BRAIN ABSCESS

20,561 views

Published on

Published in: Education, Health & Medicine
0 Comments
14 Likes
Statistics
Notes
  • Be the first to comment

No Downloads
Views
Total views
20,561
On SlideShare
0
From Embeds
0
Number of Embeds
7,862
Actions
Shares
0
Downloads
768
Comments
0
Likes
14
Embeds 0
No embeds

No notes for slide

BRAIN ABSCESS

  1. 1. BRAIN ABSCESS
  2. 2. PRESENTED BY:- JASPREET KAUR SODHI
  3. 4. BRAIN ABSCESS <ul><li>The advent of antibiotics and improved treatment of ear diseases has lead to a reduction in intracranial abscess formation ,but the incidence is still 2-3 patients /million/year </li></ul>
  4. 5. Brain Abscess <ul><li>Microorgansims reach the brain by </li></ul><ul><li>i. Direct extension </li></ul><ul><li>ii. Hematogenous spread </li></ul><ul><li>Iii. Direct inoculation from penetrating trauma or neurosurgical intervention </li></ul>
  5. 6. Brain Abscess <ul><li>Younger patients affected (<40 years) </li></ul><ul><li>Presence of predisposing condition in 80% of cases </li></ul><ul><li>Immunocompromised states from AIDS and immunosuppressive drugs in organ transplant recipents </li></ul>
  6. 7. Most Common Pathogens <ul><li>Otitis media, mastoiditis  Streptococci </li></ul><ul><li>Paranasal sinusitis  Streptococci </li></ul><ul><li>Pulmonary infection  Strep, Actionomyces </li></ul><ul><li>Dental  Mixed, Bacteroides spp. </li></ul><ul><li>CHD  Strep </li></ul><ul><li>Penetrating/Post-crani  S. aureus </li></ul><ul><li>HIV  Toxoplasma gondii </li></ul><ul><li>Transplant  Aspergillus, Candida </li></ul>
  7. 8. BRAIN ABSCESS <ul><li>Causes : </li></ul><ul><li>1. complication of bacterial meningitis </li></ul><ul><li>2. bacterial endocarditis </li></ul><ul><li>3. pulmonary sepsis : peumonia……etc </li></ul><ul><li>4. other sepsis </li></ul><ul><li>Brain abscess cause a space occupying lesion in the brain </li></ul>
  8. 9. PREDISPOSING FACTORS <ul><li>Congenital heart disease (6.1%) </li></ul><ul><li>HIV infection (1.2%) </li></ul><ul><li>Immunosuppression (3.7%) </li></ul><ul><li>Diabetes mellitus (3.1%) </li></ul>
  9. 10. Brain Abscess <ul><li>Pathophysiology </li></ul><ul><li>A collection of infectious material within the tissue of the brain </li></ul><ul><li>Infection  </li></ul><ul><li>I-ICP  </li></ul><ul><li>Brain shift </li></ul>
  10. 11. Brain Abscess <ul><li>2 ways infection can enter the brain </li></ul><ul><li>Direct invasion </li></ul><ul><li>Spread from nearby sight </li></ul><ul><ul><li>Sinuses </li></ul></ul><ul><ul><li>Ears </li></ul></ul><ul><ul><li>Teeth </li></ul></ul>
  11. 12. Tongue piercing causes brain abscess <ul><li>13 December 2001 New Scientist </li></ul><ul><li>Parents now have another reason to frown on tongue piercing - a potentially fatal brain abscess suffered by a young woman in Connecticut. </li></ul><ul><li>The woman's tongue became sore and swollen two or three days after it was pierced, and she reported a foul-tasting discharge from the pierced region. The infection healed in a few days after she removed the stud from her tongue, but a month later she suffered severe headaches, fever, nausea and vomiting. </li></ul><ul><li>A scan at the Yale University hospital revealed the brain abscess, which physicians drained. She recovered after six weeks of intravenous antibiotic treatment. </li></ul>
