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Brain abscess
- 1. BRAIN ABSCESS DR. PUSPAR. KOIRALA ASSISTANT PROFESSOR NEUROSURGERY POKHARA ACADEMY OF HEALTH SCIENCES POKHARA, NEPAL
- 2. Introduction Brain abscess(BA) - focal intracranial infection that is initiated as an area of cerebritis and evolves into a collection of pus surrounded by a vascularized capsule Universal health problem with a high morbidity and mortality rate
- 3. History Henry IIking of France – died from an orbital wound Infection had spread to brain along the orbital veins forming an abscess under the cortex Oscar wilde in 1900 died of an otogenic brain abscess
- 4. History The firstsurgery for brain abscess was performed by French surgeon S.F. Morand in 1752 on a temperoethmoidal abscess. “ Pyogenic Disease of the Brain and Spinal Cord, Meningitis, Abscess of the Brain, Infective Sinus Thrombosis”, published in 1893, William Macewen 1918, Warringtoninvestigated the etiological factors in 2 groups King(1924)- Marsupialization Dandy (1926)-Aspiration Sargent (1928) – Enucletion Vincent (1936)-Complete excision Heinman et al (1971) – Successful medical management
- 5. Epidemiology Significant problemin the developing world due to poverty, illiteracy, and lack of hygiene. The incidence of BAs is approx. 8% of intracranial masses in developing countries and 1-2% in the western countries* M:F=2-3:1 Median age – 30-40 yrs 25% of children –otitic focus /CHD 0.2% of cranial operations *Muzumdar D, Jhawar S, Goel A. Brain abscess: An overview. Int J Surg. 2011
- 6. Pathogenesis Organisms canreach the brain through Spread from a contiguous source of infection -25% to 50% Hematogenous dissemination -20% to 35% Trauma/neurosurgical procedures -2.5 to10.9% Cryptogenic - 10% to 35% Immunocompromised(infected with HIV, receiving chemotherapy for cancer, receiving immunosuppressive therapy after organ transplantation)
- 7. Contiguous spread Routes ofcontiguous spread : Direct extension through osteitis/osteomyelitis Retrograde thrombophlebitis via diploic or emissary veins Via local lymphatics Localisation : Otitis media/mastoiditis –Temporal lobe / cerebellum PNS/frontal – Frontal lobe Sphenoid sinusitis –Temporal lobe / sella Dental infection (molars) – Frontal lobe (M.C) / temporal
- 8. Otogenic source wasthe most common. Temporal lobe was the most common abscess location
- 9. Hematogenous Multiple ,multiloculated abscess- increases mortality M.C. source - 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. IE <5% despite the presence of continuous bacteremia *Brouwer MC, Coutinho JM, van de Beek D. Clinical characteristics and outcome of brain abscess: systematic review and meta- analysis. Neurology. 2014;82:806-813.
