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CNS ABSCESSES

CNS ABSCESSES. M.MOLAVI MD. CNS ABSCESSES. Focal pyogenic infections of the central nervous system Exert their effects mainly by: Direct involvement & destruction of the brain or spinal cord Compression of parenchyma Elevation of intracranial pressure Interfering with blood &/or CSF flow

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CNS ABSCESSES

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  1. CNS ABSCESSES M.MOLAVI MD

  2. CNS ABSCESSES • Focal pyogenic infections of the central nervous system • Exert their effects mainly by: • Direct involvement & destruction of the brain or spinal cord • Compression of parenchyma • Elevation of intracranial pressure • Interfering with blood &/or CSF flow • Include: Brain abscess, subdural empyema,intracranial epidural abscess, spinal epidural abscess, spinal cord abscess

  3. BRAIN ABSCESS • Accounts for ~ 1 in 10,000 hospital admissions in US (1500-2500 cases/yr) • Major improvements realized in diagnosis & management the last century, & especially over the past three decades, with:

  4. BRAIN ABSCESS • Was uniformly fatal before the late 1800’s • Mortality down to 30-60% from WWII-1970’s • Introduction of abx (penicillin, chloramphenicol...) • newer surgical techniques • Mortality down to 0-24% over the past three decades, with: • Advent of CT scanning (1974), MRI • Stereotactic brain biopsy/aspiration techniques • Further improvement in surgery • Newer abx (e.g. cephalosporins, metronidazole..) • Better treatment of predisposing conditions

  5. CHANGES IN EPIDEMIOLOGY OF BRAIN ABSCESS (in the last 2-3 decades) • Marked drop in mortality overall • Lower incidence of otogenic brain abscesses • improved treatment of chronic ear infections • With increase in No. of immunosuppressed patients: • increased incidence of brain abscessseen in that population (Transplant, AIDS,…) • More incidence of brain abscess caused by opportunistic pathogens (fungi, toxo…)

  6. PATHOPHYSIOLOGY • Begins as localized cerebritis (1-2 wks) • Evolves into a collection of pus surrounded by a well-vascularized capsule (3-4 wks) • Lesion evolution (based on experimental animal models): • Days 1-3: “early cerebritis stage” • Days 4-9: “late cerebritis stage” • Days 10-14: “early capsule stage” • > day14: “late capsule stage”

  7. PATHOGENESIS • Direct spread from contiguous foci (40-50%) • Hematogenous (25-35%) • Penetrating trauma/surgery (10%) • Cryptogenic (15-20%)

  8. Occurs by: Direct extension through infected bone Spread through emissary veins, diploic veins, local lymphatics The contiguous foci include: Otitis media/mastoiditis Sinusitis Dental infection (<10%), typically with molar infections Meningitis rarely complicated by brain abscess (more common in neonates with Citrobacter diversus meningitis, of whom 70% develop brain abscess) DIRECT SPREAD(from contiguous foci)

  9. HEMATOGENOUS SPREAD(from remote foci) • Sources: • Empyema, lung abscess, bronchiectasis, endocarditis, wound infections, pelvic infections, intra-abdominal source, etc… • may be facilitated by cyanotic HD, AVM. • Results in brain abscess(es) at middle cerebral artery distribution • Often multiple

  10. PREDISPOSING CONDITION &LOCATION OF BRAIN ABSCESS

  11. Microbiology of Brain Abscess • Dependent upon: • Site of primary infection • Patient’s underlying condition • Geographic location • Usually streptococci and anaerobes • Staph aureus, aerobic GNR common after trauma or surgery • 30-60 % are polymicrobial

  12. Predisposing Conditions & Microbiology of Brain Abscess Predisposing ConditionUsual Microbial Isolates Otitis media or mastoiditis Streptococci (anaerobic or aerobic), Bacteroides and Prevotella spp., Enterobacteriaceae Sinusitis (frontoethmoid or sphenoid) Streptococci, Bacteroides spp., Enterobacteriaceae, Staph. aureus, Haemophilus spp. Dental sepsis Fusobacterium, Prevotella and Bacteroides spp., streptococci Penetrating trauma or postneurosurgical S. aureus, streptococci, Enterobacteriaceae, Clostridium spp. PPID,2000

  13. PREDISPOSING CONDITIONUSUAL MICROBIAL ISOLATES Lung abscess, empyema, bronchiectasis Fusobacterium, Actinomyces, Bacteroides Prevotellaspp., streptococci, Nocardia Bacterial endocarditis S. aureus, streptococci Congenital heart disease Streptococci, Haemophilus spp. Neutropenia Aerobic gram-negative bacilli, Aspergillus Mucorales, Candidaspp. Transplantation Aspergillus spp., Candida spp., Mucorales, Enterobacteriaceae, Nocardia spp., Toxoplasma gondii HIV infection Toxoplasma gondii, Nocardia spp., Mycobacterium spp., Listeria monocytogenes, Cryptococcus neoformans PPID, 2000

