Intracranial Infection- Diagnosis And Management.

1. INTRACRANIAL
INFECTION-
DIAGNOSIS AND
MANAGEMENT:
Dr Shaheer Anwar.
Resident Neurosurgery Department.

2. Objectives: • Acute Bacterial Meningitis.
• Viral Meningitis.
• Tuberculous Meningitis
• Post Neurosurgical Procedure Meningitis.
• Post CraniospinalTrauma Meningitis.
• BrainAbscess.
• MedicalVs Surgical Management.
• CNS ComplicationOf AIDS.
• Subdural Empyema.

3. Meningitis: Types:
Acute Bacterial Meningitis.
Viral Meningitis.
Tuberculous Meningitis.
Post Neurosurgical Procedure meningitis.
Post cranio-spinal trauma meningitis(Post traumatic
meningitis).
Recurrent Meningitis.
Chronic Meningitis.

4. Acute
Bacterial
Meningitis:
• Meningitis is the inflammation of the meninges, caused by
bacterial/viral infection, and marked by intense headache
and fever, sensitivity to light, and muscular rigidity.
• Depending on the duration of symptoms, meningitis may
be classified as acute or chronic:
• Acute meningitis evolution of symptoms within hours to
several days,Acute meningitis (<1 d) is almost always a
bacterial infection. Expedient diagnosis is essential-
Medical emergency
• Patients with acute bacterial meningitis may
decompensate very quickly and so they require
emergency care, including antimicrobial therapy, ideally
within 30 minutes of emergency department (ED)
presentation.
• Most bacterial meningitis is not acute. Approximately 75%
of patients with bacterial meningitis present subacutely
with symptoms beginning several days prior.

5. Causes Of
Bacterial
Meningitis:
• Beyond the neonatal period, the 3 most common
organisms that cause acute bacterial meningitis are
Streptococcus pneumoniae, Neisseria meningitidis,
and Haemophilus influenzae type b (Hib).
• Neonates - Group B or D streptococci, nongroup B
streptococci, Escherichia coli, and L monocytogenes
• Infants and children -H influenzae (48%), S
pneumoniae (13%), and N meningitidis
• Adults -S pneumoniae, (30-50%), H influenzae (1-3%),
N meningitidis (10-35%), gram-negative bacilli (1-
10%), staphylococci (5-15%), streptococci (5%), and
Listeria species (5%)

6. Presentatio
n Of
Bacterial
Meningitis:
• The classic presentation of meningitis includes the
triad fever, severe neck stiffness/rigidity, called
meningismus, and change in mental status (eg,
lethargy, confusion, irritability, delirium, and coma) .
• Signs of meningeal irritation are observed in only
approximately 50% of patients with bacterial
meningitis.

7. Diagnosis: • The cornerstone in the diagnosis of meningitis is
examination of the CSF.
• Measure the opening pressure and send the fluid for
cell count (and differential count), chemistry (ie, CSF
glucose and protein), and microbiology (ie, Gram stain
and cultures).The opening pressure of CSF should be
measured in older children. Similarly, the color of the
CSF (e.g, turbid, clear, bloody) should be recorded

8. CSF
Differences
in different
types of
Meningitis:

9. Viral
Meningitis:
• Uncomplicated viral meningitis, usually self-limited,
with complete recovery in 7-10 days.
Causes
• Enteroviruses account for more than 85% of all cases of
viral meningitis.
• Herpes family viruses.
• Lymphocytic chorio-meningitis virus
• Adenovirus
• Measles
• Mumps

10. Management
:
• Mostly supportive-Rest, hydration, antipyretics, and
analgesics or anti-inflammatory medications.The
most important decision is whether to initiate
antimicrobial therapy empirically for bacterial
meningitis while waiting for the cause to be identified.
Patients with signs and symptoms of
meningoencephalitis should receive acyclovir early to
possibly curtail HSV encephalitis.
• Enteroviruses and HSV are both capable of causing
viral septic shock in newborns and infants. In these
young patients, broad-spectrum antibacterial
coverage and acyclovir should be instituted as soon as
the diagnosis is confirmed.

11. Tuberculous
Meningitis:
• Tuberculous meningitis: tuberculosis infection of the meninges.
Causative agent: Mycobacterium tuberculosis is an aerobic gram-
positive rod.
Frequency
• TheWorld HealthOrganization (WHO) estimates that one third
of the world's population is infected by M. tuberculosis.
Clinical Manifestations
• Tuberculous meningitis progresses rapidly with headache, fever,
tremor, and cranial nerve deficts. Focal neurological deficits may
include monoplegia, hemiplegia, aphasia.Vasculitis with
resultant thrombosis and hemorrhagic infarction may develop in
vessels .Visual findings-Papilledema is the most common visual
effect ofTBM.
• The clinical picture in primary spinal meningitis is often
characterized by myelopathy, with radicular pain and
progressive paraplegia.

