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Meningitis




                                   Dr. Kalpana Malla
                                       MD Pediatrics
                           Manipal Teaching Hospital

Download more documents and slide shows on The Medical Post [ www.themedicalpost.net ]
Definitions
• Meningitis : inflammation of the lepto-meninges
  covering the brain and the spinal cord

• Encephalitis : inflammation of brain parenchyma, with
  cerebral dysfunction.

• Encephalopathy : cerebral dysfunction , due to
  toxins, metabolites, poisons etc , affecting neurons
  without inflammatory response.
Classification:
1)   Viral
2)   Bacterial
3)   Tubercular
4)   Others:
      Parasitic: malarial, amebic, toxoplamosis
        Fungal: candiadiasis, cryptococcal,
               histoplasmosis
Bacterial Meningitis
• Causes:
• 0-2months: - Group B & D streptococcus
           - Gram neg enteric bacilli - E.coli,
                         Klebsiella pneumoniae
            - L. monocytogenes
            - Sometimes H influenza
2mo-5years: - H. influenzae typeb
          - Strep. Pneumoniae
            - N. meningitidis
>5 years: - S. pnemoniae
           - N. meningitidis
May spread to the meninges either
Hematogenously, or by contiguous spread
Predisposing factors include:
1) Septicemia
2) Septic foci in skin, lungs, bones
3) Trauma ie. Fracture base of the skull
4) Neural tube defects
5) Suppurative ear, mastoid infec
Etiology
• N meningitis – epidemics
• S. Pneumoniae – epidemics
• H influenza – uncommon after 3 years,
  incidence decreased after Hib vaccine.
• Less common – staph – seen in vp shunt
• Less common – E. coli, pseudo, proteus –
  neonates, immuno compromised.
PATHOGENESIS
Host :
• Young age , close contact with bacteria , altered
  immunoglobulin response, defect of complement
  system – C5-8 – recurrent meningococcal inf.,
• Defect of properdin system : meningococcal inf.,
• Splenic dysfunction : pnemococcal and H influenza
• T lymphocyte defect : L monocytogens
• Altered mucocutaneous barrier : cribiform plate
  damage, middle ear inf. – pneumococcal
• Lumbosacral myelocele : staph and gram neg. enteric
  bacilli
BACTERIAL COLONISATION OF NASOPHARYNX with pathogenic bacteria
 (eg N meningitis and H influenza attach to mucosal surface by pilli
             and enter circulation)

 DIRECT INVASION                   Blood stream               BLOOD CYTOKININE
                               Invasion / Bacteremia              RELEASE

                      THROUGH choroid plexus
                                                                  Intravascular
                       Lat ventricle, meninges
  CNS PENETRATION                                              Volume decreases


    Bacteria rapidly multiply                                      ↓CSF flow
   As CSF conc. Of complement
      And antibody LOW
                                                                   Endothelial
Complement system activation           CSF cytokine            Leukocyte activation
                                       release
                                                                    Release of
    PMN STIMULATION             BBB disturbed     ↓CSF flow     Secondary mediators

  FREE RADICAL RELEASE          Meningeal inflammation
                                                                   Brain damage
                                   Brain edema
Clinical features:
• Constitutional symptoms :
  Lethargy, irritability , anorexia, vomiting,
 fever – mild, high, hypothermia in infants, Poor
   feeding, Arthralgia, myalgia

Meningeal features:
 Neck rigidity, kernig’s, brudzinski’s sign.
These may be absent in infants, Neck pain,
Clinical features:
• Features of raised ICP:
 - HTN with bradycardia,
 - Apnea or hyperventilation,
 - Head ache , photophobia,
 - Vomiting- projectile
 - Buldging AF if open, 6th nerve palsy
 - Hypertonia, extensor plantars
 - Decorticate/decerebrate posturing
 - Papilledema
Raised ICP due to:
1) Cell death (cytotoxic cerebral edema)
2) Cytokine induced increased vascular
   permeability(vasogenic cerebral edema)
3) Increased hydrostatic pressure after
   obstructed reabsorption of CSF in the villus
   or obstruction of the flow of fluid from the
   ventricle
4) SIADH
Clinical features:

Features of parenchymal involvement:
  Altered sensorium, seizures, Coma and focal
  neurological signs
• Cutaneous features: erythamatous macular
  rashes, petechiae
Clinical features:

• Extra CNS manifestations:
  Rashes, petechiae, athralgia, shock, DIC,
  depending on etiology



In very young, immunocompromised, severely
 malnourished child signs of overt meningitis
 may be absent
Meningitis in neonates and infants
• Vacant stare, persistent vomiting, refusal to
  suck, poor tone, poor cry, shock, circulatory
  collapse, hypothermia/fever, convulsions, neur
  ological signs.