- 10. Trauma Open cranialfracture 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* Nosocomial brain abscess - halo pin insertion, electrode insertion to localize seizure foci, placement of Gliadel wafers in malignant glioma patients, after placement of deep brain stimulation hardware , intracranial pressure monitors *Tay JS, Garland JS. Serious head injuries from lawn darts. Pediatrics. 1987
- 11. Etiology The probableinfecting pathogen depends on the pathogenesis of the infection and the presence of various predisposing conditions Predisposing conditions Possible microbial causes Otitis media/Mastoiditis Streptococci ; bacteroids spp. Penetrating trauma/ 20 to neurosurgical procedures Staphylococcus aeurus , staph. epidermidis Lung abscess , empyema Streptococcus spp. , actinomyces Cyanotic congenital heart disease streptococci Bacterial endocarditis Staph aeureus , streptococcus viridans Immunocompromised states Transplantation Enterobacteriaceae, L. monocytogenes HIV infection T. gondii, L. monocytogenes, nocardia
- 12. Pathology Britt and Enzmannclassification Early cerebritis (1-4 days) Late cerebritis (5-10 days) Early capsule (10-14 days) Late capsule (>2 weeks)
- 13. Early cerebritis Acuteinflammatory infiltrate Thrombosis of the local vasculature, perivascular cuffing and perilesional oedema No visible necrosis/ capsule Poorly marginated cortical/subcortical hypodensity with mass effect with no enhancement
- 14. Late cerebritis Patchynecrotic foci with suppurative mass Poorly organized irregular rim of granulation tissue -- inflammatory cells , macrophages, fibroblasts Edema is maximal
- 15. Early capsule Capsuleis formed through the accumulation of fibroblasts and neovascularization. T2: High signal center, low-signal rim, surrounding high signal of edema FLAIR: Increased signal within and surrounding the lesion DWI/ADC: Central increased DWI signal and decreased ADC signal The ventricular side of the capsule is often thinner and more prone to rupture
- 16. Late capsule Collagencapsule complete Increased density and thickness of the capsule Diminished hypodense central cavity ,decreased surrounding oedema
- 17. Intrventricular abscess rupture?? C/F: sudden-onset headache, meningeal irritation, an abrupt deterioration in mental status Risk factors : * Deep location, location close to a ventricle wall Multiloculated abscess Difference between vascularity between cortical grey and white mater ---- -Increased fibroblast proliferation on cortical side----- capsule less formed on ventricular surface ------tendancy for intraventricular rupture *Lee TH et al . Clinical features and predictive factors of intraventricular rupture in patients who have bacterial brain abscesses. J Neurol Neurosurg Psychiatry. 2007
- 18. Clinical Features Symptom orSign Frequency Range (%) Headache 49-97 Fever 32-79 Focal Neurologic deficits 20-66 Altered mental status 28-91 Seizures 13-35 Nausea and vomiting 27-85 Nuchal rigidity 5-52 Papilloedema 9-51 Variable and non specific The classic triad, fever, headache, and focal neurological deficits, is seen in less than 50% of patients with brain abscess * *Klein M et al. Brain abscess. Infections of the Central Nervous System; 2014
- 19. Clinical Features Depends onthe origin of infection, site, size, number of lesions, specific brain structures involved, the neighborhood anatomical disturbances involving cisterns, ventricles, and the dural venous sinuses
- 20. Investigations-CT scan Early detection,determination of number, size and staging of the abscess Hydrocephalus, raised ICP, edema and associated infections like subdural empyema, ventriculitis helps in treatment planning Assessment of adequacy of treatment and sequential follow up NCCT –initially hypodense lesion with mass effect. Later phase , complete peripheral ring may be seen CECT – smooth , thin , regular wall with decreased density both in the centre and surrounding
- 21. MRI Investigation ofchoice- MRI with I/V contrast with DWI Advantages: Early detection of cerebritis, shows spread of inflammation into the ventricles and subarachnoid space, and earlier detection of satellite lesions , lack of bony artifacts, multiple imaging planes
- 22. MRI - T1WI Abscess capsule appears as a discrete rim that is isointense to mildly hyperintense Central low intensity (hyperintense to CSF) Peripheral low intensity (vasogenic edema) Ring enhancement
- 23. T2WI MRI Centralhigh intensity Peripheral high intensity (vasogenic oedema) The capsule appears as a well defined hypointense rim at the margin of the abscess “Dual rim” sign Hypointense along the periphery of the capsule and hyperintense along the inner portion of the capsule
- 24. DWI / ADC Restricteddiffusion (bright on DWI, dark on ADC) throughout the necrotic core Diffusion-weighted imaging (DWI) MRI can differentiate brain abscesses from cystic brain lesions with sensitivity and specificity of 96%* *Matthijs C. Brouwer, M.D., Ph.D.et al.Brain abscess NEJM 2014
- 25. MRS Powerful toolto non-invasively differentiate a brain abscess from a tumour. Central necrotic area show presence of amino acids (0.9 ppm), lactate (1.3 ppm), acetate (1.9 ppm), succinate (2.4 ppm); metabolites usually not present in tumor
- 26.
