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Pathophysiology of Meningitis
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Neurology CNS Infections Characteristics of CNS Infection - Occur within a closed anatomic space - The brain is well-protected by the skull - Natural history often differs from other infectious illness at other sites, even if the same organism is the cause - Clinical manifestations differ - Associated with high mortality Definition of Terms 1. Meningitis - Inflammation of the subarachnoid space - Usually pertains to the leptomeninges 2. Encephalitis - Inflammation of the brain tissue 3. Meningoencephalitis - Meningitis & encephalitis occurs - Both meninges & brain parenchyma Notes: ** Usually if you have meningitis, it follows that there will be i nfection of the brain parenchyma. parenchyma. Patient may present with seizures which which connotes the involvement of the brain tissue. ** Etiological differences: - Virus is the only one that causes encephalitis while bacteria rarely causes encephalitis - Bacteria & virus can both cause meningitis ** The brain is an immune-privileged part part of the body. Infection may only be localized especially if bacteria is the pathogen because of the limiting activity of the immune system ** Pathological differences: - Only bacteria can cause abscess in the brain - Virus affectation leads to brain tissue involvement - Some viruses affect only one part of the brain; some c an affect the whole brain (this is due to differences in receptors - Herpes zoster – special affectation in the anterior root ganglion - Virus-causing poliomyelitis poliomyelitis go only to certain parts of the brain; does not affect the whole brain Routes of Infection - Hematogenous - From distant foci of infection - By parenteral entry - Direct extension - Sinusitis - Otitis - Mastoiditis - Dental infections - Direct introduction - Head trauma - Neurosurgical Neurosurgical procedure - Lumbar puncture - Spinal anesthesia
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4 Cardinal Manifestations of CNS Infection 1. Fever - Very important - But there may be some infection in the CNS wh not prominent - Generally, CNS infections has to have fever 2. Headache 3. Alteration in consciousness 4. Focal neurologic signs - If there is brain substance involvement - May be in the form of weakness, seizures, or be changes especially if the frontal lobe is involved
Note: Because of the vague presentation of CNS infections down the differential diagnosis diagnosis will be possible if age, local year & other epidemiologic factors are considered Ex. Influenza infection – more common in children Pneumococcal Pneumococcal infection – more common in adults Hx of travel to Palawan – consider malaria (fever, c Travel from Leyte – Schistosoma infection Travel in the United States – depending on the sea may present with predilection to viral or bacterial m Clinical Manifestations of Meningitis - Meningeal Meningeal irritation - Encephalopathy - Increased ICP 1. Meningeal Meningeal Irritation Headache/vomiting Headache/vomiting with: a. Nuchal rigidity b. (+) Brudzinski c. (+) Kernig
** Brudzinski & Kernig sign are important maneuvers children and infants who cannot relate their feelings.
2. Encephalopathy - Altered mental state - May start with lethargy, then becoming stu they go into coma - Seizure - May be because of cortical irritation of the - Focal neurologic deficits, usually bilateral - Weakness or hemiparesis due to vasc secondary to infection - Language problem due to involvement of t hemisphere
3. Increased ICP Headache/vomiting: a. Papilledema (pale (pale optic disc, distorted blood ve funduscopy) b. Diplopia with internal squint (lateral rectus palsy to CN VI nerve lesion) - Most patients Sign up to vote on will thishave titlea difficulty walking double vision or diplopia Not useful c. Useful Deterioration in the level of consciousness - Patient may start sleeping & drowsy and th able to correct their ICP, they can become d. Bulging fontanel, separation of sutures, rapid en
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CSF Analysis Normal CSF • Clear, colorless (water-like) • Not more than 180mm of water • WBC less than 5cell/cu.mm • Total protein 15-45 mg/dL • Sugar 40-50% of the RBS • Negative for microorganism growth on culture
Abnormal CSF • Pleocytosis of >1000 cells/cumm with predominance of PMNs suggests bacterial meningitis or acute purulent meningitis • Fewer WBC <1000 cells/cumm with a predominance of lymphocytes suggests viral, mycobacterial or fungal meningitis RBS – random blood sugar (Compare CSF results with RBS) ** Sugar content: Bacterial, mycobacterial & fungi meningitis – low sugar content Viral meningitis – normal sugar c ontent ** Protein content: Acute purulent bacterial meningitis – protein is markedly elevated Viral meningitis – protein is slight elevated only ** Color/consistency Xanthochromic – consider hemorrhage Turbid – consider infection ** Pleocytosis >5-10 cells/cumm; in acute purulent bacterial meningitis, it is elevated at >1000
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Note: ** In some cases, you may also have infarction because th blood vessels have been involved. In this case, px may pre stroke-like complication due to the microorganism or obstru blood supply of the brain.