12. Diagnosis: • Diagnosis ofTB meningitis is made by analysing
cerebrospinal fluid collected by lumbar puncture. A
spider-web clot in the collected CSF is characteristic of
TB meningitis, but is a rare finding.
• Culture for M. tuberculosis takes 2 weeks. More
than half of cases ofTB meningitis cannot be
confirmed microbiologically, and these patients are
treated on the basis of clinical suspicion only before
the diagnosis is confirmed.

13. Tuberculom
as On MRI
Scan:

14. Management
:
• The treatment ofTB meningitis is isoniazid, rifampicin,
pyrazinamide and ethambutol for two months,
followed by isoniazid and rifampicin alone for a further
10 months.
• Treatment must be started as soon as there is a
reasonable suspicion of the diagnosis.Treatment must
not be delayed while waiting for confirmation of the
diagnosis.

15. Post
neurosurgical
procedure
meningitis:
Causative Organisms:
Coagulase negative StaphAureus.
Enterobacteriaceae.
Psuedomonas sp.
Pneumococci usually with basal skull
fractures/otorhinologic surgery.

16. Management
:
Management includes:
Systemic Empiric antibiotics:
• Vancomycin(to cover MRSA).
• Cefepime to cover other organisms.
Intrathecal antibiotic daily if the infection is very severe:
• Vancomycin.
• Amikacin.
• Tobramycin/Gentamicin.
• Colistin.

17. Post
Craniospinal
Trauma
Meningitis:
• Epidemiology:Occurs in 1-20% patients with moderate
to severe head injuries and occurs mostly within 2
weeks of trauma.
• 75% cases have demonstrable basal skull fractures.
• 58% cases have obvious CSF rhinorrhea.

18. Pathogens: • Gram positiveCocci(Strep. Epidermidis, Strep
Pneumonia).
• Gram negative bacilli (E.coli, Klebsiella pneumonia,
Acinetobacter anitratus).

19. Treatment: • Appropriate empirical therapy is started on the basis of
history and location of trauma whether the patient is
havingCSF rhinorrhea or otorhea.
• Surgical vs conservative management, very
controversial. Because some surgeons feel that CSF
rhinorrhea should be explored as all cases of
spontaneous cessation represent with obscuration by
incarcerated brain, called “sham healing” with
potential for later CSF leak or meningitis. Some
surgeons believe that cessation is acceptable.
• Continue antibiotics for 1 week after CSF is sterilized, If
rhinorrhea persists at this time then repair is
recommended.

20. Recurrent
Meningitis:
Patients presented with recurrent meningitis must be
evaluated for abnormal intracranial or intraspinal
communication.
Etiology includes:
• Dermal sinus.
• CSF fistula.
• Neurenteric cyst.

21. Chronic
Meningitis:
Chronic meningitis is usually due to one of the following:
• Tuberculosis.
• Fungal infections.
• Cysticersosis,
• neurocysticercosis.
Differential diagnosis includes:
• Sarcoidosis.
• Meningeal carcinomatosis.

22. Antibiotics
for specific
organisms
in
meningitis:
1. S. pneumoniae: PCN G (2nd choice: chloramphenicol)
a) if MIC≤0.06: PCN G or ampicillin, alternative: third
generation cephalosporin (ceftriaxone)
b) if MIC≥ 0.12: third generation cephalosporin
(ceftriaxone)
c) if cephalosporin resistance: vancomycin.
d) alternative: moxifloxacin
2. N. meningitidis: PCN G (2nd choice: chloramphenicol)
a) If MIC≤0.1: PCN G or ampicillin.
b) if MIC≥ 0.1: third generation cephalosporin
(ceftriaxone).
c) alternative: moxifloxacin, meropenem.
.

23. 3. H. influenza:
• a) beta lactamase negative: ampicillin
• b) beta lactamase positive: third generation cephalosporin
(ceftriaxone)
• alternative: aztreonam, ciprofloxacin
4. Group B strep
• Ampicillin
• b) alternative: vancomycin
5. L.monocytogenes
a) ampicillin ± IV gentamicin) alternative: IV
sulfamethoxazole/trimethoprim
6. S.aureus
• if methicillin susceptible
• oxacillin or nafcillin
• PCN allergy: vancomycin

24. Length of
the
Treatment
for
meningitis:
• Length of the treatment for meningitis is to continue
antibiotics for 10-14 days total.
• Duration is mostly dependent upon the organism and
clinical response.
• Treatment should be 21 days for Listeria, group B strep
and some GN bacilli.

25. Cerebral
Abscess:
Epidemilogy:
• Approximately 1500-2500 cases per year in developed
countries.
• Incidence is higher in developing Countries.
Risk factors:
1. Pulmonary abnormalities like infections andAV
fistulas.
2. Congenital cyanotic diseases
3. Bacterial endocarditis.
4. Penetrating head trauma.
5. Chronic sinusitis.
6. Otitis media.
7. Immunocompromised host.

26. Sources Of
Brain
Abscess:
• Hematogenous Spread.
• Contigous Spread.
• Following penetrating cranial trauma.
• Following neurosurgical procedure.

