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OUTLINE• Introduction• Epidemiology• Aetiology• Predisposing factors• Pathogenesis• Pathology/Pathophysiology• Clinical manifestations• Diagnosis• Treatment• Complications• Prognosis• Prevention/Prophylaxis• Conclusion
INTRODUCTION
• Pyogenic meningitis implies an inflammation of the leptomeninges.
• It is a potentially fatal infection that can affect any age group.
• It is associated with significant morbidity and mortality.
DEFINITION.
• Inflammation of the meninges which may be caused by bacteria, viruses, fungi, protozoa or chemicals.
• Commonest form seen is bacterial meningitis- PYOGENIC Meningitis.
• Peak age in infancy. 95% of cases of meningitis occur <5yr.
• Higher incidence in pts with impaired splenic function- HbSS, Nephrotic syndrome, congenital asplenia, post-splenectomy, as a result of increased susceptibility to infections by encapsulated organisms e.g. H.flu, Strept pneumo
EPIDEMIOLOGY
• Up to About 80-95% of cases occur in children <5 yrs.• 25% of babies with neonatal sepsis may have meningitis.• Accounts for about 0.9-5.1% of emergency room
admissions.• Affects males more than females.• Incidence has reduced in developed countries due to
vaccine use.
AETIOLOGY• Neonates : E. coli is commonest then GBS particularly in
the first week. Later, klebsiella spp. P. aeuroginosa, L. monocytogenes, proteus spp.
• Beyond the neonatal group 72-96% of cases are caused by H.influenza type b, S. pnemoniae and N. meningitidis.
• For infants 2-3 months , organisms from both groups could be implicated.
AETIOLOGY (contd)
• H.influenza, Gram neg. pleomorphic coccobacillus.
• Affects children 3mnths-4yrs
• Infection can occur in epidemics.
AETIOLOGY (contd)
• S.pneumonia: Gram pos. cocci.
• Incidence increases after 4yrs.
• Commoner in the south.• Has various serotypes.
AETIOLOGY (contd)• N.meningitidis: Gram neg intracellulaar diplococcus.
• Cause of infection more in the North.
• Can occur sporadically and in epidemics.
• Epidemics occur in meningitic belt 5-15N
PREDISPOSING / RISK FACTORS• In neonates: maternal infections, Chorioamnionitis, Spina
bifida, LBW babies• Overcrowding,• Male gender• Splenic Dysfunction• Otitis media, mastoiditis, basal skull fracture• Abnormalities of the immune system• Burns
Pathogens vary with age.
Pyogenic meningitis
NEONATES
G -ve BacilliGrp B StreptococcusStaph aureusLysteria monocytogenes
1-2 MONTHS Org in neonates +Org in age 3mo- 12yr
3mo – 12yrsHaemophilus influenzaeStreptococcus pneumoniaeNeisseria meningitidis
Pathogenesis
URTI
Bacteraemia
Invasion of the meninges
Meningitis
Sequele
Release of acute phase reactantsIL-1, TNF, Cytokines
Contiguous spread: Otitis mediaMastoditisPen. Head injuryMyelomeningocoele
Septicaemia
Penetration of BBB
PATHOGENESIS• Usually results from haematogenous spread.• May also follow direct inoculation • Capsules help resist phagocytosis• Reduced concentration of complement and antibodies in
CSF encourages proliferation• Inflammatory response occurs with production of
cytokines and subsequent alteration of BBB.
PATHOLOGY/PATHOPHYSIOLOGY• Purulent exudate within the meninges which may spread
to the ventricles.• Cerebral infarction may be due to vascular occlusion• Inflammation of spinal and cranial nerves• Raised ICP due to a combination of vasogenic, cytotoxic
and interstitial oedema, SIADH maybe a contributing factor.
PATHOPHYSIOLOGY (contd)
• Raised CSF protein due to increased vascular permeability.• Hypoglychorrachia due to decreased glucose transport by
cerebral tissues
CLINICAL FEATURES
Non-specific:
FeverLethargyVomitingIrritabilityRefusal of feedsCoughCattarrh
Specific:
Convulsion- 20-30%Bulging AFNeck painPhotophobiaHeadacheComa+ Features of raised ICP
Features of Raised ICP: Bulging AF Abnormal pupils:unequalVomiting dilatedPapilloedemaHypertensionBradycardiaAbn. Respiration- apnoea,hyperventilation
CLINICAL MANIFESTATIONS• High index of suspicion needed particularly for neonates and
younger children.• There are no specific sign or symptoms attributable to
meningitis in neonates• Up to a 3rd of patients < 2yrs don’t show typical signs and
symptoms.• May be insidious or fulminant in presentation
CLINICAL MANIFESTATIONS• A preceding history of URTI or gastroenteritis may be
present.• Seizures are present in up to 30% prior admission and up
to 75% convulse during the illness.• Focal neurological signs are present in 7-15% SP >NM
Signs of meningeal irritation
Unusual finding in infants & young children. Diagnosis of meningitis in this age group thus requires a high index of suspicion.
