1 / 24

TUBERCULOUS MENINGITIS

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…….

corbin
Download Presentation

TUBERCULOUS MENINGITIS

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. TUBERCULOUS MENINGITIS Dr ShreedharPaudel April, 2009

  2. 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

  3. TUBERCULOUS MENINGITIS…… • PATHOGENESIS • Usually reaches the meninges through hematogenous route • May occur as a part of miliary tuberculosis

  4. 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

  5. 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

  6. 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

  7. Diagnosis….. • CT Head • May identify • Basal exudates • Inflammatory granuloma • Infarct lesions • Hydrocephalus • PCR for Mycobacterium • Other tests: Chest X- Ray, HIV ELISA

  8. TUBERCULOUS MENINGITIS • Differential Diagnosis • PURULENT MENINGITIS, • PARTIALLY TREATED MENINGITIS • ENCEPHALITIS, • TYPHOID ENCEPHALOPATHY, • BRAIN ABSCESS, • BRAIN TUMOR, • CHRONIC SUBDURAL HEMATOMA, • AMEBIC MENINGOENCEPHALITIS.

  9. 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

  10. 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

  11. 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

  12. ENCEPHALITIS An inflammatory process of the central nervous system with dysfunction of the brain

  13. ENCEPHALITIS… • Encephalopathy is the cerebral dysfunction due to other causes than inflammatory response • Due to circulating toxins • Poisions • Abnormal metabolites • Intrinsic biochemical disorders

  14. 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

  15. 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

  16. Clinical Features … • DECEREBRATION, • DECORTICATION, • EXTRAPYRAMIDAL SYMPTOMS: JAPANEASE B • TEMPORAL OR FRONTAL LOBE FEATURES: HSV

  17. ENCEPHALITIS • DIAGNOSIS • HISTORY OF EXPOSURE • LP • CSF EVALUATION • PCR • SEROLOGICAL TESTS • TOXICOLOGICAL SCREENING • CT/ MRI

  18. 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

  19. 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

  20. 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

  21. CLINICAL FEATURES • STAGE I - MILD CONFUSION, VOMITING, ANOREXIA • STAGE II – DELIRIUM, IRRITATION, DISORIENTATION • STAGE III – COMA • STAGE IV – APNEA, NON REACTING PUPIL, SHOCK

  22. DIAGNOSIS • HYPERAMMONEMIA, • ABNORMAL LFT, • INCREASED PROTHROMBIN TIME • GENERALISED SLOW WAVES IN EEG • HYPOGLYCEMIA • LIVER BIOPSY SHOWS FATTY CHANGES AND GLYCOGEN DEPLETION BUT NO NECROSIS

  23. 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

  24. PROGNOSIS • POOR PROGNOSIS • 25-70% MORTALITY • SURVIVORS MAY HAVE NEUROLOGICAL SEQUALE

More Related