• More risk if – premature, LBW, coplicated
  labour, PROM, maternal sepsis……
Signs:

• Neck rigidity
• Kernig’s sign
• Brudzinski’s sign
• Bulged fontanelle
• Sutural diastasis
• Cranial n. palsies (oculomotor, abducens,
  facial, auditory)
• photophobia
Tubercular Meningitis
• Most serious complication & fatal without Rx
• Commonly affects children from 6mo- 4years
  of age
• Rapid progression occur in infants & young
  children
TBM
• Pathogenesis:
1) Rupture of subependymal tubercles – TB
  bacilli in subarachnoid space
2) Lymphohematogenous dissemination of
  primary infection
First stage
• Over 1-2 weeks – 2-8 weeks
• Stage of invasion/prodromal stage
• Nonspecific and vague
  Fever               Headache
  Irritability         Drowsiness
  Malaise             Shrill cry
100% cure
Second stage - Stage of meningitis
•   Over 1-2 wks
•   More abrupt
•   Lethargy                   - Projectile vomiting
•   Nuchal rigidity              - Bulging frontanelle
•   Seizures                - Cranial nerve palsies
•   Kernig/brudzinisky’s sign +
•   25% mortality, 25 % sequelae
•   Hypertonia
•   Cranil N palsies 3rd-7th
•   Ocular paralysis
•   Strabismus, nystagmus
•   Hemiplegia/quadriplegia
•   Semicoma/coma
Third stage - Stage of coma
• Unconscious- Coma
• Repeated convulsions
• High fever: “terminal fever”
• Severe neurological involvements –
                - Hemiplegia/paraplegia
                - Quadriplegia/ decerebrate rigidity
                - Decerebrate posturing
                - Opsithotonus
               - Deteriorating mental status
• Deteroration of vital signs- Hypertension
• 50% mortality
• 50% cure but almost all have sequelae
Disabilities of TBM
• Blindness         deafness
  paraplegia /hemiplegia
  squint            MR
  epilepsy          CP
  CN palsies
  Endocrine disturbances
INVESTIGATIONS
1)Lumbar puncture: should be done before any
    antibiotics started
      precautions: C/I for an immediate LP :
      - EVIDENCE OF increased ICT ( other than
        bulging fontanels). - Fundoscopy, to rule
                            out papilloedema -
      -infections overlying the site of      puncture
      -Relative C/I - Thrombocytopenia
      -Cardiopulmonary compromise & shock
LP
• DO RBS 30 min before LP.
• CHILD IN LATERAL POSITION with knee, hip, head
  flexed.
• Clean site L4-5, L3-4.
• LP stilleted needle, with direction towards umblicus
  , perpendicular to spine.
• Collect CSF – TUBE 1 – cell count, type
• Tube 2 – C/S.
• TUBE 3 – glucose, protein
• Tube 4 – latex fixation tests
• 0.5 to 1 ml each tube.
Investigations
2) Blood Culture:
3) Chest Roentogram
4) S. electrolytes
5) CBC, CRP
6) Skin scraping for C/S
7) Mantoux Test
7) Serology: Latex agglutination, counter
  current immunoelectrophoresis
8) CT,MRI- for detection of hydrocephalus,
  abcess, effusion, exudates, edema
Normal     PYOGENIC VIRAL      MYCOBACT FUNGAL
                               ERIAL


 GROSS     TURBID     CLEAR    COBWEB   CLEAR-
 CLEAR                                  TURBID




Pressure    100-300   80-150     >80      >80
Mm H20
 50-80
PYOGENIC VIRAL        MYCOBA FUNGAL
                                CTERIAL

SUGAR     <40(<50%   N ( < 40     <50       <50
 MG/DL    OF RBS)       IN
>50(75%              MUMPS
OF RBS                   )


PROTEI     100-500   50-200     100-3000   25-500
   N
MG/DL
 20-45
PYOGENIC     VIRAL    MYCOBA FUNGAL
                               CTERIAL