- 27. Neoplasm vs abscess AbscessNeoplasm Enhancement of wall Smooth , regular Nodular, irregular Surrounding edema Relatively extensive May be less extensive Rim thickness <5mm >5mm DWI High signal on DWI, low ADC Low signal on DWI, high ADC MR Spectroscopy Elevated lactate and cytosolic aminoacids and acetate Elevated lactate and choline peaks
- 28. Management The mainstayof treatment for brain abscesses is a combination of antibiotic treatment and surgical intervention The nature of the abscess, its anatomic location, the number of abscesses and their size and stage, the age and initial neurological status of the patient all influence the treatment strategy If < 2.5 cm antibiotics only If > 2.5 cm surgical evacuation and antibiotics Steroids for edema and mass effect AEDs
- 29. Lab-Investigations TC- Normal/mild increment ESR – Increased (90%) CRP – Increased Blood culture - + ve in IE/mycotic aneurysms CSF analysis – non specific Mild pleocytosis CSF protein slightly increased Glucose Normal
- 30. Lab Investigations : Stains Gram stain Acid-fast stain (AFB stain) Modified acid-fast stain (for Nocardia) looking for branching acid fast bacillus Special fungal stains (e.g., methenamine silver, mucicarmine) Cultures: Cultures are negative in 14%-34% of samples* Routine cultures: aerobic and anaerobic Fungal culture TB culture Additional : Chest Xray, chest CT, Echo *Nathoo N et al. Brain abscess: management and outcome analysis of a computed tomography era experience with 973 patients. World Neurosurg. 2011
- 31. Surgical treatment Goals toconfirm the diagnosis to reduce intracranial pressure to obtain pus for microbiological diagnosis to enhance the efficacy of antibiotic therapy to avoid spread of infection into the ventricles. Options Freehand aspiration, stereotactic aspiration or endoscopic aspiration Craniotomy with excision
- 32. Indications for surgicaltreatment Significant mass effect exerted by lesion (on CT or MRI) Difficulty in diagnosis (especially in adults) Proximity to ventricle Evidence of significantly increased intracranial pressure Poor neurologic condition Traumatic abscess associated with foreign material Fungal abscess Multiloculated abscess Follow-up CT/MRI scans cannot be obtained every 1-2 weeks
- 33. Aspiration Stereotactic aspirationparticularly helpful in the aspiration of deep-seated abscesses and those in eloquent locations.* Complications Subarachnoid or subdural leakage of pus, resulting in empyema or meningitis, or intraventricular rupture of the abscess.** Damage to the friable hyperaemic capsule, which causes bleeding. Abscess capsule is left intact and removal of purulent material is frequently incomplete * Kocherry XG et al. Efficacy of stereotactic aspiration in deep-seated and eloquent-region intracranial pyogenic abscesses. Neurosurg Focus. 2008 **Hall WA et al. The surgical management of infections involving the cerebrum. Neurosurgery. 2008
- 34. Indications for Craniotomyand excision Multiloculated abscesses in whom aspiration techniques have failed Abscesses that failed aspiration procedures 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 Suspected fungal abscess, gas containing abscess
- 35. Aspiration vs Craniotomy No prospective randomized trial Aspiration 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. A recent meta-analysis comparing abscess excision with aspiration showed a lower rate of mortality using aspiration (6.6% versus 12.7%)* *Ratnaike TE et al. A review of brain abscess surgical treatment-78 years: Aspiration versus excision. World Neurosurg. 2011
- 36. Intraventricular abscess t/t Rapidevacuation and debridement of the abscess cavity via urgent craniotomy or aspiration Lavage of the ventricles, ventriculostomy for drainage Combination of intrathecal and intravenous administration of antibiotics recommended
- 37. Medical therapy alone Poor surgical candidates Multiple small abscesses Abscesses in a deep or dominant location Coexisting meningitis/ependymitis Early reduction of the abscess with clinical improvement after antimicrobial therapy Abscess size < 2.5 cm
- 38. Medical management Theprinciples of antimicrobial therapy for bacterial brain abscess are to use agents that are able to penetrate the abscess cavity and have activity against the isolated pathogen
- 39. Duration of antibiotics Bacterial brain abscess – 6-8 weeks IV → 2-3 months oral 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** *Lu Chet al. Strategies for the management of bacterial brain abscess. J Clin Neurosci. 2006. **Mamelak AN et al. Improved management of multiple brain abscesses: a combined surgical and medical approach. Neurosurgery. 1995.
