This document summarizes key information about pyogenic brain abscesses: - They are focal collections of pus within the brain, most commonly caused by contiguous infections from the ear, sinuses, or mouth spreading via veins. - Symptoms vary depending on size and location but often include headache, fever, and neurological deficits. Diagnosis involves CT or MRI imaging and treatment involves antibiotics plus surgical drainage for larger abscesses.

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