CNS infection 2018

1. CNS INFECTION
EXTERN. SARISA SOOTTIWONG
6TH
YEARS MEDICAL STUDENT,THAILAND 2018
Tel. +66846299844

2. SKULL OSTEOMYELITIS

3. SKULL OSTEOMYELITIS
Skull is highly vascular and resistant to infections
Pathogen
 S. aureus
 S. epidermidis
Pathogenesis
 Direct inoculation(More common) ex. pyogenic sinus
disease, infected penetrating trauma
 Hematogenous spreading

4. SKULL OSTEOMYELITIS
Clinical feature
Fever
Signs of inflammation
Fluid collection/Discharge
Pott’s puffy tumor

5. SKULL OSTEOMYELITIS
Diagnosis
 Hx, PE
 Elevate ESR, CRP (Non specific)
 Fluid collection for G/S, C/S
Treatment
 Combination
 Surgical debridement
 Antibiotic i.v. first 2 wks then high dose oral form after surgery 6-
12 wks

6. ATB FOR CSF PENETRATING

7. EPIDURAL ABSCESS OF BRAIN

8. EPIDURAL ABSCESS OF BRAIN
 Pathogen
 S. aureus
 S. epidermidis
 Pathogenesis
 เเเเเเเเเเเเเเเเเเเเเเเเเเเเเเเเเเเเเเ
เเเเเเเเเ เเเเ Air sinus infection, Skull osteomyelitis

9. EPIDURAL ABSCESS OF BRAIN
Clinical feature
 Fever, headache
 Focal neurologic deficit
 Signs of increased intracranial pressure
 Meningeal irritation signs
 Stiff neck
 Seizure

10. EPIDURAL ABSCESS OF BRAIN
 Diagnosis
 CT/MRI c contrast
 Finding -> Extradural enhancing collection
 (LP frequently fails to yield the offending organism and risks
herniation due to mass effect)
 Treatment
 Emergency condition
 Craniectomy + Drainage
 ATB 6-12 wks

11. EPIDURAL ABSCESS OF BRAIN
Brain magnetic resonance images without and with contrast
Metastatic Epidural Bacterial Abscess

12. SUBDURAL EMPYEMA

13. SUBDURAL EMPYEMA
Collection of pus in the subdural space
Widely spreading more than Epidural and Brain
abscess
Pathogenesis
 contiguous spread ex Air sinus infection, ear infection,
Mastoiditis, Epidural abscess
 After surgery/ device insertion beneath Dura
 Infection of pre-existing subdural blood: septicemia

14. SUBDURAL EMPYEMA
Pathogens:
 Aerobic streptococcus 30-50%
 Staphylococcus 15-20%
 Microanaerobic and anaerobic 15-25%
Streptococci
 Aerobic gram negative rods 5-10%
 Other anaerobe 5-10%

15. SUBDURAL EMPYEMA
 Clinical feature
 More severe than Epidural abscess
 Rapidly progressive
 Lacks significant barriers ex compartmentalization, septation
 Status epilepticus may occur
 Diagnosis
 CT/MRI c contrast
 Enhancing collection in subdural space
 Severe brain edema

16. SUBDURAL EMPYEMA
Magnetic resonance imaging revealing
a right subdural empyema with
meningeal enhancement

17. SUBDURAL EMPYEMA

18. SUBDURAL EMPYEMA
 Treatment
 Emergency -> Drainage + lavage to decrease inflammatory material
causing CorticalVein thrombosis
 Burr hole drainage or small craniotomy
 1 to 2 months of antibiotics
 10% to 20% mortality risk
 chronic sequelae : seizure disorder, residual hemiparesis.

19. BRAIN ABSCESS

20. BRAIN ABSCESS
• A focal intracranial infection that is initiated as an area of
cerebritis and evolves into a collection of pus surrounded
by a vascularized capsule

21. EPIDEMIOLOGY
 Higher incidence in developing countries
 Men more common than women
 Differences in age are based on the primary site of infection
 Otitic focus : < 20 years or > 40 years
 Paranasal sinuses : 30 - 40 years.

22. RISK FACTORS
 pulmonary abnormalities
 congenital cyanotic heart disease
 bacterial endocarditis
 penetrating head trauma
 AIDS

23. PATHOGENESIS

24. PATHOGENESIS
o Contiguous source of infection
o Usually single brain abscess
o Infections in the middle ear , mastoid cells , or paranasal sinuses
• Otitis media : temporal lobe or cerebellum
• Paranasal sinusitis : frontal lobe
• Sphenoid sinusitis : temporal lobe or sella turcica
• Dental infections (molar teeth) : frontal lobe

25. PATHOGENESIS
 Hematogenous (10-15%)
• Multiple , multiloculated abscesses , grey-white matter
junction(site of greatest blood flow)
• The most common sources : lung
• Chronic pyogenic lung diseases : lung abscess
• Bronchiectasis
• Empyema
• Cystic fibrosis

