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TUBERCULOUS MENINGITIS. Dr Shreedhar Paudel April, 2009. TUBERCULOUS MENINGITIS……. Infection of meninges by Mycobacterrium Serious complication of childhood tuberculosis Common between 6 months to 24 months age May lead to serious disabling neurological sequale. TUBERCULOUS MENINGITIS…….

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tuberculous meningitis

TUBERCULOUS MENINGITIS

Dr ShreedharPaudel

April, 2009

tuberculous meningitis2
TUBERCULOUS MENINGITIS……
  • Infection of meninges by Mycobacterrium
  • Serious complication of childhood tuberculosis
  • Common between 6 months to 24 months age
  • May lead to serious disabling neurological sequale
tuberculous meningitis3
TUBERCULOUS MENINGITIS……
  • PATHOGENESIS
    • Usually reaches the meninges through hematogenous route
    • May occur as a part of miliary tuberculosis
tuberculous meningitis4
TUBERCULOUS MENINGITIS……
  • PATHOLOGY
    • The meningeal surface is covered with yellow grayish exudates and tubercles
    • The subarachnoid space and arachnoid villi are obliterated leading to poor absorption of CSF
    • The thick exudates may block the CSF pathway causing hydrocephalus
    • There might be thrombophlebitis and tuberculous encephalopathy
clinical features
Clinical Features
  • Prodromal stage ( stage of invasion)
    • Insidious onset with vauge symptoms
    • Fever, anorexia, disturbed sleep
    • Frequent vomiting, headache, photophobia
  • Stage of meningitis
    • Features of meningitis with focal neuroligical deficits
  • Stage of coma
    • Fever, loss of consciousness and altered respiratory pattern
diagnosis
Diagnosis…..
  • LP and evaluation of CSF
    • Raised CSF pressure: 30-40 CM of water ( normal 3-4 CM of water)
    • CSF may be clear with formation of cobweb coagulum on standing ( like suspended pellicle )
    • Protein: >40 mg/dl
    • Sugar: < 2/3rd of blood sugar level
    • Cell count: 100-400/μL, predomonance of lymphocytes
    • AFB stain and C/S
diagnosis7
Diagnosis…..
  • CT Head
    • May identify
      • Basal exudates
      • Inflammatory granuloma
      • Infarct lesions
      • Hydrocephalus
  • PCR for Mycobacterium
  • Other tests: Chest X- Ray, HIV ELISA
tuberculous meningitis8
TUBERCULOUS MENINGITIS
  • Differential Diagnosis
    • PURULENT MENINGITIS,
    • PARTIALLY TREATED MENINGITIS
    • ENCEPHALITIS,
    • TYPHOID ENCEPHALOPATHY,
    • BRAIN ABSCESS,
    • BRAIN TUMOR,
    • CHRONIC SUBDURAL HEMATOMA,
    • AMEBIC MENINGOENCEPHALITIS.
treatment of tuberculosis meningitis
TREATMENT OF TUBERCULOSIS MENINGITIS
  • Antitubercular treatment for 12 weeks
  • INITIAL PHASE-- 2 MTHS: HRZE
  • CONTINUATION PHASE--10 MTHS: HRE
    • DOSE OF DRUGS
      • ISONIAZID: 5mg/kg/day
      • RIFAMPICIN: 10mg/kg/day
      • ETHAMBUTOL: 15-20mg/kg/day
      • PYRAZINAMIDE: 30-40mg/kg/day
treatment of tuberculosis meningitis10
TREATMENT OF TUBERCULOSIS MENINGITIS……
  • STEROID THERAPY
    • DEXAMETHASONE IV- 1-2 WEEKS
    • ORAL PREDNISONE FOR 6 WEEKS
    • TAPER SLOWLY OVER 2 WEEKS
      • REDUCE THE INTENSITY OF CEREBRAL EDEMA
      • REDUCE THE DEVELOPMENT OF ARACHNOIDITIS
      • REDUCE FIBROSIS AND SPINAL BLOCK

SUPPORTIVE AND SYMPTOMATIC THERAPY

prognosis
Prognosis
  • Depends on
    • Age of the patient
    • Stage of the disease at diagnosis
    • Adequacy of treatment
    • Presence of complications
  • Untreated cases die within 4-8 weeks
  • 20-25% mortality and 25% of survivors would have neurological deficits in stage 2
  • 50% mortality and 100% neurological deficits among survivors in stage 3
encephalitis

