Understanding Brain Abscess: Causes, Symptoms, Diagnosis, and Management

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