Brain abscess neurosurgery presentation ppt

Brain abscess

1. Brain Abscess
YOUMANS Chapter 43

2. Outline
•Epidemiology
•Etiology
•Initiation of infection
•Stage of infection
•Clinical finding
•Diagnosis
•Management

3. Epidemiology
•0.3 -1.3 cases per 100,000 person
•Male : Female 2:1
•Median age 30-40 years
–Otitic focus : < 20 Yrs , >40 Yrs
–Paranasal sinus : 30 – 40 Yrs
•After cranial operation : 0.2 % of 1587 , 10 of 16540
•Commonly in Immunocompromised : infected with
HIV, receiving chemotherapy for cancer, receiving
immunosuppressive therapy after organ
transplantation, or after prolonged use of
corticosteroids.

4. Risk factor
•Pulmonary abnormality
–Infection
–AV fistula
•Congenital cyanotic heart disease
•Bacterial endocarditis
•Penetrating trauma
•Chronic sinusitis or otitis media
•AIDS

5. Pathogenesis
•Organism transmit
–contiguous source of infection, 25-30 % of case
–hematogenous dissemination 20-35% of cases
–trauma

6. Pathogenesis
•Contiguous source : middle ear, mastoid cells,
paranasal sinuses
•From purulent sinusitis : spread by osteomyelitis or
by phlebitis of emissary vein
•Rare in infant because they lack aerated paranasal
and mastoid air cells
•Localize of Contiguous source
–Otitis media : temporal lobe or cerebellum
–Paranasal sinusitis : frontal lobe
–Sphenoid sinusitis(less common for sinusitis ) : temporal
lobe, sella turcica
–Dental infection(most common molar) : frontal lobe

7. Pathogenesis
•Hematogenous dissemination : multiple,
multiloculated abscesses, higher mortality rate
•Most common source in adult
–Most common : pyogenic lung diseases (especially lung
abscess)
–bronchiectasis
–Empyema
–cystic fibrosis
–Skin infection, osteomyelitis, pelvic infections, and intra-
abdominal infections

8. Pathogenesis
•In children
•Cyanotic congenital heart disease (tetralogy of Fallot)
because increase Hct and low PO2 provide and hypoxic
environment suitable for abscess proliferation
•Right to left shunt
•Streptococcal oral flora from oral dental procedure

9. Pathogenesis
•Trauma : open cranial fracture with dural breach or
foreign body injury or as a sequela of neurosurgery
•Nosocomial brain abscess : halo pin insertion,after
electrode insertion to localize seizure foci,and in
malignant glioma patients treated by placement
of Gliadel wafers in the tumor bed to release
carmustine

10. Etiology
•Bacterial : most common, streptococci (aerobic,
anaerobic, and microaerophilic), 70%
•Streptococcus anginosus (milleri) : oral cavity,
appendix, and female genital tract
•Staphylococcus aureus : cranial trauma or infective
endocarditis
•Enteric gram-negative bacilli ,25-30% (e.g., Proteus
spp., Escherichia coli, Klebsiellaspp., Pseudomonas
aeruginosa, and Enterobacterspp.) : otitis media,
bacteremia, neurosurgical procedures, and the
immunocompromised state

11. •Negative culture : 0-43% (previous use ATB)
•Listeria monocytogenesis uncommon (<1% of cases),
considered in patient who are immunocompromised
(e.g., leukemia, lymphoma, HIV infection, and
conditions requiring corticosteroids or other agents
that cause immunosuppression)
•Salmonella, Nocardia, Streptococcus pneumoniae,
Haemophilus influenzae, Burkholderia pseudomallei,
and Actinomyces species
Etiology

12. Etiology
•the incidence of fungal brain abscess has been
rising as a result of the increased use of
corticosteroid therapy, broad-spectrum
antimicrobial therapy, and immunosuppressive
agents
•Candida : microabscesses, macroabscesses,
noncaseating granulomas, and diffuse glial nodule

13. Etiology
•Risk factors for candidal brain abscess include the
use of broad-spectrum antimicrobial agents,
corticosteroids, and hyperalimentation; premature
birth; malignancy; neutropenia; chronic
granulomatous disease; diabetes mellitus; thermal
injury; and the presence of a central venous catheter
•Aspergillosis : neutropenia, hepatic disease, diabetes
mellitus, chronic granulomatous disease, Cushing’s
syndrome, HIV infection, injection drug use, organ
transplantation, and bone marrow transplantation

