Brain abscess 2012

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  • Frontal LobeFrontal and Ethmoidal SinusesSellaTurcicaSphenoidal sinusesTemporal LobeMiddle Ear, Mastoid, Maxillary SinusesCerebellum, Brain StemMiddle Ear, Mastoid
  • Streptococci, both microaerophilic and anaerobic especially the Streptococcus milleri group are recently more prevalent up to 70% of cases (Tunkel et al., 2000). Bacteroidesspecies and gram-negative bacilli are other frequent causes In recent years abscesses due to, fungi, and parasites have been encountered more frequently, especially in patients with AIDSTunkelv A.R. et al. (2000). Brain Abscess. In: Principles and Practice of Infectious Diseases, 5th ed. (Mandell, Bennett and Dolin, eds.) pp. 1016–1028.
  • The causes are rather diverse in terms of etiologic organisms, but certain organisms predominate, especially in certain settings. Srevenc. Bausermanandk. Gillnaul (2001). Bacterial, fungal, and parasitic diseases of the central nervous system. In: Principles and practice of neuropathology, 2nded (James S. Nelson, Hernando Mena, Joseph E. Parisi and Sydney S. Schochet) Oxford University Press, Inc. pp.45-77
  • Age: May occur at any age Most common during third and fourth decades, but 25% occur in patients < 15 years Risk factors: Predisposing conditions to some extent predict causative organisms as follows: Decreased cell-mediated immunity is associated with Toxoplasma, Nocardia, Cryptococcus, Listeria, and mycobacterial species; Neutropenia/ neutrophilic functional defects are associated with aerobic gram-negative organisms, Aspergillusspecies, Zygomycetes (mucor), and Candida species.
  • Site:typically arise in the white matter or at the gray–white junction. They are most common in the distribution of the middle cerebral artery zones involving frontal, temporal, and parietal lobes. Infratentorial in about 14%. Brainstem and ganglionic involvement is rare. (Eur J Clin Microbiol Infect Dis (2007) 26:1–11) Size: Variable 5mm - severalNumber: Multiple brain abscesses are identified in 10%–50% of cases since high-quality imaging studies have been available (Tunkel et al., 2000).Tunkelv A.R. et al. (2000). Brain Abscess. In: Principles and Practice of Infectious Diseases, 5th ed. (Mandell, Bennett and Dolin, eds.) pp. 1016–1028.
  • Site:typically arise in the white matter or at the gray–white junction. They are most common in the distribution of the middle cerebral artery zones involving frontal, temporal, and parietal lobes. Infratentorial in about 14%. Brainstem and ganglionic involvement is rare. (Eur J Clin Microbiol Infect Dis (2007) 26:1–11) Size: Variable 5mm - severalNumber: Multiple brain abscesses are identified in 10%–50% of cases since high-quality imaging studies have been available (Tunkel et al., 2000).Tunkelv A.R. et al. (2000). Brain Abscess. In: Principles and Practice of Infectious Diseases, 5th ed. (Mandell, Bennett and Dolin, eds.) pp. 1016–1028.
