The document provides an overview of brain abscesses, covering their incidence, etiology, pathogenesis, clinical presentation, diagnosis, and management strategies. It highlights the typical pathogens involved, outlines stages of development, and discusses treatment options including antimicrobial agents and surgical interventions. Moreover, it presents information on related complications such as subdural and epidural empyema, emphasizing the importance of proper diagnosis and tailored management for successful outcomes.

1. BENJAMIN KIZITO BIRUNGI
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Brain Abscess

2. BRAIN ABSCESS
By the end of this session you will be able to:
• Describe the stages of development and pathogenesis of brain
abscesses
• Identify the typical spectrum of pathogens implicated in the
aetiology of brain abscess
• Define the nonspecific nature of the clinical features of brain
abscess
• List the appropriate investigation of possible brain abscess and
to identify the important radiological features on CT and MR
scanning
• Develop a management plan for patients with brain abscess,
including antimicrobial treatment, surgical interventions and
adjunctive therapies
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3. • INCIDENCE:
• ETIOLOGY
• MICROBIOLOGY
• PATHOGENESIS
• CLINICAL PRESENTATION
• DIAGNOSIS
• MANAGEMENT
• OUTCOME
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Brain Abscess

4. INCIDENCE
• Is 1-2% of SOL in brain (USA)
• Is 8% (INDIA)
• Decreased incidence (because of antibiotic
and improved life)
• Lastly increased incidence because of
opportunistic infection in immune
compromised patient .
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Brain Abscess

5. ETIOLOGY
To establish intracranial infection, bacteria reach the brain via three main routes:
1. Extension from a contiguous focus of infection, typically the middle ear or
paranasal sinuses
2. Haematogenous (metastatic) spread from a distant extracranial source
3. Direct inoculation following neurosurgery or penetrating trauma
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Brain Abscess
Otogenic and paranasal sinus

7. Hematogenous spread
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Typically, multiple or multi-loculated abscesses are seen, occurring predominantly
within the territory of the middle cerebral artery, often at the grey white matter
interface where blood flow is most marginal

8. Hematogenous: other sources
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9. Penetrating trauma
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10. • Whilst in immunocompetent individuals brain
abscess are usually caused by pyogenic bacteria,
in the immunosuppressed, a much broader array
of organisms is implicated.
• These include:
– Toxoplasma gondi (shown below)
– Aspergillus species
– Candida species
– Nocardia
– Mycobacterium tuberculosis
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Brain Abscess
Brain Abscesses in Immunosuppressed
Patients

11. PATHOGENESIS AND HISTOPATHOLOGY OF
BRAIN ABSCESS
• Brain abscesses occur at focal points of bacterial
multiplication within the brain parenchyma; they begin as a
localised area of cerebritis and later progress into a
collection of pus surrounded by a vascularised capsule.
• By virtue of the impermeability of the blood-brain barrier,
the brain parenchyma is relatively resistant to the
establishment of focal bacterial infection.
• An area of necrosis caused by for example micro-infarction
or hypoxaemia is necessary to act as a nidus for bacterial
multiplication.
• Several stages of development en route to the formation of
a mature encapsulated brain abscess following bacterial
ingress have been defined by neuroimaging studies
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12. 1. Early Cerebritis
Days 1-3: Perivascular inflammation, characterised by neutrophil infiltration,
occurs around the site of focal infection with a surrounding area of
oedema.
2. Late Cerebritis
Days 4-9: A central area of necrosis develops as the surrounding oedema
progresses. Peripheral accumulation of fibroblasts preludes the
development of a capsule.
3. Early Capsule
Days 10-14: Establishment of a ring-enhancing capsule of well-
vascularised tissue with further fibroblast migration and adjacent reactive
astrocytosis.
4. Late Capsule
Day 14 and beyond: Collagen fibre and granulation tissue deposition leads
to a thickening of the capsule effectively walling off the area of focal
suppurative infection.
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Stages of Development and Pathogenesis of
Brain Abscesses