  12. 13. Brain Abscess <ul><li>Clinical manifestations </li></ul><ul><li>I-ICP </li></ul><ul><li>Infection </li></ul><ul><li>Fever? </li></ul><ul><ul><li>Sometimes </li></ul></ul><ul><ul><li>Sometimes not! </li></ul></ul>
  13. 14. PATHOGENESIS <ul><li>Direct spread from contiguous foci (40-50%) </li></ul><ul><li>Hematogenous (25-35%) </li></ul><ul><li>Penetrating trauma/surgery (10%) </li></ul><ul><li>Cryptogenic (15-20%) </li></ul>
  14. 15. DIRECT SPREAD (from contiguous foci) <ul><li>Occurs by: </li></ul><ul><ul><li>Direct extension through infected bone </li></ul></ul><ul><ul><li>Spread through emissary veins, diploic veins, local lymphatics </li></ul></ul><ul><li>The contiguous foci include : </li></ul><ul><ul><ul><li>Otitis media/mastoiditis </li></ul></ul></ul><ul><ul><ul><li>Sinusitis </li></ul></ul></ul><ul><ul><ul><li>Dental infection (<10%), typically with molar infections </li></ul></ul></ul><ul><ul><ul><li>Meningitis rarely complicated by brain abscess (more common in neonates with Citrobacter diversus meningitis, of whom 70% develop brain abscess) </li></ul></ul></ul>
  15. 16. HEMATOGENOUS SPREAD (from remote foci) <ul><li>Sources: </li></ul><ul><ul><li>Empyema, lung abscess, bronchiectasis, endocarditis, wound infections, pelvic infections, intra-abdominal source, etc… </li></ul></ul><ul><ul><li>may be facilitated by cyanotic HD, AVM. </li></ul></ul><ul><li>Results in brain abscess(es) at middle cerebral artery distribution </li></ul><ul><li>Often multiple </li></ul>
  16. 17. PREDISPOSING CONDITION & LOCATION OF BRAIN ABSCESS Otitis/mastoiditis Temporal lobe, Cerebellum Frontal/ethmoid sinusitis Frontal lobe Sphenoidal sinusitis Frontal lobe, Sella turcica Dental infection Frontal > temporal lobe. Remote source Middle cerebral artery distribution (often multiple)
  17. 18. Microbiology of Brain Abscess <ul><li>Dependent upon: </li></ul><ul><ul><ul><li>Site of primary infection </li></ul></ul></ul><ul><ul><ul><li>Patient’s underlying condition </li></ul></ul></ul><ul><ul><ul><li>Geographic location </li></ul></ul></ul><ul><li>Usually streptococci and anaerobes </li></ul><ul><li>Staph aureus, aerobic GNR common after trauma or surgery </li></ul><ul><li>30-60 % are polymicrobial </li></ul>
  18. 19. Brain Abscess <ul><li>Medical Management </li></ul><ul><li>Antimicrobial therapy </li></ul><ul><ul><li>Large IV doses </li></ul></ul><ul><li>Surgery </li></ul><ul><li>Anti-convulsant </li></ul>
  19. 20. Brain Abscess <ul><li>Microorgansims reach the brain by </li></ul><ul><li>i. Direct extension </li></ul><ul><li>ii. Hematogenous spread </li></ul><ul><li>Iii. Direct inoculation from penetrating trauma or neurosurgical intervention </li></ul>
  20. 24. PATHOPHYSIOLOGY <ul><li>Begins as localized cerebritis (1-2 wks) </li></ul><ul><li>Evolves into a collection of pus surrounded by a well-vascularized capsule (3-4 wks) </li></ul><ul><li>Lesion evolution ( based on experimental animal models ): </li></ul><ul><ul><li>Days 1-3: “early cerebritis stage” </li></ul></ul><ul><ul><li>Days 4-9: “late cerebritis stage” </li></ul></ul><ul><ul><li>Days 10-14: “early capsule stage” </li></ul></ul><ul><ul><li>> day14: “late capsule stage” </li></ul></ul>