- 40. Role of steroids ↓ host defense mechanisms and ↓ penetration of some antimicrobial agents into the brain abscess cavity Decrease vasogenic edema -improvement of neurological symptoms and signs. Indications: * Associated edema and mass effect Progressive neurological deterioration Impending cerebral herniation. Dexamethasone, 10 mg every 6 hours administered initially and then tapered once the patient has stabilized. * Hakan T. Management of bacterial brain abscesses. Neurosurg Focus. 2008
- 41. Epilepsy and brainabscess Epilepsy frequently occurs at presentation. Incidence of seizures after brain abscess -70% * Seizure prophylaxis and continuation of anticonvulsive therapy for an extended period are recommended for patients with brain abscesses.** Discontinuation - when patient is seizure free for at least 2 years after surgery and EEG shows no epileptic activity. *Dattatraya Mazumdar et al. Brain abscess:An overview. International Journal of Surgery.2010 **Lu CH et al: Strategies for the management of bacterial brain abscess. J Clin Neurosci ,2006
- 42. Fungal brain abscess Highmortality rate despite combined medical and surgical therapy. Candidal - Amphotericin B preparation + 5-flucytosine Aspergillus – voriconazole / Liposomal amphotericin B CNS Mucormycosis - Liposomal amphotericin B
- 43. Outcome and prognosis Poor prognostic indicators Delayed diagnosis, rapidly progressing disease,low mental status on initial evaluation, coma, multiple lesions, intraventricular rupture, fungal etiology , immunocompromised Before 1970, overall mortality was 30-80%; New antibacterial approaches and the use of new imaging technologies diminish the mortality ( 8% -25% )* * Helweg-Larsen J et al. Pyogenic brain abscess, a 15 year survey. BMC Infect Dis. 2012.
- 44. Outcome and prognosis A significant proportion of treated patients recover completely and survive without residual neurologic symptoms Long-term sequelae - hemiparesis, persistent visual field defects, cognitive dysfunction, learning disorders, hydrocephalus, seizures Routine follow-up is necessary
Editor's Notes
- #4 Oscar wilde – famous irish poet and playwright
- #5 “ Pyogenic Disease of the Brain and Spinal Cord, Meningitis, Abscess of the Brain, Infective Sinus Thrombosis”, published in 1893, William Macewen advised draining the abscess and treating the underlying causative sinus infections. 1918, Warrington investigated the etiological factors in 2 groups: 1) infections from foci in the contiguous structures; 2) infections spread through the bloodstream from a distant site
- #6 The introduction of newer broad spectrum antibiotics, improved imaging technology, and intensive care facilities significantly altered the natural history of CNS infections
- #7 Over the period of last 10-15 years, the incidence of otogenic abscess has reduced while the posttraumatic or postoperative brain abscess has increased
- #10 Intracardiac right to left shunt allowing direct entry of blood containing bacteria to the cerebral circulation bypassing the pulmonary filter, hypoxaemia, metabolic acidosis, increased blood viscosity from compensatory polycythaemia resulting in low perfusion areas (microinfarcts) in the brain provide the perfect milieu where micro-organisms settle down and multiply to form an abscess Occurs in the distribution of middle cerebral artery , at grey white mater junction where the brain capillary flow is slowest Hereditary hemorrhagic telangiectasia (with coexisting pulmonary AVM) - allows septic emboli to cross the pulmonary circulation without capillary filtration – 5-9% risk
- #12 The most common bacterial causes of brain abscess are streptococci (aerobic, anaerobic, and microaerophilic), which are isolated in up to 70% of cases
- #13 Brain abscess natural history divided into four stages
- #14 T1: Ill-defined area of decreased signal T2/FLAIR: Ill-defined area of increased signal DWI/ADC: increased signal on both (edema, NOT restricted diffusion) T1 post-contrast: Patchy enhancement Unencapsulated edema and petechial hemorrhage
