Brain abscess

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Brain abscess - a detailed review regarding diagnosis, stages and management

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Brain abscess

  1. 1. Dr. Joe M Das Senior Resident Dept. of Neurosurgery Brain abscess
  2. 2.  History  Definition  Epidemiology  Pathogenesis  Clinical features  Investigations  Treatment  Special abscesses
  3. 3. History  Hippocrates – Purulent otorrhea and delerium  The first successful operation for brain abscess - S.F. Morand (France) in 1752 on a temperoethmoidal abscess.  “Pyogenic Disease of the Brain and Spinal Cord, Meningitis, Abscess of the Brain, Infective SinusThrombosis” (1893) - William Macewen – Father of modern day abscess management  King (1924) – marsupialization  Dandy (1926) – aspiration  Sargent (1928) – enucleation  Vincent (1936) – complete excision  Heineman et al (1971) – successful medical management
  4. 4.  Henry II, King of France  Death was predicted by Nostradamus  Died from an orbital wound  The skull was not penetrated but infection spread intracranially  Infection had spread to the brain along the orbital veins, forming an abscess under the cortex.
  5. 5.  OscarWilde  Irish writer and poet  Died of otogenic brain abscess
  6. 6. Definition Mathisen GE, Johnson JP: Brain abscess. Clin Infect Dis 1997; 25:763-781. A focal intracranial infection that is initiated as an area of cerebritis and evolves into a collection of pus surrounded by a vascularized capsule.
  7. 7. Epidemiology  1500-2500 cases per year in the US  8% of ICSOL in developing countries  ♂: ♀ = 2-3 : 1  Median age – 30 – 40 yrs  2° to otitic focus - <20 / > 40 yrs  2° to PNS infection – 30-40 yrs  25% in children – otitic focus / CHD  0.2% of cranial operations  Immunosuppression
  8. 8. Pathogenesis  Sources:  Contiguous source – 25-50 %  Hematogenous dissemination / trauma – 20-35 %  Cryptogenic – 10-35 %
  9. 9. Contiguous spread  Routes of contiguous spread:  Direct extension through osteitis / osteomyelitis  Retrograde thrombophlebitis via diploic or emissary vein  Via local lymphatics  Localisation:  Otitis media –Temporal lobe / cerebellum  PNS – Frontal lobe  Sphenoid sinusitis –Temporal lobe / sella  Dental infection (molars) – Frontal lobe (M.C) / temporal
  10. 10.  India – M.C source – Middle ear suppuration  Western countries – M.C source – Spread from PNS  Sites of bone dehiscence:  Post wall of frontal sinus  Tegmen tympani  Trautmann’s triangle
  11. 11. Hematogenous  Multiple, multiloculated abscesses - ↑ mortality  M.C sources in adults – chronic pyogenic lung diseases (especially lung abscess), bronchiectasis, empyema, and CF.  Distant sources – wound & skin infections, osteomyelitis, pelvic intra-abdominal infections; after esophageal dilation or sclerosing therapy for esophageal varices.  CCHD (TOF/TGV) – 5-15% of brain abscess cases.  <5% of patients with IE despite the presence of continuous bacteremia  Hereditary hemorrhagic telangiectasia (with coexisting pulmonary AVM) - allows septic emboli to cross the pulmonary circulation without capillary filtration – 5-9% risk
  12. 12. How does TOF lead to brain abscess? TOF  Chronic hypoxemia  Polycythemia  ↑ viscosity  Multiple infarcts at grey-white junction  Milieu for bacterial growth
  13. 13. Trauma  Open cranial fracture with dural breach / foreign body injury / as a sequel of neurosurgery  Civilian population - 2.5-10.9 %  Includes those 2° to compound depressed skull fractures, dog bites, rooster pecking, tongue piercing  Nosocomial brain abscess - halo pin insertion, electrode insertion to localize seizure foci, and in malignant glioma patients treated by placement of Gliadel wafers
  14. 14.  In military populations - 3-17 %  Usually occur secondary to retained bone fragments or contamination of initially uninfected missile sites with bacteria from skin, clothes, or the environment  The retained foreign bodies did not seem to increase the infection rate except in patients who suffered an in- driven cluster of bone fragments or leakage of cerebrospinal fluid.