  21. 25. STAGES <ul><li>1. Early cerebritis stage (D1-3):focal area of inflammation and edema </li></ul><ul><li>2 . Late cerebritis stage (D4-9):development of a necrotic central focus </li></ul><ul><li>3. Early capsule stage (D10-14):ring-enhancing capsule of well-vascularized tissue with early appearance of peripheral fibrosis </li></ul><ul><li>4. Late capsule stage (>D14):host defenses lead to a well-formed capsule </li></ul>
  22. 26. PATHOGENESIS <ul><li>Bacterial invasion of brain </li></ul><ul><li>(Parenchyma ) </li></ul><ul><li>Preexisting or concomitant : </li></ul><ul><li>Ischemia & </li></ul><ul><li>Necrosis & </li></ul><ul><li>Hypoxia of brain tissue </li></ul>
  23. 27. PATHOGENESIS <ul><li>Early cerebritis ( days 1 to 3 ) </li></ul><ul><li>Prevascular infiltration of inflammatory cells </li></ul><ul><li>Central core of coagulative necrosis </li></ul><ul><li>Marked edema surrounds the lesions </li></ul>Stage 1
  24. 28. Early Cerebritis
  25. 29. Early cerebritis
  26. 30. <ul><li>Late cerebritis( days 4 to 9 ) </li></ul><ul><li>Pus formation ( necrotic center ) </li></ul><ul><li>Macrophages & Fibroblasts </li></ul><ul><li>Thin capsule( Fibroblast & Reticular fibers ) </li></ul><ul><li>Marked edema around the lesions </li></ul>Stage 2
  27. 31. Late Cerebritis
  28. 32. <ul><li>Early Capsule formation ( days 10 to13 ) </li></ul><ul><li>Capsule formation </li></ul><ul><li>Ring-enhancing capsule ( Imaging ) </li></ul>Stage 3
  29. 34. Early Capsule formation
  30. 35. Stage 4 <ul><li>Late Capsule formation ( > 14 days ) </li></ul><ul><li>Well formed necrotic center </li></ul><ul><li>Dense peripheral collagenous capsule </li></ul><ul><li>No cerebral edema </li></ul><ul><li>Marked gliosis & reactive astrocytes </li></ul><ul><li>Gliosis  Seizures </li></ul>
  31. 37. CLINICAL PRESENTATIONS Brain abscess presents as an Expanding Intracranial mass <ul><li>Headache > 75% </li></ul><ul><li>Constant, Dull, </li></ul><ul><li>Aching sensation </li></ul><ul><li>Hemicranial or General </li></ul><ul><li>Progressive  Refractory </li></ul><ul><li>Fever: 50% & Low grade </li></ul><ul><li>Seizure: New onset </li></ul><ul><li>Focal or Generalized </li></ul>
  32. 38. CLINICAL PRESENTATIONS <ul><li>Increased Intracranial Pressure: </li></ul><ul><li>Papilledema </li></ul><ul><li>Nausea </li></ul><ul><li>Vomiting </li></ul><ul><li>Drowsiness </li></ul><ul><li>Confusion </li></ul><ul><li>Meningismus: </li></ul><ul><li>When it has ruptured into </li></ul><ul><li>Ventricle or subarachnoid space </li></ul>
  33. 39. CLINICAL PRESENTATIONS
  34. 40. CLINICAL MANIFESTATIONS <ul><li>Non-specific symptoms </li></ul><ul><li>Mainly due to the presence of a space-occupying lesion </li></ul><ul><ul><ul><li>H/A, N/V, lethargy, focal neuro signs , seizures </li></ul></ul></ul><ul><li>Signs/symptoms influenced by </li></ul><ul><ul><ul><li>Location </li></ul></ul></ul><ul><ul><ul><li>Size </li></ul></ul></ul><ul><ul><ul><li>Virulence of organism </li></ul></ul></ul><ul><ul><ul><li>Presence of underlying condition </li></ul></ul></ul>
  35. 41. 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
  36. 42. CLINICAL MANIFESTATIONS <ul><ul><ul><li>Headache </li></ul></ul></ul><ul><ul><ul><li>Often dull, poorly localized (hemicranial?), non-specific </li></ul></ul></ul><ul><ul><ul><ul><li>Abrupt, extremely severe H/A: think meningitis, SAH. </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Sudden worsening in H/A w meningismus: think rupture of brain abscess into ventricle (often fatal) </li></ul></ul></ul></ul>
