9.29.09 Davis-Hovda TB Meningitis

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    TB Meningitis9/29/2009 Morning Report

    Maggie Davis Hovda

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    Incidence

    2005: In the US there were 186 cases of

    meningeal TB, which accounted for 6.3% of

    all extrapulmonary TB In NC, there were 5 cases, 6.9%

    2007: In the US, there were 170 cases of

    meningeal TB, again 6.3% of cases

    In NC, there were 5 cases, 6.9%

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    Incidence

    In underdeveloped countries with higher

    overall incidence of TB, TB meningitis is

    more of a pediatric disease whereas indeveloped countries with lower incidence of

    TB, meningitis is more of an adult disease.

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    Pathogenesis

    TB Bacillemia (primary or late reactivation)

    subependymal tubercles rupture into

    the subarachnoid space

    meningitis

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    Pathogenesis

    Dense gelatinous exudate develops at the

    base of the brain surround arteries and

    CN at the base of the brain

    hydrocephalus, vasculitisinfarction,

    hemiplegia, quadriplegia

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    neuropathology.neoucom.edu

    Tuberculous Meningitis. Donald and Shoerman,

    NEJM. 351:17. 10/21/2004

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    Clinical Presentation

    3 Stages

    1 - Pts lucid at presentation w/o focal neuro signs

    or hydrocephalus; prodromal, lasts 2-3 wks and

    characterized by insidious onset of malaise, HA,

    low-grade fever

    2 Meningitic phase w/ meningismus, V,

    lethargy, confusion, CN palsies, hemiparesis 3 Paralytic phase advance to stupor, coma,

    seizure, hemiparesis.

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    Clinical Presentation

    Most common clinical findings:

    Fever

    HA Vomiting

    Nuchal Rigidity

    AMS

    CN Palsies, esp CN III

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    Diagnosis

    CSF Examination

    Usually lymphocytic pleocytosis

    Paradoxic change from lymphocytic to neutrophilicpredominance over 48 hr pathognomonic for TB

    meningitis

    Elevated protein with severely depressed

    glucose Repeated specimens for AFB culture necessary

    ADA level

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    Diagnosis

    Other Studies

    Brain imaging demonstrates hydrocephalus,

    basi lar exudates and inf lammation,

    tuberculoma, cerebral edema, cerebral infarction

    CXR

    Abnormal, sometimes miliary pattern

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    Differential Diagnosis

    Fungal Meningitis Crypto, Histo, Blasto, Cocci

    Viral meningoencephalitis HSV, mumps

    Parameningeal Infection Sphenoid sinusitis, brain abscess, spinal epidural abscess

    Incompletely treated Bacterial meningitis

    Neurosynphilis

    Neoplastic Meningitis

    Lymphoma Neurosarcoid

    Neurobrucellosis

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    Treatment: Antimicrobial Therapy

    Start as soon as there is suspicion for TBmeningitis

    Same Guidelines as those for pulmonaryTB Intensive Phase: 4 drug regimen of Isoniazid,

    Rifampin, Pyrazinamide, and Ethambutol orStreptomycin for 2 months

    Continuation Phase: Isoniazid and Rifampin foranother 7 10 months

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    Treatment: Adjunctive Therapy

    Glucocorticoids Indicated with:

    rapid progression from one stage to the next

    elevated OP on LP, CT evidence of cerebral edema

    worsening clinical signs after starting antiTb meds

    increased basilar enhancement, or moderate to advancing

    hydrocephalus on head CT

    Glucocorticoid Dosing: Dexamethasone 12

    mg/d x 3 weeks followed by a slow taper

    Surgery: Ventriculostomy placement

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    TB Meningitis in HIV population

    Study in S Africa compared 20 HIV + pts vs. 17 HIV - pts

    Similar findings in both groups:

    Presentation: HA, neck stiffness, fever

    CSF analysis: Similar amounts of lymphocytes, neutrophils,protein, glucose, ADA levels

    Outcomes predicted by GCS score upon admission

    -Differences

    Both groups showed same incidence of abnormal Head CT, butHIV + more likely to have ventricular dilatation and infarct

    HIV + patients were more likely to suffer no neurologic deficit ondischarge than HIV - pts

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    Outcomes

    Overall Poor

    Pts presenting in Stage I have 19% mortality

    Pts presenting in Stage III have 69% mortality Only 1/3 - 1/2 of patients demonstrate complete

    neurologic recovery

    Up to 1/3 of patients have residual severe

    neurologic deficits such as hemiparesis,blindness, seizure DO

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    References

    http://www.cdc.gov/TB/statistics/reports/surv2005/PDF/table27.pdf

    Donald, PR and Schoerman, JF. Tuberculous Meningitis.NEJM, 351:17. 2004.

    Schutte, CM. Clincial, Cerebrospinal Fluid and PathologicalFindings and Outcomes in HIV-Positive and HIV-negativePatients with Tuberculous Meningitis. Infection 2001: 29:213-217.

    Jacob, H et al. Acute Forms of Tuberculosis in Adults. TheAmerican Journal of Medicine (2009) 122, 12-17.

    Principles and Practice of Infectious Diseases. 4th Ed, c1995.

    Central Nervous System Tuberculosis. www.uptodate.com

    http://www.cdc.gov/TB/statistics/reports/surv2005/PDF/table27.pdfhttp://www.cdc.gov/TB/statistics/reports/surv2005/PDF/table27.pdfhttp://www.cdc.gov/TB/statistics/reports/surv2005/PDF/table27.pdfhttp://www.cdc.gov/TB/statistics/reports/surv2005/PDF/table27.pdf