  15. 15. Predisposing Conditions and Probable Etiologic Agents in Brain Abscess
  16. 16. Predisposing Conditions and Empirical Antimicrobial Therapy in Patients with Presumed Bacterial Brain Abscess
  17. 17. Antimicrobial Therapy for Brain Abscess Based on Isolated Pathogen
  18. 18. Recommended Dosages of Antimicrobial Agents in Adults with Brain Abscess and Normal Renal and Hepatic Function
  19. 19. Stages of abscess formation  A canine model after inoculation of α-hemolytic Streptococci Britt RH, Enzmann DR,YeagerAS. Neuropathological and computerized tomographic findings in experimental brain abscess. J Neurosurg. 1981 Oct;55(4):590-603.
  20. 20. Stages of abscess formation
  21. 21. Histopathologic findings in the stages of brain abscess formation Data from Tunkel AR, Scheld WM. Pathogenesis and pathophysiology of bacterial infections. In: Scheld WM, Whitley RJ, Durack, DT, eds. Infections of the Central Nervous System, tind ed. Philadelphia: Lippincott-Raven; 1997;297-312; and Britt RH, Enzmann DR, Yeager AS. Neuropathological and computerized tomographic findings in experimental brain abscess. J Neurosurg. 1981;55:590-603.
  22. 22. Early cerebritis  Acute inflammatory infiltrate  Marked edema  Invisible on CT OR  Poorly marginated cortical /subcortical hypodensity with mass effect with no enhancement
  23. 23. Late cerebritis  Central necrosis  Macrophages and fibroblasts  Vascular proliferation  Maximum edema  Irregular rim enhancing lesion with hypodense center, better defined than early cerebritis
  24. 24. Early capsule formation  Necrotic centre ↓  Collagenous capsule  Edema starts to regress  Well-defined rim enhancing mass; an outer hypodense and inner hyperdense rim (double rim sign)
  25. 25. Late capsule formation  Collagen capsule complete  ↑ density and thickness  Rim enhancing lesion with thickened capsule and diminished hypodense central cavity
  26. 26. Layers of abscess
  27. 27. Immunopathogenesis
  28. 28. Why does abscess often rupture intraventricularly? Difference in vascularity between cortical grey and white matter  ↑ fibroblast proliferation on cortical side  Capsule less formed on ventricular surface  Tendency for intraventricular rupture
  29. 29. Initial Symptoms and Signs in Patients with Brain Abscess
  30. 30. Initial Findings in Patients with Brain Abscess Based on Intracranial Location  Frontal >Temporal > Parietal > Cerebellum > Occipital
  31. 31.  Classic triad of headache, fever, and focal neurologic deficit is rarely seen (< 5-20% of cases in case series)  1/3rd – polymicrobial  Incidence of negative cultures - 25-30%  Sudden worsening of a preexisting headache accompanied with meningismus may be indicative of a catastrophic event—rupture of the abscess into the ventricular space.
  32. 32.  When there is no obvious source (up to 25% of cases), upper respiratory tract flora and anaerobes are often isolated.  Several sources have identified a patent foramen ovale by echocardiogram in these cases and propose this as a possible mechanism for seeding oral flora to the brain. Khouzam RN, El-DoklaAM, Menkes DL. Undiagnosed patent foramen ovale presenting as a cryptogenic brain abscess: case report and review of the literature. Heart Lung. Mar-Apr 2006;35(2):108-11.
  33. 33. Investigations  X-ray skull:  Often normal  Post-traumatic – air inside cranial cavity  Sinusitis/mastoiditis  CT brain:  Diagnosis, localisation and treatment  Sinisitis/mastoiditis  Staging, HCP, ↑ICP, edema, associated subdural empyema, meningitis, ventriculitis, multiplicity  NCCT - Isodense / hyperdense  CECT - Smooth, thin, regular wall with decreased density both in the centre and surrounding
  34. 34. MRI Brain  T1  Central low intensity (hyperintense to CSF)  Peripheral low intensity (vasogenic oedema)  Ring enhancement  Ventriculitis may be present, in which case hydrocephalus will commonly also be seen  T2 / FLAIR  Central high intensity (hypointense to CSF, does not attenuate on FLAIR)  Peripheral high intensity (vasogenic oedema)  The abscess capsule may be visible as a intermediate to slightly low signal thin rim  DWI / ADC  High DWI signal is usually present centrally  Low signal onADC
  35. 35.  SWI  Low intensity rim  Complete in 75%  Smooth in 90%  Mostly overlaps with contrast enhancing rim  Dual rim sign - a hyperintense line located inside the low intensity rim  MR perfusion - RCBV is reduced in the surrounding oedema c.f. to both normal white matter and tumour oedema seen in high grade gliomas  MR spectroscopy - elevation of a succinate peak is relatively specific but not present in all abscesses ; high lactate, acetate, alanine, valine, leucine, and isoleucine levels peak may be present ; cho / crn and NAA peaks are reduced
  36. 36. What are the imaging differential diagnoses?
