3. Acute Bacterial Meningitis
3
Definition-Inflammation of the leptominges
surrounding the brain and spinal cord: pia,
arachnoid and subarachnoid matter
Occurs at all ages but is commonest during
infancy (greatest risk 6-12 months)
7. EPIDEMIOLOGY
7
Predisposing Factors
Major risk –Lack of immunity to specific pathogens
associated with young age
Additional risk factors
Recent colonization with pathogenic bacteria
Close contact with patients having invasive
disease caused by N. meningitidis and H.
influenzae type b,
Crowding
Poverty
Male sex
Person to person contact through respiratory
8. 8
Congenital or acquired CSF leak
Cranial or midline facial defects (cribriform plate)
Middle ear or inner ear fistulas
Basal skull fracture into the cribriform plate or
paranasal sinus- increased risk of pneumococcal
meningitis.
Lumbosacral dermal sinus and meningomyelocele:
staphylococcal and gram-negative enteric meningitis.
VP shunts-increase the risk staphylococcal meningitis
(especially CONS) and other low virulence bacteria
that typically colonize the skin.
9. Streptococcus pneumonia
9
Commonly occurs during the first 2yrs of life
Peak 6-12 months
Highest in children with
HIV- infection
Anatomic or functional asplenia
Other risk factors include
Otitis media
Sinusitis
Pneumonia
CSF otorrhea or rhinorrhea
10. Neisseria Meningitides
10
Occurs
Sporadically or as epidemics
Serogroups A,B,C,Y, W-135,X are responsible
Common in the winter and spring
Nasopharyngeal carriage occurs in adults
Contact infection
Epidemics is defined as the occurrence of 3 cases in
3 months time with attack rate of 10 cases per
100,000 population in the same community
Epidemics is usually caused by serogrup A
12. Haemophilus influenza type B
12
Primarily occurs in infants 2month to 2 yrs
50% of cases occur in the 1st year of life
Peak at 6-9 months of age
Risk increased
among family or day care center contacts of patients
with HIB disease.
unvaccinated and
those with blunted immunologic responses to vaccine
( HIV- Infection)
13. Pathogenesis
Routes of infection
13
Hematogenous dissemination of micro-organisms
from a distant site of infection-Most common
route.
Direct invasion of the CNS from
contiguous focus of infection: otitis media, mastoditis,
sinusitis,osteomyelitis (cranial,vertebral)
through anatomic abnormalities
head trauma
neurosurgical procedures
14. Pathogenesis…..
14
Bacteria gain entry to the CSF
Multiply rapidly and incite local inflammatory response,
with poly morphonuclear cell infiltration.
Marked inflammatory response with local production of
TNF, IL-1, and other cytokines
Inflammatory response in characterized by
Neutrophilic infiltration
Altered BBB
Increased vascular permeability
Vascular thrombosis and vasculitis
Inflammation of spinal nerves and roots produces
meningeal signs
Inflammation of the cranial nerves produces cranial
neuropathies
15. Nasopharyngeal colonization
Local invasion
Bacteremia
Meningeal invasion
Bacterial replication in the subarachnoid space
Release of bacterial components (cell wall, LOS)
Cerebral microvascular endothelium Macrophages, neutrophils, other CNS Cells
Cytokines
Subarachnoid space inflammation
Cerebral
vasculitis
Increased CSF outflow resistance
Hydrocephalus
Interstitial edema
Increased intracranial pressure
Decreased cerebral blood flow and loss of cerebrovascular autoregulation
Cytotoxic edema
Cerebral
infarction
Increased BBB
permeability
Vasogenic edema
15
17. Clinical manifestations…..
17
Older children
Classic signs are preceded upper respiratory or GIT
symptoms
Fever
Headache
Projectile Vomiting
Poor feeding
Seizures are common-20-30% of patients before or
during the first 3 days after diagnosis
19. 19
Alterations of mental status
Irritability, lethargy to coma may be due to:
Increased ICP
Cerebritis
Hypotension
Factors that lead to Death or Brain Damage in
Meningitis
SIADH secretion With resultant Hyponatremia
Brain edema → Acute Brainstem Compression
Subdural Effusion/Empyema/Brain Abscess
Seizures
21. Diagnosis
21
Lumbar Puncture- CSF analysis
Leukocyte count (>1000/mm3) with neutrophilic
predominance (75–95%).
Turbid CSF when WBC count is >200–400/mm3.
<250/mm3in as many as 20% of patients
pleocytosis may be absent in severe overwhelming
sepsis and meningitis and is a poor prognostic sign
lymphocyte predominance may be present during
the early stage
Elevated protein
Hypoglycorrhachia
Gram stain-positive in 70–90% of untreated
patients
Culture
22. 22
Condition
s
Pressure
(mmH2O)
Leukocyte
(mm3)
Protein
(mg/dl)
Glucose
(mg/dl)
Normal 50-80 <5, ≥75%
Lymphocytes
20-45 >50 (or 75%
Serum
Glucose)
Acute
Bacterial
Usually
elevated
(100 -300)
>100-10,000 ;
usually 300-2,000;
PMNs
Usually
100-500
usually <40
(or <50%
serum
glucose)
Partially
Rxed Bact.
