PYOGENIC BRAIN ABSCESS

1. Pyogenic Brain Abscess
Dr Himanshu Soni

2. pathogenesis
• pyogenic brain abscess is a focal
collection of pus withing thebrain.
• the incidence is 8% of intracranial
masses.
• largely because of the brain natural
resistance to infection, mediated by
– abundant blood supply
– relative impermeability of blood brain barrier
– improvement in the treatment of ear, sinus
and orofacial infections
• peak ages vary

3. • pediatric peak - 4 to 7 years, found in
congenital heart disease
• causes :
– trauma
– contiguous spread from a suppurative focus
– hematogenous dissemination from a distant
infection
• 40-60% are result of contiguous infection
from middle ear, oropharynx and sinuses

4. • these are usually solitary lesions
• seeding via te valveless emissary veins
draining the contiguous areas, allowing the
entry into venous sinus system.
• Temporal lobe / Cerebellar abscesses
– chronic otitis media, mastoiditis
• frontal or temporal lobe
– paranasal sinusitis
• penetrating cranial trauma with dural
tear account for 10% of the abscesses

6. post operative brain abscess
• infrequent, approx 0.1% after clean
procedure
• at the time of surgery, infect the wound /
bone flap

7. metastatic brain abscess
• seeding from a distant site - 25% of brain
abscesses
• locations
– in the distribution of MCA
– parietal-occipital junction
– corticomedullary junction where the capillary flow is
slowest
• sources
– pulmonary lesions - AV fistulas occuring in hereditary
telangiectasis
– infective endocarditis
– deep seated infections such as osteomyelitis,
pulmonary empyema, pelvic infections &
intraabdominal infections

8. other causes
• iv drug users
• cyanotic heart diseases - in 2 to 6% cases
• Tetralogy of Fallot and transposition of
great vessels most causes
• intrasellar abscesses
– pituitary / sellar adenomas,
craniopharyngiomas, Rathke's cysts or a
complication of TS surgery
– sphenoid sinusitis

11. • determined by the site of infection
• Streptococci ( milleri and viridans )
– most common cause, nearly 2/3rd cases,
mostly extending from naso/oropharynx,
viridans in endocarditis
• Staphylococcus aureus - 10 to 21%
– trauma postoperative, endocarditis
– MRSA in hospitalized patients
• Actinomyeces
• pulmonary and odontogenic infections

12. • GNB like proteus, klebsiella,
pseudomonas, E. coli, serratia
– genitourinary or intraabdominal infections
• pseudomonas
– otitis media / externa
• clostridium
– underlying malignancy or hemolytic-uremic
syndrome
• propionibacterium
– post neurosurgical patient

13. • bacillus like salmonella
– intracerebral hematoma
• Nocardia (asteroides and farcinica) - 1 to
2%, carry 31% mortality rate
– immunicompromised patients
– isolated or disseminated pathology
• fungal (candida, cryptococcus, dimorphic
fungus or molds)
– immunicompromised states
• protozoa / helminths
– cat exposure or endemic areas

14. • Neonatal meningitis caused by Proteus
and Citrobacter, result in abscess in 40-
75% cases

15. PATHOLOGY
• evolution studied using a-
streptococci in canine model
• early cerebritis - day 1 to 3
– poorly circumscribed lesion
– acute inflammation and cerebral
edema associated with bacterial
invasion
• Expansion - day 4 to 9
– zone of cerebritis expands
– necrosis develops with pus
formation
– CT scan reveals some ring
enhancement with diffusion of
contrast into the necrotic center

16. • early capsule state - days 10 to 13
– establishment and maturation of well formed
collagenous capsule
– reduction in degree of ceribritis and edema
• Late capsule stage - day 14 and beyond
– continued maturation of thick capsule with
extracapsular gliosis
– dense ring enhancement on CT contrast

20. CAPSULE CHARACTERISTICS
• capsule formation and ring enhancement -
thinner and less complete on the
ventricular side
• related to poor vascularity of the deep
white matter and reduced migration of
fibroblasts
• tinner area predisposis to ventricular
rupture
• nature of the organism influences
encapsulation