- #15 T1: low signal center, iso-intense rim T2: high signal center, hypointense rim (presumed to be due to high concentration of free oxygen radicals causing local disruption of the magnetic field and loss of signal) FLAIR: increased signal within and surrounding the lesion DWI/ADC: increased signal within and surrounding the lesion on both (edema, transitioning to restricted diffusion) T1 post-contrast: irregular rim enhancement
- #16 (restricted diffusion due to high degree of cellular debris – bacteria and inflammatory response cells). The ventricular side of the capsule is often thinner and more prone to rupture, allowing for the development of satellite abscesses and intraventricular extension. The cause is felt to be relatively poorer blood flow and poorer fibroblast migration from the deep white matter. Inner rim of granulation tissue and outer rim of multiple concentric layers of fibroblasts and collagen
- #17 T1: Thicker capsule, decreased size of the cavity T2/FLAIR: decreased surrounding edema DWI/ADC: Persistent restricted diffusion in the necrotic center (high DWI, low ADC), decreased surrounding edema (high DWI and high ADC) T1 post-contrast: Thick enhancing capsule, decreased size of the non-enhancing central cavity
- #18 Intraventricular rupture of the abscess is the most important complication of brain abscesses ;mortality rates have ranged from 27% to 85% Imaging is notable for hydrocephalus, ependymal enhancement, septation of the ventricle, meningeal enhancement, or the presence of ventricular debris. Small abscesses abutting the ventricular space are no less likely to rupture than larger abscesses
- #19 The clinical signs and symptoms of brain abscesses are nonspecific. So high clinical suspicion is necessary for prompt diagnosis. Patients typically present with signs and symptoms due to mass effects, accompanied by high fever and seizure. In immunocompromised patients, the clinical findings may be masked by the diminished inflammatory response.
- #20 Sudden worsening of preexisting headache accompanied with meningismus may be indicative of catastrophic event – rupture of the abscess into the ventricular space Diagnosis can be challenging, as abscess presentation is highly variable and routine studies frequently lack specificity
- #21 It is readily available, inexpensive, and fast.
- #22 more sensitive than computed tomography (CT) and offers significant advantages in the early detection of cerebritis, more conspicuous demonstration of spread of inflammation into the ventricles and subarachnoid space, and earlier detection of satellite lesions
- #23 On T1-weighted images, the abscess capsule often appears as a discrete rim that is isointense to mildly hyperintense; administration of gadolinium– diethylenetriaminepentaacetic acid helps clearly differentiate the central abscess, surrounding enhancing rim, and cerebral edema Ventriculitis may be present, in which case hydrocephalus will commonly also be seen
- #24 Inner rim of enhancement tends to be quite smooth, helping to differentiate from the irregular enhancement in the necrotic center of high grade tumors
- #25 This is in contrast to restricted diffusion seen in hypercellular viable tumor, in which the necrotic center (unless hemorrhagic) only rarely demonstrates restricted diffusion
- #26 when combined with diffusion-weighted imaging, MR spectroscopy can significantly increase the diagnostic accuracy of conventional MRI Spectroscopy allows for the detection of products of bacterial metabolism (lactate, acetate, and succinate) and neutrophil proteolysis (cytosolic amino acids).
- #27 Metastasis , ADEM, GBM, Stroke, radionecrosis , tuberculomas Bacterial abscess can mimic most ring enhancing lesions, but classically can be differentiated by central diffusion restriction and potential secondary causative etiologies, such as mastoiditis or sinusitis.