- 80% of bacterial meningitis are caused by the followin organisms: 1. S. pneumoniae 2. N. meningitidis 3. S. Aureus 4. H. influenza type B
How do you differentiate those 4 organisms? (Examples) ** If an outbreak of meningitis occurs in a refugee center (b flash floods), most common cause would be meningococca ** Take note of the patient’s age, situation to delineate whi is responsible for the meningitis Pathophysiology of Bacterial Meningitis
Etiologic Agents 1. Bacteria 2. Fungi 3. Virus 4. Others - Spirochete - Rickettsia, mycoplasma, chlamydia - Parasite (Helminths, Protozoa) General Syndromes You're Reading a Preview - Acute Meningitis Syndrome - Subacute or Chronic Meningitis Syndrome Unlock full access with a free trial. - Acute Encephalitis Syndrome - Chronic Encephalitis Syndrome - Space-occupying Lesion Syndrome Download With Free Trial - Toxic-mediated Syndrome - Encephalopathy with Sys temic Infection - Postinfectious Syndrome - Slow Viral Diseases – s imulates the degenerative disorders ACUTE MENINGITIS - Most familiar & most feared - Acute onset (few hours to a few days) - Symptoms: - High fever - Headache - Photophobia - Stiff neck - Altered mental state - Etiology: (specific predisposing conditions) - Bacterial infection of the paranasal sinuses or mastoids - Recent neurosurgical procedure - Bacteria & viruses (“aseptic meningitis”) – the 2 leading causes - Viral meningitis is c onsidered “aseptic” because when you culture CSF, it is usually s terile or you won’t be able to
Patient Characteristic Neonate
Biological Organis Group B streptococcus E. coli (UTI) Children H. influenza N. meningitides Adults S. pneum Older (>50) S. pneumoniae Sign up to vote on thisEnteric title gram (-) bacilli (E. coli, pseudomon Useful Not useful Neurosurgical pxs Staphylococci (cranial trauma) Gram (-) bacilli Immunosuppressed Gram (-) enteric bacilli
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Pathophysiology of Meningitis
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Streptococcus pneumoniae - Most common etiologic organisms of community-acquired bacterial meningitis in children & adults - Caused by: (associated conditions) - Pneumonia - Otitis media - Sinusitis - CSF fistulae - Alcoholism - Head injury Neisseria meningitidis - Nonspore-forming, nonmotile, oxidase-positive, gram (-) cocci or kidney-shaped diplococci - Disease exclusive to humans - Nasopharynx is the natural reservoir - N. meningitidis is naturally present i n the nasopharynx. But somehow, something happened that made it spread to the brain - Transmission by airborne droplets or close contact - Time from nasopharyngeal acquisition to bloodstream invasion is short (~10days) - Once the organism is blood-borne over 90% of meningococcal disease is manifested as meningitis &/or meningococcemia - At this stage, the disease is very contagious. Everybody who had contact with this px should receive prophylaxis. Gram (-) bacilli - ~84% of cases of neonatal meningitis & sepsis attributed to E. coli - Neurosurgical, alcoholics & in pxs with underlying lung CA, diabetes, CHF, chronic pulmonary disease, hepatic & renal disease Listeria monocytogenes - Common among immunocompromised pxs S. aureus - In neurosurgical procedures
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Clinical Manifestations by Age Group - Neonates & Infants - Fever (50%) - Lethargy - Poor feeding - Irritability - Vomiting & diarrhea - Apnea - Seizures - Bulging fontanel - Children & adults - Fever - Headache - Photophobia - Nuchal rigidity - Lethargy, stupor, confusion, coma - Seizures - Focal neurological deficits - Nausea & vomiting - Older adults - Fever - Headache - Nuchal rigidity - Confusion or coma - Seizures
Diagnosis of Bacterial Meningitis Routine CSF Examination Purulent meningitis Normal values opening pressure <180-200 mmH 2O Gross appearance turbid or Clear & colorless purulent You're Reading aPreview WBC (mostly PMN) <5 mononuclears (-) polymorphonuclears Unlock full access witha protein free trial. 15-45 mg% Low glucose (<50% RBS) 50-60 mg% or