22. • bacteroides - delayed capsule formation
with multiple daughter abscesses
• S. aureus - larger, delayed healing with
markec extracapsular abnormalities
• contiguous spread - better encapsulation
• hematogenous spread - less extensive
• immunisuppresion - incomplete
encapsulation

23. CLINICAL PRESENTATION
• symptoms < 2 weeks
• depend on
– size & location
– virulence of the agent
– immunologic status of the host
– cerebral edema

25. • triad - fever, headache & focal neurological
deficit - present in < 50%
• headache
– dull and poorly localised
– 50-70% cases and is nonspecific
– sudden worsening of a prexisting headache in
a ptient with abscess, with meningeal signs,
suggest herniation or intraventricular rupture

26. • fever
– 25-50% cases, more common in children
• deficits
– altered sensorium often present
– frontal and parietal abscesses
• hemiparesis, aphasia
– temporal lobe
• aphasia, visual field defects
– intrasellar
• mimic pituitary tumors
– cerebellar
– ataxia and nystagmus

27. LABORATORY FINDINGS
• moderate leucocytosis
• blood cultures are only 10% positive
• ESR and CRP are elevated, help in
monitoring response
• LP is strongly contraindicated
• tissue and pus samples - best during
surgery
• bacterial r-DNA PCR - crucial, more
sensitive, esp in patient's already on
antibiotics

28. CT SCAN
• hypodense lesion, surrounded by ring
enhancement with variable zone of edema
• sensitivity is 95-99%
• specificity is compromised
• cant differentiate with metastatic tumor or
some vascular lesions
• Indium - 111 labelled leucocyte scanning
helpful, radioleucocytes accumulate in the
area of active inflammation
• delayed contrast - value in cerebritis

30. MRI
• more sensitive in
– early cerebritis
– extent of central liquefaction necrosis
– early satellite lesions
– extraparenchymal extension (subdural
empyema)
• insentive to differentiate
– cystic or necrotic high grade glioma
– metastasis

31. • T1 - pus is hypointense
• T2 - pus is hyperintense
• FLAIR - nullifies free water signal, caused
by increased protein content
– reported in brain tumors, abscesses and
vascular insults
• Diffusion weighted imaging (DWI) and
apparent diffusion coefficient (ADC) -
based on movements of water molecules
– to measure degree of water movements, ADC
maps are useful

32. – abscess contains bacteria, proteins and pus.
Hence shows restricted water motion
– DWI shows incresed signal with low ADC
values
– most necrotic tumors have serous fluid and
fewer inflammatory cells. Hence shows low-
intermediate intensity on DWI and high ADC
values due to serous fluid

36. MR SPECTROSCOPY
• helps differentiate cystic tumors and
abscesses
• detects the metabolic profile of teh brain
• cytosolic amino acids (leucine, isoleucine
and valine) are usually detected in
cerebral abscesses and absent in tumors
• however their abscence does not rule out
pyogenic abscess.
• acetate with/out succinate supports an
anaerobic abscess

37. • in fungal abscess, amino acids are low
• response to treatment is followed by serial
changes in metabolite patterns
• lactate and amino acids - present
regardless of teh treatment
• acetate and pyruvate - disappeared after 1
week of therapy

38. PET
• the mechanism of FDG uptake is related
to the degree of inflammatory cells in the
abscess
• increased uptake corresponded to the
enhanced area
• after treatment the area showed
decreased uptake

39. MEDICAL MANAGEMENT
• empiric antibiotic - as early as possible
• cover gram positive, gram negative &
anerobes.
• 3rd or 4th Gen cephalosporin,
metronidazole and vancomycin - choice
• culture and modify accordingly
• MRSA - vancomycin and clindamycin

40. ANTIBIOTIC CONSIDERATIONS
• anti-infective agents should be
– acting against probable pathogens
– able to penetrate into the abscess
– achieve high levels in abscess pus
• Penicilin G at high doses, metronidazole,
cotrimoxazole, chloramphenicol - achieve
therapeutic concentrations
• metronidazole - high levels in abscess -
important component of most regimens