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14. Occur in majorities in the first 2 decades of life
• Males more affected ( cause is unknown )
• adults depend on immune status
• Infants : increase in head circumference , bulging fontanel ,
separation of cranial sutures , vomiting , irritability , seizures
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Clinical presentation :

15. • Symptoms :
1. Head ache ( 90 %)
2. Change in conscious level ( 60 %)
3. FND ( 60 %)
 Parietal lobe : hemiparesis
 Temporal lobe : dysphasia
 Cerebellar : ataxia and nystagmus
4.Fever (more than 50 %)
5. Nausea and vomiting ( 50 %)
6. Seizure ( 50 %)
7.Papilledema and meningismus
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16. Laboratory findings
1. WBC : normal or mild increase
2. ESR : increase in 90%
3. CSF : not specific
1. Opening pressure
2. Protein
3. Glucose
4. Culture
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17. 4. radiological characteristic of brain abscess
1. Brain CTS with contrast
• ring enhancement
• Multi loculation
• Multiplicity
• Finding of gas
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18. • MRI :
• T1 :
• necrotic center ( hypointense)
• Capsule ( hyperintence)
• Edema ( hypointence)
• T2 :
• necrotic center ( hyperintence)
• Capsule ( hypointence)
• Edema ( hyperintence
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24. management
The main treatment strategies are:
• Antimicrobial agents
• Needle aspiration - often using stereotactic guidance
• Complete surgical excision
In addition, adjunctive therapies such as corticosteroids and anticonvulsant agents are variably used.
A combination of antimicrobial therapy and aspiration is now used for the majority of cases, with
medical therapy alone and complete surgical excision reserved for particular circumstances
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25. Management
1. Antibiotic therapy :
• Antibiotic is mandatory and should given
• Antibiotics depends on C/S
• Imperial treatment depend on the etiology
– Sinusitis : ( penicillin + metronidazole )
– Otitis : ( penicillin + metronidazole + 3rd generation cephalosporin)
– Metastatic abscess :(metronidazole + 3rd generation cephalosporin)
– Post traumatic abscess ( vancomycin)
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26. It may also be considered for…
• Multiple small abscesses
• Abscesses located in surgically unaccessible or eloquent areas
It is most likely to be successful if…
• Abscesses are small (i.e. <1.5cm)
• In cerebritis stage
• Located in a well vascularised cortical area
Frequent interval scans should be performed to assess therapeutic response and to
identify complications requiring definitive surgical management.
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antibiotic therapy

