2. Acute CNS infection

3. • 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?

4. Significance
• Significant morbidity & mortality in
children [1.2m cases worldwide]
• Diagnosis, challenging in young children
• High incidence of sequalae

5. • Fever with altered sensorium
• Virus > bacteria > fungi & parasite
• Meningitis
• Meningoencephalitis
• Brain abscess
• Common symptoms
photophobia, neckpain/rigidity, fits,
stupor
• Diagnosis by CSF

7. Pyogenic meningitis

8. Etiology
• < 2months
• Maternal flora, NICU/PNW flora;
• GBS, GDS, gram-ve, listeria, HIB,
• 2m-12m
• Pneumococci, meningococci, HIB[now less]
• Pseudomonos, staph.aureus, CONS.

9. Reasons for infection
• Less immunity
• Contact with people with invasive disease
• Occult bacteremia [infants]
• Immunodeficiency
• Splenic dysfunction
• CSF leak , Meningomyelocele
• CSF shunt infection

10. Risk of infection
• Pneumococci
OM, sinusitis, pneumonia, CSF rhinorrhea.
• Meningococci
contact with adults, nasopharyngeal carriage
• HIB
Contact in daycare center

11. Pathogenesis
• Colonisation of nasopharynx
• Prior/concurrent viral URTI
• Bacteremia
• Hematogenous dissemination
• Contiguous spread from sinus, otitis, orbit
vertebral trauma, meningocele.

12. Why few only get meningitis?
• Defective opsonic phagocytosis
– Developmental defects
– Absent preformed anticapsular antibodies
– Deficient complement/properdin system
– Splenic dysfunction

13. 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

14. 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

15. Clinical features
• Nonspecific
– Fever,anorexia,myalgia,arthralgia,headache,
– Purpura , petechiae, rash, photophobia.
• Meningeal signs
– Neck rigidity, backache.
– Kernig sign
– Brudzinski sign
– Crossed leg sign

19. ICT signs
 Headache, vomiting, drowsy, Fits
 Ptosis, squint,
 AF bulge, widened sutures
 Hypertension, bradycardia
 Stupor, coma
 Abnormal posturing
 Papilloedema [only in chronic ICT]

20. • Focal neurological deficit
• Cranial neuropathy
– 3rd
nerve
– 6th
nerve
– 7th
nerve
– 8th
nerve

21. Diagnosis
• LP & CSF analysis
– Gram stain
– Culture
– Cell count
– Glucose, protein
– [Contraindications for LP]
• Blood culture

23. 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

28. CSF analysis in prior antibiotic
therapy
• Culture, gramstain altered
• Pleocytosis, protein, glucose unaltered

29. Traumatic LP
• Cell count, protein level altered
• Glucose, bacteriology unaltered.

30. 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

31. Treatment
• Rapidly progressive [ ~24h]
LP  antibiotics
ICT , FND  CTbrain & antibiotics
Manage shock, ARDS
• Subacute course [4-7d]
• Assess for ICT, FND
• Antibiotics  CT  LP

32. 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

33. Antibiotic therapy
• Vancomycin & cefataxime/ceftrioxone
– Pneumococci,meningococci,HIB.
• Ampicillin / cotrimaxazole I.V
– Listeria
• Ceftazidime & aminoglycoside
– Immunocompromised

34. 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.

35. Repeat LP
• After 48h
• For ; resistant pneumococci,
gram-ve meningitis

36. 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.

37. Complications
• ICT, Herniation
• Fits, Cranial N palsy
• Dural Vein sinus thrombosis
• Subdural effusion
• SIADH
• Pericarditis, Arthritis
• Anemia, DIC

38. 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,

39. 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

40. 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.

41. • Brainstem affected
• Cranial N dysfunction
• Hydrocephalus
• Infarcts
• Cerebral edema
• SIADH
• Dyselectrolytemia

42. 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

43. Diagnosis
• Contact with adult TB
• Mx nonreactive 50%
• CSF – lymphocytes
• Glucose <40mg/dl
• Protein high: 400-5000mg/dl
• AFB +ve 30%

44. Thank you

45. Meningoencephalitis

46. • Encephalitis
• Encephalopathy
• Meningitis
• Myelitis
• Radiculitis

47. Meningoencephalitis
• Acute inflammation of meninges & brain
tissue
• CSF – pleocytosis
• Gram stain & culture negative
• Mostly self limiting

48. Etiology
• Enterovirus
• Arbovirus
• Herpes virus

52. Pathogenesis
• Direct invasion & destruction by virus
• Host reaction to viral antigens
• Meningeal congestion
• Mononuclear infiltration
• Neuronal disruption
• Neuronophagia
• Demyelination

53. Structures affected
• HSV; temporal lobe
• Arbovirus; entire brain
• Rabies; basal parts

54. 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]

55. DD
• Meningitis of various organisms

56. 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

57. 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

58. MRI brain (T2W image): right
temporal lobe high signal in a patient
with herpes encephalitis

60. Treatment
• Acyclovir for HSV
• Non aspirin analgesic
• Nursing in a quiet room