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Meningitis
Meningitis
Meningitis
Meningitis
Meningitis
Meningitis
Meningitis
Meningitis
Meningitis
Meningitis
Meningitis
Meningitis
Meningitis
Meningitis
Meningitis
Meningitis
Meningitis
Meningitis
Meningitis
Meningitis
Meningitis
Meningitis
Meningitis
Meningitis
Meningitis
Meningitis
Meningitis
Meningitis
Meningitis
Meningitis
Meningitis
Meningitis
Meningitis
Meningitis
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Meningitis
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Meningitis
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Meningitis

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  • 1. Meningitis Dr. Kalpana Malla MD Pediatrics Manipal Teaching HospitalDownload 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) Viral2) Bacterial3) Tubercular4) 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 influenza2mo-5years: - H. influenzae typeb - Strep. Pneumoniae - N. meningitidis>5 years: - S. pnemoniae - N. meningitidis
  • 5. May spread to the meninges eitherHematogenously, or by contiguous spreadPredisposing factors include:1) Septicemia2) Septic foci in skin, lungs, bones3) Trauma ie. Fracture base of the skull4) Neural tube defects5) 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. PATHOGENESISHost :• 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 EndothelialComplement 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 ventricle4) 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 space2) 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 cry100% 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. INVESTIGATIONS1)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. Investigations2) Blood Culture:3) Chest Roentogram4) S. electrolytes5) CBC, CRP6) Skin scraping for C/S7) Mantoux Test7) Serology: Latex agglutination, counter current immunoelectrophoresis8) CT,MRI- for detection of hydrocephalus, abcess, effusion, exudates, edema
  • 26. Normal PYOGENIC VIRAL MYCOBACT FUNGAL ERIAL GROSS TURBID CLEAR COBWEB CLEAR- CLEAR TURBIDPressure 100-300 80-150 >80 >80Mm H20 50-80
  • 27. PYOGENIC VIRAL MYCOBA FUNGAL CTERIALSUGAR <40(<50% N ( < 40 <50 <50 MG/DL OF RBS) IN>50(75% MUMPSOF RBS )PROTEI 100-500 50-200 100-3000 25-500 NMG/DL 20-45
  • 28. PYOGENIC VIRAL MYCOBA FUNGAL CTERIALTOTAL 100-10,000 100 10-500 5-500 CELL <5PREDO 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 DURATIONUNKNOW EMPERIC 10 DAYS 1)CEFTRIAXONE 100-150N MG/KGDAY 2)CEFOTAXIME 4 LAC 3)AMPI/PENCILLIN U/KG/DAY G + CHRAMPHENi 100 MG/KGDAYMENINGOC Pencillin G 3-4 lac 7DAYSOCCUs U/KG/DAY
  • 32. ORGANISM ANTIBIOTIC DOSE DURATIONPneumococcu Pencillin G or if 40 10DAYSs resistance – MG/KG/D Ceftriaxone plus VancomycinGram neg. Ceftriaxone/cefo 21DAYS taxime plus aminoglycogide
  • 33. ORGANISM ANTIBIOTIC DOSE DURATIONPseudomonas Ceftazidime 150 14-21DAYS MG/KG/DStaphyloco Vancomycin 40 28DAYScci MG/KGD AYH 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 careSeizures• 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 days2.Meningococcus : Rifampicin : 20 mg/kg/day, in 2 divided doses for 2 days Or Ciprofloxacin- single dose 500mg
  • 45. Thank youDownload more documents and slide shows on The Medical Post [ www.themedicalpost.net ]

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