27. Corticosteroids
– Adjuvant corticosteroids are often used to reduce vasogenic oedema
associated with brain abscesses.
There are important concerns regarding steroid use…
• Effectiveness in reducing oedema and mass effect not established in human
clinical trials
• May retard abscess capsule development
• May reduce antimicrobial penetration
• Give false impression of a therapeutic response by reducing ring-
enhancement on follow-up scans
Most authors recommend that corticosteroids are reserved for situations of
raised intracranial pressure resulting in a clear risk of brainstem herniation or
other significant neurological deficit.
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28. Anticonvulsants
– Seizures are a frequent complication of brain abscess both in the acute setting
and for a prolonged period after the resolution of the acute infection.
– Some advocate the use of seizure prophylaxis for extended periods in every
case of brain abscess
– If commenced, anticonvulsants should probably be continued for 6-12 months
and then only withdrawn if the patient is seizure-free, the EEG normal and no
signs of on going inflammation on neuroimaging.
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29. Aspiration
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30. Excision of brain abscess
• Advantages
1. Traumatic abscess ( contain foreign body and bone fragment )
2. Fungal abscess
3. Gas containing abscess
• Disadvantages
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31. Follow up
• CT weekly during antibiotic therapy
• And then monthly CT
• 2-3 week decrease size of abscess
• 3-4 months complete resolution of abscess
• 6-9 months no residual contrast
enhancement
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32. Outcome of abscess :
Mortality influenced by ( herniation , rupture of
abscess to the ventricle , clinical course of the
patient, type of abscess, neurological state of
patient at time of diagnosis)
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33. 1. Long term morbidity : ( seizure , FND,
Cognitive dysfunction)
2. Recurrence: ( 5-10%) causes ( inadequate
antibiotic therapy, incorrect choice of AB,
presence of foreign body , failure to eradicate
source of the abscess)
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34. SUBDURAL AND EPIDURAL
EMPYEMA
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35. Subdural empyema
• This is an intracranial focal collection of pus
between the dura mater and the arachnoid
• Subdural empyema is usually unilateral
• There is tendecy to spread rapidly in the sub
dural space until limited by specific
boundaries( falx cerebr, tentorium cerebelli,
foramen magnum
• Causative bacteria same as those in prev slides
of brain abscess
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36. Pathophysiology
• Subdural empyema has a tendecy to behave like an
expanding mass
• This causes increased intracranial pressure and
cerebral intraparenchymal penetration
• Cerebral edema and hydrocephalus maybe develop
secondary to disruption in blood flow or CSF flow
• Cerebral infarction may develop due to thrombosis of
the the cortical veins or the carvenous sinus or from
septic venous thrombosis
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37. Pathophysisology
• In children, its often a complication of
meningitis. Therefore its important to
differentiate it from reactive subdural effusion.
• In older children and adults, it occurs as a
complication of paranasal sinusitis, otitis media
or mastoiditis
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38. Clinical presentation
• From history
– Fever above 38
– Headache: initially focal and later generalised
– Recent hx of sinusitis, otitis media, mastoiditis, meningitis,
cranial surgery, trauma, pulmonary infection,
– Confusion, drowsiness, stupor or coma
– Hemiparesis or hemiplegia
– Seizures: focal or generalized
– Nausea and vomiting
– Blurred vision: ambylopia
– Speech difficulty (dysphasia)
– Hx of intracranial abscess
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39. Physical examination
• Altered mental state
• Signs of meningeal irritation
• Focal neurologic deficits
• Aphasia or dysarthria
• Seizure
• Features of sinusitis
• Features of increased ICP
• Palsies of CN 3, 5, 6
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40. Investigations
• Labaratory studies
– CBC : leukocytosis
– Elevated ESR
– Blood culture
– Preoperative test: BUN, LFTs, electrolyts
Imaging studies
Cranial MRI is the choice( it outlines the extent of
subdyral empyema and greater morphological
details than CT scan
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41. • CT scan : shows hypodense area over the
hemisphere or along the falx
• Cranial ultrasound: important in
differentiating subdural empyema from
anechoic reactive subdural effusion in infants
with meningitis
• Other tests: EEG, chest radiograph,
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42. Treatment
• Maintain adequate airway and ensure
breathing and circulation
• Antibiotic therapy alone adequate in small
subdural empyema <1.5cm diameter
• Prophylactic anticonvulsants
• Treatment for increased ICP
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43. • Immediate surgical drainage should be
considered
– Craniotomy: best option
– Stereotatic burr hole placement with drainage and
irrigation
Grainage and debreidement of the primary source
of infection maybe necessary
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44. complications
• Seizures
• Cavernous sinus thrombosis from septic
thrombosis
• Increased ICP
• Hydrocephalous
• Cerebral infarction
• Cranial osteomyelitis
• Focal neurological deficits
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45. Epidural empyemaabscess
• Rare but pontentially life threatening
• Occus between the dura dnthe skull
• There are two types
– Spinal epidural abscess
– Intracranial epidural abscess
• The difference is where they develop and
some variationsi in risk factors
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46. Spinal epidural empyema
• Read more about it
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47. Intracranial epidural abscess
• Usually associated with subdural empyema
because the pus can cross the brain dura
along emissary veins
• Risk factirs include prior craniotomy, head
injury, sinusitis, otits media and mastoiditis.
• Common in males in the 2nd and 3rd decades
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48. Clinical presentation
• Fever
• Headache
• Malaise
• Lethargy
• Nausea and vomiting
• Focal neurological deficits
• Altered mental state
• evidence of infection
• seizure
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49. Management
• Craniotomy
• Antibiotic therapy
• Anticonvulsants
• corticosteroids
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