It discuss meningitis and the likes

1. Management of Intracranial
Infection
Dr. N.A Adeleke

2. Outline
 Introduction
 Classifications
 Aetiology
 Epidemiology
 Pathophysiology
 Clinical features
 Investigations
 Treatment
 Prognosis
 Conclusion

3. Introduction
 CNS infection is the infection of any
component of the CNS and their
coverings by pathogenic organism
 Importance
◦ Common and difficult to manage
◦ May be the reason for presentation
◦ May complicate neurosurgical procedures

4. Bacterial meningitis
 Bacterial meningitis has been reported in up to
17% of neurosurgical patients
 The majority of cases of bacterial meningitis in
the neurosurgical patient result from direct
inoculation
 Retro-grade propagation from contiguous
structures through emissary veins

5.  Meningitis most commonly occurs in one of the
following clinical settings:
◦ Post-operatively
◦ Penetrating CNS trauma
◦ Following basilar skull fracture associated with CSF leak
◦ CSF shunt devices infection
◦ Spinal bifida- i.e ruptured myelomeningocele and
persistent dermal sinus tracts

6.  Risk factors for postop meninigitis
◦ Non-elective surgery,
◦ Clean-contaminated and dirty wounds,
◦ Operative time greater than four hours and
more recent neurosurgery

7. Pathogenesis of bacterial meningitis after
neurosurgical procedures
 Involves direct inoculation of bacteria at the time of
surgery
 Common organisms are gram-negative enteric bacilli or
staphylococci
 The organisms are often resistant to multiple antibiotics
 It is most common after approaches to the posterior
fossa and is often associated with CSF leak

8. Clinical presentation
 Headache, nuchal rigidity and altered sensorium
are less reliable in meningitis in neurosurgical
patients
 Pre-existing neurological deficits and effects of
surgery may cloud the clinical picture
 Investigations :
◦ CSF culture
◦ CSF analysis

9. Treatment
 Antibiotics- IV for 2-4wk and oral for 4-
6wks
 Surgery –indicated in;
◦ Bone flap infection,
◦ Subdural empyema or
◦ Cerebral abscess

10. Brain Abscess
 Brain abscess is accumulation of pus within brain
parenchyma surrounded by tissue reaction(capsule
formation)
 Accounts 1-2% of all ICSOL in developed world
 Incidence is on the rise with the advent of AIDS
 Current literature suggests a shift in peak incidence toward
the third to fifth decades of life
 Male to female ratio- 2:1

11. Aetiopathogenesis
 Organisms-varies depends on the route
of infection
◦ 1/3 cases are polymicrobial
◦ Bacteroides and anaerobic streptococci are
the most common causative bacteria
◦ S. aureus commonest in the preantibiotic era

12. Route of infection
 Hematogenous route from a remote site give rise
to metastatic abscesses.
◦ They are often multiple and typically occur at the junction of
the white and gray matter
◦ They are more commonly seen in the distribution of the
middle cerebral arteries
◦ The common systemic sites are chronic pulmonary
infections, skin pustules, bacterial endocarditis and
osteomyelitis

13. Route of infection contd.
 Contagious spread – from adjacent
infection site e.g otitis media, sinusitis,
dental abscess, mastoiditis
 Direct inoculation/Dural disruption
– e.g surgery, trauma and congenital
defect

14. Stages of cerebral abscess
 Early cerebritis on days 1–3;There is perivascular
infiltration of inflammatory cells composed of
polymorphonuclear leukocytes, plasma cells and
mononuclear cells that surround a central core of
coagulative necrosis
 Late cerebritis on days 4–9
 Early capsule formation on days 10–13
 Late capsule formation after day 14

16. Clinical Features
 Seizures
 Focal deficits
 Features of raised ICP such as headache and
vomiting
 Low grade fever
 Signs of meningism seen with spread of abscess
to the ventricle or subarachnoid space

17. Investigation
 A brain CT scan reveals a contrast enhancing ring
lesion with non-enhancing hypodense center and
surrounding edema
 MRI scan delineates the lesion better and also reveals
additional microabscesses, if any. Cranial MRI scanning
is superior to cranial CT scanning in detecting a lesion
in the early cerebritis stage
 FBC, ESR , CRP

19. Treatment
 Goals of treatment
◦ Decrease the mass effect associated with the
abscess by draining the pus
◦ Use antimicrobial therapy to treat the abscess
and the primary source of infection

20. Medical therapy
• Indications for non-surgical treatment
 Patients who have a small abscess (less than 3 cm
in diameter)
 Patients who have no signs of raised ICP
 Clinically stable patient with no neurological signs
 Patient with multiple lesions
 Patients having high-risk for surgery and
anaesthesia.

21. Medical therapy
 Antibiotic therapy started early during
the cerebritis stage or in small abscesses
may result in complete cure.
 Antibiotic choice depends on some
factors
 Use of corticosteroid?