  37. 37. How to differentiate between peripherally enhancing neoplasm and abscess radiologically?
  38. 38. Laboratory investigations  TC – Normal / mild ↑ (↑ if meningitis / acute systemic infection)  ESR - ↑ in >90%  CRP - ↑. Useful marker to differentiate between brain abscess and slowly progressive ICSOLs  Blood culture - +ve in IE / mycotic aneurysms  CSF analysis – Non-specific.  Mild pleocytosis. CSF potein – mild ↑  Glu – Normal  LP – dangerous  PCR analysis of 16S rDNA – to identify to species level  111In-labelled leukocytes
  39. 39. Treatment
  40. 40. Surgical therapy  The optimal approach to patients with bacterial brain abscess  Aspiration after bur-hole placement or complete excision after craniotomy (no prospective trial comparing these two)  May be performed under stereotactic neuroimaging guidance  Stereotactic aspiration is a useful approach even for abscesses located in eloquent or inaccessible regions; repeat aspiration should be considered if the initial aspiration proves ineffective or partially effective.  Intraoperative ultrasound - for the aspiration of small abscesses and can delineate abscess pockets,  Recurrence rates after stereotactic aspiration range from 0-24 %.
  41. 41. Pus has been aspirated. What all investigations are to be sent? A. Stains A. Gram stain B. Acid-fast stain (AFB stain) for Mycobacterium C. Modified acid-fast stain (for Nocardia) looking for branching acid fast bacillus D. Special fungal stains (e.g., methenamine silver, mucicarmine) B. Cultures A. Routine cultures: aerobic and anaerobic B. Fungal culture: this is not only helpful for identifying fungal infections, but since these cultures are kept for longer period and any growth that occurs will be further characterized, fastidious or indolent bacterial organisms may sometimes be identified C. TB culture
  42. 42. What are the indications for initial surgical treatment? 1. Significant mass effect exerted by lesion (on CT or MRI) 2. Difficulty in diagnosis (especially in adults) 3. Proximity to ventricle: indicates likelihood of intraventricular rupture which is associated with poor outcome 4. Evidence of significantly increased intracranial pressure 5. Poor neurologic condition (patients responds only to pain, or does not even response to pain) 6. Traumatic abscess associated with foreign material 7. Fungal abscess 8. Multiloculated abscess 9. Follow-up CT/MRI scans cannot be obtained every 1-2 weeks
  43. 43. What are the indications for complete excision by craniotomy ?  Multiloculated abscesses in whom aspiration techniques have failed  Abscesses containing gas  Abscesses that fail to resolve  Posttraumatic abscesses that contain foreign bodies or retained bone fragments to prevent recurrence  Abscesses that result from fistulous communications (e.g., secondary to trauma or congenital dermal sinuses)  Abscess localized to one lobe of the brain and contiguous with a primary focus.  Cerebellar abscess in children  Difficulty in diagnosis  Suspected fungal abscess
  44. 44. What are the contraindications for craniotomy and evacuation?  Abscess in the cerebritis stage  Deep-seated abscess in eloquent area  Multiple abscesses
  45. 45. Aspiration vs. Craniotomy  Craniotomy is now rarely practiced as the first line of treatment.  Aspiration repeated as necessary or with drainage, has widely replaced attempts at complete excision.  Several reports have advocated excision as the procedure of choice because it is often followed by a lower incidence of recurrence and shorter hospitalization.  Xiao et al reported that favorable outcome was not significantly different between the patients treated by excision or aspiration. However, the mortality rate was significantly lower in the patients treated with excision than the patients treated with aspiration.  This is probably due to the better general condition and/or more favorable location of abscess that could be excised surgically in such patients.  Stereotactic aspiration should be considered the treatment of choice in all but the most superficial and the largest cerebral abscesses.