TOTAL    100-10,000    100     10-500    5-500
 CELL
  <5

PREDO      PMN        lympho   Lympho   Monnucl
 MINAT                 cytes              ear
 TYPE
 ,>75%
Lympho
PARTIALLY TREATED MENINGITIS
• Culture : sterile in 48 hrs
• Sugar normalize by 48 hrs
• Cells may increase initially, persistence of
  neutrophil indicates poor response.
• Protein : take longer time to normalize, thus
  not good parameter for adequacy of
  treatment.
RAPID DIAGNOSTIC TESTS
• PCR – for diagnosis of infections ( herpes, TB,
  meningococci)

• Latex agglutination and ELISA- antigen
  antibody detection

• CSF C-RP, LDH, lactic acid – to differentiate
  pyogenic from non pyogenic.
ORGANISM ANTIBIOTIC           DOSE       DURATION




UNKNOW     EMPERIC                       10 DAYS
           1)CEFTRIAXONE      100-150
N                             MG/KGDAY
           2)CEFOTAXIME
                              4 LAC
           3)AMPI/PENCILLIN
                              U/KG/DAY
           G + CHRAMPHENi
                              100
                              MG/KGDAY


MENINGOC Pencillin G          3-4 lac  7DAYS
OCCUs                         U/KG/DAY
ORGANISM ANTIBIOTIC              DOSE DURATION



Pneumococcu Pencillin G or if    40      10DAYS
s           resistance –         MG/KG/D
            Ceftriaxone plus
            Vancomycin
Gram neg.     Ceftriaxone/cefo          21DAYS
              taxime plus
              aminoglycogide
ORGANISM ANTIBIOTIC         DOSE    DURATION



Pseudomonas   Ceftazidime   150     14-21DAYS
                            MG/KG/D


Staphyloco    Vancomycin    40     28DAYS
cci                         MG/KGD
                            AY

H influenza   Ceftriaxone           10-14
                                    DAYS
              Cefotaxime
2) Anti inflammatory therapy
  Dexamethasone: 0.15mg/kg/dose 6hrly for 2
   days
   First dose should be given prior to starting
   antibiotics
  In case of TBM: prednisolone;4-6wks
STEROID THERAPY
• Rationale : to decrease cytokine related damage ,
  esp . To 8th nerve .
• Decrease ICT
• ESP. useful for children older than 6 weeks with
  suspected H influenza.
• Current recommendation :
• Dexamethasone : 1-2 hr before first antibiotic dose
• 0.15mg/kg/dose every 6 hrly for 2 days.
General Care
- Fluid and electrolytes homeostasis -Check for shock –
   fluid bolus NS
• NPO
• Oral feeds if sensorium –ok
• Care of oral cavity, eyes, bladder,bowel and skin
• IF suspecting SIADH – give 2/3rd maintenance
• Symptomatic Management:
   Paracetamol
    Diazepam, Phenytoin, Phenobarbitone
Supportive care

Seizures
• No role for prophylactic use of AED
• For immediate control : lorazepam/diazepam,
• Load on phenytion to reduce recurrence.
• Phenytoin preferred than pheno as produces less
  CNS depression and permits assessment of levels
  of consciousness.
Treatment of raised intracranial pressure
• Head end elevation to 30 degree
• Fluid – 2/3 rd maintaiance
• Do not use hypotonic fluids
• 20% mannitol
• Frusemide
• Acetazolamide
• Glycerol
4) Treatment of complications:
  Shock: Volume expander, FFP,
      Dopamine
  Subdural effusion: Aspiration
  Hydrocephalus: Shunt Operation (VP)
Complications - immediate
• Seizure              • Ventriculitis
• Raised ICP           • Brain abscess
• Stroke               • Hydrocephalus
• Cerebral or          • DIC
  Cerebellar           • Cranial Nerve Palsy
  herniation           • Thrombosis of dural
• Sub Dural Effusion     sinuses
• SIADH                • Shock
CHRONIC –late
• Permanent brain damage with
      - CP,Mental retardation,
     - Epilepsy
     - Deafness
     - Blindness
     - Hemiplegia
     - Hydrocephalus
• EHAVIOUR PROBLEMS
POOR PROGNOSIS
• SEIZURES THAT PERSIST after 4 days of illness
  and are difficult to treat
• Coma
• CSF pleocytosis may be absent in
  overwhelming meningitis and sepsis.
• < 6 months
• Focal deficit at presentation
• Pnemococcal organism
PREVENTION

