Brain abscess gk


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Brain abscess gk

  1. 1. Brain abscess
  2. 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. 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. 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. 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 abscess seen in that population (Transplant, AIDS,…) • More incidence of brain abscess caused by opportunistic pathogens (fungi, toxo…)
  6. 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. 7. PATHOGENESIS• Direct spread from contiguous foci (40-50%)• Hematogenous (25-35%)• Penetrating trauma/surgery (10%)• Cryptogenic (15-20%)
  8. 8. DIRECT SPREAD (from contiguous foci)• 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)
  9. 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. 10. PREDISPOSING CONDITION & LOCATION OF BRAIN ABSCESSOtitis/mastoiditis Temporal lobe, CerebellumFrontal/ethmoid sinusitis Frontal lobeSphenoidal sinusitis Frontal lobe, Sella turcicaDental infection Frontal > temporal lobe.Remote source Middle cerebral artery distribution (often multiple)
  11. 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. 12. Predisposing Conditions & Microbiology of Brain AbscessPredisposing Condition Usual Microbial IsolatesOtitis media or mastoiditis Streptococci (anaerobic or aerobic), Bacteroides and Prevotella spp., EnterobacteriaceaeSinusitis (frontoethmoid or sphenoid) Streptococci, Bacteroides spp., Enterobacteriaceae, Staph. aureus, Haemophilus spp.Dental sepsis Fusobacterium, Prevotella and Bacteroides spp., streptococciPenetrating trauma or postneurosurgical S. aureus, streptococci, Enterobacteriaceae, Clostridium spp.PPID,2000
  13. 13. PREDISPOSING CONDITION USUAL MICROBIAL ISOLATESLung abscess, empyema, bronchiectasis Fusobacterium, Actinomyces, Bacteroides Prevotellaspp., streptococci, NocardiaBacterial endocarditis S. aureus, streptococciCongenital heart disease Streptococci, Haemophilus spp.Neutropenia Aerobic gram-negative bacilli, Aspergillus Mucorales, Candidaspp.Transplantation Aspergillus spp., Candida spp., Mucorales, Enterobacteriaceae, Nocardia spp., Toxoplasma gondiiHIV infection Toxoplasma gondii, Nocardia spp., Mycobacterium spp., Listeria monocytogenes, Cryptococcus neoformansPPID, 2000
  14. 14. MICROBIOLOGY OF BRAIN ABSCESSAGENT FREQUENCY (%)Streptococci (S. intermedius, including S. anginosus) 60–70Bacteroides and Prevotella spp. 20–40Enterobacteriaceae 23–33Staphylococcus aureus 10–15Fungi * 10–15Streptococcus pneumoniae <1Haemophilus influenzae <1Protozoa, helminths † (vary geographically) <1*Yeasts, fungi (Aspergillus Agents of mucor Candida Cryptococci CoccidiodoidesCladosporium trichoides Pseudallescheria boydii)†Protozoa, helminths (Entamoeba histolytica, Schistosomes Paragonimus Cysticerci) CTID,2001
  15. 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. 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 25CTID,2001. PPID,2000
  17. 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. 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. 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. 20. DIAGNOSIS• High index of suspicion• Contrast CT or MRI• Drainage/biopsy, if ring enhancing lesion(s) are seen
  21. 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. 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•LP Contraindicated in 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. 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. 24. Armstrong ID, Mosby inc 1999
  25. 25. MEDICAL TREATMENT ONLY• 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]
  26. 26. CTID,2001
  28. 28. Before RxAfter completion of Rx Armstrong ID,Mosby inc 1999
  29. 29. 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
  30. 30. EPIDURAL ABSCESSES• Spinal > intracranial (9:1)• Intracranially, the dura is adherent to bone• True spinal epidural space is present posteriorly throughout the spine, thus posterior longitudinal spread of infection is common. – Anterior spinal epidural very rare (usually below L1 & cervical)
  31. 31. American Family Physician April 1, 2002
  32. 32. SPINAL EPIDURAL ABSCESS INTRODUCTION• Rare, 0.2-1.2 per 10,000 hospital admissions• Median age 50 yrs (35 yrs in IVDU)• Thoracic>lumbar>cervical• Majority are acquired hematogenously
  33. 33. COMMON PREDISPOSING CONDITIONS• HEMATOGENOUS SPREAD: from remote infections & w IVDU• DIRECT SPREAD: Vertebral osteomyelitis, diskitis, decubitus ulcers, penetrating trauma, surgery, epidural catheters• Via paravertebral venous plexus: from abdominal/pelvic infections