  46. 46. IV rupture with ventriculitis and HCP – What to do? Rapid evacuation and débridement of the abscess cavity via urgent craniotomy + Ventricular drainage + Intravenous or intrathecal administration of appropriate antimicrobial agents
  47. 47. When to opt for medical therapy alone?  Patients with medical conditions that increase the risk associated with surgery  Multiple abscesses  Abscesses in a deep or dominant location  Coexisting meningitis or ependymitis  Early reduction of the abscess with clinical improvement after antimicrobial therapy  Abscess size < 3 cm
  48. 48. What is the optimal duration of medical treatment?  Bacterial brain abscess – 6-8 weeks IV → 2-3 months oral antimicrobial therapy  Post-surgical excision - Courses of 3 to 4 weeks of antimicrobial therapy  Medical therapy alone - up to 12 weeks with parenteral agents  A combination of surgical aspiration or removal of all abscesses larger than 2.5 cm in diameter → 6 weeks or more of antimicrobial therapy, and weekly neuroimaging to document abscess resolution  Repeat neuroimaging studies - biweekly for up to 3 months after completion of therapy
  49. 49. How will you follow up an abscess case radiographically?  CT scans weekly during the course of therapy   One week after discontinuation of antibiotics   Scan one month later   Monthly or bimonthly till radiographic resolution  Time course for abscess resolution:  ↓ in abscess size – 2-3 weeks after initiating therapy  Complete resolution of abscess cavity, mass effect – 3-4 months  Residual contrast enhancement – 6-9 months
  50. 50. Brain abscess – Management algorithm
  51. 51. Any role for steroids?  ↓ host defense mechanisms and ↓ penetration of some antimicrobial agents into the brain abscess cavity  May result in improvement of neurological symptoms and signs.  Therapy started in abscess patients with:  Associated edema and mass effect  Progressive neurological deterioration  Impending cerebral herniation.  Dose:  Dexamethasone, 10 mg every 6 hours is generally administered initially and then tapered once the patient has stabilized.  The use of prolonged courses of corticosteroids is discouraged.  May also decrease contrast enhancement of the abscess capsule in the early stages of infection, thereby being a false indicator of radiologic improvement.
  52. 52. What is the role of anticonvulsants?  Initiated immediately and continued at least 1 year due to high risk in the brain abscesses.  The treatment can be discontinued if no significant epileptogenic activity can be shown in electroencephalogram (EEG).
  53. 53. How to treat otogenic brain abscess? Initial neurosurgical removal of abscess, which after improvement of general condition of the patient should be followed by radical otosurgical removal of the process from the ear. Otogenic brain abscess: diagnostic and treatment experience. D Djeric NArsovic V Djukic. International Congress Series, 2003; 1240 (61-65) Brain abscesses of otogenic origin. [Article in Serbian] NesićV1, Janosević L, Stojicić G, Janosević L, Babac S, Sladoje R. SrpArh Celok Lek. 2002 Nov-Dec;130(11-12):389-93.
  54. 54. How to manage multiple brain abscesses?  Incidence – 10-50%  Emergent stereotactic aspiration for all lesions > 2.5 cm diameter and those causing mass effect, located deep in brain stem or close to ventricular wall  If all the lesions are < 2.5 cm and not producing mass effect, the largest one should be aspirated for diagnostic cultures.  Antibiotics withheld till culture results  Antibiotics for 3 months (Immunosuppressed – 1 yr)  Repeat surgical aspiration if  radiographic enlargement after 2 weeks of therapy  Failure to diminish in size after 4 weeks of antibiotics  Clinical deterioration
  55. 55. How to treat Nocardial brain abscess?  A sulfonamide ± trimethoprim, is recommended.  Alternative agents include minocycline,imipenem, amikacin, third- generation cephalosporins, and linezolid  In immunocompromised patients or those in whom therapy fails  a third-generation cephalosporin or imipenem + a sulfonamide or amikacin  Nocardia farcinica,a species that may be highly resistant to various antimicrobial agents, successful treatment has included moxifloxacin.  Craniotomy with total excision is difficult in patients with Nocardia brain abscess because these abscesses are often multiloculated.  The duration of therapy - 3 to 12 months, but it should probably be continued up to 1 year in those who are immunocompromised.