• Immuno prophylaxis :
 - Hib vaccine - routine
- Meningococcal vaccine -
          epidemics
PREVENTION
• Chemo prophylaxis: ( for house hold contacts)
1. H influenza : Rifampicin : 20 mg/kg/day,
  single dose/day for 4 days
2.Meningococcus : Rifampicin : 20 mg/kg/day, in
  2 divided doses for 2 days
                    Or
  Ciprofloxacin- single dose 500mg
Thank you
Download more documents and slide shows on The Medical Post
               [ www.themedicalpost.net ]

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Meningitis

  • 1. Meningitis Dr. Kalpana Malla MD Pediatrics Manipal Teaching Hospital Download more documents and slide shows on The Medical Post [ www.themedicalpost.net ]
  • 2. Definitions • Meningitis : inflammation of the lepto-meninges covering the brain and the spinal cord • Encephalitis : inflammation of brain parenchyma, with cerebral dysfunction. • Encephalopathy : cerebral dysfunction , due to toxins, metabolites, poisons etc , affecting neurons without inflammatory response.
  • 3. Classification: 1) Viral 2) Bacterial 3) Tubercular 4) Others: Parasitic: malarial, amebic, toxoplamosis Fungal: candiadiasis, cryptococcal, histoplasmosis
  • 4. Bacterial Meningitis • Causes: • 0-2months: - Group B & D streptococcus - Gram neg enteric bacilli - E.coli, Klebsiella pneumoniae - L. monocytogenes - Sometimes H influenza 2mo-5years: - H. influenzae typeb - Strep. Pneumoniae - N. meningitidis >5 years: - S. pnemoniae - N. meningitidis
  • 5. May spread to the meninges either Hematogenously, or by contiguous spread Predisposing factors include: 1) Septicemia 2) Septic foci in skin, lungs, bones 3) Trauma ie. Fracture base of the skull 4) Neural tube defects 5) Suppurative ear, mastoid infec
  • 6. Etiology • N meningitis – epidemics • S. Pneumoniae – epidemics • H influenza – uncommon after 3 years, incidence decreased after Hib vaccine. • Less common – staph – seen in vp shunt • Less common – E. coli, pseudo, proteus – neonates, immuno compromised.
  • 7. PATHOGENESIS Host : • Young age , close contact with bacteria , altered immunoglobulin response, defect of complement system – C5-8 – recurrent meningococcal inf., • Defect of properdin system : meningococcal inf., • Splenic dysfunction : pnemococcal and H influenza • T lymphocyte defect : L monocytogens • Altered mucocutaneous barrier : cribiform plate damage, middle ear inf. – pneumococcal • Lumbosacral myelocele : staph and gram neg. enteric bacilli
  • 8. BACTERIAL COLONISATION OF NASOPHARYNX with pathogenic bacteria (eg N meningitis and H influenza attach to mucosal surface by pilli and enter circulation) DIRECT INVASION Blood stream BLOOD CYTOKININE Invasion / Bacteremia RELEASE THROUGH choroid plexus Intravascular Lat ventricle, meninges CNS PENETRATION Volume decreases Bacteria rapidly multiply ↓CSF flow As CSF conc. Of complement And antibody LOW Endothelial Complement system activation CSF cytokine Leukocyte activation release Release of PMN STIMULATION BBB disturbed ↓CSF flow Secondary mediators FREE RADICAL RELEASE Meningeal inflammation Brain damage Brain edema
  • 9. Clinical features: • Constitutional symptoms : Lethargy, irritability , anorexia, vomiting, fever – mild, high, hypothermia in infants, Poor feeding, Arthralgia, myalgia Meningeal features: Neck rigidity, kernig’s, brudzinski’s sign. These may be absent in infants, Neck pain,
  • 10. Clinical features: • Features of raised ICP: - HTN with bradycardia, - Apnea or hyperventilation, - Head ache , photophobia, - Vomiting- projectile - Buldging AF if open, 6th nerve palsy - Hypertonia, extensor plantars - Decorticate/decerebrate posturing - Papilledema