  • Early cerebritis (3-5 days) Infection is focal but not localizedUnencapsulated mass of PMNs, edema, scattered foci of necrosis and petechial hemorrhage Late cerebritis (4-5 days up to 2 weeks) Necrotic foci coalesce Rim of inflammatory cells, macrophages, granulation tissue, fibroblasts surrounds central necrotic core Vascular proliferation, surrounding vasogenic edema Early capsule (begins at around 2 weeks): Histologically three zones are characterized in the mature abscess: The central suppurative focus, A zone of acute and chronic inflammation and well-delineated collagenous capsule. The neovascularization and appearance of fibroblasts herald the early organization/encapsulation stage, with capsule being 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. The proliferating endothelial cells in the capsule do not form a competent blood–brain barrier and lead to continuing vasogenic edema Peripherally edematous, gliotic parenchyma Late capsule (weeks to months) Central cavity shrinks Thick wall (collagen, granulation tissue, macrophages, gliosis). The encapsulation, even at a late stage, is usually less than a few millimeters in thickness, developing at approximately 1 mm in a month’s time
  • CT appeareance dependent on stage Early cerebritis: Ill-defined hypodensesubcortical lesion with mass effect; may be normal early. +/- Mild patchy enhancement Late cerebritic stage:Central low density area; peripheral edema, mass effect increase. Irregular peripheral rim enhancement. Early Capsular stage: Hypodense mass with moderate vasogenic edema and mass. thin, distinct enhancing capsule. Deep part of capsule is thinnest while thickest near cortex Late capsule: Edema, mass effect diminish. With contrast cavity shrinks, capsule thickens. May be multiloculated and have "daughter“ abscessesMRI TlWI Early cerebritis: Poorly marginated, mixed hypointense/isointense mass Late cerebritis: Hypointense center, isointense/mildly hyperintense rim Early capsule: Rim isointense to hyperintense to WM; center hyperintense to CSF Late capsule: Cavity shrinks, capsule thickens T2WI Early cerebritis: Ill-defined hyperintense mass Late cerebritis: Hyperintense center, hypointense rim; hyperintense edema Early capsule: Hypointense rim. Related to collagen, hemorrhage, or paramagnetic free radicals Late capsule: Edema and mass effect diminish Resolving abscess: Hyperintense on T2WI, FLAIR DWI Increased signal intensity in cerebritis and abscessTl C+ Early cerebritis: Patchy enhancement Late cerebritis: Intense but irregular rim enhancement Early capsule: Well-defined, thin-walled enhancing rim Late capsule: Cavity collapses, thickened enhancement of capsule. Capsule is thinnest on the ventricular side Resolving abscess: Small ring/punctate enhancing focus may persist for monthsMRS: Central necrotic area may show presence of acetate, lactate, alanine, succinate, pyruvate, and amino acids
  • CT appeareance dependent on stage Early cerebritis: Ill-defined hypodensesubcortical lesion with mass effect; may be normal early. +/- Mild patchy enhancement Late cerebritic stage:Central low density area; peripheral edema, mass effect increase. Irregular peripheral rim enhancement. Early Capsular stage: Hypodense mass with moderate vasogenic edema and mass. thin, distinct enhancing capsule. Deep part of capsule is thinnest while thickest near cortex Late capsule: Edema, mass effect diminish. With contrast cavity shrinks, capsule thickens. May be multiloculated and have "daughter“ abscessesMRI TlWI Early cerebritis: Poorly marginated, mixed hypointense/isointense mass Late cerebritis: Hypointense center, isointense/mildly hyperintense rim Early capsule: Rim isointense to hyperintense to WM; center hyperintense to CSF Late capsule: Cavity shrinks, capsule thickens T2WI Early cerebritis: Ill-defined hyperintense mass Late cerebritis: Hyperintense center, hypointense rim; hyperintense edema Early capsule: Hypointense rim. Related to collagen, hemorrhage, or paramagnetic free radicals Late capsule: Edema and mass effect diminish Resolving abscess: Hyperintense on T2WI, FLAIR DWI Increased signal intensity in cerebritis and abscessTl C+ Early cerebritis: Patchy enhancement Late cerebritis: Intense but irregular rim enhancement Early capsule: Well-defined, thin-walled enhancing rim Late capsule: Cavity collapses, thickened enhancement of capsule. Capsule is thinnest on the ventricular side Resolving abscess: Small ring/punctate enhancing focus may persist for monthsMRS: Central necrotic area may show presence of acetate, lactate, alanine, succinate, pyruvate, and amino acids