Streptococcus agalactiae or GBS - Leading cause of bacterial meningitis & s epsis in neonates Download H. influenza type B - Most common causative organism of bacterial meningitis i n children - Small, gram (-) pleomorphic coccobacilli - Grows best in anaerobic medium Classic CSF Analysis of Bacterial Meningitis - ↑ opening pressure - Pleocytosis of PMN leukocytes (10-10,000 cells/cumm) - ↓ glucose concentration (<45mg/dL) - ↑ protein concentration ** Use Latex agglutination (LA) test for detection of bacterial antigens. Also gram staining & culture & sensitivity are appropriate diagnostic tests. ** Before getting these lab results, you should already have a suspicion & antibiotics are imperative to have been started soon. You cannot delay treatment to avoid complications. J ust change antibiotics when
With Free Trial procedures: Other diagnostic Gram stain Culture & sensitivity Bacterial antigens
** CSF may appear cloudy or turbid, greenish or yellowish especially in purulent meningitis. (Pineapple juice-like)
Base of the brain in a of pneumococcal me showing abundant pu exudate especially pr the cisterns ** Bulk ofthe exudate Sign up to vote on this title usually in the convex cerebrum Useful Not useful ** For more prolonge exudates appear in th the brain
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Ventriculitis, shunt infection
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Immunocompromised or older pxs (impaired cellular immunity) Diffuse pial meningeal enhancement
Focal left cerebral meningitis
** What we do before a lumbar puncture is administer antibiotics and request for CT or MRI. Absence of abscess or any space-occupying lesion is a go signal for the lumbar puncture. But if these are present, lumbar puncture is a contraindication. ** If CT or MRI is not available (like i n the remotes areas), Mannitol can be used to decompress the brain before doing the lumbar puncture to prevent complication of herniation. Principles of Treatment in Meningitis 1. Always treat as a medical emergency. 2. Prompt and appropriate antibiotic therapy. 3. Cerebral metabolism should be protected. 4. Monitor ↑ ICP by clinical sings including BP, serial measurements of head and if available, intracranial sensors 5. Prevention and control of seizures 6. Fluid management should strive for normovolemia of SIADH and hypovolemia of dehydration. 7. Control of hyperpyrexia because it increases cerebral metabolic demand. Antibiotic Penetration into CSF from Blood Antibiotic
Normal Meninges Poor
Penicillin G Ampicillin Nafcillin Poor Ticarcillin/Piperacillin Fair Ceftriaxone Fair Cefotaxime Fair Ceftazidime Fair Gentamicin Poor Amikacin Tetracycline Poor Doxycycline Poor- air Chloramphenic ol Good Rifampicin Fair Vancomycin Poor Erythromycin Poor Sulfonamides Fair-good Clindamycin Poor Aprofloxacin Ofloxacin Good
S. epidermidis, S. aureus, Gram (-) Enterobac, P.aeruginosa L. monocytogenes Gram (-) Enterobac, P. aeruginosa, Pneumococci
Mero Van
3 ceph Amp Van
Antibiotics Commonly Used in the Treatment of Bacter Meningitis in Children & Adults Medication Dose Ampicillin Child: 300-400 mg/kg/d (q4h) Adult: 12-15 g/d (q4-6) Ceftriaxone Child: 80-100 mg/kg/d (q12h) Adult: 4 g/d (q12h) Cefotaxime Child: 300 mg/kg/d (q6h) Adult: 12 g/d (q4h) Ceftazidime Child: 6 g/d (q8h) Cefepime Adult: 4 g/d (q12h) Fosfomycin 15 g/d (q8h) Meropenem 6 g/d (q8h) Nafcillin Child: 200-300 mg/kg/d (q4h) Adult: 9-12 g/d Rifampin 600-1200 mg/d (q12h) Gentamicin, 6 mg/kg/d (q8h) tobramycin TMP-SMX 15-20 mg/kg/d of TMP component Metronidazole 1500-2000 mg (q8h) Vancomycin Child: 60 mg/kg/d (q6h) Adult: 2-3 g/d (q6-12h)
