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BRAIN ABSCESS PowerPoint Presentation

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  • Slide 1 - CNS ABSCESSES Nov 10, 2003 Gebre K Tseggay, MD
  • Slide 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
  • Slide 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:
  • Slide 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
  • Slide 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 abscess seen in that population (Transplant, AIDS,…) More incidence of brain abscess caused by opportunistic pathogens (fungi, toxo…)
  • Slide 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”
  • Slide 7 - PATHOGENESIS Direct spread from contiguous foci (40-50%) Hematogenous (25-35%) Penetrating trauma/surgery (10%) Cryptogenic (15-20%)
  • Slide 8 - 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 (<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)
  • Slide 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
  • Slide 10 - PREDISPOSING CONDITION & LOCATION OF BRAIN ABSCESS
  • Slide 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
  • Slide 12 - Predisposing Conditions & Microbiology of Brain Abscess Predisposing Condition Usual 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
  • Slide 13 - 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
  • Slide 14 - MICROBIOLOGY OF BRAIN ABSCESS AGENT FREQUENCY (%) 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
  • Slide 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
  • Slide 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
  • Slide 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)
  • Slide 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
  • Slide 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
  • Slide 20 - DIAGNOSIS High index of suspicion Contrast CT or MRI Drainage/biopsy, if ring enhancing lesion(s) are seen
  • Slide 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
  • Slide 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 LP Contraindicated in 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
  • Slide 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
  • Slide 24 - Armstrong ID, Mosby inc 1999
  • Slide 25 - MEDICAL TREATMENT ONLY 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]
  • Slide 26 - CTID,2001
  • Slide 27 - SERIAL IMAGING IMPORTANT TO MONITOR RESPONSE
  • Slide 28 - Before Rx After completion of Rx Armstrong ID,Mosby inc 1999
  • Slide 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
  • Slide 30 - ppt slide no 30 content not found
  • Slide 31 - 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)
  • Slide 32 - American Family Physician April 1, 2002
  • Slide 33 - 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
  • Slide 34 - 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
  • Slide 35 - 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
  • Slide 36 - 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)
  • Slide 37 - 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
  • Slide 38 - 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
  • Slide 39 - D/DXSPINAL EPIDURAL ABSCESS Metastases Vertebral diskitis and osteomyelitis Meningitis Herpes Zoster infection Other disc/bone disease
  • Slide 40 - 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
  • Slide 41 - (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
  • Slide 42 - ppt slide no 42 content not found
  • Slide 43 - 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
  • Slide 44 - 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%
  • Slide 45 - 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
  • Slide 46 - 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)
  • Slide 47 - (Armstrong, ID,1999, Mosby Inc)
  • Slide 48 - ppt slide no 48 content not found
  • Slide 49 - PARASITIC BRAIN ABSCESS Toxoplasmosis Neurocysticercosis Amebic Echinococcal
  • Slide 50 - 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
  • Slide 51 - BRAIN ABSCESS IN AIDS Toxoplasmosis is the most common Seropositive d/dx lymphoma Often empiric Rx given & biopsy only non- responders Listeria, Nocardia, tb, fungi…
  • Slide 52 - BRAIN TB Rare cause of brain abscess Usually in immunocompromised Tuberculoma is a granuloma (not a true abscess ) Biopsy/drainage (send for PCR too )
  • Slide 53 - FUNGAL BRAIN ABSCESS (Aspergillus, Mucor ...) IMMUNOCOMPROMISED Poor inflammatory response, less enhancement on CT. May present w much more advanced disease (seizure, stroke more common) High mortality Rx: aggressive surgery + antifungal
  • Slide 54 - BRAIN ABSCESS SEQUELAE Seizure in 30-60% Neuro deficits 30-50% Mortality 4-20%
  • Slide 55 - YIELD OF CULTURESSPINAL EPIDURAL ABSCESS SOURCE YIELD Abscess fluid aspirate 90% Blood culture 62% CSF* 19% *LP often contraindicated
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