1 / 34

CNS INFECTIONS – BRAIN ABSCESS

CNS INFECTIONS – BRAIN ABSCESS. Prof.Arjun Shetty Dept Of Neurosurgery Yenepoya Medical College. Brain abscess. Occurs when micro organisms are introduced into the cerebral tissues commonly as a result of 1.trauma 2.contiguous infection 3.hematogenous dissemination of infection.

greeves
Télécharger la présentation

CNS INFECTIONS – BRAIN ABSCESS

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript


  1. CNS INFECTIONS – BRAIN ABSCESS Prof.Arjun Shetty Dept Of Neurosurgery Yenepoya Medical College

  2. Brain abscess • Occurs when micro organisms are introduced into the cerebral tissues commonly as a result of • 1.trauma • 2.contiguous infection • 3.hematogenous dissemination of infection

  3. Slide for prc 330.1 and 3285

  4. Frontal sinus infection • Retrograde thrombophlebitis of diploic vein • Direct extension secondary to osteomyelitis • Abscess in frontal lobe base

  5. Middle ear infection • Direct spread through tegmen tympani • Trans-labyrinthine spread through round/oval window • Direct spread of mastoid sinus infection • Abscess in temporal lobe • Abscess secondary to mastoiditis can occur in the cerebellum

  6. Abscesses due to sinusitis or otitis tend to be single and superficial

  7. Hematogenous spread of infection • Skin pustules • Pulmonary infection • Osteomyelitis • Dental abscess • Diverticulitis • Infective bacterial endocarditis

  8. Hematogenous abscesses occur usually in M.C.A territory • These abscesses occur in the cortico medullary junction – slow blood flow • Can be multiple • Blood brain barrier usually prevents abscess formation secondary to transient bacteremia

  9. Brain abscess can be associated with cyanotic heart disease especially right to left shunt

  10. Right to left shunt • Pulmonary capillary filtration is bypassed • Hypoxia leads to polycythemia and increased blood viscosity which causes micro infarcts – nidus for infection

  11. Abscess secondary to cyanotic heart disease have usually single unlike those associated with bacterial endocarditis • Fallot’s tetrology – 50% • Transposition of great vessels • Tricuspid atresia • ASD , VSD

  12. microbiology • In the pre-antibiotic era - staph aureus • Anaerobes are now becoming common • Bacteroids • Anaerobic streptococci • Peptococcus • actinomycosis

  13. aerobes • Staph aureus • Streptococcus enterobactericiae • Haemophilus • 1/3 cases have mixed infection especially secondary to otogenic infection • Neonates – proteus and citrobacter

  14. Immunocompromised patients • Fungal infections – candida,aspergillus,cryptococcus neoformans • Toxoplasmosis – commonest non viral infection in HIV patients

  15. pathology • Stage of early cerebritis : • 1-3 days • necrotic center • local inflammation around the vessels

  16. Stage of late cerebritis : • 4-9 days • Increased necrotic center • Zone of inflammatory cells and macrophages • Fibroblasts lay down reticulin

  17. Stage of early capsule formation : • Day 10-13 • Reticulin network forms capsule

  18. Stage of late capsule formation : • >14 days • Necrotic center • Inflammatory zone and fibroblasts • Capsule • Neo-vasculature surrounding capsule • Zone of edema and reactive gliosis

  19. Clinical features • Male predominance • Symptoms of raised ICP • Fever – tends to be low grade – 50% may be associated with meningeal signs • Focal neurological deficits • Seizures ( 30-50%)

  20. investigations • Laboratory : • 1.WBC count – normal or mildly elevated • 2.ESR – raised, • polycythemia decreases it hence it is unreliable in cyanotic heart disease • 3.lumbar puncture – avoid in SOL with increased ICP, significant only in meningitis

  21. Radiological : • 1.X-ray – PNS , mastoid evaluation for sinusitis, evidence of osteomyelitis , trauma

  22. CT Early cerebritis – hypo dense area with minimal contrast enhancement Late cerebritis – hypo dense area with ring enhancement which diffuses medially Early capsule – well defined ring enhancement with hypo dense center Late capsule – hyper dense capsule demonstrated with non contrast films

  23. MRI • T1 – central hypo intensity , capsules are iso to hyper intense , edema is hypo intense • T2 – necrotic area is iso to hyper intense,capsule is hypo intense,edema is hyper intense

  24. MRI may be better in differentiating edema from necrosis

  25. Differential diagnosis • Glioma , metastasis , resolving hematoma , radiation necrosis • Ir 111 labelled radionucleotide scan – useful to differentiate abscess from malignant lesion (sensitivity 100% , specificity 96%)

  26. management

  27. antibiotics • Antibiotics alone – empirical • Not effective in abscess above 2.5cm

  28. Initial treatment • Penicillins , metronidazole ,3rd gen.cephalosporins – covers anaerobes,streptococci,gram negative aerobes • Later antibiotics to be continued as per c/s

  29. Duration of antibiotics – usually 6 weeks to 3 months • If follow up scan shows residual contrast enhancement, follow up CT recommended for every 3 months.antibiotics are reinstated if enhancement increases • Residual tumor enhancement in itself does not indicate need to continue antibiotics • Stoppage of steroids may be associated with an increase in contrast enhancement – this does not indicate re-growth of abscess

  30. Corticosteroids : • 1.decreases edema • 2.decreases mass effect • 3.used only in cases where mass effect is significant problem

  31. Surgery – excision vs aspiration • Excision : • Traumatic abscess with retained fragments • Fungal abscess • Multiple loculated abscesses

  32. Aspiration : • In cerebritis stage • Abscess in deep seated areas • Cyanotic heart disease

  33. sequelae • Epilepsy – 20 to 30% , increased association with excision than aspiration • Hemiparesis & cognitive deficits – increased in excision • Children fare poorly

  34. Abscess in immunocompromised patients: • Toxoplasma gondii – pyrimethamine +sulfamethoxazole+folinic acid • Cryptococcal infection – amphotericin B +s.tancytosine • Pseudomonas – amikacin or tobramicin + cephalosporin • Multiple abscesses without bacteriological diagnosis – may need upto 3 months of iv antibiotics

More Related