22. Surgical therapy
 Indications
◦ To get culture specimen
◦ Significant mass effect exerted by lesion
◦ Cerebellar abscess
◦ Post-traumatic, evidence of foreign body or gas containing abscesses
◦ Proximity to ventricle
◦ Poor neurological condition
◦ Inability to obtain weekly CT scans
◦ In patient undergoing medical treatment
 if neurological deterioration occurs,
 if abscess increase in size,
 if there is no decrease in abscess size by 4 weeks of treatment

23.  Options
◦ Burr hole drainage
◦ Craniotomy plus excision

24. Poor prognostic factors in cerebral
abscess
• Hematogenous spread of infection
• Underlying systemic illness, including
immunodeficiency, and comorbid conditions (eg,
malignancy, diabetes mellitus)
• Multifocal abscess
• Ventricular rupture
• Depressed mental status at time of presentation

25. Complications of Cerebral abscess
 Epilepsy
 Neurological deficit
 Hydrocephalus
 Ventriculitis

26. Subdural Empyema
 This is presence of pus in the subdural
space
 Epidemiology
◦ Common between 6-20yr
◦ M:F – 3:2
◦ Common in the developing countries

27. Locations
 Supratentorial vs Infratentorial
 Convexity vs Parafalcine

28. Pathogenesis
 Rhinogenic infection: results from paranasal
sinusitis.Accounts for 59-67% of cases
 Meningitis- accounts for 10% of SDE
 Otogenic infection: usually from mastoiditis
accounting for 9% of suprtentorial SDE and 80%
of infratentorial SDE
 Penetrating trauma

29. Clinical features
 Fever
 Neck stiffness
 Seizure
 Focal neurologic deficit

30. Investigations
 Cranial CT
 MRI

31. Treatment
 Principle of treatment
◦ Early removal of infection source
◦ Drainage of subdural pus
 Craniotomy vs Burr hole drainage
◦ Appropriate antibiotic use

32. Prognosis
 Supratentorial has a mortality of 8-12%
which is correlated with level of
consciousness at presentation
 Infratentorial SDE has mortality rate of
33-57% with no correlation with GCS at
presentation

33. Neurocysticercosis (NCC)
 Neurocysticercosis is the most common
parasitic infection of the brain worldwide
 Neurocysticercosis is caused by the encysted
larval stage of the tapeworm Taenia solium
 They can present either in the parenchymal
form or extraparenchymal or mixed form

34. Location of the cysts tends to fall into 1
of 4 groups
 :
 Meningeal: found in 27–56% of cases with neural involvement.
Cysts are adherent or free-floating and are located either in:
◦ Dorsolateral subarachnoid space : usually C. cellulosae type causing minimal
symptoms
◦ Basal subarachnoid space: usually the expanding C.racemosus form producing
arachnoiditis and fibrosis comprising a chronic meningitis with hypoglycorrhachia.
Extremely high mortality with this form
 Parenchymal: found in 30–63%; focal or generalized seizures occurs
in ≈ 50% of cases (up to 92% in some series)

35.  Ventricular: found in 12–18%, possibly gaining
access via the choroid plexus. Pedunculated or
free floating cysts occur, can block CSF flow and
cause hydrocephalus with intermittent intracranial
hypertension (Brun syndrome).There may be
adjacent ependymal enhancement (ependymitis)
 Mixed lesions: found in ≈ 23%

36. Clinical Presentation
 Seizures
 Signs of elevated ICP (Increased ICP may be due to hydrocephalus or
to giant cysts).
 Focal deficits related to the location of the cyst
 Altered mental status are the most common findings
 Symptoms may also be produced by the immunologic reaction to the
infestation (cysticercotic encephalitis)
 Cranial nerve palsies can occur with basal arachnoiditis
 Subcutaneous nodules may sometimes be felt

37. Diagnosis
 Diagnosis is usually made by imaging studies and confirmatory serologic
tests.
 Serology
◦ Enzyme linked immunoelectrotransfer blot ELITB
 100% specific and 98% sensitive
 May be used on serum or CSF
 Less sensitive with solitary cyst
◦ ELISA where titer is considered
 significant at 1:64 in serum, and 1:8 in the CSF
 Serum test more sensitive
 CSF titer more specific
 False negative rates are higher in cases without meningitis.

38. Radiographic evaluation
 X-Ray
◦ Soft-tissue X-rays may show calcifications in
subcutaneous nodules, and in thigh and shoulder
muscles.
◦ Skull X-rays show calcifications in 13–15% of cases
with neurocysticercosis. May be single or multiple.
Usually circular or oval in shape.

39.  CT
◦ The following findings on brain CT have been described
◦ Ring-enhancing cysts of various sizes representing living cysticerci.
Little inflammatory response (edema) occurs as long as larva is
alive.
 Characteristic finding:
 Larva stage- small (< 2.5 cm) low density cysts with eccentric punctate high
density that may represent the scolex
 Intermediate stage - low density with ring enhancement with periliesional
oededma. Often
 Dead parasites- ring-enhancing intraparenchymal punctate calcifications
(granuloma) sometimes with, but usually without surrounding enhancement
◦ Hydrocephalus sometimes with intraventricular type.

40.  MRI
◦ Early findings: nonenhancing cystic structure(s)
with eccentricT1WI hyperintensity (scolex)
with no inflammatory response
◦ Lesions may be seen in parenchyma, ventricle,
and subarachnoid space

41. Treatment Overview
 Combination of:
◦ Antihelmintic medication: antiparasitic and/or cysticidal regimens
◦ Antiepileptics: to treat seizures, which may sometimes be medically refractory
◦ Steroids
 Surgery:
◦ Surgical resection of lesions when appropriate
◦ Ventricular CSF diversionary procedures
◦ Surgery may sometimes be necessary to establish the diagnosis. Stereotactic
biopsy may be well suited for some cases, especially with deep lesions

42. Other intracranial infections
 Tuberculous meningitis/ tuberculoma
 hydatid disease
 Cerebral schistosomiasis
 intracranial fungal infections