Neck stiffness +ve Kerning's sign +ve Brudzinski sign
Diagnosis Lumbar Puncture mandatory. CSF analysis shows- o Pleocytosis with preponderance of neutrophilso Elevated CSF protein contento Reduced CSF: Blood sugar ratio (Hypoglycorrhachia)o +/- Orgs. on Gram staino +/- Culture.
DIAGNOSIS • Lumbar puncture• Blood culture• PCV• E/U• FBC• RBS• CT Scan• Rapid diagnostic tests: CIE, ELISA, Limulus lysate
Contra-indications to LP
• 1. Raised ICP• 2.Thrombocytopaenia• 3. Coagulopathy• 4. Infection of overlying skin at LP site• 5. Very ill patients with imminent cardio respiratory collapse
•
•
Typical CSF picture in the various forms of Meningitis
Normal CSF
PyogenicMeningitis
PartiallyTreated
ViralMeningit
TBMeningit
Appearance
ClearColourless
Purulent Turbid,Hazy
TurbidHazy
Clear Colourless
Xanthochromic, clear
WBC <5/mm3 Increased++N >L
Increased+ L>N
Increased+ L >N
Increased L>N
RBC nil nil nil + / - nil
Protein 10-40mg/dl Increased + +
Increased + / ++
Increased +
Increased +++
CSF: BSRatio
½ - 2/3 < 1/2 <1/2 Normal <1/2
GramStain
No org seen
+ /- -ve -ve -ve
TREATMENT
Parenteral Antibiotic Therapy is the treatment of choice. Drugs must be given IV.
NEONATES - Combination of a 3rd Generation Cephalosporin & an Aminoglycoside. IV Ceftriaxone or Cefotaxime or Ceftazidime + IM Gentamycin or IV Amikacin Lysteria monocytogenes- IV AMPICILLIN
INFANTS 1-2 MO - Treat as Neonate.
Age >2mo - IV Crystalline Penicillin 0.04MU/kg/D + IV Chloramphenicol 100mg/kg/D
Steroid Therapy- Controversial. IV Dexamethasone 0.15mg/kg 6hrly X 48hr. First dose
must be given at least 30min before 1st dose of antibiotic.
Duration of antibiotic therapy depends on the causative organism:
• G-ve bacilli - 21days• N.meningitidis - 5-7days• H.flu - 7-10days• Strept pneumo - 10-14days
• Neonatal meningitis – 21 days
o SUPPORTIVE THERAPY - ABC of resuscitation - Anticonvulsants - N-G Tube feeding - Control Raised ICP- Mannitol, Hypervent - Frequent Turning - Strict input / output monitoring
DIFFERENTIAL DIAGNOSIS• Cerebral malaria• TB meningitis• Aseptic meningitis• Encephalitis• Lead encephalopathy• CNS spread of Malignancies• Brain tumors• Causes of meningism
COMPLICATIONS• Deafness - commonest comp. of meningitis• Subdural effusion• SIADH• Visual impairment• Hydrocephalus- usually non-obstructive type• Seizure disorder• Speech defects• Mental retardation• Cerebral palsy• Ataxia
TREATMENT• Standard duration of treatment: Hib 7-10 days, NM-- 7 days,
SP 10 days GNB- 3 weeks• Role of corticosteroids: decreased duration o fever, CSF
protein, frequency of seizures, and frequency of hemiparesis and hearing deficits.
TREATMENT
• Supportive care:• Regular monitoring of the vital signs• Control of seizures• Fluid restriction• Treatment of raised intracranial pressure• Treatment of shock
COMPLICATIONS• Acute complications: seizures , raised ICP, CN palsies
• Subdural effusion• SIADH• Hydrocephalus • Neurologic deficits• Persistent or prolonged fever• Athritis or pericarditis• Long term sequelae
PROGNOSIS
• Poorer in neonates• Mortality is higher in SP>NM>Hib• Delayed diagnosis and inadequate treatment• Delayed CSF sterilization• Seizures after the 4th day of therapy
Prevention
IMMUNISATION Hib vaccine Conjugate pneumovax CSM Vaccine- given during epidemics
Good hygiene and hand washing practices in neonatal units.
CHEMOPROPHYLAXIS P.O. Rifampicin- given to household & close contacts of patients
with H.flu or meningococcal meningitis. rifampin 10 mg/kg/dose every 12 hr (maximum dose of 600 mg) for 2
days as soon as possible after identification of a case of suspected meningococcal meningitis or sepsis
CONCLUSION• Pyogenic meningitis still causes significant morbidity and mortality in our environment and the incidence can be reduced by improved social conditions.
• Though the use of vaccines has reduced the incidence in developed countries when it does occur it si still associated with significant morbidity. Ways of improving the outcome with regards to sequelae need to be sought.