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CNS ABSCESSES

CNS ABSCESSES. Nov 10, 2003 Gebre K Tseggay, MD. CNS ABSCESSES. Focal pyogenic infections of the central nervous system Exert their effects mainly by: Direct involvement & destruction of the brain or spinal cord Compression of parenchyma Elevation of intracranial pressure

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CNS ABSCESSES

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  1. CNS ABSCESSES Nov 10, 2003 Gebre K Tseggay, MD

  2. CNS ABSCESSES • Focal pyogenic infections of the central nervous system • Exert their effects mainly by: • Direct involvement & destruction of the brain or spinal cord • Compression of parenchyma • Elevation of intracranial pressure • Interfering with blood &/or CSF flow • Include: Brain abscess, subdural empyema,intracranial epidural abscess, spinal epidural abscess, spinal cord abscess

  3. BRAIN ABSCESS • Accounts for ~ 1 in 10,000 hospital admissions in US (1500-2500 cases/yr) • Major improvements realized in diagnosis & management the last century, & especially over the past three decades, with:

  4. BRAIN ABSCESS • Was uniformly fatal before the late 1800’s • Mortality down to 30-60% from WWII-1970’s • Introduction of abx (penicillin, chloramphenicol...) • newer surgical techniques • Mortality down to 0-24% over the past three decades, with: • Advent of CT scanning (1974), MRI • Stereotactic brain biopsy/aspiration techniques • Further improvement in surgery • Newer abx (e.g. cephalosporins, metronidazole..) • Better treatment of predisposing conditions

  5. CHANGES IN EPIDEMIOLOGY OF BRAIN ABSCESS (in the last 2-3 decades) • Marked drop in mortality overall • Lower incidence of otogenic brain abscesses • improved treatment of chronic ear infections • With increase in No. of immunosuppressed patients: • increased incidence of brain abscessseen in that population (Transplant, AIDS,…) • More incidence of brain abscess caused by opportunistic pathogens (fungi, toxo…)

  6. PATHOPHYSIOLOGY • Begins as localized cerebritis (1-2 wks) • Evolves into a collection of pus surrounded by a well-vascularized capsule (3-4 wks) • Lesion evolution (based on experimental animal models): • Days 1-3: “early cerebritis stage” • Days 4-9: “late cerebritis stage” • Days 10-14: “early capsule stage” • > day14: “late capsule stage”

  7. PATHOGENESIS • Direct spread from contiguous foci (40-50%) • Hematogenous (25-35%) • Penetrating trauma/surgery (10%) • Cryptogenic (15-20%)

  8. Occurs by: Direct extension through infected bone Spread through emissary veins, diploic veins, local lymphatics The contiguous foci include: Otitis media/mastoiditis Sinusitis Dental infection (<10%), typically with molar infections Meningitis rarely complicated by brain abscess (more common in neonates with Citrobacter diversus meningitis, of whom 70% develop brain abscess) DIRECT SPREAD(from contiguous foci)

  9. HEMATOGENOUS SPREAD(from remote foci) • Sources: • Empyema, lung abscess, bronchiectasis, endocarditis, wound infections, pelvic infections, intra-abdominal source, etc… • may be facilitated by cyanotic HD, AVM. • Results in brain abscess(es) at middle cerebral artery distribution • Often multiple

  10. PREDISPOSING CONDITION &LOCATION OF BRAIN ABSCESS

  11. Microbiology of Brain Abscess • Dependent upon: • Site of primary infection • Patient’s underlying condition • Geographic location • Usually streptococci and anaerobes • Staph aureus, aerobic GNR common after trauma or surgery • 30-60 % are polymicrobial

  12. Predisposing Conditions & Microbiology of Brain Abscess Predisposing ConditionUsual Microbial Isolates Otitis media or mastoiditis Streptococci (anaerobic or aerobic), Bacteroides and Prevotella spp., Enterobacteriaceae Sinusitis (frontoethmoid or sphenoid) Streptococci, Bacteroides spp., Enterobacteriaceae, Staph. aureus, Haemophilus spp. Dental sepsis Fusobacterium, Prevotella and Bacteroides spp., streptococci Penetrating trauma or postneurosurgical S. aureus, streptococci, Enterobacteriaceae, Clostridium spp. PPID,2000

  13. PREDISPOSING CONDITIONUSUAL MICROBIAL ISOLATES Lung abscess, empyema, bronchiectasis Fusobacterium, Actinomyces, Bacteroides Prevotellaspp., streptococci, Nocardia Bacterial endocarditis S. aureus, streptococci Congenital heart disease Streptococci, Haemophilus spp. Neutropenia Aerobic gram-negative bacilli, Aspergillus Mucorales, Candidaspp. Transplantation Aspergillus spp., Candida spp., Mucorales, Enterobacteriaceae, Nocardia spp., Toxoplasma gondii HIV infection Toxoplasma gondii, Nocardia spp., Mycobacterium spp., Listeria monocytogenes, Cryptococcus neoformans PPID, 2000