  56. 56. What are the treatment options for fungal brain abscess?  Patients with fungal brain abscess, especially those who are immunocompromised, have a high mortality rate despite combined medical and surgical therapy.  Candidal brain abscess -Amphotericin B preparation + 5- flucytosine  The therapy of choice for Aspergillus brain abscess is voriconazole.  Alternative agents include an amphotericin B preparation, posaconazole, and itraconazole.  Itraconazole - as an extension of successful treatment rather than as primary therapy.  Excisional surgery or drainage is a key factor in the successful management of CNS aspergillosis.
  57. 57.  CNS mucormycosis - Amphotericin B deoxycholate or a lipid formulation of amphotericin  Correction of the underlying metabolic derangements and aggressive surgical débridement  The etiologic agents of mucormycosis invade blood vessels, tissue infarction occurs and impairs the delivery of antifungal agents to the site of infection; this often leaves surgery as the only modality that may effectively eliminate the infecting microorganism.  In patients not responding to or intolerant of an amphotericin B formulation, posaconazole can be used as salvage therapy.  HBO - useful adjunct  Surgery is the cornerstone of therapy for brain abscesses caused by Scedosporium species  Voriconazole is the agent of choice.
  58. 58. What is meant by delayed “glue abscess”?  Delayed multiloculated abscess after embolization ofAVM nidus  The duration of the procedure and repeated handling of the catheters along with use of large amount foreign material or Hysto-acryl “glue” can precipitate infection.  Cure of the lesion can only be obtained by surgical excision of the infected and partially embolizedAVM.  Antibiotic prophylaxis with all endovascular procedures is recommended Mourier L, Bellec C, Lot G, Reizine D, Gelbert F, Dematons C, et al. Pyogenic parenchymatous and nidus infection after embolization of an arteriovenous malformation: an unusual complication. Case report. Acta Neurochir (Wien) 1993;122:130-3. Pendarkar H, KrishnamoorthyT, Purkayastha S, GuptaAK. Pyogenic cerebral abscess with discharging sinus complicating an embolized arteriovenous malformation. J Neuroradiol 2006;33:133-8
  59. 59. What are the factors to be considered in a patient with cyanotic heart disease developing a brain abscess?  5-18% population with CHD. 10 times more prone. M.C –TOF  Intracardiac right to left shunt by-pass allows direct entry of blood containing bacteria to the cerebral circulation without pulmonary filtration.  Anaerobic streptococci (Sterile cultures are reported in 16-68%)  Cardiopulmonary risk, coagulation defects and variable degree of immunodeficient states  A deeply located parieto-occipital abscess larger than 2 cm diameter which causes mass effect, should be aspirated immediately even in late cerebritits stage using stereotactic or CT guided methods to decrease intra-cranial pressure and avoid intraventricular rupture of brain abscess.  Intravenous Beta-lactam antibiotics are started immediately.
  60. 60. Cerebellar abscess  6-35% of all brain abscesses  Often ominously silent and carry significant mortality  Can cause sudden total occlusion of CSF pathways early in the course of disease.  Presence of periventricular lucency is an absolute indication of immediate ventricular drainage regardless of level of consciousness i.e. even if patient is fully conscious.  Burr hole aspiration has emerged as a satisfactory method
  61. 61. Sequelae  30-50% of survivors are found to have neurological sequelae.  The incidence of residual neural deficits - hemiparesis, cognitive and learning deficits in children, is less with aspiration than excision.  About 72% of patients can have epileptic seizures upto five years of diagnosis.This incidence is less with aspiration than excision.  5 to 10% abscesses recur due to inadequate or inappropriate antibiotics, failure of removal of foreign body, dural fistula or failure of eradication of primary source.  Hydrocephalus may also develop
  62. 62.  What is the difference between otogenic and odontogenic brain abscess?  Unlike otogenic abscess, odontogenic abscess occurs as a sequel of acute rather than chronic infection  What is the most common site of metastatic abscess?  In the distribution of MCA – Parietal & frontal (left side) Grey-white junction – capillary flow slowest  Does a high velocity bullet injury cause an abscess?  The fragments do not present a significant risk because of heat sterilisation and do not require removal

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