1. Ilos Enumerate the commonest causative organism of thebrain abscess. Discuss the pathogenesis of brain abscess Discuss the epidemiology of the commonest CNSbacterial abscess. Describe the gross & histopathological features ofthe different stages of brain abscess. Describe the radiological features. Describe the possible clinical presentation Discuss diagnosis & differential diagnosis Discuss in details treatment of brain abscess

2. ACUTE FOCAL SUPPURATIVE CNS INFECTIONS Brain abscess Subdural Empyema Extradural Abscess Spinal epidural abscess Spondylodiscitis epidural abscess 3. 1) Cell of origin & pathogenesis 2) Epidemiology 3) Macroscopic features 4) Microscopic features 5) Immunohistochemistry 6) Genetic & Ultra structures features 7) Radiological features 8) Pattern of growth & Spread 9) Staging & behavior 10) Prognosis 4. Pathogenesis 50% - Local Source Otitis media, sinusitis, dental infection Direct extension through infected bone Spread through emissary/diploic veins, local lymphatics 25% Hematogenous spread adults - lung abscess, bronchiectasis and empyema children - cyanotic congenital heart disease (4-7%) pulmonary AVM - Osler-Weber-Rendu syndrome (5%) rarely bacterial endocarditis 10% trauma / surgery 15-20% cryptogenic 5. MicrobiologyAGENT FREQUENCY (%)Streptococci (S. intermedius, including S. anginosus)6070 %Bacteroides and Prevotella spp. 2040Enterobacteriaceae2333Staphylococcus aureus 1015Fungi * 1015Streptococcus pneumoniae other lobes Size: Variable, 5 mm several cms Number: 10-50 % are multiple PREDISPOSING LOCATION OF ABSCESSCONDITION Character: According to stages Otitis/mastoiditis - poorly demarcated Cerebellum Early cerebritisTemporal lobe, from surrounding brain Frontal/ethmoidFrontal lobe Early (Late Stage)Later Cerebritic /Abscess Stage Late cerebritis - reticular marix (collagen precursor) and Mature abscess sinusitis developing necrotic center Sphenoidal sinusitis Frontal lobe, Sellanecrotic center, Early capsule formation - neovascularity, turcica developing capsule Dental infection Frontal > temporal lobe. Late capsule formation - collagen capsule, necrotic center, Remote source gliosis surrounding capsule cerebral arteryMiddle distribution (often multiple) 13. 1) Cell of origin & pathogenesis 2) Epidemiology 3) Macroscopic features 4) Microscopic features 5) Immunohistochemistry 6) Genetic & Ultra structures features 7) Radiological features 8) Pattern of growth & Spread 9) Staging & behavior 10) Prognosis 14. Microscopic features 15. 1) Cell of origin & pathogenesis 2) Epidemiology 3) Macroscopic features 4) Microscopic features 5) Immunohistochemistry 6) Genetic & Ultra structures features 7) Radiological features 8) Pattern of growth & Spread 9) Staging & behavior 10) Prognosis 16. 1) Cell of origin & pathogenesis 2) Epidemiology 3) Macroscopic features 4) Microscopic features 5) Immunohistochemistry 6) Genetic & Ultra structures features 7) Radiological features 8) Pattern of growth & Spread 9) Staging & behavior 10) Prognosis 17. 1) Cell of origin & pathogenesis 2) Epidemiology 3) Macroscopic features 4) Microscopic features 5) Immunohistochemistry 6) Genetic & Ultra structures features 7) Radiological features 8) Pattern of growth & Spread 9) Staging & behavior 10) Prognosis 18. Radiological features: CT 19. Radiological features: MRI Early cerebritis 20. Radiological features: MRIEarly capsule 21. Radiological features: MRI Late capsule 22. Pattern of growth & Spread 1) Cell of origin & pathogenesis 2) Epidemiology 3) Macroscopic features 4) Microscopic features 5) Immunohistochemistry 6) Genetic & Ultra structures features 7) Radiological features 8) Pattern of growth & Spread 9) Staging & behavior 10) Prognosis 23. Capsulebeing thinner on the deep aspect unfortunately promoting possible rupture into the ventricular system. Because differences in vascularity between cortical gray and white matter allowed greater fibroblast proliferation on the cortical side of the abscess 24. 1) Cell of origin & pathogenesis 2) Epidemiology 3) Macroscopic features 4) Microscopic features 5) Immunohistochemistry 6) Genetic & Ultra structures features 7) Radiological features 8) Pattern of growth & Spread 9) Staging & behavior 10) Prognosis 25. 