Pyogenic meningitis in child

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  • Inf most common,
  • Seizures, fnd, mr, deaf, blind, coma,death, 2= not localising enough, sudden deteriorate, die before you diagnose..
  • Unusual self, incessant cry,
  • Pyogenic meningitis in child

    1. 1. Acute CNS infection
    2. 2. • What is it? • What causes it? • What happens in the system? • How to recognize it? • How to prove it? • How to treat it? • How to prevent?
    3. 3. Significance • Significant morbidity & mortality in children [1.2m cases worldwide] • Diagnosis, challenging in young children • High incidence of sequalae
    4. 4. • Fever with altered sensorium • Virus > bacteria > fungi & parasite • Meningitis • Meningoencephalitis • Brain abscess • Common symptoms photophobia, neckpain/rigidity, fits, stupor • Diagnosis by CSF
    5. 5. Pyogenic meningitis
    6. 6. Etiology • < 2months • Maternal flora, NICU/PNW flora; • GBS, GDS, gram-ve, listeria, HIB, • 2m-12m • Pneumococci, meningococci, HIB[now less] • Pseudomonos, staph.aureus, CONS.
    7. 7. Reasons for infection • Less immunity • Contact with people with invasive disease • Occult bacteremia [infants] • Immunodeficiency • Splenic dysfunction • CSF leak , Meningomyelocele • CSF shunt infection
    8. 8. Risk of infection • Pneumococci OM, sinusitis, pneumonia, CSF rhinorrhea. • Meningococci contact with adults, nasopharyngeal carriage • HIB Contact in daycare center
    9. 9. Pathogenesis • Colonisation of nasopharynx • Prior/concurrent viral URTI • Bacteremia • Hematogenous dissemination • Contiguous spread from sinus, otitis, orbit vertebral trauma, meningocele.
    10. 10. Why few only get meningitis? • Defective opsonic phagocytosis – Developmental defects – Absent preformed anticapsular antibodies – Deficient complement/properdin system – Splenic dysfunction
    11. 11. Pathogenesis • Bacteria enter through choroid plexus of LV • Circulate to extra cerebral CSF & subarachnoid space • Rapidly multiply in CSF • Release of inflammatory mediators • Neutrophilic infiltrates • Increase vascular permeability • Altered BBB • Vascular thrombosis
    12. 12. Pathology • Thick exudate covering all areas • Ventriculitis, arteritis, thrombosis • Vascular occlusion, sinus occlusion. • Cortical necrosis, cerebral infarct • Subarachnoid hemorrhage • Hydrocephalus • ICT, inflammation of spinal nerves
    13. 13. Clinical features • Nonspecific – Fever,anorexia,myalgia,arthralgia,headache, – Purpura , petechiae, rash, photophobia. • Meningeal signs – Neck rigidity, backache. – Kernig sign – Brudzinski sign – Crossed leg sign
    14. 14. ICT signs  Headache, vomiting, drowsy, Fits  Ptosis, squint,  AF bulge, widened sutures  Hypertension, bradycardia  Stupor, coma  Abnormal posturing  Papilloedema [only in chronic ICT]
    15. 15. • Focal neurological deficit • Cranial neuropathy – 3rd nerve – 6th nerve – 7th nerve – 8th nerve
    16. 16. Diagnosis • LP & CSF analysis – Gram stain – Culture – Cell count – Glucose, protein – [Contraindications for LP] • Blood culture
    17. 17. CSF analysis • Cell count – Normal • NB >30/mm3 • Child >5/mm3 – Meningitis >1000/mm3 • Turbid 200-400/mm3 • Early; lymphocytic predominance • Later; neutrophilic predominance • low in severe sepsis
    18. 18. CSF analysis in prior antibiotic therapy • Culture, gramstain altered • Pleocytosis, protein, glucose unaltered
    19. 19. Traumatic LP • Cell count, protein level altered • Glucose, bacteriology unaltered.
    20. 20. Condition Pressure mm-h2o Cell count/mm3 Glucose mg/dl Protein mg/dl microbiology Normal 50-80 <5,lymphocyte >50, 75% of blood level 20-40mg Bacterial meningitis 100-300 100-1000, >75% neutrophils <40mg 100-500 Gram stain+ve Partially treated meningitis N / elevated 5-1000, Lymphocytes? N /decreased 100-500 Gramstain , c/s maybe -ve Antigens +ve Viral meningitis Normal Less cells, lymphocytes N, less in mumps <200 TBM More <500, lymphocytes <40 100-3000 Stain –ve Culture ± ve Fungal More 5-500 N More? Culture
    21. 21. Treatment • Rapidly progressive [ ~24h] LP  antibiotics ICT , FND  CTbrain & antibiotics Manage shock, ARDS • Subacute course [4-7d] • Assess for ICT, FND • Antibiotics  CT  LP