  • CT appeareance dependent on stage Early cerebritis: Ill-defined hypodensesubcortical lesion with mass effect; may be normal early. +/- Mild patchy enhancement Late cerebritic stage:Central low density area; peripheral edema, mass effect increase. Irregular peripheral rim enhancement. Early Capsular stage: Hypodense mass with moderate vasogenic edema and mass. thin, distinct enhancing capsule. Deep part of capsule is thinnest while thickest near cortex Late capsule: Edema, mass effect diminish. With contrast cavity shrinks, capsule thickens. May be multiloculated and have "daughter“ abscessesMRI TlWI Early cerebritis: Poorly marginated, mixed hypointense/isointense mass Late cerebritis: Hypointense center, isointense/mildly hyperintense rim Early capsule: Rim isointense to hyperintense to WM; center hyperintense to CSF Late capsule: Cavity shrinks, capsule thickens T2WI Early cerebritis: Ill-defined hyperintense mass Late cerebritis: Hyperintense center, hypointense rim; hyperintense edema Early capsule: Hypointense rim. Related to collagen, hemorrhage, or paramagnetic free radicals Late capsule: Edema and mass effect diminish Resolving abscess: Hyperintense on T2WI, FLAIR DWI Increased signal intensity in cerebritis and abscessTl C+ Early cerebritis: Patchy enhancement Late cerebritis: Intense but irregular rim enhancement Early capsule: Well-defined, thin-walled enhancing rim Late capsule: Cavity collapses, thickened enhancement of capsule. Capsule is thinnest on the ventricular side Resolving abscess: Small ring/punctate enhancing focus may persist for monthsMRS: Central necrotic area may show presence of acetate, lactate, alanine, succinate, pyruvate, and amino acids
  • CT appeareance dependent on stage Early cerebritis: Ill-defined hypodensesubcortical lesion with mass effect; may be normal early. +/- Mild patchy enhancement Late cerebritic stage:Central low density area; peripheral edema, mass effect increase. Irregular peripheral rim enhancement. Early Capsular stage: Hypodense mass with moderate vasogenic edema and mass. thin, distinct enhancing capsule. Deep part of capsule is thinnest while thickest near cortex Late capsule: Edema, mass effect diminish. With contrast cavity shrinks, capsule thickens. May be multiloculated and have "daughter“ abscessesMRI TlWI Early cerebritis: Poorly marginated, mixed hypointense/isointense mass Late cerebritis: Hypointense center, isointense/mildly hyperintense rim Early capsule: Rim isointense to hyperintense to WM; center hyperintense to CSF Late capsule: Cavity shrinks, capsule thickens T2WI Early cerebritis: Ill-defined hyperintense mass Late cerebritis: Hyperintense center, hypointense rim; hyperintense edema Early capsule: Hypointense rim. Related to collagen, hemorrhage, or paramagnetic free radicals Late capsule: Edema and mass effect diminish Resolving abscess: Hyperintense on T2WI, FLAIR DWI Increased signal intensity in cerebritis and abscessTl C+ Early cerebritis: Patchy enhancement Late cerebritis: Intense but irregular rim enhancement Early capsule: Well-defined, thin-walled enhancing rim Late capsule: Cavity collapses, thickened enhancement of capsule. Capsule is thinnest on the ventricular side Resolving abscess: Small ring/punctate enhancing focus may persist for monthsMRS: Central necrotic area may show presence of acetate, lactate, alanine, succinate, pyruvate, and amino acids
  • capsule being 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.
  • Mortality from brain abscess is generally secondary to herniation, and less commonly is due to rupture into the ventricular system.Mortality down to 0-24% over the past three decades, with:Advances in radiography [CT scanning (1974), MRI] Advances in surgeryStereotactic brain biopsy/aspiration techniquesNewer abx(e.g. cephalosporins, metronidazole..)Better treatment of predisposing conditions
  • Manifestations are influenced by Location of abscessSize of abscessVirulence of organismPresence of underlying condition
  • At the time of aspiration,specimens should be sent for􀁺 Gram stain􀁺 aerobic and anaerobic cultures􀁺 cultures for mycobacteria and fungi􀁺􀁺 acid-fast stains for mycobacteria􀁺 modified acid-fast stains for Nocardia􀁺􀁺 special stains (e.g., mucicarmine, methenamine silver) for fungiMandell, Bennett, & Dolin: Principles and Practice of Infectious Diseases, 6th ed.