  34. 34. PATHOGENESIS SPINAL EPIDURAL ABSCESS• Often begins as a focal disc or disc-vertebral junction infection• Damage of spinal cord can be caused by: – Direct compression – Thrombosis, thrombophlebitis – Interruption of arterial blood supply – Focal vasculitis – Bacterial toxins/mediators of inflammation• Even a small SEA may cause serious sequelae
  35. 35. MICROBIOLOGY SPINAL EPIDURAL ABSCESSThe most common pathogens are:• Staph aureus >60%• Streptococci 18%• Aerobic GNR 13%• Polymicrobial 10%(Note: TB may cause up to 25% in some areas)
  36. 36. CLINICAL MANIFESTATIONS SPINAL EPIDURAL ABSCESSFour clinical stages have been described: 1. Fever and focal back pain; 2. Nerve root compression with nerve root pain; “shooting pain” 3. Spinal cord compression with accompanying deficits in motor/sensory nerves, bowel/bladder sphincter function; 4. Paralysis (respiratory compromise may also be present if the cervical cord is involved).Armstrong, ID, Mosby inc,2000
  37. 37. DIAGNOSIS SPINAL EPIDURAL ABSCESS (Thinking of it is key, in a pt with fever, severe, focal back pain)• MRI, CT• Abscess drainage• Blood cultures• Routine Labs rarely helpful • ESR,CRP usually elevated, BUT non-specific • WBC may or may not be elevated• LP contraindicated
  38. 38. D/DX SPINAL EPIDURAL ABSCESS• Metastases• Vertebral diskitis and osteomyelitis• Meningitis• Herpes Zoster infection• Other disc/bone disease
  39. 39. TREATMENT SPINAL EPIDURAL ABSCESS• Early surgical decompression/drainage (preferably within first 24h)• Antibiotics – Empiric abx should cover Staph, strep, & GNR – Duration of Rx : 4-6 weeks
  40. 40. (SEA/SDE)• 90% epidural abscesses are spinal• Most SEA occur in thoracic (the longest)• Majority of SEA (>70%) are posterior to the cord• Most SEA caused hematogenous spread & Staph aureus is the leading cause.• 95% SDE are in intracranial• Majority of SDE pts have associated sinusitis
  41. 41. INTRACRANIAL EPIDURAL ABSCESS• Less common & less acute than SEA• Rounded, well-localized (because dura is firmly adherent to bone)• Pathogenesis: – Direct ext. from contiguous foci (sinusitis, otitis/mastoiditis) – trauma,or surgery
  42. 42. INTRACRANIAL EPIDURAL ABSCESS• MICROBIOLOGY: Micraerophillic Strep, Propioni, Peptostrept, few aerobic gNR, fungi. Postop: Staph, GNR.• CLINICAL MANIFESTATION: from SOL/ systmic igns of infection – Fever, HA, N/V, lethargy• DX:- Think of it, imaging, drainage• D/Dx: Tumor, other ICAbscesses• Rx: Surgery + abx• Mortality w appropriate Rx < 10%
  43. 43. SUBDURAL EMPYEMA• 15-20 % of all focal intracranial infections• Motly a complication of sinusitis, otitis media, mastoiditis.• Most common complication of sinusitis (60% of such cases), mostly from frontal/ethmoid sinusitis.• Trauma/post-op & rarely hematogenous• M>F
  44. 44. SUBDURAL EMPYEMA Clinical Manifestations• Fever• Headache• Focal Neuro defects• Vomiting• Mental status changes• Seizures• Mass effect more common w SDE than w ICEADX: CT, MRI (LP contraindicated)Rx: Surgery . Abx (3-6 wks)
  45. 45. (Armstrong, ID,1999, Mosby Inc)
  46. 46. PARASITIC BRAIN ABSCESS• Toxoplasmosis• Neurocysticercosis• Amebic• Echinococcal
  47. 47. NOCARDIA BRAIN ABSCESS• Usually in immunosuppresed (CMI)• >50% no known predisposing factor• All pts w pulmonary nocardiosis should undergo brain imaging to r/o subclinical CNS nocardiosis• Rx: Sulfa (T/S invitro synergy), imipenem, ceftriaxone, amikacin, minocin – Duration of abx <a year. – Needle aspiration or surgical excision needed in most.• Relapse common
  48. 48. BRAIN ABSCESS IN AIDS• Toxoplasmosis is the most common • Seropositive • d/dx lymphoma • Often empiric Rx given & biopsy only non- responders• Listeria, Nocardia, tb, fungi…
  49. 49. BRAIN TB• Rare cause of brain abscess• Usually in immunocompromised• Tuberculoma is a granuloma (not a true abscess )• Biopsy/drainage (send for PCR too )
  50. 50. FUNGAL BRAIN ABSCESS (Aspergillus, Mucor ...)• IMMUNOCOMPROMISED• Poor inflammatory response, less enhancement on CT.• May present w much more advanced disease (seizure, stroke more common)• High mortality• Rx: aggressive surgery + antifungal
  51. 51. BRAIN ABSCESS SEQUELAE• Seizure in 30-60%• Neuro deficits 30-50%• Mortality 4-20%
  52. 52. YIELD OF CULTURES SPINAL EPIDURAL ABSCESS SOURCE YIELD• Abscess fluid aspirate 90%• Blood culture 62%• CSF* 19% *LP often contraindicated