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Meningitis
 

Meningitis

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date:19/09/2011

date:19/09/2011

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    Meningitis Meningitis Presentation Transcript

    • MENINGITIS
      Dr .PRAVEEN NAGULA
    • MENINGITIS
      MENINGITIS
    • Introduction
      Infection predominantly involves the subarachnoid space---MENINGITIS.
      Brain tissue directly involved is called as ENCEPHALITIS.
      Focal bacterial,fungal,parasitic infection involving brain tissue – CEREBRITIS –absence of capsule,ABSCESS presence of capsule.
      Nuchal rigidity (STIFF NECK ) – pathognomonic sign of meningeal irritation-resistance to passive flexion.
      Classical signs of meningeal irritation –KERNIG’S,BRUDZINSKI’S sign.
    • MENINGES
    • Meninges
    • What is ?
      MENINGISM :the symptoms and signs of meningeal irritation assosciated with acute febrile illness or dehydration without actual infection of the meninges…also called meningismus…PSEUDOMENINGITIS.
    • KERNIG’S SIGN
      Patient to be in supine position.
      Thigh flexed on abdomen.
      Knee flexed.
      Attempt to passively extend knee elicit pain when irritation is present.
    • BRUDZINSKI’S sign
      Supine position.
      Passive flexion of neck –spontaneous flexion of hips and knees.
      Specificity and sensitivity of these tests –UNCERTAIN.
    • Where they could be absent are?
      Immunocompromised
      Very young or elderly.
      Severely depressed mental state.
      False positive – cervical spine disease..
    • IMPORTANT POINTS..
      It is an emergency.
      Empirical antibiotics to be started.
      Do CT scan/MRI in case of immunocompromised,recent head trauma,focal neurological deficits ---LP – but AB not to be delayed.
      No depressed level of consciousness –think of viral meningitis.
      Immunocompetent ,consciousness good –can be treated on OP basis.
      Failure of a patient to improve < 48 hrs – reevaluate the patient,repeat LP ,lab studies and neurological examination.
    • ACUTE BACTERIAL
      MENINGITIS
      ACUTE BACTERIALMENINGITIS
    • It is an acute purulent infection within the subarachnoid space.
    • Most common orgnaisms responsible for community acquired bacterial meningitis
      S.pneumoniae 50%
      N.meningitidis 25%
      Group B streptococci - 15%
      Listeriamonocytogenes 10%
      Hemophilusinfluenzae  10%
    • Based on age
    • TRIAD OF MENINGITIS
    • ETIOLOGY
      PNEUMOCOCCAL –
      from pneumonia,otitis media,alcoholism,diabetes,splenectomy,hypogammaglobulinemia,complement deficiency,head trauma.
      20% mortality depsite antimicrobial Rx.
      N.meningitidis-25% of all cases.
      Petechiae or purpuric skin rash.
      Fulminant –death within hours
      ENTERIC gram negative – chronic debilitating diseases.
      S.agalacticae -- >50 yrs of age.
      L.monocytogenes–ingestion of food contaminated.
    • PATHOGENESIS
      Nasopharyngeal colonization –asymptomatic carrier.
      Invasive meningeal disease
      Depends on bacterial virulence factor ,host immune defense mechanisms
      Deficiency of complement
      Highly susceptible
    • pathogenesis
    • Much of the pathophysiology is due to direct consequence of chemokines,cytokines.
    • Clinical features
      Decreased level of consciousness >75%
      Nausea,vomiting,photphobia common
      Classical triad –less sensitivity
      Only two may be present nearly in all cases.
      Seizure –initial presentation in 20-40% cases
      Focal –focal arterial ischemia,cortical venous thrombosis,focal edema
      GTCS– hyponatremia,anoxia,high dose penicillin.
      RAISED ICP- >90 % have CSF pressure – 180mmH20
      20% -- 400mm H20
      Rash of meningococcemia – diffuse,petechial;
    • DIAGNOSIS
      CSF analysis
      Blood cultures
      CT scan/MRI --- LP
      Latex agglutination – S.pneumoniae,N.meningitidis
      Lumuluslysate –gram negative
      In case of immunocompetent,no h/o head trauma,no evidence of papilledema –LP without CT scan
      AB therapy to be started hrs before LP –no change in analysis,or visualization of organisms
    • CSF analysis
    • CSF glucose may be zero –
      CSF/serum glucose corrects for hyperglycemia
