Meningitis

Serious infection of the meninges, the outer membranes covering the brain and spinal cord

Aetiology

Bacterial meningitis

Age-specific common causes
  • ­Neonates: Listeria monocytogenes, group B Streptococci, E. coli
  • ­Infants and young children: H. influenza
  • ­Ages 10 to 21: Neisseria meningitidis, Streptococcus
    pneumoniae
  • ­Age over 21: Streptococcus pneumoniae, Neisseria
    meningitidis
  • ­Over 65 : Streptococcus pneumoniae, Listeria monocytogenes
Causes associated with specific patient factors
  • ­Decreased cell-mediated immunity: Listeria monocytogenes
  • Neurosurgery/ head trauma: Staphylococcus, Gram negative
    bacilli (Klebsiella pneumoniae, E.coli, Pseudomonas aeruginosa)
  • Fracture of the cribiform plate: Streptococcus pneumoniae

Viral meningitis

  • Most common cause of meningitis
  • Common causative organanisms include: enteroviruses (echovirus, Coxsackievirus), mumps, HSV and herpes zoster virus, HIV, measles, influenza, arboviruses
    • Enteroviruses are the most common cause of meningitis in immunocompetent adults in the UK

Aseptic meningitis

  • CSF has cells but is Gram-stain negative and no bacteria can be cultured on standard media
  • Viral meningitis will be aseptic
  • Other (rarer) causes include fugal infection, parasites, atypical TB, syphilis, Lyme disease, Kawaskaki disease

Pathophysiology

Aquisition of infection

  • Microorganisms reach the meninges either by direct extension from the ears, nasopharynx, cranial injury or congenital meningeal defect, or by bloodstream spread

Acute bacterial meningitis

  • The pia-arachnoid is congested with polymorphs
  • A layer of pus forms
  • This may organize to form adhesions, causing cranial nerve palsies and hydrocephalus
  • Cerebral oedema occurs in any bacterial meningitis

Chronic infection (e.g. TB)

  • The brain is covered in a viscous grey–green exudate with numerous meningeal tubercles
  • Adhesions are invariable
  • Cerebral oedema occurs in any bacterial meningitis

Viral meningitis

  • In viral meningitis there is a predominantly lymphocytic inflammatory cerebrospinal fluid (CSF) reaction without pus formation, polymorphs or adhesions
  • There is little or no cerebral oedema unless encephalitis develops

Clinical presentation

  • Triad of headache, neck stifness, and fever
  • Photophobia and vomiting are often present
  • Acute bacterial meningitis
    • Onset is typically sudden, with rigors and high fever
    • Meningococcal septicaemia is associated with a non-blanching rash
  • Meningoencephalitis
    • Headache, fever and neck stiffness PLUS features of encephalitis

Investigations

Lumbar puncture

  • Ideally LP should be performed within an hour of arrival at hospital and treatment commenced immediately afterwards
  • Samples of CSF are usually sent for white blood cell count and differential, Gram stain, glucose, protein, lactate, culture, and meningococcal and pneumococcal polymerase chain reaction (PCR)
  • Further tests on saved CSF can be performed if no aetiology is found at first, such as virology
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Management

Viral meningitis

  • Treatment is generally supportive - self-limiting condition lasting 4–10 days

Bacterial meningitis

  • When meningococcal meningitis is diagnosed clinically by the petechial rash, immediate intravenous antibiotics should be given and blood cultures taken (lumbar puncture is unnecessary)
Adults
  • Ceftriaxone IV 2g bd + Dexamethasone IV 10mg qds (started with or just before first dose of antibiotics for 4 days)
    • Do not give steroids in post-surgical meningitis, severe immunocompromise, meningococcal or septic shock or those hypersensitive to steroids
  • Add Aciclovir IV (10mg/kg tds) if encephalitis suspected
  • Add Amoxicillin IV 2g 4 hourly if ≥ 60 years or immunocompromised
Children
  • <3 months Cefotaxime + Amoxicillin
  • > 3 months 1st dose Cefotaxime followed 6 hours later with once daily Ceftriaxone
  • +/- Dexamethasone IV starting before or with first dose of antibiotic
  • Chloramphenicol if penicillin allergic

Complications

  • Purulence
    • ­Clusters at the base of the brain
    • ­Convexities of rolandic and sylvian sulci
    • ­Exudate around nerves (III, VI cranial nerves particularly vulnerable)
  • Invasion
    • ­Pia prevents meningitis becoming abscess
    • ­Abscesses can cause secondary ventriculitis and hence meningitis
  • Cerebral oedema (temporal lobe vs cerebellar)
  • Ventriculitis / hydrocephalus (communicating vs non-communicating)