  37. 43. LOCATION & CLINICAL FEATURES <ul><li>FRONTAL LOBE : H/A, drowsiness, inattention, hemiparesis, motor speech disorder, AMS </li></ul><ul><li>TEMPORAL LOBE : Ipsilateral H/A, aphasia, visual field defect </li></ul><ul><li>PARIETAL LOBE : H/A, visual field defects, endocrine disturbances </li></ul><ul><li>CEREBELLUM : Nystagmus, ataxia, vomiting, dysmetria </li></ul>
  38. 44. Brain Abscess <ul><li>Diagnostic findings </li></ul><ul><li>CT </li></ul><ul><li>MRI </li></ul>
  39. 45. DIAGNOSIS <ul><li>High index of suspicion </li></ul><ul><li>Contrast CT or MRI </li></ul><ul><li>Drainage/biopsy, if ring enhancing lesion (s) are seen </li></ul>
  40. 46. TREATMENT <ul><li>Combined medical & surgical </li></ul><ul><ul><ul><li>Aspiration or excision </li></ul></ul></ul><ul><ul><ul><li>empirical abx </li></ul></ul></ul><ul><li>Empirical antibiotics are selected based on: </li></ul><ul><ul><ul><li>Likely pathogen (consider primary source, underlying condition, & geography) </li></ul></ul></ul><ul><ul><ul><li>Antibiotic characteristics: usual MICs, CNS penetration, activity in abscess cavity </li></ul></ul></ul><ul><li>Modify abx based on stains </li></ul><ul><li>Duration: usually 6-8 wks </li></ul><ul><ul><ul><li>after surgical excision, a shorter course may suffice </li></ul></ul></ul>
  41. 47. Armstrong ID, Mosby inc 1999
  42. 48. MEDICAL TREATMENT ONLY <ul><li>Only in pts with prohibitive surgical risk: </li></ul><ul><ul><li>poor surgical candidate, </li></ul></ul><ul><ul><li>multiple abscesses, </li></ul></ul><ul><ul><li>in a dominant location, </li></ul></ul><ul><ul><li>Abscess size < 2.5 cm </li></ul></ul><ul><ul><li>concomitant meningitis, ependymitis, </li></ul></ul><ul><ul><li>early abscess (cerebritis?) </li></ul></ul><ul><ul><li>with improvement on abx, </li></ul></ul><ul><li>[Better-vascularized cortical lesions more likely to respond to abx alone] </li></ul><ul><li>[ Subcortical/white-matter lesions are poorly vascularized] </li></ul>
  43. 49. Treatment <ul><li>I.V. Antibiotics 6 weeks </li></ul><ul><li>Steroids </li></ul><ul><li>Surgical intervention: Stereotactic aspiration vs. craniotomy </li></ul>
  44. 50. ANTIBIOTICS <ul><li>CEFTRIAXONE i.v 3-4 g/day </li></ul><ul><li>METRONIDAZOLE i.v 500 mg tds </li></ul><ul><li>+ amoxicillin iv 2g 4 hourly (for middle ear source) </li></ul><ul><li>I f ENDOCARDITIS OR CONGENITAL HEART FAILURE DISEASES , </li></ul><ul><li>+ benzylpenicillin i.v 1.8-2.4 g 6hourly </li></ul><ul><li>IF A PENETRATING TRAUMA, </li></ul><ul><li>FLUCLOXACILLIN-i.v 2g 4 hourly. </li></ul><ul><li>GENTAMICIN –i.v 5 mg/kg/day(monitor levels) </li></ul>
  45. 51. ABSCESS DRAINAGE <ul><li>Primary excision of the whole abscess </li></ul><ul><li>Burr hole aspiration of pus,guided by ultrasound & frameless sterotaxy,with repeated aspirations if required. </li></ul><ul><li>Evacuation of abscess contents under direct vision, leaving capsule remnants . </li></ul>
  46. 52. TREATMENT OF INFECTION SITE <ul><li>Mastoditis and sinusitis require immediate surgery. </li></ul><ul><li>Use of steroids is controversial. </li></ul><ul><li>Conservative management </li></ul>
  47. 53. <ul><li>FEW PICTURES RELATED TO BRAIN ABSCESS </li></ul>

×