14. Etiology
•Mucorales group : Diabetes mellitus, patients with
acidemia from profound systemic illness (e.g., sepsis,
severe dehydration, severe diarrhea, chronic
kidney disease)
•Scedosporium : immunocompetent and
immunocompromised hosts
•Cryptococcus neoformans, the endemic mycoses
(Coccidioides spp., Histoplasma spp., and
Blastomyces dermatitidis)

15. Etiology

16. Initiation of infection
•The brain appears to be significantly more sensitive
to infection than many other tissues.
•The brain may also be more susceptible to
infection by different organisms

17. Stages of infection

18. Stages of infection

19. Host defence mechanism
•Although the brain is generally protected from
infection by an intact blood-brain barrier, once
infection is established, immune defenses are
usually inadequate to control the infection
•Encapsulate bacteria : E.coli, B.fragilis

20. Clinical finding

21. Clinical finding
•Newborn
–Patent suture
–Seizure
–Meningitis
–Irritabilitiy
–Increasing OFC(occipital-frontal circumference)
–Failure to thrive
–May afebrile

22. Clinical finding

23. Clinical finding
•Intraventricular rupture of brain abscess : severe
headaches and signs of meningeal irritation were
prominent findings before rupture
•Intraventricular rupture appears to be more likely
if the abscess is deep-seated, multiloculated, and in
close proximity to the ventricular wall

24. Clinical finding
•Related to pathogen
–Nocardia : concomitant pulmonary, skin, or muscle
lesions
–Aspergillus brain abscess : commonly manifest signs of a
stroke syndrome as a result of ischemia or intracerebral
hemorrhage, or both
–rhinocerebral mucormycosis : symptoms referable to
the eyes or sinuses and complaints of headache, facial
pain, diplopia, lacrimation, and nasal stuffiness or epistaxis
 cranial nerve involvement  blindness

25. Clinical finding
•Related to pathogen
–Scedosporium apiospermum brain abscess :
•occur in immunocompromised patients or in
individuals 15 to 30 days after an episode of near-
drowning
•cerebrum, cerebellum, or brainstem
•Clinical finding : seizures, altered consciousness,
headache, meningeal irritation, focal neurological
deficits, abnormal behavior, and aphasi

26. Diagnosis
•WBC : mildly elevate (>10,000)
•Blood C/S : should be obtain (usually negative)
•ESR : may be normal
•CRP : may arise
•LP : dubious, OP increase, WBC count, Protein
elevate, risk for tantentorial herniation

27. Diagnosis
•MRI is more sensitivity than CT, early detection of
cerebritis, more conspicuous spread of inflammation
into the ventricles and subarachnoid space, and
earlier detection of satellite lesions
•T1 : the abscess capsule often appears as a discrete
rim that is isointense to mildly hyperintense
•T1 c Gad : rim enhancement, cerebral edema
•T2 : zone of edema : hyperintensity, capsule : ill-
defined hypointensity
•DWI : restricted diffusion (bright signal) may be seen
•ADC : Dark

28. Diagnosis

29. Diagnosis
•Aspergillosis : finding of a cerebral infarct, which
typically develops into either single or multiple
abscesses, in immunocompromised patients, there
may be little or no contrast enhancement on MRI
•Rhinocerebral mucormycosis : sinus opacification,
erosion of bone, and obliteration of deep fascial
planes; cavernous sinus thrombosis

30. Diagnosis
•stereotactic MRI- or CT-guided aspiration
•Specimens sent for : Gram stain, routine aerobic
and anaerobic culture, modified acid-fast smears,
acidfast smears and culture, and fungal smears and
culture
•Aspergillus brain abscess : septate hyphae with
acute-angle, dichotomous branching
•Mucormycosis : irregular hyphae with right-angle
branching.

31. Diagnosis

32. Diagnosis
•Scedosporiumspecies are indistinguishable from
those caused by Aspergillus species. The hyphae of
dematiaceous fungi may be brownish on
hematoxylin-eosin staining but are not
distinguishable from those of other molds.