Chemoprophylaxis of Meningococcal Meningitis ** To those individuals who are exposed to people with infection Fair-goodYou're Reading a Preview Antibiotic, Age group Dosage Poor Fair-good Unlock full access withRifampin a free trial. Fair Adults 600 mg q12 for 2 day Fair-good 10 mg/kg q12 for 2 da Infants ≥ 1 mo Good 5 mg/kg q12 for 2 day ≤ Infants 1 mo Download With Free Trial Good Ciprofloxacin Good Adults 500 mg as single Poor- air Ceftriaxone Poor Poor 250 mg as single dos Adults & children ≥ 15 y/o Fair 125 mg as single dos Children < 15 y/o Fair Good Dexamethasone Good Fair-good Rationale: Poor- air – May ↓ ICP by ↓ meningeal inflammation and brain w Good – May ↓ sensorineural hearing loss and other neurolog Fair complications Good Good – May modulate production of cytokines, which in turn, Good meningeal inflammatory response Meningitis
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Initial Empiric Antibiotic Therapy of Bacterial Meningitis Age group/clinical setting
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Recommended Initial Antibiotic
Indications:Useful Not useful – H. influenzae meningitis – May be considered in pneumococcal and meningoco meningitis, although its efficacy for these infections is
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Pathophysiology of Meningitis
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Cerebral Complications of Bacterial Meningitis 1. Brain edema with risk of herniation 2. Cerebrovascular involvement—most frequent - Cerebral arterial complications: - Arteritis - Vasospasm - Focal cortical hyperperfusion - Disturbed cerebral autoregulation - Septic sinus thrombosis & cortical venous thrombosis 3. Hydrocephalus (communicating or obstructive type) - Especially if meningitis is prolonged & unresponsive to medication - Because of the thickening of the CSF 4. Vestibulocochlear involvement (hearing impairment, vestibulopathy) 5. Cranial nerve palsies—CN II, III, VI, VII, VIII 6. Cerebritis 7. Sterile subdural effusion 8. Rarely as a c onsequence of meningitis: brain abscess, subdural empyema - If infection is not controlled promptly & properly
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VIRAL MENINGITIS Pathogenesis: Steps in Hematogenous Spread of Virus 1. Entry into host through inoculation, respiratory or ente 2. Growth in extraneural tissues 3. Viremia 4. Viral crossing from the blood a. small vessels to brain (encephalitis) b. choroids plexus to CSF ( meningitis)
Etiology A. Viral Meningitis 1. Enterovirus (coxsackie, echovirus) – most commo 2. Mumps 3. Herpes simplex type 2 4. Lymphocyte choriomeningitis (LCM) 5. Adenovirus
B. Viral Encephalitis 1. Arthropod-borne (Japanese B Encephalitis) 2. HSV Type 1 (labialis) 3. HSV Type 2 (genitalis) 4. Varicella Zoster Virus 5. Cytomegalovirus 6. EBV 7. HIV 8. Other viruses ** HSV is the only microorganism that is responsive to trea others are usually self-resolving or microorganisms die eve
Spectrum of Complications in Pneumococcal Meningitis 1. Septic shock 2. Diffuse brain edema 3. Seizures 4. Hydrocephalus 5. Arterial CV complication 6. Venous CV complication 7. Spontaneous intracranial hemorrhage Diagnosis 8. Cerebritis 1. CSF Examination 9. CN palsies a. Clear colorless 10. Spinal cord dysfunction - May be bloody in herpes simplex encepha 11. Hearing loss b. Slight to moderate pleocytosis with either PMN 12. DIC mononuclear predominance (Cell counts do not 13. Renal failure counts. Only until 200-300. Unlike in purulent, w You're Reading a Preview 14. Requiring hemofiltration reaches up to 1000 cell counts) 15. Adult RDS Proteins mild to moderate increase occasionally Unlock full access with a free c. trial. IgG concentration ** 1, 2, 3 are the top 3 complications d. Glucose normal but decreased in mumps, herpe and lymphocytic choriomeningitis Download With Free Trial Mortality Rates of Bacterial Meningitis in Adults 2. PCR 3. Viral culture ** A completely normal CSF does not rule out encephalitis Bacterial Pathogens Mortality Rate (%) Pneumococcal meningitis 