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Meningitis
By: Darya Osman Hussein Daoud
Introduction
• Meningitis is an acute inflammation
of the meninges (i.e. the protective
membranes covering the brain and
spinal cord)
• Can be bacterial, viral or fungal
• The causative organism depends on
the age of the individual
• May also be caused by some drugs
Bacterial meningitis – causative organisms
1. Birth – 4 wks:
• Streptococci group B, E. coli, Listeria
2. 4 – 12 wks:
• Streptococci group B, Pneumococcus Salmonella, Listeria, H. influenza type B
3. 3 mths – 3 yrs:
• Pneumococcus, Neisseria meningitidis, H. influenza
4. 3yrs – adult:
• Pneumococcus, Meningococcus
Viral meningitis
• Most common infection of CNS especially in <1yr
• Causative organisms:
• Herpes, influenza, rubella, echo, coxsackie, EBV, adenovirus
• Tretatment is sympromatic
• Complcations associated with envephalitis and ICP
TB Meningitis
• Usually insidious: difficult to diagnose in early stages (fever 30%, URTI 20%)
• Rare in children in developed countries
• If untreated is usally fatal
• Meningitis usually occurs 3-6 mnths after primary infection
• 1st stage: lasts 1-2 weeks, fever malaise, headache
• 2nd stage: +/- suddenly, menigal signs
• 3rd stage: worsening neurological condition, death
Meningitis – Pathogenesis
• Begins with infection of upper respiratory tract by bacteria, viral of fungal
infection
• Infection progresses and invasion of the blood streem occurs
• Microbe enters the subarachnoid space in places where the BBB isvulnerable
(e.g. choroid plexus)
• The presence of invador is detected by immune cells of the brain (astrocytes
and microglia) which react by releasing large amounts of cytokines
stimulating the inflammatory response of the immunesystem
• The BBB becomes more permeable leading to vasogenic cerebral edema
• Large numbers of WBCs enter the CSF causing inflammation and interstitial
edema
• Cerebral vasculitis occurs which leads to decreased blood flow and cytotoxic
edema
• The three forms of edema all lead to increased intracranial pressure leading
to decreased blood entering the brain and hypoxia induced apoptosis
Meningitis – Pathogenesis cont.
Clinical features – Infants
• Non specific in newborns and infants
• Fever
• Irritability
• Lethargy
• Poor feeding
• High pitched cry
• Convulsions
Clinical features – Older children
• Severe headache
• Stiff neck
• Photophobia
• Fever and vomiting
• Drowsy and less responsive/vacant
• Rash
Clinical features - Adults
• Headache, fever and vomiting
• Neck rigidity and photophobia
• Pain in posterior thigh or lumbar
region
• Rash on skin and joint pain
• Lethargy, seizures, confusion, coma,
focal deficits and cranial nerve
palsies(if not treated immediately)
Physical exam – Kernig’s sign
• Patient in supine position with leg
flexed at hip and knee
• Extension of leg while hip still
flexed
• Patient will experience pain and
hamstring muscle spasm if
meningeal irritiation/inflammation
is present
Physical exam – Brudzinski’s neck sign
• Patient is in supine position
• Head is raised towards the chest
slowly
• If hips and knees flex in response
to the passive neck flexion (as
shown) there is menengial
irritiation/inflammation
Physical exam – Glass test
• When a rash is present if it does
not fade when a glass is pressed to
it
• A sign of meningococcal infection
and septicaemia
Diagnostic tests – Lumbar Puncture
• CSF from lumbar puncture is used
to culture cells, glucose level,
protein, cell count and differential
and gram test
Diagnostic tests – LP findings
Bacterial Viral Fungal TB Malignant
Cell number 10 – 100,000 <2000 <2000 250 – 500 ---
Cell type Polys Lymphocytes --- Lymphocytes Lymphocytes
Glucose Low Normal Low Very Low Low
Protein High Normal or high High High High
G-Stain G +ve G –ve G –ve G +ve Zn ---
Management and Treatment
• Medical emergency
• Early diagnosis essential
• Immediate pharmacological
treatement/intervension
• Intensive supportive treatment
• Prophylaxis for family
• Notification to GP and Public health autority
Management/Treatment cont.
