes
Increasingly important cause of meningitis in
neonate, pregnant women, >60 years, and
immunocompromised
Contaminated milk, soft cheeses, and several
types of fast food
Staphylococcus aureus and coagulase-
negative staphylococci

Shunting procedures for hydrocephalus

Administration of intrathecal chemotherapy.


Group B Streptococcus
Listeria monocytogenes
Streptococcus pneumoniae
Neisseria meningitidis
Haemophilus influenzae.
PATHOPHYSIOLOGY
• Attachment to nasopharyngeal epithelial cells

• Transport or invasion to the intravascular space

• Prevention of Phagocytosis

• Reach and infect choroid plexus epithelial cells,


and gain access to the CSF

• Multiply rapidly within CSF


Mechanism of neuronal injury

Directly by the bacteria

Immune response

Neurologic injury can progress even after the


CSF has been sterilized by antibiotic therapy
Main starting point of immune response
is the lysis of bacterial cells

Inducers of immune response


LPS of gram negative organisms

Teichoic acid and peptidoglycans of S.


pneumoniae
Elevated levels of CSF cytokines and
chemokines is responsible for the
pathophysiology

TNF and IL4-1


Increase the permeability of the blood-brain
barrier, resulting in induction of vasogenic
edema and the leakage of serum proteins into
the subarachnoid space

The subarachnoid exudate leads to


Obstructive and communicating
hydrocephalus
Interstitial edema.
Cytokines Increased leukocyte adherence to
vascular endothelial cells and subsequent
migration into the CSF Inreased permeability
of blood vessels, allowing for the leakage of
plasma proteins into the CSF, which adds to the
inflammatory exudate.

Neutrophil degranulation Leads to


Cytotoxic edema
Cell injury and death.

CSF leukocytes probably do little to


contribute to the clearance of CSF bacterial
infection.
During the very early stages of meningitis there is
an increase in cerebral blood flow, soon followed
by a decrease in cerebral blood

Causes of Stroke
Cerebral vasculitis ischaemia and infarction
Thrombosis of MCA
Thrombosis of the major cerebral venous sinuses
Thrombophlebitis of the cerebral cortical veins

Cerebral edema
Combination of Interstitial, Vasogenic and cytotoxic
edema
Clinical features
Classical triad
– Fever
– Headache
– Neck rigidity

Other symptoms
Nausea, vomiting, altered sensorium,
photophobia
Seizures in 20 to 40%

Focal seizures 
• Focal arterial ischemia or infarction
• CVT with hemorrhage or focal edema

Generalized seizure activity and status


epilepticus
• Hyponatremia
• Cerebral anoxia
• Toxic effects of antimicrobial agents such
as high-dose penicillin.
Features of Raised ICP
Deteriorating or reduced level of consciousness
Papilledema
Dilated poorly reactive pupils
VI nerve palsy
Decerebrate posturing
Cushing reflex (bradycardia, hypertension, and
irregular respirations).

Cerebral herniation  occurs in 1-8%  Death !!


Specific diagnostic features

Rash of Meningococcemia
Diagnosis
Once clinically suspected….Take Blood
sample for culture and start Empirical
antibiotic…

Gold standard for diagnosis  CSF


analysis

Imaging CT, MRI  When ?


CSF
PMN leukocytosis >100 cells/uL in 90
Decreased Glucose <40 mg/dL or < 2/3 of
blood glucose
Increased protein concentration>45 mg/dL
Increased opening pressure >180 mmH2O

CSF bacterial cultures are +ve in >80% of patients


CSF Gram's stain demonstrates organisms in
>60%.
It takes from 30 min to several hours for
CSF glucose concentration to reach
equilibrium with blood glucose
concentrations

The Gram staining should be done by the


treating physician himself to avoid the
lab delay……..
Other diagnostic tests
Latex agglutination
• Specificity of 95 to 100% for S. pneumoniae and N.
meningitidis
• Sensitivity of the CSF LA test is only 70 to 100%
for detection of S. pneumoniae and 33 to 70% for
detection of N. meningitidis

Limulus amebocyte lysate assay


• For rapid detection of gram negative endotoxin in
CSF

Imaging

Biopsy of purpuric rash


Differential diagnosis
• H.simplex meningoencephalitis

Differentiating points
1. Prominent altered sensorium and seizures

3. No evidence of Severe meningeal irritation

5. Normal sugar and Predominant lymphocytosis in


CSF

7. Parenchymal changes, especially in orbitofrontal


and medial temporal lobes in MRI

9. Typical EEG pattern


Differential diagnosis
1. RMSF (not common in our place)
Differentiating features

• Rash is beginning in wrists and


ankles

• Immunofluorescence of skin biopsy


Differential diagnosis
Focal suppurative CNS infections focal
signs

Noninfectious CNS disorders mimicing


bacterial meningitis
SAH
Chemical meningitis
Drug-induced hypersensitivity meningitis
Carinomatous or lymphomatous meningitis
Sarcoid, SLE and Behcet disease;
Pituitary apoplexy
Differential diagnosis
1. Subacutely evolving meningitis
Mycobacterium tuberculosis
Cryptococcus neoformans
Histoplasma capsulatum
Coccidioides immitis and Treponema
pallidum
Treatment
Empirical Treatment

Specific antimicrobial therapy


Empirical
Infants 1-3 mos Ampicillin + cefotaxime or
ceftriaxone
Immunocompetent children > 3 mos
and adults <55 Cefotaxime or ceftriaxone +
vancomycin
Adults > 55 and adults of any age
with alcoholism or other debilitating Ampicillin + cefotaxime or
illnesses ceftriaxone + vancomycin