20-35 Pathology Meningococcal meningitis 3-10 - Parenchymal brain infection almost invariably associa Listeria meningitis 20-30 meningeal inflammation Staphylococcal aureus meningitis 20-40 - Perivascular and parenchymal mononuclear cel Gram (-) meningitis 20-30 - Microglial nodule - Neuronophagia ** In a recent s tudy, dexamethasone significantly reduced mortality Herpes simplex encephalitis: rates of pneumococcal meningitis in adults to 14% (34% in the placebo Hemorrhage group) - Necrotizing encephalitis - Most severe along the inferior & medial surface lobes orbitofrontal Sign up and to vote on thisgyri title - Due to the involvement of these areas, pa useful altered sensorium Useful Notchanges, with behavioral seizures Herpes Simplex Encephalitis
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SUBACUTE OR CHRONIC MENINGITIS SYNDROME - Course over weeks, months or years - Clinical findings are same as acute meningitis but the time course is quite different - Fever tends to be lower & hectic - Focal neurological findings are common - Caused by a variety of microorganism (TB, Cryptococcus, spirochetes, etc) - Meningeal TB is more difficult to diagnose or exclude, often it should be treated empirically while evaluation continues TB Meningitis - 8M years - Brain damage if untreated - Tuberculoma – 10-20% - First few days of anti-TB does not affect the ability to culture MTb from the CSF – do not withheld tx - Solid media culture – 4-6wks - BACTEC radiometric system (Middlebrook 7H10, LowensteinJensen or liquid culture system – 1-3wks) - PCR assay – rapid method of detecting TB DNA; but not very efficient Pathogenesis of TB Meningitis Initial infection
Late reactivation of foci outside the CNS Bacteremia
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Petechial hemorrhages in the subcortical white matter of the brain as a result of TB meningitis-associated vasculitis
Extensive right bas & internal capsule after the appearan vasculitis in the thalamoperforating a child treated for T meningitis
Note: ** Px presents with 2 wks of fever, headache, and lethargic When you do a lumbar tap, pressure is 250-300. CSF is thi If lab results confirm meningitis, immediately start with anti treatment right away
** Infarcts in TB meningitis - Blood vessels will traverse the subarachnoid spac chronic infection of the CSF, then you develop vas because of its proximity obstruction thrombo infarct
General Principles in the Treatment of TB Meningitis – Multiple antimicrobial drugs are required – Drugs must adequately cross the BBB – Drugs should be taken on a regular basis Isolated miliary tubercles throughout theYou're substanceReading of the – Drugs should be taken for a sufficient period to eradic a Preview brain & meninges infection TB meningitis does not develop by direct & immediate hematogenous invasion in the meninges
Unlock full access with a free trial. Treatment of TB Meningitis - Drug resistance to MTb is low Large caseous foci - Suspect if px has been previously treated for TB Download With Free Trial come from a part of the world with high prevalen resistance If located adjacent to ependyma may rupture into First line drug regimen – INH, Rifampicin, Pyrazinami subarachnoid space ( “rich foci”) addition of Streptomycin or Ethambutol - 9-12 mos – most circumstances Diagnosis - 6 mos – excellent clinical response - 18-24 mos – poor response CSF Examination 1. INH 1. Opening pressure—increased - Bactericidal 2. Gross appearance—clear or turbid (pellicl e formation) - Impairs TB DNA synthesis 3. Increased WBC—mostly lymphocytes 2. Rifampicin 4. Increased protein - Bactericidal 5. Low glucose - Impairs TB RNA synthesis 6. (+) AFB stain 3. PZA 7. Culture & sensitivity slowlyon metabolizing - Kills 8. TB Bactec Sign up to vote this title mycobacteria 4. Streptomycin Useful Not useful - Bactericidal - Given for 2 mos only due to s ensorineural 5. Ethambutol Bacteristatic