• Mechanical ventilation may beneeded if lowlevelof consciousness orevidence
of respiratory failure
• Monitoring intracranial pressure andcerebral perfusion
• Hydrocephalus (obstuctedflow of CSF) may require insertion of temporary
or long-term drainage device(e.g. cerebral shunt)
Pharmacological Intervention – Antibiotics
• Empiric antibiotics should be started immediately even before LP results
• Recommended to administer benzylpenicillin before transfter to hospital
• Treatment starts with a 3rd generation Cefalosporin (eg. Cefotaxime) with
possible addition of Vancomycin
• Can also use Chloramphenicol as monotherapy or in combination with
Ampicillin
Pharmacological
Intervention –
Antibiotic
treatment
• The drug used depends
on susceptibility of
causative organism as
well as the age of the
patient
Organism Age Group Antibiotic
Unknown Infants <1mths Ampicillin, Cefotaxime, Gentamicin
Unknown Children >1mths and Adults Ampicillin, Cefotaxime, Vancomycin
Gram-positive organisms
(unidentified)
Children and Adults Ceftriaxone, Vancomycin, Ampicillin
Gram-negative bacilli
(unidentified)
Children and Adults Cefazidime, Gentamicin
Haemophilus influenza type b Children and Adults Ceftriaxone
Meningococci Children and Adults Penicillin G plus ceftriaxone
Streptococci Children and Adults
Vancomcin, Nafcillin (with or without
rifampin)
Listeria sp Children and Adults
Ampicillin, Gentamicin, Trimethoprim-
sulfamethoxaxzole
Enteric gram-negative
bacteria(Escherichia coli,
Proteus sp, Klebsiella sp)
Children and Adults Ceftriaxone, Gentamicin
Pseudomonas Children and Adults
Ceftazidime, Cefepime (may be used
with the addition of aminoglycoside)
Staphyococci Children and Adults
Vancomycin, Nafcillin (with or without
rifampin)
Pharmacological Intervension – Other drugs
Other medication may be used to
control/relieve symptoms
1. Steroids:
i. Used to control alterations of CSF flow
ii. Dexamethasone – decreased
subarachnoids space inflammation
2. Antiepileptic agents
i. Used to control seizure activity
3. Mannitol
i. Used to decease intracranial pressure
4. Antivirals
i. Used for viral meningitis
5. Antifungals
i. E.g amphotericin B and Flucytosine
ii. Used for fungal meningitis
Pharmacological Intervention- Prophylaxis
• Rifampicin
• Children: 5mg/Kg bd x 2/7
• Adults: 600mg bd x 2/7
• Pregnant contact
• Cefuroxime IM x 1 dose
• Vaccine
• Available against H. influenza, Pneumococcal
conjugate, and meningicoccus,
Paritally treated meningitis
• 50% of cases have prior antibiotic use which can alter findings
• Acture history is vital
• CSF mainly lyphocytic (not usually polys)
• Can have normal glucose
• +ve cultures reduced by 30%
• Gram stain reduced by 20%
Complications
• Septic shock
• Verebral oedema
• Seizure
• Arteritis/venous
thrombosis
• Subdural effusions
• Hyrocephalus
• Abscess
• Brain damange
• deafness
Mortality/Morbidity
• Bacterial: overall mortality 5-10%
• Neonatal meningitis: 15-20%
• Older children: 3-10%
• S. pneumonia: 26-30%
• H.influenza type B: 7-10%
• N. meningitides: 3.5 – 10%
• 30% neurological complications
• 4% profound b/l hearing loss
Mortality/Morbidity cont.