Hospital-acquired meningitis,
posttraumatic or postneurosurgery
meningitis, neutropenic patients, or
patients with impaired cell- Ampicillin + ceftazidime +
mediated immunity vancomycin
Ceftazidime should be substituted for
ceftriaxone or cefotaxime in
neurosurgical patients and in
neutropenic patients
Specific treatment
N.meningitidis

Penicillin sensitive Penicillin G or Ampicillin

Penicillin-resistant Ceftriaxone or cefotaxime


Chemoprophylaxis for N.meningitidis

Rifampin 600 mg every 12 h for 2 days in


adults and 10 mg/kg every 12 h for 2 days in
children >1 year

Or

One dose of ciprofloxacin (750 mg)


One dose of azithromycin (500 mg)
One intramuscular dose of ceftriaxone (250 mg)

Rifampicin is not recommended in pregnant


women.
Pneumococci

Penicillin-sensitive Penicillin G

Penicillin-intermediate  Ceftriaxone or
cefotaxime

Penicillin-resistant  (Ceftriaxone or
cefotaxime) + vancomycin

Repeat LP at 24 – 36 hrs
Gram-negative bacilli (except Pseudomonas
spp.)  Ceftriaxone or cefotaxime

Pseudomonas aeruginosa  Ceftazidime


Staphylococci spp.
Methicillin-sensitive  Nafcillin
Methicillin-resistant  Vancomycin

Listeria monocytogenes  Ampicillin + gentamicin


Haemophilus influenzae  Ceftriaxone or
cefotaxime
Streptococcus agalactiae Penicillin G or
ampicillin
Bacteroides fragilis  Metronidazole
Fusobacterium spp.  Metronidazole
Duration of treatment
N.meningitidis  1 week

S.pneumoniae  2 weeks

Listeria  3 weeks

Gram negative Bacillary  3 weeks


Adjunctive therapy
Dexamethasone
20 mts before or alongwith 1st dose of antibiotic

Raised ICP
Head raised to 30˚ - 45˚
Hyperventilation
Mannitol

Fluid and electrolyte balance

Bladder and Skin care


PROGNOSIS
Mortality

3 to 7% for H. influenzae, N. meningitidis, or


group B streptococci

15% for that due to L. monocytogenes

20% for S. pneumoniae


PROGNOSIS
Risk of death increases with
Decreased level of consciousness on admission
Onset of seizures within 24 h of admission
Signs of increased ICP
Extremes of Age
Comorbid conditions including shock and/or the
need for mechanical ventilation
Delay in the initiation of treatment
Sequelae  25%
Decreased intellectual function
Memory impairment
Seizures
Hearing loss
Gait disturbances
Viral meningitis
Etiology
Enteroviruses 75 to 90%
Adeno
HSV
LCMV
Mumps
HIV
Arboviridae
Rabies
Rota
Influenza
A specific viral cause can be found in 75
to 90% of cases of viral meningitis by
using
CSF PCR
Culture
Serology
Lab
CSF
Lymphocytic pleocytosis (25 to 500 cells/uL)
Normal or slightly elevated protein
concentration (20 to 80 mg/dL)
Normal glucose concentration
Normal or mildly elevated opening pressure
(100 to 350 mmH2O)

Organisms are not seen on Gram's or acid-


fast stained smears or india ink preparations
of CSF
Viral meningitis with PMN in CSF in early
period
Echovirus 9
West Nile virus
Mumps

Viral meningitis with low sugar in CSF


LCMV
10 – 30 % of mumps

As a rule, a lymphocytic pleocytosis with a low glucose


concentration should suggest fungal, listerial, or
tuberculous meningitis or noninfectious disorders
Other investigations
PCR

CSF culture

Other sources of Viral isolation

Serology
Differential diagnosis
Bacterial meningitis and other infectious
meningidities

Parameningeal infections or partially treated


bacterial meningitis

Nonviral infectious meningitides where cultures


may be negative (e.g., fungal, tuberculous,
parasitic, or syphilitic disease)

Neoplastic meningitis

Noninfectious inflammatory diseases


Treatment
Supportive care
Seizure
Fever
Fluid and electrolyte balance
Antiviral treatment
Acyclovir
Experimental drug  Pleconaril for
enterovirus
Prevention

Measles
Mumps
Polio
Varicella zoster
Prognosis
Excellent in adults
Occasional sequel in infants
Subacute and chronic meningitis

M. tuberculosis
C. neoformans
H. capsulatum
C. immitis
T. pallidum
TBM
Subependymal caseous foci cause
meningitis via discharge of bacilli and
tuberculous antigens into the SAS

Intense inflammatory reaction that leads


to the production of a thick exudate that
fills the basilar cisterns and surrounds
the cranial nerves and major blood
vessels at the base of the brain
Complications

Cranial nerve palsies

Cerebral vasculitis  stroke

Hydrocephalus
CSF
Elevated opening pressure
Lymphocytic pleocytosis (10 to 500 cells/uL)
Elevated protein concentration (10 to 500
mg/dL)
Decreased glucose concentration (20 to 40
mg/dL)
“Cobweb”

Most common cause of Chronic meningitis in


our place
Positive smears  in only 10 to 40% of
cases of tuberculous meningitis

Cultures are positive in  50 %

Culture – gold standard


Treatment
Antituberculous therapy

Steroid

Supportive measures
Cryptococcal meningitis
Association with Immunodeficiency

Indian Ink preparation

Latex agglutination test for cryptococcal


polysaccharide for rapid test

Lymphocytic predominance
Read in detail…
Herpes simplex meningoencephalitis

Cryptococcal meningitis

Differentiation of TBM, Viral, and Bacterial


Meningitis by CSF picture

Indian ink preparation

CSF Gram staining

Chemoprophylaxis

Empirical drug therapy


Thank you