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Time course First 2 months
Drugs Isoniazid Rifampicin Pyrazinamide Ethambutol Streptomycin
Next 7-10 months (Total of 9-12 mos)
Drug Isoniazid
Rifampicin Ethambutol Pyrazinamide Streptomycin
of 9
Isoniazid Rifampicin
Doses Daily 10-15 10-20 25-30 15-25 15-40 Daily 10-15 10-20
mg/kg/d mg/kg/d mg/kg/d mg/kg/d mg/kg/d
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Treatment of Cryptococcal Meningitis Phase Drug Initial 4-8 wks Amphotericin B Flucytosine Maintenance
mg/kg/d mg/kg/d
Adverse Effect/s Hepatic Toxicity Peripheral neuropathy (can be prevented with pyridoxine) Phenytoin toxicity Hepatic toxicity Interstitial nephritis Optic neuropathy Hepatic toxicity Arthralgia with hyperuricemia Vestibular toxicity
- Prednisone 1-2 mg/kg/d or its equivalent for 6-8wks to reduce vasculitis, inflammation, and ultimately intracranial pressure - Hydrocephalus: use ventriculoperitoneal shunt - Supportive measures - Segregation from infection source
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Fluconazole
Adverse Nephrotoxici Anaphylaxis Bone marrow suppression
Hepatotoxic SJS Anaphylaxis
** Cryptoccocal meningitis is very indolent. Be very v igilan treating this.
ACUTE ENCEPHALITIS SYNDROME - Often co-exist with acute meningitis (meningoenceph - Lesion may either be focal or diffuse - Early abnormalities of mental status (prior to the onse obtundation or coma) and seizure is higher compared meningitis - Herpes Simplex Encephalitis - only treatable viral
CHRONIC ENCEPHALITIS SYNDROME - Shares many clinical features with AES however, the gradual and the course is less hectic. - Less dramatic findings and less severe but often they gradually to severe disability or death. - Patient presents a picture of greater debility rather tha illness. - Complications are more common (pressure sore, con dementia) during the course
Cryptococcal Meningitis - Most common form of fungal meningitis SPACE-OCCUPYING LESION SYNDROME - Seen in human immunodeficiency virus (HIV), and among immunocompromised patients Brain Abscess - Pathogen: Cryptococcal neoformans - Focal intracranial infections most challenging neurolo You're Reading a Preview - Respiratory tract – typical portal entry condition – diagnosis and management - 90% - headache Difficult fullof access with a free trial.to localize at early s tage - 50-60% - fever, nausea, vomiting, altered sensoriumUnlock with signs - Requires coordinated effort to s everal disciplines (neu inc. ICP intensivist, infectious disease specialist)
Download With Free Trial Pathogenesis
CSF Examination
Etiopathogenesis - Direct bacterial implantation as in t rauma or surgery - By contiguity from infections of the mastoid or parana - Sinusitis frontal lobe - Mastoiditis temporal lobe or cerebellum - By hematogenous route: - from remote infection as a consequence of seps - in association with a cardiopulmonary malfuncti cyanotic congenital heart defects - If from the heart, usually from the middle c artery since it has the direct connection w system; can go anywhere - unknown
Etiology Sign up to vote on this title - Most common: Streptococcus Useful and Not useful streptococci - Anaerobic microaerophilic - Fusobacterium species - β-hemolytic streptococci S. aureus
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Predisposing Conditions & Likely Pathogens in the Brain Abscess
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Predisposing Conditions Ear infection
Dental sinuses Trauma, surgery Abdominal, pelvic streptococci Endocarditis
HIV/T-cell dysfunction
Neutrophil dysfunction
Likely Pathogens Anaerobes, gram (-) aerobes, streptococci, H. influenza (children) Streptococcus, anaerobes S. aureus, S. epidermidis, Gram (-) aerobes Anaerobes, gram (-) aerobes, infections S. aureus, S. epidermidis, Gram (-) anaerobes, Streptococci, drug usage, Fungi Toxoplasma, Aspergillus, Candida, Nocardia, Mycobacteria, Listeria, Salmonella, Cryptococcus (& lymphoma-mimicking abscess) S. aureus, gram (-) anaerobes, aspergillus, Zygomycetes, Candida