• Viral meningoencephalitis: Enteroviral
fewer complications
• Tuberculous meningitis: related to stage of
disease
• Stage I - 30%
• Stage II - 56%
• Stage III - 94%
Meningitis

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Meningitis

  • 2. Introduction • Meningitis is an acute inflammation of the meninges (i.e. the protective membranes covering the brain and spinal cord) • Can be bacterial, viral or fungal • The causative organism depends on the age of the individual • May also be caused by some drugs
  • 3. Bacterial meningitis – causative organisms 1. Birth – 4 wks: • Streptococci group B, E. coli, Listeria 2. 4 – 12 wks: • Streptococci group B, Pneumococcus Salmonella, Listeria, H. influenza type B 3. 3 mths – 3 yrs: • Pneumococcus, Neisseria meningitidis, H. influenza 4. 3yrs – adult: • Pneumococcus, Meningococcus
  • 4. Viral meningitis • Most common infection of CNS especially in <1yr • Causative organisms: • Herpes, influenza, rubella, echo, coxsackie, EBV, adenovirus • Tretatment is sympromatic • Complcations associated with envephalitis and ICP
  • 5. TB Meningitis • Usually insidious: difficult to diagnose in early stages (fever 30%, URTI 20%) • Rare in children in developed countries • If untreated is usally fatal • Meningitis usually occurs 3-6 mnths after primary infection • 1st stage: lasts 1-2 weeks, fever malaise, headache • 2nd stage: +/- suddenly, menigal signs • 3rd stage: worsening neurological condition, death
  • 6. Meningitis – Pathogenesis • Begins with infection of upper respiratory tract by bacteria, viral of fungal infection • Infection progresses and invasion of the blood streem occurs • Microbe enters the subarachnoid space in places where the BBB isvulnerable (e.g. choroid plexus) • The presence of invador is detected by immune cells of the brain (astrocytes and microglia) which react by releasing large amounts of cytokines stimulating the inflammatory response of the immunesystem
  • 7. • The BBB becomes more permeable leading to vasogenic cerebral edema • Large numbers of WBCs enter the CSF causing inflammation and interstitial edema • Cerebral vasculitis occurs which leads to decreased blood flow and cytotoxic edema • The three forms of edema all lead to increased intracranial pressure leading to decreased blood entering the brain and hypoxia induced apoptosis Meningitis – Pathogenesis cont.
  • 8. Clinical features – Infants • Non specific in newborns and infants • Fever • Irritability • Lethargy • Poor feeding • High pitched cry • Convulsions
  • 9. Clinical features – Older children • Severe headache • Stiff neck • Photophobia • Fever and vomiting • Drowsy and less responsive/vacant • Rash
  • 10. Clinical features - Adults • Headache, fever and vomiting • Neck rigidity and photophobia • Pain in posterior thigh or lumbar region • Rash on skin and joint pain • Lethargy, seizures, confusion, coma, focal deficits and cranial nerve palsies(if not treated immediately)
  • 11. Physical exam – Kernig’s sign • Patient in supine position with leg flexed at hip and knee • Extension of leg while hip still flexed • Patient will experience pain and hamstring muscle spasm if meningeal irritiation/inflammation is present
  • 12. Physical exam – Brudzinski’s neck sign • Patient is in supine position • Head is raised towards the chest slowly • If hips and knees flex in response to the passive neck flexion (as shown) there is menengial irritiation/inflammation
  • 13. Physical exam – Glass test • When a rash is present if it does not fade when a glass is pressed to it • A sign of meningococcal infection and septicaemia
  • 14. Diagnostic tests – Lumbar Puncture • CSF from lumbar puncture is used to culture cells, glucose level, protein, cell count and differential and gram test