  • MRI of the brain reveals a 2-cm, round, ring-enhancing lesion in the right lentiform nucleus with associated vasogenic edema and midline shift to the left. A, T1-weighted image reveals an ill-defined area of low attenuation. B, T1-weighted image after administration of gadolinium, which reveals ring enhancement of the abscess. C, T2-weighted image demonstrates hypointensity of the rim of the abscess with a large area of high signal intensity consistent with cerebral edema.PPID,2005
  • DWI yielded􀁺􀁺 a sensitivity of 93.33%􀁺 a specificity of 90.91%
  • DWI yielded􀁺􀁺 a sensitivity of 93.33%􀁺 a specificity of 90.91%
  • DWI yielded􀁺􀁺 a sensitivity of 93.33%􀁺 a specificity of 90.91%
  • DWI yielded􀁺􀁺 a sensitivity of 93.33%􀁺 a specificity of 90.91%
  • DWI yielded􀁺􀁺 a sensitivity of 93.33%􀁺 a specificity of 90.91%
  • DWI yielded􀁺􀁺 a sensitivity of 93.33%􀁺 a specificity of 90.91%
  • Spectral patterns from in vivo MR spectroscopy may permit differentiation of brain abscess from necrotic or cystic tumor.
  • Spectral patterns from in vivo MR spectroscopy may permit differentiation of brain abscess from necrotic or cystic tumor.
  • Primary or metastatic neoplasm• Thick, nodular enhancing wall typical• Low signal on DWI (occasionally high, can mimicabscess)Resolving hematoma• History of trauma or vascular lesion• Blood products presentDemyelination• Enhancement often incomplete ring• Characteristic lesions elsewhere in brain• Small amount of mass effect for size of lesionSubacute infarct• History of stroke• Vascular distribution, gyriform enhancement
  • CorticosteroidsAdvantagespts with increased intracranial pressurepotentially lifethreatening complications, such as impending cerebral herniationDisadvantages: (1) Reduction in contrast enhancement on CT scan Slowing of capsule formation Increasing the risk of ventricular rupture Decreasing the penetration of antibiotics into the abscessDose: Dexamethasone is administered at a loading dose 10 mg IV followed by 4 mg every six hours.Anticonvulsant therapy: Incidence of subsequent seizures after brain abscess approached 70%. Seizure prophylaxis or anti-epileptic medication should be given in every case and continued for extended periods (1) Quartey, GR, Johnston, JA, Rozdilsky, B. Decadron in the treatment of cerebral abscess. An experimental study. J Neurosurg 1976; 45:301.
  • Cavuşoglu, H, Kaya, RA, Türkmenoglu, ON, et al. Brain abscess: analysis of results in a series of 51 patients with a combined surgical and medical approach during an 11-year period. Neurosurg Focus 2008; 24:E9.
  • Duration of Antimicrobial therapyhigh-dose iv antibiotics has traditionally been administered for 6 to 8 weeks in pts with bacterial brain abscesses Often followed by oral antibiotic therapy for 2- 6 months, although the efficacy and necessity of this approach has not been established.Shorter courses (3-4 wks) of antimicrobial therapy may be adequate for pts who have undergone surgical excision of the abscess.Mandell, Bennett, & Dolin: Principles and Practice of Infectious Diseases, 6th ed.
  • 3rd cephalosporin recommendCefotaxime (claforan), ceftriaxone (Rocephin), or cefepime (Maxipime)Use ceftazidime (fortum) or cefepime (Maxipime) as the 3rd generation cephalosporin if Pseudomonas aeruginosa is suspected (as in post operative abscess).Trimethoprim-sulfamethoxazole if a Nocardiaspecies is suspectMetronidazole “Flagyl (15 mg/kg IV as a loading dose, followed by 7.5 mg/kg IV every eight hours; not to exceed 4 g per day)Ceftriaxone “Rociphen”: Adult dose 2 / 12 hours. Pediatric dose 50mg/kg /12 hCefotaxime “Claforan”: Adult dose (50 kg or more) 12 g/d on 4-6 doses. Pediatric dose (less than 50 kg): 50 to 180 mg/kg/d divided into 4-6 dosesCefepime “Maxipime”: adult dose: 2 g IV every eight hours. Pediatric dose: 50mg/kg every 8 hoursVancomycin (30 mg/kg IV daily in two equally divided doses adjusted for renal function) If susceptibility testing reveals methicillin-sensitive S. aureus, vancomycin should be replaced with nafcillin (2 g IV every four hours) or oxacillin (2 g IV every four hours) since these agents have better CNS penetration than vancomycinCeftazidime “Fortum”: 2 g IV every eight hours. Pediatric dose: 25-100 mg/kg/day in three divided doses (in less than one year pediatric can be given in two divided doses)Mandell, Bennett, & Dolin: Principles and Practice of Infectious Diseases, 6th ed.
