Acute Bacterial Meningitis

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Acute Bacterial Meningitis

• Neonates bacteria in the birth canal. Group B
  streptococci (s. agalactiae), Listeria
  monocytogenes, E.coli, other GNR, enterococci.
• Age 1-23 months, Strep pneumoniae and Neiseeria
  meningitidis
• Children 2-5 years used to have high rate of
  Haemophilus influenzae tybe b. Declined after
  HIB vaccine introduced.

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Acute Bacterial Meningitis

• Children 2-18, N. meningitidis
• Adults up to age 60, S. pneumo followed by N.
  meningitidis.
• Adults over 60, S. pneumo, L. monocytogenes.,
  Gram negatives
• Adults over 80, nosocomial G(-)
• Polymicrobial meningitis extremely rare,
  usually an event secondary to a contiguous
  infection in the head and neck or (2 case
  reports) colorectal surgery.

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Pathogenesis

• Colonization of the nasopharynx with potential
  pathogens
• Mucosal invasion, bacteremia, invasion of the CSF
  via choroid plexus
• Host factors Lack of opsonizing antibody (post
  splenectomy), deficiencies of complement
• Activation of inflammatory mediators

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Clinical Presentation

• Very common fever (97), nuchal rigidity (87),
  headache (66)
• Common confusion (56), nausea/vomiting (55),
  decreased LOC (51)
• Less common focal neuro signs (23) rash (10),
  papilledema 2
• Look for other signs of URI infection (otitis
  media)

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Diagnostic Strategies

• CBC elevated WBC, left shift
• CT not needed unless focal neuro findings,
  papilledema, altered mentation
• Blood cultures positive in 50
• CSF glucose lt45, protein gt500, WBC gt1000
• Gram stain () in 80 of those with () CSF
  culture and up to 10 of those with (-) CSF
  culture. Can help guide therapy.
• Early acute bacterial meningitis can mimic
  aseptic meningitis in LP findings. Helpful to
  repeat LP in 8-12 hours to distinguish.

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Complications

• Children overall mortality 4.8 (varies by
  organism), 83 recover with no sequelae.
  Deafness 10, MR 4, spasticity/paresis 3,
  seizures 4.
• Adults overall mortality 18.6, complication
  rate as high as 50. CVA 15, cerebral edema
  14, hydrocephalus 11, septic shock 11, DIC 8,
  ARDS 3

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Cerebral Salt Wasting Syndrome

• Hyponatremia is common in pts with CNS events.
• Mechanism SIADH vs. cerebral salt wasting.
• SIADH is euvolemic or hypervolemic, with a
  persistently low Uosms in the face of low Sosms.
• SIADH can be thought of as the inability to
  excrete free water and therefore the treatment
  is water restriction.

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Cerebral Salt Wasting Syndrome

• Cerebral salt wasting is the result of renal
  wasting of sodium. Main distinction is that
  patients are volume depleted. Respond to saline
  infusion.
• Possible mechanisms ACTH disruption, leading to
  loss of mineralocorticoid effect release of ANP
  and BMP by certain areas of the brain
  ouabain-like compound inhibition of sympathic
  output to kidneys.
• Overlap exists. One small series both plasma ADH
  and ANP levels were elevated for 5 days after
  insult but only ANP levels remained elevated at
  13 and 28 days.

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