  • 11. Raised ICP due to: 1) Cell death (cytotoxic cerebral edema) 2) Cytokine induced increased vascular permeability(vasogenic cerebral edema) 3) Increased hydrostatic pressure after obstructed reabsorption of CSF in the villus or obstruction of the flow of fluid from the ventricle 4) SIADH
  • 12. Clinical features: Features of parenchymal involvement: Altered sensorium, seizures, Coma and focal neurological signs • Cutaneous features: erythamatous macular rashes, petechiae
  • 13. Clinical features: • Extra CNS manifestations: Rashes, petechiae, athralgia, shock, DIC, depending on etiology In very young, immunocompromised, severely malnourished child signs of overt meningitis may be absent
  • 14. Meningitis in neonates and infants • Vacant stare, persistent vomiting, refusal to suck, poor tone, poor cry, shock, circulatory collapse, hypothermia/fever, convulsions, neur ological signs. • More risk if – premature, LBW, coplicated labour, PROM, maternal sepsis……
  • 15. Signs: • Neck rigidity • Kernig’s sign • Brudzinski’s sign • Bulged fontanelle • Sutural diastasis • Cranial n. palsies (oculomotor, abducens, facial, auditory) • photophobia
  • 16. Tubercular Meningitis • Most serious complication & fatal without Rx • Commonly affects children from 6mo- 4years of age • Rapid progression occur in infants & young children
  • 17. TBM • Pathogenesis: 1) Rupture of subependymal tubercles – TB bacilli in subarachnoid space 2) Lymphohematogenous dissemination of primary infection
  • 18. First stage • Over 1-2 weeks – 2-8 weeks • Stage of invasion/prodromal stage • Nonspecific and vague Fever Headache Irritability Drowsiness Malaise Shrill cry 100% cure
  • 19. Second stage - Stage of meningitis • Over 1-2 wks • More abrupt • Lethargy - Projectile vomiting • Nuchal rigidity - Bulging frontanelle • Seizures - Cranial nerve palsies • Kernig/brudzinisky’s sign + • 25% mortality, 25 % sequelae
  • 20. Hypertonia • Cranil N palsies 3rd-7th • Ocular paralysis • Strabismus, nystagmus • Hemiplegia/quadriplegia • Semicoma/coma
  • 21. Third stage - Stage of coma • Unconscious- Coma • Repeated convulsions • High fever: “terminal fever” • Severe neurological involvements – - Hemiplegia/paraplegia - Quadriplegia/ decerebrate rigidity - Decerebrate posturing - Opsithotonus - Deteriorating mental status • Deteroration of vital signs- Hypertension • 50% mortality • 50% cure but almost all have sequelae
  • 22. Disabilities of TBM • Blindness deafness paraplegia /hemiplegia squint MR epilepsy CP CN palsies Endocrine disturbances
  • 23. INVESTIGATIONS 1)Lumbar puncture: should be done before any antibiotics started precautions: C/I for an immediate LP : - EVIDENCE OF increased ICT ( other than bulging fontanels). - Fundoscopy, to rule out papilloedema - -infections overlying the site of puncture -Relative C/I - Thrombocytopenia -Cardiopulmonary compromise & shock
  • 24. LP • DO RBS 30 min before LP. • CHILD IN LATERAL POSITION with knee, hip, head flexed. • Clean site L4-5, L3-4. • LP stilleted needle, with direction towards umblicus , perpendicular to spine. • Collect CSF – TUBE 1 – cell count, type • Tube 2 – C/S. • TUBE 3 – glucose, protein • Tube 4 – latex fixation tests • 0.5 to 1 ml each tube.
  • 25. Investigations 2) Blood Culture: 3) Chest Roentogram 4) S. electrolytes 5) CBC, CRP 6) Skin scraping for C/S 7) Mantoux Test 7) Serology: Latex agglutination, counter current immunoelectrophoresis 8) CT,MRI- for detection of hydrocephalus, abcess, effusion, exudates, edema
  • 26. Normal PYOGENIC VIRAL MYCOBACT FUNGAL ERIAL GROSS TURBID CLEAR COBWEB CLEAR- CLEAR TURBID Pressure 100-300 80-150 >80 >80 Mm H20 50-80
  • 27. PYOGENIC VIRAL MYCOBA FUNGAL CTERIAL SUGAR <40(<50% N ( < 40 <50 <50 MG/DL OF RBS) IN >50(75% MUMPS OF RBS ) PROTEI 100-500 50-200 100-3000 25-500 N MG/DL 20-45