Normal or
elevated
5-10,000; PMNs
early/Mon dominate
most of the course
Usually
100-500
Normal or
decreased
Viral Normal/slightl
y (80-150)
Rarely >1,000, Mon
predominate
Usually 50-
200
Generally
normal; but
mumps
Tuberculou
s
Usually
elevated
10–500;lymp
predominate
through most of the
100-3,000;
may be
higher
<50 in most
cases
23. Diagnosis……
23
CBC- Leukocytosis, with polymorph
predominance
Blood culture- reveals organisms in ~80-
90% of cases
o CXR if pneumonia or TB is suspected
24. Contra-indications for Lumbar Puncture
24
Elevated ICP and focal Neurologic deficit
Severe cardio respiratory compromise –
postpone LP
Infection of the overlying skin
Thrombocytopenia ( relative)
26. Management
26
I. Supportive Measures
Vital Signs _ 15-30 min.
Frequent Neurologic assessment -Follow patient with
neurosign chart
Level of consciousness(GCS)
Pupillary size and reactivity
Pattern of breathing
Posture
Occulocephalic reflex
Seizure
Cranial nerve palsies or focal Neurologic deficits
Daily HC measurement –for children<18 months
27. Management…..
27
Strict input/output recording
Serum electrolytes
Body weight
Antipyretics ,Cold sponging
Fluid restriction to 2/3rd maintenance for fear of
syndrome of inappropriate ADH secretion
- fluid restriction should be avoided in the presence of
hypotension
Coma care- bowel, bladder, skin, air way
Seizure control
Active SZ –arrest with diazepam 0.1 -0.3 mg/kg/IV
or PR
Prevention of recurrence of seizure
o Phenytoin- 20mg/kg loading then 5mg/kg/
24 hrs – bid
Phenobarbitone can be added for refractory
SZ
29. Antibiotic therapy
29
Empirical treatment
Cyst.pencillin plus
Chloramphenicol or
Ceftriaxone 100mg/kg/24hrs Bid
Vancomycin – penicillin/ceftriaxone resistant
S.pneumoniae
According to culture and sensitivity result
30. Antibiotics
30
Duration of therapy
5-7 days for meningococcal meningitis
7-10 days for H. influenzae meningitis
10-14 days for pneumococcal meningitis
Gram-negative meningitis should be treated for
3 wk or for at least 2 wk after CSF sterilization
31. Corticosteroids
31
Corticosteroid:
decrease ICP by decreasing meningeal
inflammation and brain water content
modulate the production Of cytokines,
lessens the meningeal inflammatory
response
decrease incidence of sensorineural
hearing loss or other neurologic
complications
Dexamthasone
• 0.15 mg/kg/dose Qid for 2 days before the
1st dose of antibiotic for those older than
32. Complications
32
Increased Intracranial pressure(ICP)-
Common acute complication
Increase ICP is due to:-
Cytotoxic cerebral edema- due to cell swellingcell death
Vasogenic cerebral edema- due to cytokine induced increased
capillary vascular permeability
Interstitial cerebral edema- increased hydrostatic pressure
after impaired reabsorption or obstruction of CSF flow
(Hydrocephalus)
33. 33
Management of Increased ICP
Elevating head by 300
20%Manitol 0.5-1g/kg/dose over 30min, Q6hrs or
Frusemide 1mg/kg or hypertonic saline(3% Saline)
Dexamethasone 0.25 -0.5mg/kg QID
Endotracheal intubation and hyperventilation (Pco2 25-
30mmHG)
Treat fever aggressively
34. 34
Hydrocephalus
Communicating
Ocurrs most commonly
due to adhesive thickening of arachnoid villi around
the cisterns - impaired CSF reabsorption
Obstructive
Less often
due to fibrosis and gliosis of the aqueduct of sylvius
36. 36
Subdural effusion/empyema
10-30% & 1% of cases respective
Highest in infants ,and H.influenzae
meningitis(45% of cases)
85-90% are asymptomatic
C/Fs
o bulging fontanel
o diastasis of sutures
o enlarging HC
o Persistence /recurrence of emesis
o Persistent/focal seizures
o persistence of fever
Symptomatic - subdural tap
37. Complications…..
37
Cranial nerve palsies
Inflammation of cranial nerves results cranial
neuropathies of Optic ,Oculomotor, Facial ,Auditory
Nerves
Increased ICP Produces oculomotor and abducens nerve
palsies
Seizure
focal or generalized
20–30% of patients
occurs due to cerebritis, infarction, or
electrolyte disturbances
_ on presentation or within the 1st 4 days of
onset is usually of no prognostic
significance
40. Prognosis
Poor prognostic factors
40
Infants <6 months
Delayed/Late presentation
>106 CFU/ml of CSF
Seizure that persist after 4 days of illness and
difficult to treat/control
Coma or focal Neurologic signs at presentation.
pneumococcal meningitis
Delayed sterilization of CSF
42. Prevention…
42
H. Influenza
Rifampin 20mg/kg/daily for 4 day for all close
contacts
if any close family member younger than 48 mo has
not been fully immunized or if an
immunocompromised person, of any age, resides in
the household
HIB vaccine - Prevents development of HIB
Infection – If given for all < 2yrs
Pneumococcal
Conjugate vaccine against S.pneumoniae (
PCV10) for all younger than 2 yrs.
43. References
43
Nelson Text book of pediatrics, 19th ed
Mandell, Bennett, & Dolin: Principles and
Practice of Infectious Diseases, 6th ed
Feigin and Cherry’s Text book of pediatrics
infectous disease
UpTodate 21.2
Most infections of children are acquired from a contact in a daycare facility, a colonized adult family member, or an ill patient with meningococcal disease.
Designed by Lapeysonnie
BBB (arachnoid membrane, choroid plexus epithelium, and cerebral microvascular endothelium)
A household contact is one who lives in the residence of the index case or who has spent a minimum of 4 hr with the index case for at least 5 of the 7 days preceding the patient's hospitalization
