CNS ABSCESSES. Focal pyogenic infections of the central nervous system Exert their effects mainly...

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Transcript of CNS ABSCESSES. Focal pyogenic infections of the central nervous system Exert their effects mainly...

  • Slide 1
  • CNS ABSCESSES
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  • 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
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  • 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:
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  • BRAIN ABSCESS Was uniformly fatal before the late 1800s Mortality down to 30-60% from WWII-1970s 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
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  • 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 abscess seen in that population (Transplant, AIDS,) More incidence of brain abscess caused by opportunistic pathogens (fungi, toxo)
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  • 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
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  • PATHOGENESIS Direct spread from contiguous foci (40-50%) Hematogenous (25-35%) Penetrating trauma/surgery (10%) Cryptogenic (15-20%)
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  • DIRECT SPREAD (from contiguous foci) 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 (
  • PREDISPOSING CONDITION & LOCATION OF BRAIN ABSCESS Otitis/mastoiditisTemporal lobe, Cerebellum Frontal/ethmoid sinusitisFrontal lobe Sphenoidal sinusitisFrontal lobe, Sella turcica Dental infectionFrontal > temporal lobe. Remote source Middle cerebral artery distribution (often multiple)
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  • Microbiology of Brain Abscess Dependent upon: Site of primary infection Patients underlying condition Geographic location Usually streptococci and anaerobes Staph aureus, aerobic GNR common after trauma or surgery 30-60 % are polymicrobial
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  • Predisposing Conditions & Microbiology of Brain Abscess Predisposing Condition Usual Microbial Isolates Otitis media or mastoiditisStreptococci (anaerobic or aerobic), Bacteroides and Prevotella spp., Enterobacteriaceae Sinusitis (frontoethmoid or sphenoid)Streptococci, Bacteroides spp., Enterobacteriaceae, Staph. aureus, Haemophilus spp. Dental sepsisFusobacterium, Prevotella and Bacteroides spp., streptococci Penetrating trauma or postneurosurgicalS. aureus, streptococci, Enterobacteriaceae, Clostridium spp. PPID,2000
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  • PREDISPOSING CONDITION USUAL 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
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  • MICROBIOLOGY OFBRAIN ABSCESS MICROBIOLOGY OF BRAIN ABSCESS AGENT FREQUENCY (%) Streptococci ( S. intermedius, including S. anginosus )6070 Bacteroides and Prevotella spp.2040 Enterobacteriaceae2333 Staphylococcus aureus1015 Fungi * 1015* Streptococcus pneumoniae
  • 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)
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  • American Family Physician April 1, 2002
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  • SPINAL EPIDURAL ABSCESS INTRODUCTION 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
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  • 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
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  • PATHOGENESIS PATHOGENESIS SPINAL 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
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  • MICROBIOLOGY SPINAL EPIDURAL ABSCESS The most common pathogens are: Staph aureus >60% Streptococci18% Aerobic GNR13% Polymicrobial 10% (Note: TB may cause up to 25% in some areas)
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  • CLINICAL MANIFESTATIONS SPINAL EPIDURAL ABSCESS Four clinical stages have been described: 1. Fever and focal back pain; 2. Nerve root compression with nerve root pain; shooting pain 3. Spinal cord compression with accompanying deficits in motor/sensory nerves, bowel/bladder sphincter function; 4. Paralysis (respiratory compromise may also be present if the cervical cord is involved). Armstrong, ID, Mosby inc,2000
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  • DIAGNOSIS SPINAL 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
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  • D/DX D/DX SPINAL EPIDURAL ABSCESS Metastases Vertebral diskitis and osteomyelitis Meningitis Herpes Zoster infection Other disc/bone disease
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  • TREATMENT TREATMENT SPINAL EPIDURAL ABSCESS Early surgical decompression/drainage (preferably within first 24h) Antibiotics Empiric abx should cover Staph, strep, & GNR Duration of Rx : 4-6 weeks
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  • (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
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  • 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
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  • 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%
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  • 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
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  • SUBDURAL EMPYEMA Clinical 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)
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  • (Armstrong, ID,1999, Mosby Inc)
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  • PARASITIC PARASITIC BRAIN ABSCESS Toxoplasmosis Neurocysticercosis Amebic Echinococcal
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  • 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