  • 15. Diagnostic tests – LP findings Bacterial Viral Fungal TB Malignant Cell number 10 – 100,000 <2000 <2000 250 – 500 --- Cell type Polys Lymphocytes --- Lymphocytes Lymphocytes Glucose Low Normal Low Very Low Low Protein High Normal or high High High High G-Stain G +ve G –ve G –ve G +ve Zn ---
  • 16. Management and Treatment • Medical emergency • Early diagnosis essential • Immediate pharmacological treatement/intervension • Intensive supportive treatment • Prophylaxis for family • Notification to GP and Public health autority
  • 17. Management/Treatment cont. • Mechanical ventilation may beneeded if lowlevelof consciousness orevidence of respiratory failure • Monitoring intracranial pressure andcerebral perfusion • Hydrocephalus (obstuctedflow of CSF) may require insertion of temporary or long-term drainage device(e.g. cerebral shunt)
  • 18. Pharmacological Intervention – Antibiotics • Empiric antibiotics should be started immediately even before LP results • Recommended to administer benzylpenicillin before transfter to hospital • Treatment starts with a 3rd generation Cefalosporin (eg. Cefotaxime) with possible addition of Vancomycin • Can also use Chloramphenicol as monotherapy or in combination with Ampicillin
  • 19. Pharmacological Intervention – Antibiotic treatment • The drug used depends on susceptibility of causative organism as well as the age of the patient Organism Age Group Antibiotic Unknown Infants <1mths Ampicillin, Cefotaxime, Gentamicin Unknown Children >1mths and Adults Ampicillin, Cefotaxime, Vancomycin Gram-positive organisms (unidentified) Children and Adults Ceftriaxone, Vancomycin, Ampicillin Gram-negative bacilli (unidentified) Children and Adults Cefazidime, Gentamicin Haemophilus influenza type b Children and Adults Ceftriaxone Meningococci Children and Adults Penicillin G plus ceftriaxone Streptococci Children and Adults Vancomcin, Nafcillin (with or without rifampin) Listeria sp Children and Adults Ampicillin, Gentamicin, Trimethoprim- sulfamethoxaxzole Enteric gram-negative bacteria(Escherichia coli, Proteus sp, Klebsiella sp) Children and Adults Ceftriaxone, Gentamicin Pseudomonas Children and Adults Ceftazidime, Cefepime (may be used with the addition of aminoglycoside) Staphyococci Children and Adults Vancomycin, Nafcillin (with or without rifampin)
  • 20. Pharmacological Intervension – Other drugs Other medication may be used to control/relieve symptoms 1. Steroids: i. Used to control alterations of CSF flow ii. Dexamethasone – decreased subarachnoids space inflammation 2. Antiepileptic agents i. Used to control seizure activity 3. Mannitol i. Used to decease intracranial pressure 4. Antivirals i. Used for viral meningitis 5. Antifungals i. E.g amphotericin B and Flucytosine ii. Used for fungal meningitis
  • 21. Pharmacological Intervention- Prophylaxis • Rifampicin • Children: 5mg/Kg bd x 2/7 • Adults: 600mg bd x 2/7 • Pregnant contact • Cefuroxime IM x 1 dose • Vaccine • Available against H. influenza, Pneumococcal conjugate, and meningicoccus,
  • 22. Paritally treated meningitis • 50% of cases have prior antibiotic use which can alter findings • Acture history is vital • CSF mainly lyphocytic (not usually polys) • Can have normal glucose • +ve cultures reduced by 30% • Gram stain reduced by 20%
  • 23. Complications • Septic shock • Verebral oedema • Seizure • Arteritis/venous thrombosis • Subdural effusions • Hyrocephalus • Abscess • Brain damange • deafness
  • 24. Mortality/Morbidity • Bacterial: overall mortality 5-10% • Neonatal meningitis: 15-20% • Older children: 3-10% • S. pneumonia: 26-30% • H.influenza type B: 7-10% • N. meningitides: 3.5 – 10% • 30% neurological complications • 4% profound b/l hearing loss
  • 25. Mortality/Morbidity cont. • Viral meningoencephalitis: Enteroviral fewer complications • Tuberculous meningitis: related to stage of disease • Stage I - 30% • Stage II - 56% • Stage III - 94%