27. Pathogens: • Cultures from cerebral Abscesses are sterile in about
25% of the cases.
• Organisms recovered depends upon the primary
source of infection.
• In general Streptococcus id the most common
organism.
• Post traumatic mostly due to S.Aureus or
Enterobacteriaceae.
• Odontogenic source may be associated with
Actinomyces.
• Following Neurosurgical procedure, Staph epidermidis
and aureus may be seen.
• In infants,Gram negatives are common because IgM
antibodies dnt cross the placenta.

28. Presentation
:
• In Adults no findings are specific for abscess, and many
are due to edema surrounding the lesion.
• Most symptoms are due to increase in ICP.
• Hemiparesis and Seizure may develop in 30-50% of the
cases.
• Symptoms tend to progress more rapidly than with
neoplasm.
Newborns:
• Seizures.
• Meningitis.
• irritability.
• IncreasingOFC.
• Failure to thrive.

29. Histologic
Stages Of
Cerebral
Abscess:
Stage: Histologic Characteritics Resistance to aspiration
needle:
1 Early cerebritis:(Days 1-3)
early infection &
inflammation, poorly
demarcated from
surrounding brain, toxic
changes in neurons,
perivascular infiltrates.
Intermediate resistance.
2 Late cerebritis:(Days 4-9)
reticular matrix(collagen)&
developing necrotic
center.
No resistance.
3 Early capsule:(10-13)
neovascularity, necrotic
center, reticular network
surrounds.
No resistance.
4 Late Capsule:(>14
days)collagen capsule,
necrotic center, gliosis
around the capsule.
Firm resistance “pop” on
entering.

30. Evaluation: BloodWork:
Complete Blood Examination.
Blood Cultures.
ESR.
CRP.
Lumber Puncture:
The Opening Pressure is usually increased and the WBC
count and proteins may be elevated.There is a risk of
transtentorial herniation, especially with large lesions.

31. Brain
Imaging:
• CT Scan: Ring enhancing Lesions.

32. • MRI:T1WI shows thin walled ring enhancement
surrounding low intensity central region. Fluid-Fluid
levels may be seen.
• MR Spectrosopy: Presence of
amino acids and either acetate or
lactate are diagnostic for abscess .

33. MR
Findings of
Cerebral
Abscess:

34. Treatment
Of Brain
Abscess:
• There is no single best method for treating a brain
abscess,Treatment includes:
• Surgical treatment includes needle drainage or
excision.
• Long term use of antibiotics.

35. Medical
treatment:
Medical treatment alone is more successful if:
• Treatment is begun in cerebritis stage.
• Small lesions (0.8-2.5cm) successfully treated with
medical treatment alone.
• Duration of symptoms < 2 wks.
• Patients show definite improvement within 1st week.

36. Medical
Managemen
t Alone
Considered
if:
• Poor surgical candidate.
• Multiple abscesses, especially if small.
• Abscess in poorly accessible location: brain stem.
• Concominant meningitis/ependymitis.

37. Indications
For surgical
Managemen
t:
Indications for initial surgical treatment include:
1. Significant mass effect exerted by lesion (on CTor MRI)
2. Difficulty in diagnosis (especially in adults)
3. Proximity to ventricle.
4. Evidence of significantly increased intracranial pressure
5. Poor neurologic condition (patients responds only to pain,
or does not even response to pain)
6.Traumatic abscess associated with foreign material.
7. Fungal abscess.
8. Multiloculated abscess.
9. Follow-up CT/MRI scans cannot be obtained every 1–2
weeks
10. Failure of medical management: neurological
deterioration, progression of abscess towards ven-tricles, or
after 2 wks if the abscess is enlarged. Also considered if no
decrease in size by 4 wks.

38. Steroids: Reduces edema and decreases likelihood of fibrous
encapsulation of abscess but may reduce penetration of
antibiotics into abscess and immune suppression may
also be deleterious.
Only reserved for the patients for with clinical and
imaging evidence of of deterioration from marked mass
effect, and duration of therapy should be minimized.

39. Follow up
imaging:
If therapy is successful, imaging should show decrease in:
• Degree of ring enhancement.
• Edema.
• Mass effect.
• Size of lesion (it takes 1-4wks).

40. Surgical
Treatment
Options:
• Needle aspiration.
• Surgical excision.
• External drainage.
• Instillation of antibiotics directly into the abscess.

41. Outcome
with
cerebral
abscess:
Mortality: 0-10%
Neurologic disability 45%
Late focal or generalized
seizures
27%
Hemiparesis 29%

43. Subdural
empyema:
• Subdural empyema is a suppurative infection in the
subdural space, which has no anatomic barrier to
spread over the convexity an into the interhemispheric.
Epidemiology: Less common than cerebral abscess (5:1).
Mainly over the convexity(70-80%), 10-20% are
parafalcine.

44. Biologies Of
SDE:
Location: %
Paranasal Sinuses 67-75
Otits 14
Post surgical 4
Trauma 3
Meningitis 2
Congenital heart diseases 2
Misc(Pulmonary suppuration) 4

45. Presentation
:
• Symptoms are generally due to mass effect,
inflammatory involvement of the brain and meninges.

46. Evaluation: • CT Scan witrh IV Contrast is usually helpful.

47. Thankyou.