  • “Fortum”: 2 g IV every eight hours. Pediatric dose: 25-100 mg/kg/day in three divided doses (in less than one year pediatric can be given in two divided doses)
  • Instillation of antibiotics directly into the abscess: has not been extremely effective, although it may be used as a last resort in AspergillusAspergillusabscesses.
  • Brain abscess 2012

    1. 1. Ilos Enumerate the commonest causative organism of the brain abscess. Discuss the pathogenesis of brain abscess Discuss the epidemiology of the commonest CNS bacterial abscess. Describe the gross & histopathological features of the 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. 2. ACUTE FOCAL SUPPURATIVE CNS INFECTIONS Brain abscess Subdural Empyema Extradural Abscess Spinal epidural abscess Spondylodiscitis epidural abscess
    3. 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. 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. 5. Microbiology AGENT FREQUENCY (%)Streptococci (S. intermedius, including S. anginosus) 60–70 %Bacteroides and Prevotella spp. 20–40Enterobacteriaceae 23–33Staphylococcus aureus 10–15Fungi * 10–15Streptococcus pneumoniae <1Haemophilus influenzae <1Protozoa, helminths † (vary geographically) <1*Fungi (Aspergillus Agents of mucor Candida Cryptococci CoccidiodoidesCladosporium trichoides Pseudallescheria boydii)†Protozoa, helminths (Entamoeba histolytica, Schistosomes ParagonimusCysticerci)
    6. 6. Pathogen PREDISPOSING CONDITION USUAL MICROBIAL ISOLATES otitis/mastoiditis. Mixed flora of Streptococci (anaerobic or aerobic), Bacteroides and Prevotella spp., EnterobacteriaceaeSinusitis (frontoethmoid …….+ Staph. aureus, Haemophilus spp. or sphenoid) post-traumatic or S. aureus, streptococci, Enterobacteriaceae, Clostridium spp postneurosurgical Bacterial endocarditis S. aureus, streptococciCongenital heart disease Streptococci, Haemophilus spp.Lung abscess, empyema, Fusobacterium, Actinomyces, Bacteroides , Prevotella spp., streptococci, Nocardia bronchiectasis Neutropenia Aerobic gram-negative bacilli, Aspergillus , Mucorales, Candidaspp AIDS Toxoplasmosis, Nocardia, Mycobacterium Tuberculosis Diabetic: Klebsiella pneumoniae Posttransplant Nocardia, Aspergillus, Candida Transplantation Aspergillus spp., Candida spp., Mucorales, Enterobacteriaceae, Nocardia spp., Toxoplasma gondii Neonates Citrobacter, Proteus, Pseudomonas, Serratia, Staphylococcus aureus
    7. 7. Pathogen Streptococci most commonly (70%) Bacteroides and Prevotella in 20% to 40% Enteric gram-negative bacilli (e.g., Proteus species, Escherichia coli, Klebsiella and Pseudomonas) in 23% to 33% Staphylococcus aureus for 10% to 15% Rarely <1% of cases  Haemophilus influenzae  Streptococcus pneumoniae  Listeria monocytogenes ( Immunocompromised 85%)  facultative gram-negative organisms ( Citrobacter diversus, Proteusm, Serratia marcescens, Enterobacter)
    8. 8.  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
    9. 9. Epidemiology Incidence: Sex: M:F = 2:1 Race: Age: any age but most common during 3rd-4th decades Risk factors:  IVDA (2.5%)  Congenital heart disease (6.1%)  HIV infection (1.2%)  Immunosuppression (3.7%)  Diabetes mellitus (3.1%)
    10. 10.  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
    11. 11. Macroscopic features Site: frontal > Parietal > other lobes Size: Variable, 5 mm – several cms Number: 10-50 % are multiple Character: According to stages  Early cerebritis - poorly demarcated from surrounding brain  Late cerebritis - reticular marix (collagen precursor) and developing necrotic center  Early capsule formation - neovascularity, necrotic center, developing capsule  Late capsule formation - collagen capsule, necrotic center, gliosis surrounding capsule
    12. 12. Macroscopic features Site: frontal > Parietal > other lobes Size: Variable, 5 mm – several cms Number: 10-50 % are multiple PREDISPOSING LOCATION OF ABSCESS CONDITION Character: According to stages Otitis/mastoiditis - poorly demarcated Cerebellum  Early cerebritis Temporal lobe, from surrounding brain Frontal/ethmoid Frontal 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 artery Middle distribution (often multiple)
