Successfully reported this slideshow.
We use your LinkedIn profile and activity data to personalize ads and to show you more relevant ads. You can change your ad preferences anytime.

Cnsinfection

288 views

Published on

  • Be the first to comment

  • Be the first to like this

Cnsinfection

  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. • Acute inflammation of meninges & brain tissue • CSF – pleocytosis • Gram stain & culture negative • Mostly self limiting
  37. 37. Etiology • Enterovirus • Arbovirus • Herpes virus
  38. 38. Pathogenesis • Direct invasion & destruction by virus • Host reaction to viral antigens • Meningeal congestion • Mononuclear infiltration • Neuronal disruption • Neuronophagia • Demyelination
  39. 39. Structures affected • HSV; temporal lobe • Arbovirus; entire brain • Rabies; basal parts
  40. 40. 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]
  41. 41. DD • Meningitis of various organisms
  42. 42. 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
  43. 43. Treatment • Acyclovir for HSV • Non aspirin analgesic • Nursing in a quiet room

×