1) Cell of origin & pathogenesis 2) Epidemiology 3) Macroscopic features 4) Microscopic features 5) Immunohistochemistry 6) Genetic & Ultra structures features 7) Radiological features 8) Pattern of growth & Spread 9) Staging & behavior 10) Prognosis 26. Prognosis Mortality: 0-24% Morbidity: 45% Seizure in 30-60% Neuro deficits 30-50% Late focal or generalized seizures - 27% 27. Poor Prognostic Factors Delayed or missed diagnosis Inappropriate antibiotics Multiple, deep, or multi-loculated abscesses Poor localization, especially in the posterior fossa Ventricular rupture (80%100% mortality) Fungal , resistant pathogens Degree of neurological compromise at presentation Rapidly progressive neuro. impairment Immunosuppressed host Extremes of age Modified from CTID,2001 28. Usually non-specific symptoms Increase intracranial pressure: Neurological deficits: Seizure: Ventriculitis: 29. Laboratory Aspirate: Stains: Gram/AFB/fungal stains Cultures: aerobic, anaerobic, fungal & TB cytopathology (+/-PCR for TB) WBC: Normalin 40%, only moderateleukocytosis in ~ 50%, & only 10% have WBC>20,000 CRP: almost always elevated ESR : Usually (75%) moderately elevated Blood Cultures : Often negative, BUT Shouldstill be done 30. Radiological: CT 31. Radiological: MRI 32. Radiological: MRI 33. Radiological: MRI (DWI) 34. Radiological: M RI (DWI) 35. Radiological: M RI (DWI) 36. Radiological: M RI (DWI) 37. Radiological: M RI (DWI) differentiation between abscess and mets 38. MRS 39. MRS 40. History 41. History : Diagnostic methods 42. History: Instillation of AB 43. History: Surgical Enuculation 44. Treatment Treatment of abscess: Eradication of primary infected foci 45. Medical Treatment When? Medical therapy alone is more successful if Treatment is begun before complete encapsulation Lesion is 0.8-2.5cm (3.0 cm is the typical cutoff) Duration of symptoms is < 2 weeks The patients should show improvement in the first 2 weeksof treatment What? Antibiotics: Steroids: Advantages / Disadvantages Dehydrating measures: Anticonvulsant therapy: 46. MONITOR RESPONSE CLOSELY WITH SERIAL IMAGING every week 47. Before RxContrast enhancement at the site of the abscess may persistfor several months [3]. Thus, this finding alone is not anAfter completion of Rxindication for continued antibiotic treatment or for surgicalexploration. Cavuoglu et al Neurosurg Focus 2008; 24:E9 48. Antibiotics What? Likely pathogen: considering primary source, underlyingcondition, & geography Biopsy proved: -Antibiotic characteristics: MICs for usual pathogens,CNS penetration, activity in abscess cavity For how long? Usually parental AB 6-8 wks followed by oral AB for 2-6months) After surgical excision, a shorter course may suffice 49. What ? Mandell 6th ed.Predisposing Condition Antimicrobial Regimen Vancomycin + 3rd -generationUnknown cephalosporin+ metronidazolePenetrating trauma orVancomycin + 3rd generationpostneurosurgical cephalosporinOtitis media, Metronidazole + 3rd generationmastoiditis, or Sinusitis cephalosporinVancomycin + gentamicin orBacterial endocarditis(nafcillin + ampicillin + gentamicin)Congenital heart disease 3rd-generation cephalosporinLung abscess, empyema,Penicillin + metronidazole+bronchiectasissulfonamide 50. Another way of Thinking 51. Flagyl: 15 mg/kg IV as a loading dose, Followed by 7.5 mg/kg /8h Vancomycin: 15 mg/kg/12 h Claforan: Adult dose (50 kg or more) 2 g/ 4-6 h. Pediatric dose (less than 50 kg): 50 to 180 mg/kg/ddivided into 4-6 doses Rociphen: Adult dose 2 / 12 hours. Pediatric dose 50mg/kg /12 h Maxipime: Adult dose: 2g /8h. Pediatric dose: 50mg/kg every 8 hours 52. Surgical Treatment: Indications1. Significant mass effect on CT (lesions > 2.5 cm).2. Difficulty in diagnosis.3. Proximity to ventricle.4. Significantly increased intracranial pressure.5. Poor neurological condition.6. Traumatic abscess associated with foreignmaterial7. Fungal abscess.8. Multiloculated abscess.9. CT scans can not be obtained every 1- 2 weeks10. Failure of medical treatment for at least 2 weeks 53. Surgical Treatment: Methods Needle aspiration: Free hand: Stereotactic: Deep seated. Multiple or multiloculated Local instillation of AB: Surgical excision: 54. References Anne G. Osborn et al 2004: Infection and DemyelinatingDisease. In: Diagnostic imaging Brain. First Edition.Amirsys Inc, Salt Lake City, Utah. part I/section 8/ pp 4-82 Srevenc. Bausermanandk. Gillnaul (2001). Bacterial,fungal, and parasitic diseases of the central nervoussystem. In: Principles and practice of neuropathology, 2nded (James S. Nelson, Hernando Mena, Joseph E. Parisi andSydney S. Schochet) Oxford University Press, Inc. pp.45-77 Tunkelv A.R. et al. (2000). Brain Abscess. In: Principlesand Practice of Infectious Diseases, 5th ed. (Mandell,Bennett and Dolin, eds.) pp. 10161028.