    13. 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. 14. Microscopic features
    15. 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. 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. 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. 18. Radiological features: CT
    19. 19. Radiological features: MRI Early cerebritis
    20. 20. Radiological features: MRI Early capsule
    21. 21. Radiological features: MRI Late capsule
    22. 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. 23.  Capsule being 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. 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. 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. 26. Prognosis Mortality: 0-24% Morbidity: 45%  Seizure in 30-60%  Neuro deficits 30-50% Late focal or generalized seizures - 27%
    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. 28.  Usually non-specific symptoms Increase intracranial pressure: Neurological deficits: Seizure: Ventriculitis:
    29. 29. Laboratory Aspirate:  Stains: Gram/AFB/fungal stains  Cultures: aerobic, anaerobic, fungal & TB  cytopathology (+/-PCR for TB) WBC: Normal in 40%, only moderate leukocytosis in ~ 50%, & only 10% have WBC >20,000 CRP: almost always elevated ESR : Usually (75%) moderately elevated Blood Cultures : Often negative, BUT Should still be done
    30. 30. Radiological: CT
    31. 31. Radiological: MRI
    32. 32. Radiological: MRI
    33. 33. Radiological: MRI (DWI)
    34. 34. Radiological: M RI (DWI)
    35. 35. Radiological: M RI (DWI)
    36. 36. Radiological: M RI (DWI)
    37. 37. Radiological: M RI (DWI) differentiation between abscess and mets
    38. 38. MRS
    39. 39. MRS
    40. 40. History
    41. 41. History : Diagnostic methods
    42. 42. History: Instillation of AB
    43. 43. History: Surgical Enuculation
    44. 44. Treatment Treatment of abscess: Eradication of primary infected foci
    45. 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 weeks of treatment What?  Antibiotics:  Steroids: Advantages / Disadvantages  Dehydrating measures:  Anticonvulsant therapy:
    46. 46. MONITOR RESPONSE CLOSELY WITH SERIAL IMAGING every week
    47. 47. Before RxContrast enhancement at the site of the abscess may persist for several months [3]. Thus, this finding alone is not an After completion of Rxindication for continued antibiotic treatment or for surgical exploration. Cavuşoglu et al Neurosurg Focus 2008; 24:E9
    48. 48. Antibiotics What?  Likely pathogen: considering primary source, underlying condition, & 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 2-6 months)  After surgical excision, a shorter course may suffice
    49. 49. What ? “Mandell 6th ed.”Predisposing Condition Antimicrobial Regimen Vancomycin + 3rd -generationUnknown cephalosporin+ metronidazolePenetrating trauma or Vancomycin + 3rd generationpostneurosurgical cephalosporinOtitis media, Metronidazole + 3rd generationmastoiditis, or Sinusitis cephalosporin Vancomycin + gentamicin orBacterial endocarditis (nafcillin + ampicillin + gentamicin)Congenital heart disease 3rd-generation cephalosporinLung abscess, empyema, Penicillin + metronidazole+bronchiectasis sulfonamide
    50. 50. Another way of Thinking
    51. 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/d divided 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. 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. 53. Surgical Treatment: Methods Needle aspiration:  Free hand:  Stereotactic:  Deep seated.  Multiple or multiloculated Local instillation of AB: Surgical excision:
    54. 54. References Anne G. Osborn et al 2004: Infection and Demyelinating Disease. 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 nervous system. In: Principles and practice of neuropathology, 2nd ed (James S. Nelson, Hernando Mena, Joseph E. Parisi and Sydney S. Schochet) Oxford University Press, Inc. pp.45- 77 Tunkelv A.R. et al. (2000). Brain Abscess. In: Principles and Practice of Infectious Diseases, 5th ed. (Mandell, Bennett and Dolin, eds.) pp. 1016–1028.

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