  14. MICROBIOLOGY OFBRAIN ABSCESS AGENTFREQUENCY (%) Streptococci (S. intermedius, including S. anginosus) 60–70 Bacteroides and Prevotella spp. 20–40 Enterobacteriaceae 23–33 Staphylococcus aureus 10–15 Fungi* 10–15 Streptococcus pneumoniae <1 Haemophilus influenzae <1 Protozoa, helminths†(vary geographically) <1 *Yeasts, fungi (Aspergillus Agents of mucor Candida Cryptococci Coccidiodoides Cladosporium trichoides Pseudallescheria boydii)†Protozoa, helminths (Entamoeba histolytica, Schistosomes Paragonimus Cysticerci) CTID,2001

  15. CLINICAL MANIFESTATIONS • Non-specific symptoms • Mainly due to the presence of a space-occupying lesion • H/A, N/V, lethargy, focal neuro signs , seizures • Signs/symptoms influenced by • Location • Size • Virulence of organism • Presence of underlying condition

  16. CLINICAL MANIFESTATIONS OF BRAIN ABSCESS Headache 70% Fever 50 Altered mental status 50-60 Triad of above three <50 Focal neurologic findings 50 Nausea/vomiting 25-50 Seizures 25–35 Nuchal rigidity 25 Papilledema 25 CTID,2001. PPID,2000

  17. CLINICAL MANIFESTATIONS Headache • Often dull, poorly localized (hemicranial?), non-specific • Abrupt, extremely severe H/A: think meningitis, SAH. • Sudden worsening in H/A w meningismus: think rupture of brain abscess into ventricle (often fatal)

  18. LOCATION & CLINICAL FEATURES • FRONTAL LOBE: H/A, drowsiness, inattention, hemiparesis, motor speech disorder, AMS • TEMPORAL LOBE: Ipsilateral H/A, aphasia, visual field defect • PARIETAL LOBE: H/A, visual field defects, endocrine disturbances • CEREBELLUM: Nystagmus, ataxia, vomiting, dysmetria

  19. DIFFERENTIAL DIAGNOSIS • Malignancy • Abscess has hypo-dense center, with surrounding smooth, thin-walled capsule, & areas of peripheral enhancement. • Tumor has diffuse enhancement & irregular borders. • SPECT (PET scan) may differentiate. CRP too? • CVA • Hemorrhage • Aneurysm • Subdural empyema/ICEpidural abscess

  20. DIAGNOSIS • High index of suspicion • Contrast CT or MRI • Drainage/biopsy, if ring enhancing lesion(s) are seen

  21. IMAGING STUDIES • MRI • more sensitive for early cerebritis, satellite lesions, necrosis, ring, edema, especially posterior fossa & brain stem • CT scan • 99m Tc brain scan • very sensitive; useful where CT or MRI not available • Skull x-ray :insensitive, • if air seen, consider possibility of brain abscess

  22. LABORATORY TESTS • BRAIN ABSCESS • Aspirate:Gram/AFB/fungal stains & cultures, cytopathology (+/-PCR for TB) • WBC Normal in 40% ( only moderate leukocytosis in ~ 50% • & only 10% have WBC >20,000) • CRP almost invariably elevated • ESR Usually moderately elevated • BC Often negative BUT Should still be done • LPContraindicatedin patients with known/suspected brainabscess • Risk of herniation 15-30% • If done, may have normal CSF findings, but: • Usually elevated CSF protein & cell count (lymphs) • Unremarkable glucose & CSF cultures rarely positive

  23. TREATMENT • Combined medical & surgical • Aspiration or excision • empirical abx • Empirical antibiotics are selected based on: • Likely pathogen (consider primary source, underlying condition, & geography) • Antibiotic characteristics: usual MICs, CNS penetration, activity in abscess cavity • Modify abx based on stains • Duration: usually 6-8 wks • after surgical excision, a shorter course may suffice

  24. CT Scan

  25. MRI scan

  26. MRI Scan

  27. MRI scan

  28. MR spectroscopy

  29. Tips for Dx on MRI

  30. Treatment Options

  31. Goals & advantages of stereotactic-guided surgical approach

  32. Surgical indications

  33. Contraindications

  34. Complications

  35. Outcome & prognosis

  36. Armstrong ID, Mosby inc 1999

  37. MEDICAL TREATMENTONLY • Only in pts with prohibitive surgical risk: • poor surgical candidate, • multiple abscesses, • in a dominant location, • Abscess size <2.5 cm • concomitant meningitis, ependymitis, • early abscess (cerebritis?) • with improvement on abx, [Better-vascularized cortical lesions more likely to respond to abx alone] [ Subcortical/white-matter lesions are poorly vascularized]

  38. CTID,2001

  39. SERIAL IMAGING IMPORTANT TO MONITOR RESPONSE

  40. Before Rx After completion of Rx Armstrong ID,Mosby inc 1999

  41. POOR PROGNOSTIC MARKERS • Delayed or missed diagnosis • Inappropriate antibiotics. • Multiple, deep, or multi-loculated abscesses • Ventricular rupture (80%–100% mortality) • Fungal , resistant pathogens. • Neurological compromise at presentation • Short duration w severe AMS, • Rapidly progressive neuro. Impairment • Immunosuppressed host • Poor localization, especially in the posterior fossa (before CT) • Modified from CTID,2001

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