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Case study,[object Object]
Case,[object Object],A 70year old male NKCM came with the complain of,[object Object],Low grade fever -5yrs –on & off,[object Object],Severe Headache-15-20dys,[object Object],Behavioural changes- 2wks,[object Object]
According to the attendant (son) he has been ill on & off since the past 5-6yrs when he used to develop a low grade intermittent self resolving fever. It was sudden & non specific happening bout 1-3dys & the fever free period varied from weeks to months. ,[object Object],Now since the past few weeks he had a headache which wasn’t relieved by anything. He also was restless & disoriented. His talk & behaviour was odd to the family so they brought him for treatment. He was labelled as having dementia since the past year. ,[object Object],He was a smoker *quit since some years* & had a persistent dry cough.  ,[object Object],No history of vomiting, Night sweats, loss of consciousness or loss of function but on/off nausea present. ,[object Object],Past hx- Pulmunary TB diagnosed on CXR/Sputum test 2yrs ago,[object Object],               took ATT for only 2 weeks,[object Object],               Hernia repair & Hemorrhoidectomy -6-7yrs ago. ,[object Object],Social History- Contact Hx of TB from work collegue. ,[object Object],Family History- not significant. ,[object Object]
Investigations,[object Object],CBC,[object Object],Hb-12.1, Pcv-37, TLC-5.9, Plt-267,[object Object],UCE,[object Object],Na-142, K-3.4, Co3-21, Cl-103,Urea-44, Crt-0.84,[object Object],                    SGPT- 10,  RBS-91,[object Object],Urine D/R,[object Object],PH-5.5, Protein- 10mg/dl, Sp.grav-1.025, Rbs-numerous, Blood-3+, pus-2, Epi-2, Bacteria-few,[object Object]
CSF-D/R,[object Object],Volume-10ml,[object Object],Colorless, clear,[object Object],Glucose-43 ( Serum Rbs-83),[object Object],Protein-87,[object Object],Rbc-64, 000cu/mm,[object Object],Wbc- 200cu/mm ------Neu- 6, Lymp-92, Mono-2,[object Object],ESR-32,[object Object],AFB –ve,[object Object],CXR- Fibrosis. ,[object Object]
CT scan showing basilar & Vascular enhancement,[object Object]
CT showing ventricular dilatation,[object Object]
TB Meningitis,[object Object]
Clinical features,[object Object],Principle presentaion is subacute febrile illness that progresses through three discernible phases:,[object Object]
Choroid tubercles on opthalmoscopy -multiple, ill-defined, raised yellow-white nodules (granulomas) ,[object Object],of varying size near ,[object Object],the optic disk,[object Object],CXR abnormalities- single or multiple lesions,[object Object]
Atypical features:,[object Object],Meningitic syndrome rapidly progressing-suggesting acute infection,[object Object],Dementia over months or years- personality change, social withdrawal, loss of libido, and memory deficits,[object Object],Encephalitic course with stupor, coma, and convulsions without overt signs of meningitis,[object Object]
Clinical stages,[object Object],It is useful for prognosis and therapy,[object Object],Stage I patients are lucid with no focal neurologic signs or evidence of hydrocephalus. ,[object Object],Stage II patients exhibit lethargy, confusion; may have mild focal signs, such as cranial nerve palsy or hemiparesis.,[object Object],Stage III represents advanced illness with delirium, stupor, coma, seizures, multiple cranial nerve palsies, and/or dense hemiplegia.,[object Object]
Pathogenesis & suseptibility,[object Object],Following primary infection or late reactivation TB elsewhere in the body scattered tubercles are established in the brain, meninges, or adjacent bone. Subcortical or meningeal focus from which bacilli gained access to the subarachnoid space is the critical event for development of tuberculous meningitis .More common in miliary TB because of higher chance of forming Juxta ependymal meningitis. ,[object Object],Meningitis can develop as a complicatin of primary infection in infants/children ,[object Object],Due to chronic reactivation bacillemia in older adults immune deficiency caused by aging, alcoholism, malnutrition, malignancy, or human immunodeficiency virus (HIV) infection,[object Object],Head trauma may also lead to destabilization of an established quiescent focus resulting in meningitis,[object Object]
The spillage of tubercular protein into the subarachnoid space produces an intense hypersensitivity reaction due to a dense gelatinous exudate, giving rise to inflammatory changes.,[object Object], Proliferative arachnoiditis, most marked at the base of the brain, produces a fibrous mass involving cranial nerves and penetrating vessels. ,[object Object],Vasculitis with resultant thrombosis and infarction involves vessels that traverse the basilar or spinal exudate or are located within the brain substance itself. Multiple lesions are common and a variety of stroke syndromes may result, involving the basal ganglia, cerebral cortex, pons, and cerebellum.,[object Object],Communicating hydrocephalus results from extension of the inflammatory process to the basilar cisterns and impedance of CSF circulation and resorption. Obstruction of the aqueduct develops less frequently, from contraction of exudate surrounding the brain stem or from a strategically placed brain stem tuberculoma.,[object Object]