    22. 22. Supportive care • Monitoring – Vitals – BUN,electrolytes,HCO3,IO, CBC,Platelets,Ca – Periodic neurologic assessment • PR,sensorium,power,cranial N ex, head circ, • Supportive care – IVF  restrict for ICT,SIADH, more for shock – ICT ETI & ventilation,frusemide,mannitol – Seizures  diazepam,phenytoin
    23. 23. Antibiotic therapy • Vancomycin & cefataxime/ceftrioxone – Pneumococci,meningococci,HIB. • Ampicillin / cotrimaxazole I.V – Listeria • Ceftazidime & aminoglycoside – Immunocompromised
    24. 24. Duration of therapy  Pneumococci : 7-10 days  Menigococci: 5-7 days  HIB; 7-10 days  E.coli,Pseudomonos ; 3 weeks  Antibiotics started before LP [partially treated meningitis] ; ceftrioxone 7-10 days.
    25. 25. Repeat LP • After 48h • For ; resistant pneumococci, gram-ve meningitis
    26. 26. Corticosteroids • Rapid bacterial killing • Cell lysis • Release of inflammatory mediators • Edema • Neutrophilic infiltration • 1-2h before antibiotics • Dexamathasone q6h for 2 days. • Less fever, less deafness.
    27. 27. Complications • ICT, Herniation • Fits, Cranial N palsy • Dural Vein sinus thrombosis • Subdural effusion • SIADH • Pericarditis, Arthritis • Anemia, DIC
    28. 28. Prognosis • Mortality >10% [more in pneumococci] • Prognosis poor in – Infants – Fits >4days – Coma, FND on presentation • Neurological sequalae 20% – Behavior changes 50% – Deafness [pneumo,HIB], visual loss – MR,fits,
    29. 29. Prevention • Meningococci – Rifampacin for close contacts [10mg/kg/day q12h for 2days] – Quadrivalent vaccine for high risk children • HIB – Rifampacin for contacts for 4days – Conjugate vaccine • Pneumococci – Heptavalent conjugate vaccine
    30. 30. TBM • Subacute / ?chronic meningitis • From lymphohematogenous dissemination • Caseous lesion in cortex / meninges • Discharge of TB bacilli in CSF • Thick exudate infiltrate blood vessels • Inflammation,obstruction,infarct.
    31. 31. • Brainstem affected • Cranial N dysfunction • Hydrocephalus • Infarcts • Cerebral edema • SIADH • Dyselectrolytemia
    32. 32. Features • 6m-4yrs • 3 stages • Prodrome stage; 1-2 wks, nonspecific symptoms, stagnant development • Abrupt stage;lethargy,fits,meningeal signs focal ND,cranial neuropathy,hydrocephalus. Encephalitic picture • Coma stage; posturing,hemi/paraplegia,poor vital signs
    33. 33. Diagnosis • Contact with adult TB • Mx nonreactive 50% • CSF – lymphocytes • Glucose <40mg/dl • Protein high: 400-5000mg/dl • AFB +ve 30%
    34. 34. Thank you
    35. 35. Meningoencephalitis
    36. 36. • Encephalitis • Encephalopathy • Meningitis • Myelitis • Radiculitis
    37. 37. Meningoencephalitis • Acute inflammation of meninges & brain tissue • CSF – pleocytosis • Gram stain & culture negative • Mostly self limiting
    38. 38. Etiology • Enterovirus • Arbovirus • Herpes virus
    39. 39. Pathogenesis • Direct invasion & destruction by virus • Host reaction to viral antigens • Meningeal congestion • Mononuclear infiltration • Neuronal disruption • Neuronophagia • Demyelination
    40. 40. Structures affected • HSV; temporal lobe • Arbovirus; entire brain • Rabies; basal parts
    41. 41. Clinical features • Depends on parenchymal involvement • Preceding mild febrile illness & exantheme • Acute onset of high fever, headache, irritability,lethargy,nausea,myalgia • Convulsions,stupor,coma • Fluctuating FND,emotional outburst • Ant.horn cell injuryflaccid paralysis [west nile,entero virus]
    42. 42. DD • Meningitis of various organisms
    43. 43. Diagnosis • CSF: lymphocytic predominance – Protein: normal,high in HSV – Glucose: normal,low in mumps – Culture of organism [entero V] – Viral antigen by PCR – Culture from NPswab,feces,urine • EEG: focal seizures [temporal];HSV • CT/MRI: swollen brain parenchyma
    44. 44. EEG patterns include focal slowing, spiking, and paroxysmal lateralizing epileptiform discharges.13 Focal-temporal or lateralized polymorphic delta activity is the earliest change. Diffuse slowing soon follows, with a persistence of temporal predominance. Pseudoperiodic complexes, present on serial EEGs in two-thirds of biopsy-proven cases, appear over temporal regions
    45. 45. MRI brain (T2W image): right temporal lobe high signal in a patient with herpes encephalitis
    46. 46. Treatment • Acyclovir for HSV • Non aspirin analgesic • Nursing in a quiet room

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