34. Management
•Multidisciplinary, neuroradiologist, neurosurgeon,
and infectious disease specialist
•Larger than 2.5 cm : excision
•Smaller than 2.5 cm : aspiration for definite diagnosis
•Empirical ATB : metronidazole + third-generation
cephalosporin
•S.aureus consider : add vancomycin
•gram-negative bacilli such as P. aeruginosa :
ceftazidime, cefepime, or meropenem

35. Management
•no clear predisposing factors : combination of
vancomycin, metronidazole, and a third- or fourth-
generation cephalosporin
•Once the infecting pathogen is isolated, antimicrobial
therapy can be modified for optimal treatment

36. Medical management alone
•Treatment began in cerebritis
•Small lesion 0.8-2.5 cm
•Duration of symptom < 2 Wk
•Patient show clinical improvement in 1 wk

37. Surgical treatment
•Significant mass effect exerted by lesion
•Difficult in diagnosis
•Proximity to ventricle
•Evedence of significane increase intracranial
pressure
•Poor neurological condition
•Traumatic abscees associated with foreign
material
•Fungal abscess

38. Management

39. Bacterial brain abscess
•The principles of antimicrobial therapy for bacterial
brain abscess
–penetrate the abscess cavity
–in vitro activity against the isolated pathogen
•Metronidazole
–excellent in vitro activity against strict anaerobes
–an excellent pharmacokinetic profile
–good oral absorption
–penetration into brain abscess cavities
–must always be used in combination with an agent
effective against streptococci

40. Bacterial brain abscess
•Vancomycin, The third generation cephalosporins
are common used
•Imipenem : pyogenic and nocardial brain abscess,
beware seizure
•Meropenem : Enterobacter cloacae

41. Bacterial brain abscess
•Surgical therapy : aspiration after bur-hole
placement or complete excision after craniotomy
•Stereotactic aspiration : eloquent or inaccessible
regions
•Complete excision by craniotomy
–patients with multiloculated abscesses in whom
aspiration techniques have failed
–for abscesses containing gas
–for abscesses that fail to resolve
–posttraumatic abscesses that contain foreign bodies or
retained bone fragments to prevent recurrence

42. Bacterial brain abscess
•In patients with intraventricular rupture of a
purulent brain abscess :
–rapid evacuation and débridement of the abscess cavity
via urgent craniotomy and ventricular drainage
–intravenous or intrathecal ATB
•groups of patients may be treated with medical
therapy alone
–medical conditions that increase the risk associated with
surgery
–multiple abscesses

43. Bacterial brain abscess
•groups of patients may be treated with medical
therapy alone
–abscesses in a deep or dominant location
–the presence of coexisting meningitis or ependymitis
–early reduction of the abscess with clinical improvement
after antimicrobial therapy
–abscess size less than 3 cm

44. Bacterial brain abscess
•ATB optimal duration : 6-8 Wk IV then follow by oral
ATB for 2-3 Mo
•Repeat neuroimaging studies performed biweekly for
up to 3 months after completion of therapy has been
suggested to monitor for reexpansion of the abscess
or failure of resolution

45. Nocardial brain abscess
•Sulfonamide with or without trimethoprim is
recommend
•Alternative agent : minocycline, imipenem, amikacin,
third-generation cephalosporins, and linezolid
•In immunocompromised patients or those in whom
therapy fails : combination treatment with
regimens + a third-generation cephalosporin or
imipenem + a sulfonamide or amikacin

46. Nocardial brain abscess
•Craniotomy with total excision is difficult in
patients with Nocardia brain abscess because
these abscesses are often multiloculated
•ATB duration : 3-12 Mo but in immunocompromised
should be up to 1 Yr

47. Fungal brain abscess
•Candidal brain abscess : amphotericin B preparation
plus 5-flucytosine
•Aspergillusbrain abscess : voricazole
•CNS mucormycosis : amphotericin B deoxycholate
or a lipid formulation of amphotericin B with
aggressive surgical debridment
• Scedosporiumspecies : surgery

48. Management

50. Adjunctive Therapy
•Steroid effect
–Reduced edema
–Decrese likehood of fibrous encapsulation
–May be reduced penetration of antibiotic into abscess
•Corticosteroid use
–edema and mass effect
–progressive neurological deterioration
–impending cerebral herniation
•High dose : dexamethasone 10 mg q 6 hr and
then tapered