Pathology of Brain Abscess Stage Early Cerebritis
Days 1-3
Late Cerebritis
4-9
Early capsule
10-13
Late capsule
>14
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Complications 1. Seizures - can appear anytime within 1 month and 15 year supratentorial abscess 2. Localized neurologic abnormalities 3. Mental retardation in children 4. Hydrocephalus: common complication
Prognosis Good if detected and treated early Mortality rate has declined from 30% in the pre-CT ar In infants, mortality approaches 50% Usual causes of death - cerebral herniation - fulminant meningitis when abscess ruptures into ventricles or subarachnoid space
TOXIN-MEDIATED SYNDROME - Several distinctive syndrome can occur when microb react specifically with neural tissue reach the CNS - Tetanus – clinical findings result from overstimu neural cells - Botulism – clinical findings result from interruptio transmission. - Least likely to show the four cardinal manifestations o infection
Changes Local inflammatory response ENCEPHALOPATHY WITH SYSTEMIC INFECTION seen in adventitia of blood - Usually the manifestations of the primary disease dom vessels beginning edema clinical picture. with small necrotic areas - Typhoid fever, malaria, etc Edema reaches maximum - Because of large and varied group of disease, syndro with an increase in the size of approach to diagnosis is less effective the necrotic area - Should be considered as possible underlying cause w Necrotic area is isolated from undiagnosed CNS syndrome is under evaluation. the adjacent parenchyma by You're Reading a Preview consolidation of the collagen POSTINFECTIOUS SYNDROME network around it Usual sequence begins with common, rather trivial, Unlock full access with a-free trial. Nature’s attempt to protect - Usually most patients recover uneventfully from the in the surrounding tissues from - Serious PI neurologic syndrome develops due to idios injury with more reactive Download With Freereaction Trial to primary infection. inflammatory changes - GBS, PI encephalitis or meningoencephalitis,
Clinical Manifestations - At onset, headache, vomiting, convulsions as the abscess progress, neurologic signs become readily apparent - papilledema - lateralizing signs e.g. hemiparesis, homonymous hemianopsia - more obvious signs of increased ICP - Insidious onset and slowly progressive - Sudden rupture - sudden high fever - meningeal signs - deterioration of consciousness Treatment - Medical: only if early and late Cerebritis - Surgical: only if abscess is solitary, superficial, well-encapsulated Pathogen
2011-2012 Sanderson
Agent/s
myelitis SLOW VIRAL DISEASES - Develop insidiously, over months or l onger - Show progressive sign of neuronal destruction, often motor function severely - Mortality is high - Creutzfeldt-Jacob Disease
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“If in the exam I asked you” – Dr. Poblete 1. 3 most common pathogens causing CNS infections: 36. Most common pathogen of brain abscess: Streptococ bacterial, fungal, viral 37. Brain abscess: most common presentation is focal de 2. Most common bacterial pathogens: of ICP. Temporal profile is insidious and slowly progressive S. pneumoniae, N. meningitidis which is rapid and s udden 3. Listeria monocytogenes: common pathogen in developed 38. Routine CSF cannot differentiate between TB and cryp countries meningitis. 4. Major route of CNS infection: hematogenous 39. Meningococcal meningitis: has the least mortality rat 5. In TB and fungal meningitis, inflammatory prognosis among the different types of bacterial meningitis exudates are seen at the base of the brain and the structures 40. 