41. • use in combination with an agent active
against streptococci (eg penicillin)
• clindamycin, aminoglycosides and 1stG
cephalosporins - poor penetration
• potentially effective
– ceftriaxone, ceftazidime or 3rd G cephalosp
– quinolones
– monobactams
– carbapenems

42. • duration depends on
– causative pathogen
– adequacy of drainage
• 6-8 week is recommended
• complete resolution may take 3-4 months
radiologically
• residual contrast enhancement may take
more than 6 months

44. STEROIDS
• controvertial
• suggested role
– diminish microbe entry into the CNS
– reduce the elimination of viable organisms from the
abscess cavity
– inhibit effective, ring enhancing, host inflammatory
response
– delay in encapsulation
• preponderance of evidence weighs against the
routine use of steroids as an adjunct except
when signs of raised ICP are marked

45. SEIZURE CONTROL
• incidence of seizures - 13 to 25 %
• recommended perioperative use of AED
and continue after surgery
• long term use depends on neurologic
evaluation after the abscess has resolved

46. MEDICAL MANAGEMENT
• determinants of medical management are
– neurologically stable with cerebritis or small
lesions (less than 1.5cm)
– severe concomitant medical conditions
– severe bleeding diathesis
– multiple abscesses
– surgically inaccesible, dominant or disparate
location

47. • limitations
– lack of diagnostic specimen
– empirical long term antimicrobial therapy
– potential for drug adv effects
– risk of ventricular rupture
– frequent imaging until radiographic resolution

48. SURGICAL MANAGEMENT
• diagnostic and therapeutic
• larger than 2.5cm - surgery must
• provides
– pathologic diagnosis
– bacteriological profile
– reduction in mass effect
– improves milieu for antimicrobial therapy
– removes toxic necrotic material
• options
– aspiration of the abscess
– excision of brain abscess

49. ASPIRATION
• provides specimens
• low surgery related morbidity and mortality
• post aspiration recurrence - upto 32%
• CT guided aspiration accurate within a few
mm with yield of 95%
• highly effective in definitive drainage of
abscess
• preferred treatment for deep seated
lesions or eloquent areas

50. • suitable for
– brain stem
– thalamus
– basal ganglia
• stereotactic drainage - can drain multiple
abscesses, with prolonged medical
therapy is effective
• frameless neuronavigation - best
technique to localise
• less chance of seizures and other
sequelae

51. • Ultrasound guidance
– real time
– reliable
– fewer risks
– minimally invasive and accurate
• other methods
– endoscoic stereotactic aspiration and
irrigation
• precise localisation, minimal craniotomy, multiple
lesions addressed

52. SURGICAL EXCISION
• useful in
– large (>2.5cm) abscess
– superficial abscess
– refractory aspirations
– posterior fossa lesions
– fungal abscesses
– post traumatic abscess with retained bones or
foreign bodies
– gas containing abscesses

53. • not choice in
– cerebritis stage
– deep seated abscess
– eloquent areas
• emergency surgery in
– obtunded patient
– severe neurologic deficit
– encapsulated lesion
– aim to decompress and diagnose

54. • choice procedure
– image guided keyhole approach
– small incision
– limited craniotomy
– limited brain retraction
– minimal intraop trauma
– better cosmesis
• large craniotomy and decompression
– failed conservative management
– dangerios location like posterior fossa
– extensive edema, mass effect
– impending or actual hydrocephalus

55. intraventricular rupture
• as pus increases - abscess expands - may
rupture into the ventricle
• sudden, catastrophic deterioration of the
patient
• diagnosis
– hydrocephalus
– enhancement of teh ventricular walls
• management
– immidiate ventricular drainage
– intraventricular instillation of antibiotics

56. – evacuation of teh remaining abscess
– systemic antibiotic therapy
• mortality greater than 80%
• if multiple lesions
– those > 2.5cm should be aspirated
– the largest or most accessible should be
aspirated for culture

57. OSTEOMYELITIS OF THE SKULL
• results from
– paranasal sinusitis
– otogen infection
– odontogenic infection
– penetrating truama or craniotomy