      CSF/s.glucose < 0.6
      CSF/s.glucose < 0.4 – bacterial,fungal,tuberculosis,carcinomatosis
      30 min to several hours to reach equilbrium with blood glucose levels –so can start 50 ml of 50 % D.
      PCR –useful in pretreated pts,gram stain negative
      MRI >CT for cerebral edema
      Diffuse meningeal enhancement --gadolinium –increased permeability of BBB.
    • Differential diagnosis
      HSV mimics bacterial meningitis –differentiated by CSF,EEG,neuroimaging.
      RICKETTESIAL- rash—petechiae—necrosis—gangrene,distal
      Non infectious – SAH,Chemical meningitis
      Uveomeningeal syndrome – VogtKoyangiHarada syndrome
      Subacute –M.tuberculosis,c.noeformans,h.capsulatum
    • Treatment
      BEGIN AB < 60 min
      Empirical treatment –dexamethasone,cefotaxime or ceftriaxone,vancomycin,azithromycin,acyclovir,doxycycline.
      Post op cases –ceftazidime,cefepime,meropenem,vancomycin
      Then change according to culture reports
    • Meningococcal
      PENICILLIN G is DOC
      In case of resistance – Ceftriaxone,cefotaxime
      Uncomplicated course--7 day course.
      All close contacts should receive chemoprophylaxis – 2 day regimen of rifampicin 600 mg every 12 hrs * 2days/ciprofloxacin 750 mg od/azithromyxin 500 mg OD/ceftriaxone 250 mg OD
      Who are close contacts --- nasopharyngeal secretions,kissing,toys,beverages use.
    • pneumococcal
      Cephalosporin plus vancomycin
      If resistance – vancomycin
      Rifampin can be added synergistic action
      2 week course
      Repeat LP after 24-36 hrs –sterilization of CSF –if not introventricularvancomycin
    • Listeria and others
      Ampicillin for 3 weeks
      Gentamicin 2mg/kg/d loading – 7.5 mg/kg/d every 8hrs
      TMP SMX –every 6hrs
      STAPHYLOCOCCAL –vancomycin
      Gram negative – 3 weeks of third generation cephalosporin.
    • Adjunctive therapy
      Dexamethasone – decreases synthesis of IL1,TNF,stabilises BBB
      20 min before AB Rx
      Inhibits TNF production by macrophages only before activated by endotoxin.
      Decreases penetration of vancomycin into CSF.
      10 mg IV 30 min before AB every 6hrs -4 days.
    • Raised ICP
      Elevate head end of bed 30-45
      Intubation
      Hyperventilation PaCo2 – 25-30 mm Hg
      mannitol
    • prognosis
      20% mortality –pneumococcal
      15% - listerias
      3-7% h.infleunzae,gram negative.
    • Who are at risk of poor prognosis
      Decreased level of consciousness at admission
      Seziures < 24 hrs of onset
      Raised ICP
      Young age,>50 yrs
      Mechanical ventilation
      Delay in treatment
      <40 mg /dl -glucose
      >300 mg/dl -protein
    • sequelae
      Decreased intellectual function
      Memory impairement
      Seizures
      Hearing loss
      Gait disturbances
    • SUMMARY
      Acute bacterial meningitis is an emergency
      Triad is seen less commonly
      Pathognomonic feature is neck rigidity
      Altered level of consciousness and seziures can be the presenting features.
      S pneumoniae is the most common organism overall
      Other organisms based on the age ,and clinical background
      CSF analysis after CT scan is the rule…
      PMNs,hypoglycoracchchia,raised proteins and pressure is the hallmark
      PCR to be done only in negative cases
      MRI for cerebral edema
    • Antibiotics for a week in case of uncomplicated meninogcocci,2 weeks in s pneumoniae,3 weeks listeria.
      All close contacts to be given chemoprophylaxis in case of meningococci with rifampicin 600 mg bid for 2 days.
      Triad of meningitis is fever,headache,neckstiffness
      Postoperative cases think of s aurues,gram negative.
      Ampicillin to be given in case of suspicion of listeria for 3 weeks
      S. pneumoniae has high mortality of 20%
    • Antibiotic treatment not to be delayed for the results of investigations
      Third generation cephalosporins,vancomycin,ampicillindurgs empirically will cover all organisms.
      Dexamethasone for stabilisingBBB,to be given beofre AB.
      HSV encephalitis is closest DD
      1 week therapy in case of meningococci,2 weeks pneumoniae,3 weeks –listeria
      Raised ICP –hyperventilate,raise head end,mannitol
      Sequelae decrease on early management
      20% mortality in case of s.pneumoniae
      Thank you