3rd gen cephalosporin: good penetration in both intact involved are the cranial nerves (leading to cranial nerve deficits) inflamed brain and Circle of Willis (leading to stroke-like symptoms) 41. Ceftriaxone & Cefotaxime: for gram (-) bacteria 6. Brain parenchymal infection: 42. Ceftazidime: good for Pseudomonas diffuse—encephalitis 43. Gentamicin & Amikacin: adjuncts only and not given focal—abscess monotherapy 7. Infection subarachnoid space: Leptomeningitis 44. Chloramphenicol: good penetration but bacteriostatic 8. Infection in s ubdural space: Subdural empyema 45. Cefepime & Meropenem: 4th gen cephalosporin with g 9. Infection in the epidural space: Epidural abscess coverage against Pseudomonas 10. Infection in venous sinus: Thrombophlebitis 46. Metronidazole: given to cover anaerobes 11. Spread of ethmoiditis: ethmoid, frontal, sphenoid sinuses anterior 47. Dexamethasone : used for H. influenza, pneumococca cranial fossafrontal lobe meningococcal meningitis 12. Spread of otitis and mastoiditis: 48. Dexamethasone: not indicated for partially treated men petrous sinusmiddle cranial fossa temporal lobe 49. Best timing of Dexamethasone administration is at the petrous sinusposterior cranial fossacerebellum 20 minutes before the first dose of antibacterial therap 50. 3 most common complications of pneumococcal menin 13. Infection in the cranium may spread shock, diffuse brain edema, seizure retrograde via emissary vein 14. Enterovirus: Most common viral pathogen 51. Acute meningitis: usually caused by viral and bacterial 15. Cerebellar hemispheres when affected leads to 52. TB meningitis: results only after rupture of military tube ipsilateral incoordination 53. Hepatotoxic drugs: Isoniazid, Rifampicin, Pyrazinam 16. Midline vermis when affected leads to 54. Side effect of Ethambutol is optic neuropathy truncal ataxia 55. Streptomycin is vestibulotoxic 17. 4 important clinical manifestations of meningitis are: 56. 3 drugs used to treat cryptococcal i nfection are Ampho a. meningeal irritation Flucytosine and Fluconazole b. encephalopathy 57. Amphotericin B is nephrotoxic c. increased ICP 58. Flucytosine causes bone marrow suppression d. focal neurologic deficits Fluconazole is Hepatotoxic You're Reading a59. Preview 18. Headache/Vomiting : most common symptoms 60. Most common cause of viral encephalitis is arthropod 19. Nuchal rigidity: resistance of the neck with passive flexion B enceph in the Phils) Unlock full access with(Japanese a free trial. 20. (+) Brudzinki sign: passive neck flexion leads to knee flexion 61. Bloody CSF seen in HSV encephalitis 21. Kernig’s sign: passive knee extension with hip flexed leads to 62. A completely normal CSF does not rule out encephaliti 63. Cowdry resistance to knee extension Download With Free TrialA bodies seen i n HSV encephalitis 22. HSV encephalitis: present as diffuse inflammation but with 64. Brain abscess treated medically if presents with Cerebr prominent focal deficits especially in the medial temporal and surgically if already with capsule orbitofrontal structures 65. Hydrocephalus: most common complication of brain a 23. Acyclovir : treatment of HSV encephalitis 24. The 2 most common presentations of encephalopathy: altered mental state and seizure 25. Abducens nerve: mostly affected with increased ICP due to its long intracranial course (more susceptible to stretching) 26. Abducens nerve palsy alone is a false localizing sign. 27. Abducens nerve palsy with papilledema is most likely due to increased ICP 28. 2 areas that may be affected in patients with altered consciousness are the cerebrum or the brainstem (ARAS) 29. CSF Examination is the most important diagnostic procedure to do; lumbar puncture is only the procedure to get the sample CSF Sign up to vote on this title 30. In the diagnosis of purulent meningitis, one must look at the Useful Not useful following parameters: a. opening pressure b. gross appearance cell count (most impt; characterized by pleocytosis)
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