ENCEPHALITIS

An inflammatory process of the central nervous system with dysfunction of the brain

encephalitis13
ENCEPHALITIS…
  • Encephalopathy is the cerebral dysfunction due to other causes than inflammatory response
    • Due to circulating toxins
    • Poisions
    • Abnormal metabolites
    • Intrinsic biochemical disorders
encephalitis14
ENCEPHALITIS…
  • ETIOLOGY
    • VIRAL: Measles, Mumps, Rubella, Enterovirus, HSV, CMV, EBV, Japanese B, WEST NILE, RABIES, DENGUE, HIV
  • OTHER: RICKETTSIA,
  • Cryptococcus
  • TOXOPLASMA, MALARIA
  • BACTERIAL: Mycobacterium, Salmonella, Shigella, Leptospirosis
  • REYE’S SYNDROME
clinical features15
Clinical Features
  • ONSET: SUDDEN
  • SIGNS AND SYMPTOMS: FEVER, HEADACHE, VOMITING, ALTERED MENTAL STATUS, IRRITABILITY, APATHY , COMA
  • Typical features
    • Increased ICP Papilloedema Evidence of brain stem dysfunctions
  • Focal neurological deficits,
  • Respiratory/ Cardiac arrest due to Herniation of cerebellum
clinical features16
Clinical Features …
  • DECEREBRATION,
  • DECORTICATION,
  • EXTRAPYRAMIDAL SYMPTOMS: JAPANEASE B
  • TEMPORAL OR FRONTAL LOBE FEATURES: HSV
encephalitis17
ENCEPHALITIS
  • DIAGNOSIS
    • HISTORY OF EXPOSURE
    • LP
    • CSF EVALUATION
    • PCR
    • SEROLOGICAL TESTS
    • TOXICOLOGICAL SCREENING
    • CT/ MRI
management of encephalitis
MANAGEMENT OF ENCEPHALITIS
  • MANAGEMENT OF ABC
  • SYMPTOMATIC: ICT, FEVER, SHOCK, SEIZURES
  • SPECIFIC TREATMENT
    • HSV: ACYCLOVIR 30 MG/KG/DAY IN 3 DIVIDED DOSE FOR 10 DAYS
    • Focal neurological deficits, RBCs in CSF and focal involvement of temporal lobe on CT are important diagnostic clues for herpes simplex encephalitis
reye s syndrome
REYE’S SYNDROME
  • Acute self limiting metabolic insult resulting in generalised mitochondrial dysfunction due to inhibition of fatty acid beta-oxidation.
  • Precipitated by use of aspirin in viral acute respiratory infections
reye s syndrome20
REYE’S SYNDROME
  • PATHOGENESIS
    • DYSFUNCTION OF LIVER, KIDNEY , CNS
    • GENERALISED MYOCARDIAL DYSFUNCTION
    • INHIBITION OF B-OXIDATION OF FATTY ACIDS
    • HYPERAMMONEMIA, NEUROHYPOGLYCAEMIA
    • COMMON AGE IS 2MTHS – 15 YEARS
    • RAPID PROGRESSION
clinical features21
CLINICAL FEATURES
  • STAGE I - MILD CONFUSION, VOMITING, ANOREXIA
  • STAGE II – DELIRIUM, IRRITATION, DISORIENTATION
  • STAGE III – COMA
  • STAGE IV – APNEA, NON REACTING PUPIL, SHOCK
diagnosis22
DIAGNOSIS
  • HYPERAMMONEMIA,
  • ABNORMAL LFT,
  • INCREASED PROTHROMBIN TIME
  • GENERALISED SLOW WAVES IN EEG
  • HYPOGLYCEMIA
  • LIVER BIOPSY SHOWS FATTY CHANGES AND GLYCOGEN DEPLETION BUT NO NECROSIS
treatment
TREATMENT
  • LOW PROTEIN DIET WITH ADEQUATE CALORY
  • TREATMENT OF HEPATIC FAILURE
  • TREATMENT OF RAISED ICT
  • TREATMENT OF HYPOGLYCAEMIA
  • SUPPLEMENTATION OF VITAMIN K , FFP
  • TREATMENT OF ACIDOSIS, HYPOXIA AND DYSELECTROLYTEMIA
prognosis24
PROGNOSIS
  • POOR PROGNOSIS
  • 25-70% MORTALITY
  • SURVIVORS MAY HAVE NEUROLOGICAL SEQUALE