  14. MICROBIOLOGY OFBRAIN ABSCESS AGENTFREQUENCY (%) Streptococci (S. intermedius, including S. anginosus) 60–70 Bacteroides and Prevotella spp. 20–40 Enterobacteriaceae 23–33 Staphylococcus aureus 10–15 Fungi* 10–15 Streptococcus pneumoniae <1 Haemophilus influenzae <1 Protozoa, helminths†(vary geographically) <1 *Yeasts, fungi (Aspergillus Agents of mucor Candida Cryptococci Coccidiodoides Cladosporium trichoides Pseudallescheria boydii)†Protozoa, helminths (Entamoeba histolytica, Schistosomes Paragonimus Cysticerci) CTID,2001

  15. CLINICAL MANIFESTATIONS • Non-specific symptoms • Mainly due to the presence of a space-occupying lesion • H/A, N/V, lethargy, focal neuro signs , seizures • Signs/symptoms influenced by • Location • Size • Virulence of organism • Presence of underlying condition

  16. 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 CTID,2001. PPID,2000

  17. CLINICAL MANIFESTATIONS Headache • Often dull, poorly localized (hemicranial?), non-specific • Abrupt, extremely severe H/A: think meningitis, SAH. • Sudden worsening in H/A w meningismus: think rupture of brain abscess into ventricle (often fatal)

  18. LOCATION & CLINICAL FEATURES • FRONTAL LOBE: H/A, drowsiness, inattention, hemiparesis, motor speech disorder, AMS • TEMPORAL LOBE: Ipsilateral H/A, aphasia, visual field defect • PARIETAL LOBE: H/A, visual field defects, endocrine disturbances • CEREBELLUM: Nystagmus, ataxia, vomiting, dysmetria

  19. DIFFERENTIAL DIAGNOSIS • Malignancy • Abscess has hypo-dense center, with surrounding smooth, thin-walled capsule, & areas of peripheral enhancement. • Tumor has diffuse enhancement & irregular borders. • SPECT (PET scan) may differentiate. CRP too? • CVA • Hemorrhage • Aneurysm • Subdural empyema/ICEpidural abscess

  20. DIAGNOSIS • High index of suspicion • Contrast CT or MRI • Drainage/biopsy, if ring enhancing lesion(s) are seen

  21. IMAGING STUDIES • MRI • more sensitive for early cerebritis, satellite lesions, necrosis, ring, edema, especially posterior fossa & brain stem • CT scan • 99m Tc brain scan • very sensitive; useful where CT or MRI not available • Skull x-ray :insensitive, • if air seen, consider possibility of brain abscess

  22. LABORATORY TESTS • BRAIN ABSCESS • Aspirate:Gram/AFB/fungal stains & cultures, cytopathology (+/-PCR for TB) • WBC Normal in 40% ( only moderate leukocytosis in ~ 50% • & only 10% have WBC >20,000) • CRP almost invariably elevated • ESR Usually moderately elevated • BC Often negative BUT Should still be done • LPContraindicatedin patients with known/suspected brainabscess • Risk of herniation 15-30% • If done, may have normal CSF findings, but: • Usually elevated CSF protein & cell count (lymphs) • Unremarkable glucose & CSF cultures rarely positive

  23. TREATMENT • Combined medical & surgical • Aspiration or excision • empirical abx • Empirical antibiotics are selected based on: • Likely pathogen (consider primary source, underlying condition, & geography) • Antibiotic characteristics: usual MICs, CNS penetration, activity in abscess cavity • Modify abx based on stains • Duration: usually 6-8 wks • after surgical excision, a shorter course may suffice

  24. Armstrong ID, Mosby inc 1999

  25. MEDICAL TREATMENTONLY • Only in pts with prohibitive surgical risk: • poor surgical candidate, • multiple abscesses, • in a dominant location, • Abscess size <2.5 cm • concomitant meningitis, ependymitis, • early abscess (cerebritis?) • with improvement on abx, [Better-vascularized cortical lesions more likely to respond to abx alone] [ Subcortical/white-matter lesions are poorly vascularized]

  26. CTID,2001

  27. SERIAL IMAGING IMPORTANT TO MONITOR RESPONSE

  28. Before Rx After completion of Rx Armstrong ID,Mosby inc 1999

  29. POOR PROGNOSTIC MARKERS • Delayed or missed diagnosis • Inappropriate antibiotics. • Multiple, deep, or multi-loculated abscesses • Ventricular rupture (80%–100% mortality) • Fungal , resistant pathogens. • Neurological compromise at presentation • Short duration w severe AMS, • Rapidly progressive neuro. Impairment • Immunosuppressed host • Poor localization, especially in the posterior fossa (before CT) • Modified from CTID,2001

  30. EPIDURAL ABSCESSES • Spinal > intracranial (9:1) • Intracranially, the dura is adherent to bone • True spinal epidural space is present posteriorly throughout the spine, thus posterior longitudinal spread of infection is common. • Anterior spinal epidural very rare (usually below L1 & cervical)