Ventricular dilatation is present (asterisks), as well as inflammatory exudate in the ambient cistern (black arrows) and multiple foci of vasculitis-associated subacute, ischemic necrosis,[object Object]
Diagnosis,[object Object],Cerebrospinal fluid examination:,[object Object],Protein      100-500mg/dl ,[object Object],Glucose     <45 mg/dL (80%),[object Object],Initial stages PMN predominance later changed to lymphocytic dominance. ,[object Object]
Tb Meningitis
Culture: (87% diagnostic),[object Object],CSF specimens for M. tuberculosis. The demonstration of acid-fast bacilli (AFB) in the CSF is the effective means for an early diagnosis. Minimum of 3 lumbar punctures be performed at daily intervals. ,[object Object],Polymerase chain reaction: nucleic acid-based amplification test (NAAT) relies upon the polymerase chain reaction (PCR) is 60% sensitive in rapid detection of M. tuberculosis in CSF. Recommended whenever clinical suspicion is sufficiently high for empirical therapy or AFB is negative. ,[object Object]
Neuroradiology: CT & MRI are helpful in detection. CT can present the extent of basilar arachnoiditis, cerebral edema and infarction, and the presence and course of hydrocephalus.,[object Object],Hydrocephalus combined with marked basilar enhancement is indicative of advanced meningitic disease and carries a poor prognosis. Marked basilar enhancement correlates well with vasculitis and, therefore, with a risk for basal ganglia infarction.,[object Object]
Interferon-gamma release assay (IGRA) using specific tuberculous antigens is a rapid, specific and sensitive method for the detection of tuberculous infection. The high interferon-gamma concentration in the CSF increases further after the antigen stimulation, suggesting theoretically the presence of tuberculous antigen-specific T cells.,[object Object]
DIFFERENTIAL DIAGNOSIS,[object Object],Based on CSF findings of      Glucose,  Protein & lymphocytic pleocytosis, ,[object Object],Subacute or chronic meningitis syndrome caused by cryptococcosis, Granulomatous fungal infections, brucellosis, and neurosyphilis.,[object Object],Parameningealsuppurative infection, (eg, sphenoid sinusitis, brain abscess, or spinal epidural space infection.,[object Object],Herpes encephalitis,[object Object]
Treatment,[object Object],The mainstay of treatment for TB is clinical suspicion & starting of empirical therapy. ,[object Object], First line drugs — Isoniazid (INH), rifampin (RIF), and pyrazinamide (PZA) are bactericidal, can be administered orally all having good meningeal penetration. ,[object Object]
First line drugs,[object Object]
Recommended regimen ,[object Object],  Intensive phase (Initial 2months) — A four drug regimen that includes INH, RIF, PZA, and either EMB or STM ,[object Object],  Continuation phase (7-10m) — INH and RIF alone if the isolate is fully susceptible.,[object Object],Duration of therapy —9 to 12 months in drug-sensitive infections. If PZA is omitted or cannot be tolerated, treatment should be extended to 18 months. ,[object Object]
Glucocorticoid regimen,[object Object],Dexamethasone — A total dose of 8 mg/day for children weighing <25 kg; 12 mg/day for adults and children >25 kg, for 3 weeks, then tapered off gradually over the following 3 to 4 weeks. ,[object Object],Prednisone — A dose of 2 to 4 mg/kg per day for children; 60 mg/day for adults, for 3 weeks, then tapered off gradually over the following 3 weeks.,[object Object]
Second line drugs,[object Object],Aminoglycosides: e.g., amikacin (AMK), kanamycin (KM);,[object Object],Polypeptides: e.g., capreomycin, viomycin, enviomycin;,[object Object],Fluoroquinolones: ,[object Object],e.g., ciprofloxacin (CIP), levofloxacin, moxifloxacin (MXF);,[object Object],Thioamides: e.g. ethionamide, prothionamide,[object Object],Cycloserine (the only antibiotic in its class);,[object Object],p-aminosalicylic acid (PAS or P).,[object Object]
Others,[object Object],Macrolides: e.g., clarithromycin (CLR);,[object Object],Linezolid (LZD);,[object Object],Thioacetazone (T);,[object Object],Immunomodulators- cytokine-based therapy but more research needed for other cytokines and chemokines that may enhance both the mycobacterial killing activity of effector cells and the restriction of bacterial intracellular multiplication,[object Object]
Surgical Intervention,[object Object],Patients with hydrocephalus may require surgical decompression of the ventricular system by shunt. ,[object Object]
Complications,[object Object],Hydrocephalus,[object Object],Infarctions,[object Object],Coma/stupor,[object Object],Motor deficits-CN palsies, hemiparesis , ,[object Object],Seizures, ,[object Object],Mental impairment,[object Object],Abnormal behavior,[object Object],Brain damage,[object Object],High morbidity and mortality,[object Object]
Take home message	,[object Object],Start ATT empirically when suspicion of TB,[object Object],Counsel the patient for medication/side effects,[object Object],Complete the course,[object Object],Follow up,[object Object]
The End,[object Object]

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Tb Meningitis

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