  • 28. PYOGENIC VIRAL MYCOBA FUNGAL CTERIAL TOTAL 100-10,000 100 10-500 5-500 CELL <5 PREDO PMN lympho Lympho Monnucl MINAT cytes ear TYPE ,>75% Lympho
  • 29. PARTIALLY TREATED MENINGITIS • Culture : sterile in 48 hrs • Sugar normalize by 48 hrs • Cells may increase initially, persistence of neutrophil indicates poor response. • Protein : take longer time to normalize, thus not good parameter for adequacy of treatment.
  • 30. RAPID DIAGNOSTIC TESTS • PCR – for diagnosis of infections ( herpes, TB, meningococci) • Latex agglutination and ELISA- antigen antibody detection • CSF C-RP, LDH, lactic acid – to differentiate pyogenic from non pyogenic.
  • 31. ORGANISM ANTIBIOTIC DOSE DURATION UNKNOW EMPERIC 10 DAYS 1)CEFTRIAXONE 100-150 N MG/KGDAY 2)CEFOTAXIME 4 LAC 3)AMPI/PENCILLIN U/KG/DAY G + CHRAMPHENi 100 MG/KGDAY MENINGOC Pencillin G 3-4 lac 7DAYS OCCUs U/KG/DAY
  • 32. ORGANISM ANTIBIOTIC DOSE DURATION Pneumococcu Pencillin G or if 40 10DAYS s resistance – MG/KG/D Ceftriaxone plus Vancomycin Gram neg. Ceftriaxone/cefo 21DAYS taxime plus aminoglycogide
  • 33. ORGANISM ANTIBIOTIC DOSE DURATION Pseudomonas Ceftazidime 150 14-21DAYS MG/KG/D Staphyloco Vancomycin 40 28DAYS cci MG/KGD AY H influenza Ceftriaxone 10-14 DAYS Cefotaxime
  • 34. 2) Anti inflammatory therapy Dexamethasone: 0.15mg/kg/dose 6hrly for 2 days First dose should be given prior to starting antibiotics In case of TBM: prednisolone;4-6wks
  • 35. STEROID THERAPY • Rationale : to decrease cytokine related damage , esp . To 8th nerve . • Decrease ICT • ESP. useful for children older than 6 weeks with suspected H influenza. • Current recommendation : • Dexamethasone : 1-2 hr before first antibiotic dose • 0.15mg/kg/dose every 6 hrly for 2 days.
  • 36. General Care - Fluid and electrolytes homeostasis -Check for shock – fluid bolus NS • NPO • Oral feeds if sensorium –ok • Care of oral cavity, eyes, bladder,bowel and skin • IF suspecting SIADH – give 2/3rd maintenance • Symptomatic Management: Paracetamol Diazepam, Phenytoin, Phenobarbitone
  • 37. Supportive care Seizures • No role for prophylactic use of AED • For immediate control : lorazepam/diazepam, • Load on phenytion to reduce recurrence. • Phenytoin preferred than pheno as produces less CNS depression and permits assessment of levels of consciousness.
  • 38. Treatment of raised intracranial pressure • Head end elevation to 30 degree • Fluid – 2/3 rd maintaiance • Do not use hypotonic fluids • 20% mannitol • Frusemide • Acetazolamide • Glycerol
  • 39. 4) Treatment of complications: Shock: Volume expander, FFP, Dopamine Subdural effusion: Aspiration Hydrocephalus: Shunt Operation (VP)
  • 40. Complications - immediate • Seizure • Ventriculitis • Raised ICP • Brain abscess • Stroke • Hydrocephalus • Cerebral or • DIC Cerebellar • Cranial Nerve Palsy herniation • Thrombosis of dural • Sub Dural Effusion sinuses • SIADH • Shock
  • 41. CHRONIC –late • Permanent brain damage with - CP,Mental retardation, - Epilepsy - Deafness - Blindness - Hemiplegia - Hydrocephalus • EHAVIOUR PROBLEMS
  • 42. POOR PROGNOSIS • SEIZURES THAT PERSIST after 4 days of illness and are difficult to treat • Coma • CSF pleocytosis may be absent in overwhelming meningitis and sepsis. • < 6 months • Focal deficit at presentation • Pnemococcal organism
  • 43. PREVENTION • Immuno prophylaxis : - Hib vaccine - routine - Meningococcal vaccine - epidemics
  • 44. PREVENTION • Chemo prophylaxis: ( for house hold contacts) 1. H influenza : Rifampicin : 20 mg/kg/day, single dose/day for 4 days 2.Meningococcus : Rifampicin : 20 mg/kg/day, in 2 divided doses for 2 days Or Ciprofloxacin- single dose 500mg
  • 45. Thank you Download more documents and slide shows on The Medical Post [ www.themedicalpost.net ]