  31. American Family Physician April 1, 2002

  32. SPINAL EPIDURAL ABSCESSINTRODUCTION • Rare, 0.2-1.2 per 10,000 hospital admissions • Median age 50 yrs (35 yrs in IVDU) • Thoracic>lumbar>cervical • Majority are acquired hematogenously

  33. COMMON PREDISPOSING CONDITIONS • HEMATOGENOUS SPREAD: from remote infections & w IVDU • DIRECT SPREAD: Vertebral osteomyelitis, diskitis, decubitus ulcers, penetrating trauma, surgery, epidural catheters • Via paravertebral venous plexus: from abdominal/pelvic infections

  34. PATHOGENESISSPINAL EPIDURAL ABSCESS • Often begins as a focal disc or disc-vertebral junction infection • Damage of spinal cord can be caused by: • Direct compression • Thrombosis, thrombophlebitis • Interruption of arterial blood supply • Focal vasculitis • Bacterial toxins/mediators of inflammation • Even a small SEA may cause serious sequelae

  35. MICROBIOLOGYSPINAL EPIDURAL ABSCESS The most common pathogens are: • Staph aureus >60% • Streptococci 18% • Aerobic GNR 13% • Polymicrobial 10% (Note: TB may cause up to 25% in some areas)

  36. CLINICAL MANIFESTATIONS • SPINAL EPIDURAL ABSCESS • Four clinical stages have been described: • Fever and focal back pain; • Nerve root compression with nerve root pain; “shooting pain” • Spinal cord compression with accompanying deficits in motor/sensory nerves, bowel/bladder sphincter function; • Paralysis (respiratory compromise may also be present if the cervical cord is involved). • Armstrong, ID, Mosby inc,2000

  37. DIAGNOSISSPINAL EPIDURAL ABSCESS (Thinking of it is key, in a pt with fever, severe, focal back pain) • MRI, CT • Abscess drainage • Blood cultures • Routine Labs rarely helpful • ESR,CRP usually elevated, BUT non-specific • WBC may or may not be elevated • LP contraindicated

  38. D/DXSPINAL EPIDURAL ABSCESS • Metastases • Vertebral diskitis and osteomyelitis • Meningitis • Herpes Zoster infection • Other disc/bone disease

  39. TREATMENTSPINAL EPIDURAL ABSCESS • Early surgical decompression/drainage (preferably within first 24h) • Antibiotics • Empiric abx should cover Staph, strep, & GNR • Duration of Rx : 4-6 weeks

  40. (SEA/SDE) • 90% epidural abscesses are spinal • Most SEA occur in thoracic (the longest) • Majority of SEA (>70%) are posterior to the cord • Most SEA caused hematogenous spread & Staph aureus is the leading cause. • 95% SDE are in intracranial • Majority of SDE pts have associated sinusitis

  41. INTRACRANIAL EPIDURAL ABSCESS • Less common & less acute than SEA • Rounded, well-localized (because dura is firmly adherent to bone) • Pathogenesis: • Direct ext. from contiguous foci (sinusitis, otitis/mastoiditis) • trauma,or surgery

  42. INTRACRANIAL EPIDURAL ABSCESS • MICROBIOLOGY: Micraerophillic Strep, Propioni, Peptostrept, few aerobic gNR, fungi. Postop: Staph, GNR. • CLINICAL MANIFESTATION: from SOL/ systmic igns of infection • Fever, HA, N/V, lethargy • DX:- Think of it, imaging, drainage • D/Dx: Tumor, other ICAbscesses • Rx: Surgery + abx • Mortality w appropriate Rx < 10%

  43. SUBDURAL EMPYEMA • 15-20 % of all focal intracranial infections • Motly a complication of sinusitis, otitis media, mastoiditis. • Most common complication of sinusitis (60% of such cases), mostly from frontal/ethmoid sinusitis. • Trauma/post-op & rarely hematogenous • M>F

  44. SUBDURAL EMPYEMAClinical Manifestations • Fever • Headache • Focal Neuro defects • Vomiting • Mental status changes • Seizures • Mass effect more common w SDE than w ICEA DX: CT, MRI (LP contraindicated) Rx: Surgery . Abx (3-6 wks)

  45. (Armstrong, ID,1999, Mosby Inc)

  46. PARASITICBRAIN ABSCESS • Toxoplasmosis • Neurocysticercosis • Amebic • Echinococcal

  47. NOCARDIA BRAIN ABSCESS • Usually in immunosuppresed (CMI) • >50% no known predisposing factor • All pts w pulmonary nocardiosis should undergo brain imaging to r/o subclinical CNS nocardiosis • Rx: Sulfa (T/S invitro synergy), imipenem, ceftriaxone, amikacin, minocin • Duration of abx <a year. • Needle aspiration or surgical excision needed in most. • Relapse common

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