26. PATHOGENESIS
• Hematogenous dissemination
• Other : wound & skin infections , osteomyelitis , pelvic
infections , and intra-abdominal infections
• Cyanotic heart disease (TOF ,TGA) : common cause in
pediatrics
• Bacterial endocarditis

27. PATHOGENESIS
 Direct penetrating trauma
 Open head injury
 Neurosurgical procedure
 Foreign body
 No obvious source 25%

28. MICROBIOLOGY
• Bacteria is the most common
• Streptococcus spp.
• Enteric gram-negative bacilli
• Proteus spp. , Escherichia coli, Klebsiella spp. , Pseudomonas aeruginosa
and Enterobacter spp.
• Staphylococcus aureus
• Anaerobes
• Bacteroides spp. and Prevotella spp

30. MICROBIOLOGY
• Fungus
• most common : Candida spp.
• Risk factor
• The use of broad-spectrum antimicrobial agents
• Corticosteroids
• Diabetes mellitus

32. PATHOPHYSIOLOGY
Early cerebritis
Late cerebritis
Early capsule formation
Late capsule formation

33. PATHOPHYSIOLOGY
1.Early cerebritis (Day 0-3)
 Histopathology
- Central zone of necrosis
- local inflammatory response
- Marked peri-lesion edema
- Poor demarcation from adjacent
brain
 CT
- Poor marginated area of
hypodensity
- Minimal if any enhancement with IV
contrast

34. PATHOPHYSIOLOGY
2. Late cerebritis
 Day 4-9
 Histopathology
- Pus
- Enlargement of necrotic
center
- Maximal cerebral edema
- Reticulin network as precu
rsor to capsule

35. 2. LATE CEREBRITIS(CON’T)
 CT
- Hypodensity area still
may show poor margination
- Patchy enhancement duri
ng early part of phase
- Rim-enhancement begins late
r in phase
- Central hypodense areas fil
ls in with contrast on delayed
scans

36. 3. Early capsule formation
 Day 10-14
 Histopathology
- Continue formation of pus
- Development of collagen capsule
- Cerebral edema surrounding
capsule
 CT
- Well-defined rim enhancing
- mass; an outer hypodens rim
(double rim sign)

37. 4. Late capsule formation
 Day >14
 Histopathology
5 distinct zone
(a) Necrotic center filled with pus
(b) Peripheral zone of inflammatory cell
and fibroblasts
(c) Dense collagen capsule
(d) Layer of neovascularity with residual
cerebritis
(e) Zone of edema and reactive gliosis

38. 4. Late capsule
formation(con’t)
 CT
- Rim enhancing lesion
- Thickned capsule
- Diminisned hypodense
central cavity

39. HISTOLOGIC STAGING OF CEREBRAL
ABSCESS

40. CLINICAL FEATURES
• Signs & symptom : related to size, location ,virulence of the
organism
• Classical triad <50% :
• headache
• fever
• focal neurological deficit
• Sudden worsening of the headache & new onset of
meningismus, may signify rupture of the abscess into the
ventricular space

42. INVESTIGATION
 BLOODWORK
- Peripheral WBC: may be normal or only mildly elevated in
60-70% of cases (usually > 10,000)
- Blood cultures: usually negative
- ESR: may be normal
- C-reactive protein (CRP): infection anywhere in body can
raise the level. Patients with brain tumor and other
inflammatory condition (e.g. dental abscess) may have and
elevated CRP level. Sensitivity is 90%, specificity is 77%

43. INVESTIGATION
 Lumbar puncture
 No characteristic finding diagnostic of abscess
 Open pressure is usually increase,WBC count and protein
may be elevated
 Organism can rarely identified from CSF by LP
 Risk of transtentorial herniation,especially with large
lesions
Due to the risk and the low yield of useful
information,avoid LP if not already done

44. INVESTIGATION
• Imaging
• MRI : gold standard
• CT with contrast : Rim enhancing lesion, smooth & thin wall
with surrounding edema

46. TREATMENT
 Medical
Abscess < 3 cm
Multiple small abscesses
Difficult area
Early cerebritis phase
High surgical risk
 ATB 6-8 wk
 Empirical tx :
 Vancomycin
 Cloxacillin+
Ceftriazone+
Metronidazole
 Supportive treatment
 Dexamethasone
 Anticonvulsant

48. SURGICAL MANAGEMENT
• Needle aspiration after burr-hole
• Indication
 Well encapsulated > 3 cm
 Nearly to ventricle
• No response to antibiotics
• Preferable

49. SURGICAL MANAGEMENT
• Complete excision after craniotomy
• Indication
• Multiloculated abscess
• Traumatic brain abscess (to remove bone fragment
or foreign body)
• Encapsulated fungal brain abscess
• Gas-forming lesion

51. CLINICAL COMPLICATIONS
 Abscess rupture transforms localized infection 
-Meningitis
-Ventriculitis
 Elevated ICP may cause uncal hernia and subsequently death
 Seizure

52. OUTCOME
Mortality ranged form 40-60%
With improvement in antibiotics, surgery, and the improved
ability to diagnose and follow response with CT and/or MRI,
mortality rate has been reduced to 10%
But morbidity remains high with permanent neurologic
deficit or seizures in up to 50% of cases
A worse prognosis is associated with poor neurologic
function, intraventricular rupture of abscess