51. Cranial Subdural empyema and
Epidural abscess
YOUMANS Chapter 43

52. Epidemiology and Etiology
•Cranial subdural empyema : collection of pus
between the space of the dura and arachnoid, 15-20
% intracranial lesion
•Less common than brain abscess
•SDE may be complicated by cerebral brain abcess,
cortical vein thrombosis, localized cerebritis
•Location : 70-80 % convexity, 10-20% parafalcine

53. Epidemiology and Etiology
•most common predisposing conditions :
otorhinologic infections, especially of the
paranasal sinuses
•Other predisposing conditions : skull trauma,
neurosurgical procedures, and infection of a
preexisting subdural hematoma

54. Epidemiology and Etiology
•Organisms
–aerobic streptococci (25% to 45%)
–staphylococci (10% to 15%)
–aerobic gram-negative bacilli (3% to 10%)
–anaerobic streptococci
–other anaerobes
•If the predisposing condition is postoperative or
posttraumatics : staphylococci and aerobic gram-
negative bacilli

55. Clinical finding
•Clinical manisfestation of subdural empyema
–rapidly progressive, with symptoms and signs related to
increased intracranial pressure (headache, vomiting)
–meningeal irritation
–focal cortical inflammation (hemiparesis and hemiplegia,
ocular palsies, dysphasia, homonymous hemianopia,
dilated pupils, and cerebellar signs
–Altered mental status
–Seizure
–Fever

56. Clinical finding
•Clinical manisfestation of cranial epidural abscess
–Insidious onset
–Abscess enlarge too slowly to produce a sudden onset of
major neurological deficits, as is seen in patients with
cranial subdural empyema
–Most common : fever, headache
–If the location of the epidural abscess is near the petrous
bone, Gradenigo’s syndrome may develop (involvement
of cranial nerves V and VI and manifested clinically as
unilateral facial pain and weakness of the lateral
rectus muscle)

57. Diagnosis
•Cranial subdural empyema should be suspected in
any patient with meningeal signs and a focal
neurological deficit
•CT brain : iv contrast : hypodense crescentric
•LP : potential hazardous for herniation

58. Diagnosis
•MRI in Cranial subdural empyema : crescentic or
elliptical area of hypointensity (on T1 images) below
the cranial vault or adjacent to the falx cerebri, high
signal on T2
•MRI in cranial epidural abscess : superficial,
circumscribed area of diminished intensity with
pachymeningeal enhancement.

59. Management of
Cranial subdural empyema
•Cranial subdural empyema is a surgical emergency
because antimicrobial therapy alone does not
reliably sterilize the empyema
•The goals of surgical therapy are to achieve adequate
decompression of the brain and to evacuate the
empyema completely.
•The optimal surgical approach is controversial.

60. Management of
Cranial subdural empyema
•Patients who underwent drainage via bur holes or
craniectomy required more frequent operations to
drain recurrent or remaining pus and exhibited
higher mortality rates and worse outcomes
•Drainage via bur holes or craniectomy is therefore
recommended only for
–patients in septic shock, those with localized parafalcine
collections
–children with subdural empyema secondary to
meningitis because there is usually no brain swelling and
the pus is thin

61. Management of
Cranial subdural empyema
•S. aureusis suspected : vancomycin
•suspected anaerobes : metronidazole
•aerobic gram-negative bacilli are suspected,
empirical : ceftazidime, cefepime, or meropenem
•ATB continued for 3-4 wk after drainage

62. Management of
Cranial subdural empyema
•ATB alone in
–patients with cranial subdural empyema who have
minimal or no impairment of consciousness
–no major neurological deficit
–limited extension of the empyema with no
midline shift
–early improvement with antimicrobial therapy

63. Management of
Cranial epidural abscess
•combined medical and surgical approach
•Empirical antimicrobial therapy is similar to that for
cranial subdural empyema
•For surgical drainage, craniotomy or craniectomy
is generally preferred over bur-hole placement or
aspiration of purulent material through the scalp
•ATN length 3-6 wk or longer in osteomyelitis

64. Thank you