- #29 Even with enormous advances in imaging, surgery, anesthesia, bacterial isolation techniques, and antibiotic therapy, bacterial brain abscesses can still be fatal
- #30 Such tests as leukocyte count, serum C-reactive protein level, and erythrocyte sedimentation rate are not specific but are valuable especially in the evaluation of the patient's condition during the treatment period. BA is the only CNS infection in which a lumbar puncture (LP) is never recommended and may even be contraindicated. LP does not help in the diagnosis but also because increased ICP is often present as a result of the mass effect, which increases the likelihood of herniation, complicating patient clinical status
- #31 1/3 polymicrobial Incidence of negative cultures 25-30%
- #32 It is relatively safe, and may therefore be performed even in patients who are poor surgical candidates. Endoscopic aspiration of brain abscesses is said to be more effective than other aspiration methods; in addition to facilitating retrieval of a specimen and reduction of intracerebral pressure, advantages include direct visual control and the possibility of treating multiseptate abscesses and intraventricular purulent collections
- #34 It is preferred also in patients with multiple abscesses necessitating drainage. Limitations -Abscess recurrence or failure to improve Inadequate aspiration, chronic immunosuppression, and inadequate antibiotic therapy are the clinical factors most commonly associated with failure
- #35 Open craniotomy for excision of brain abscess allows complete removal of purulent material and the surrounding abscess capsule, providing definitive treatment that may reduce the need for additional treatment and length of antibiotic therapy C/I – abscess in cerebritis stage, deep seated abscess in eloquent areas, multiple abscess
- #36 Primary excision of a BA carries the risk of serious damage to the surrounding brain with increased potential for neurological sequelae and epilepsy because the capsule often has anchor extensions into the surrounding white matter, with the surgical procedure may be caused unplanned extensive damage to adjacent viable cerebral tissue
- #38 Although the optimal approach to brain abscess most often requires a combined medical and surgical approach, certain groups of patients may be treated with medical therapy alone . The ineffectiveness of antibiotics in the stage of capsule formation is due to the acidic medium within the abscess cavity and the inability to have adequate therapeutic concentration of the antibiotic within the abscess
- #39 If the culture is negative for organism, then the broad spectrum antibiotics should be continued according to the likely predisposing cause (primary source) and the anatomic location of abscess.
- #40 Duration of antimicrobial therapy should be determined individually, based on the size of abscess, combination of surgical treatment, causative organism, and response to treatment
- #41 The use of corticosteroids in management of brain abscesses is controversial. Local vasogenic edema is the predominant type of edema leading to increased intracranial pressure and significant mortality and morbidity in patients with brain abscesses. There is no well-controlled, randomized clinical study evaluating the use of corticosteroids for controlling the cerebral edema surrounding BA 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.
- #42 Initiated immediately and continued at least 1 year due to high risk in the brain abscesses. On the basis of this high postabscess epilepsy rate, patients should be advised on the risk of seizures and consideration should be given to prophylactic anticonvulsant therapy, although no randomized trials have assessed such an approach. Early seizures predispose to late seizures and in these patients long-term anticonvulsant treatment should be considered**
- #43 Excisional surgery or drainage is a key factor in the successful management of CNS aspergillosis Because the etiologic agents of mucormycosis invade blood vessels, tissue infarction occurs and impairs the delivery of antifungal agents to the site of infection; this development often leaves surgery as the only modality that may effectively eliminate the infecting microorganism.
- #44 The major prognostic factors for brain abscesses are early diagnosis, appropriate antimicrobial treatment that is based on causative agents, the virulence of the infecting organisms, and the optimal timing of surgery. Outcome poorer in newborn and elderly Degree of neurologic compromise at initial evaluation is a strong predictive factor of ultimate outcome
- #45 Routine follow-up is necessary, as abscess recurrence is a known complication and may occur years after the initial event