54. SPINAL INFECTION

55. SPINAL ABSCESS
 Intraspinal abscess เเเเเเเเเเเเเเเเเเเเเเ
เเเเเ Morbidity เเเ Mortalityเเเ เเเเเเเเ
 Spinal epidural abscess (most common)
 Spinal subdural abscess
 Intramedullary abscess

56. SPINAL EPIDURAL ABSCESS
 Posteriorly, the epidural space contains fat, small arteries,
and the venous plexus
 Anteriorly, the epidural space is a potential space with the
dura tightly adherent to the vertebral bodies and ligaments
 Most spinal epidural abscesses occur in the thoracic area,
which is anatomically the longest of the spinal regions

57. PATHOGENESIS
 Hematogenous : bacterial endocarditis, infected indwelling
catheters, urinary tract infection, peritoneal and
retroperitoneal infections, and others. Symptoms progress
rapidly
 Direct extension : from vertebral osteomyelitis, Psoas
abscess , Epidural injections or catheters.
Slow progression of symptoms

59. PATHOGENSIS
 Staphylococcus aureus
 Staphylococcus and Pseudomonas species, Escherichia coli,
Brucella, and Mycobacterium tuberculosis.
 MRSA : history of MRSA abscesses, spinal surgery, or
implanted devices
 Fungal infections : Immunosuppressed patients

60. RISK FACTOR
 DM
 IVDU
 Alcoholism
 chronic immunosuppression, older adult
 hemodialysis patients

61. CLINICAL FEATURES
 Four phases
I. localized spinal pain
II. radicular pain and paresthesias
III. muscular weakness, sensory loss, and sphincter
dysfunction
IV. paralysis
 Fever 30%
 Headache & neck pain

62. INVESTIGATION
 Imaging
 MRI is the procedure of choice
 CT myelography : intraspinal extramedullary mass
 LP is relatively contraindicated : risk of introducing purulent
material into the subarachnoid space

63. TREATMENT
 Laminectomy + Drainage
 ATB 6-8 wk

64. TUBERCULOMA

65. TUBERCULOMA
 Tuberculoma เเเเเเเเเเเเเเเเเเเเเเเเ
เเเเเเเเเเเเเเเเเเเเเ เเเเเเเ
เเเเเเเเเเเเเเเ เเเเเเเเเเเเเเเเเ
เเเเเเ เเเเเเเเเเเเเเเเ เเเเเเเเเ
caseous necrosis

66. TUBERCULOMA
 Clinical feature
 เเเเเเเเเเเเเเเเเเเเเเเเเเเเ
 เเเเเเเเเเเเเเเเเเเเเเเเเเ
เเเเเเ
 Investigation
 CT brain c contrast
 Mass
 Hydrocephalus
 CXR -> Pulmonary TB
 Film skull -> Calcified tuberculoma

67. TUBERCULOMA

68. TUBERCULOMA
Treatment
 Anti TB drug
 Surgical removal
 เเเเเเเเเเเเเเเเเเเเเเเเเเเเเ

69. CEREBRAL CYSTICERCOSIS

70. CEREBRAL CYSTICERCOSIS
 Ingestion of eggs of Taenia solium
 Most common parasitic disease of the nervous system
 Pathogenesis
 เเเเเเเเเเเเเเเเเเเเเเเเเเเ
เเเเเเเเเเเเเเเเเเเเเเเเเเ Scolex
เเเเเเ เเเเเเเเเเเเเเเเเเเเเ เเเ
เเ infarct เเเเเเเเเเ
 เเเเเเเเเเเเเเเเเเเเเเเเเเเเเเ
เเเเเเเเเเ Hydrocephalus เเเเเเ
1.5-2 เเ เเเเเ เเเ Scolexเเเเเ เเเเเเเ
เเเเเเเเ เเ Calcified

72. CEREBRAL CYSTICERCOSIS
 Pathology 4 ชชชชชชชชชชชชชชช
 Meningeal form
 Parenchymatous form
 Ventricalar form
 Mixed form

73. CEREBRAL CYSTICERCOSIS
 Clinical feature
 Epilepsy: Most common presentation (70%)
 Headache, dizziness
 Neuropsychiatric dysfunction
 Cognitive decline
 Dysarthria
 severe dementia

74. CEREBRAL CYSTICERCOSIS
 Clinical feature
 Stool exam 10-15% taeniasis
 CSF
 Mononuclear pleocytosis
 Eosinophilia
 Normal or low glucose levels
 Elevated protein levels
 Immunology ELISA for neurocysticercosis
 CT brain

77. CEREBRAL CYSTICERCOSIS
 Medical treatment
 Anticonvulsant
 Steroid
 Anti helminthic therapy : Praziquantel
 Surgical treatment
 Indication
 Hydrocephalus
 V-P shunt,V-A shunt
 Mass effect -> Obstructive hydrocephalus
 Surgical removal