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Case presentation tb meningitis

a case of tb meningitis with presentation

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Case presentation tb meningitis

  1. 1. CASE STUDY Prajjwal Malla MDGP Resident 1st yr
  2. 2. • 62 years male, Kham Bahadur Gurung • From Syangja • Dizziness and vomiting for 10 days • Fever for 2 days along with headache and neck stiffness • He was in delirious state with behavioral changes • Bowel and bladder habits were normal • He was treated outside but did not get better.
  3. 3. • Personal history: alcoholic but non smoker • Past history : PTB 10 yrs back, treated • Surgical history : -Right hydrocele was operated 3 yrs ago -Right eye was operated 1 month back • O/E : General condition: fair, confused, GCS:14/15, febrile • Other vitals: stable
  4. 4. SYSTEMIC EXAMINATION • Respiratory: normal vesicular breath sounds in both lungs decreased air entry in right upper lobe • Cardiovascular : S1S2M0 • Per abdomen: soft, non tender, no organomegaly
  5. 5. Central Nervous System: • Higher mental function: delirious, not oriented to time, place and person • Neck rigidity : present • Ophthalmoplegia : present • Slight facial deviation on left side • Power : intact in all the four limbs • Tone : increased in upper limbs • Deep tendon reflexes : exaggerated in all four limbs • Plantar: B/L upgoing
  6. 6. LABS • WBC: 10360/mm3 • Hb: 12.3 mg/dl • Platelets: 458000 cu/mm • PMN: 82% • ESR: 14 mm • Blood culture : no growth after 72 hours • Malaria parasite: not seen • B24-negative • S. creat: 1.4 mg/dl • K+: 5.6 mmol/L • Na+: 136 mmol/L • ALP: 105 U/L • AST: 28 U/L • ALT: 10 U/L • RBS: 183 mg/dl
  7. 7. CSF FLUID ANALYSIS • WBC: 155 (↑↑) • RBC: 15 (↑↑) • POLYS: 42% • LYMPHS: 58% • GLUCOSE: 48mg/dl (↓) • PROTEIN: 176.0mg/dl (↑↑) • ADA: 17
  8. 8. CHEST XRAY
  9. 9. CT- HEAD
  11. 11. ETIOLOGY • Causative organism: Mycobacterium tuberculosis • First description of TBM credited to Robert Whyte, on the basis of his 1768 monograph, Observations of Dropsy in the Brain. • Described as a distinct pathological entity in 1836 • Robert Koch demonstrated that TB was caused by M. tuberculosis in 1882.
  12. 12. RISK FACTORS • HIV coinfection is the strongest risk factor for progression to TBM. • Unimmunized with BCG Other contributing factors • Malnutrition • Alcoholism • Substance abuse • Diabetes mellitus
  13. 13. EPIDEMIOLOGY • In populations with a low prevalence of TB, most cases of TBM occur in adults. • However, TBM is more common in children than in adults, especially in the first 5 years of life.
  14. 14. PATHOPHYSIOLOGY • 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 . • Due to chronic reactivation bacillemia occurs in older adults due to immune deficiency caused by aging, alcoholism, malnutrition, malignancy, or human immunodeficiency virus (HIV) infection • Head trauma may also lead to destabilization of an established quiescent focus resulting in meningitis
  15. 15. • 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. • Proliferative arachnoiditis, most marked at the base of the brain, produces a fibrous mass involving cranial nerves and penetrating vessels. • Vasculitis with resultant thrombosis and infarction involves vessels that traverse the basilar or spinal exudate or are located within the brain substance itself. • Variety of stroke syndromes may result, involving the basal ganglia, cerebral cortex, pons, and cerebellum. • Communicating hydrocephalus results from extension of the inflammatory process to the basilar cisterns and impedance of CSF circulation and resorption.
  16. 16. • Basal exudates
  17. 17. • Tuberculomas are coglomerate caseous foci within the substance of the brain.
  19. 19. CLINICAL PRESENTATION • TBM is difficult to diagnose and a high index of suspicion is needed to make an early diagnosis HISTORY: • Recent contact with patients of TB • Past history of TB • History of immunosuppresion from a known disease or from drug therapy • Negative history of BCG vaccination-see for scar
  20. 20. Principle presentation is subacute febrile illness that progresses through three phases:
  21. 21. • Choroid tubercles on opthalmoscopy - multiple, ill-defined, raised yellow-white nodules (granulomas) of varying size near the optic disc
  22. 22. Atypical features: • Meningitic syndrome rapidly progressing- suggesting acute infection • Dementia over months or years- personality change, social withdrawal, loss of libido, and memory deficits • Encephalitic course with stupor, coma, and convulsions without overt signs of meningitis
  23. 23. PHYSICAL EXAMINATION • Look for BCG vaccination scar • Visual findings: papilledema or a small grayish white choroidal nodule • cranial neuropathies: VI most affected, then III, IV, VII and less commonly II, VIII, X, XI, XII. • Kernig’s sign and Brudzinki’s sign • Tremor is the most common movement disorder seen in the course of TBM. • In a smaller percentage of patients, abnormal movements, including choreoathetosis and hemiballismus, have been observed, suggesting of deep vascular lesions.
  24. 24. • Stage I - apathy, irritability, headache, malaise, fever, anorexia, nausea, and vomiting, without any alteration in the level of consciousness. • Stage II - altered consciousness without coma or delirium but with minor focal neurological signs; symptoms and signs of meningism and meningitis are present, in addition to focal neurological deficits, isolated CN palsies, and abnormal involuntary movements. • Stage III - advanced state with stupor or coma, dense neurological deficits, seizures, posturing, and/or abnormal movements CLINICAL STAGING
  25. 25. DIFFERENTIAL DIAGNOSES Based on CSF findings of ↓Glucose, ↑Protein & lymphocytic pleocytosis • Subacute or chronic meningitis syndrome caused by Cryptococcosis, Granulomatous fungal infections, Brucellosis, and Neurosyphilis. • Parameningeal suppurative infection, eg.brain abscess, or spinal epidural space infection. • Herpes encephalitis
  26. 26. WORK UP • Electrolyte concentrations: - mild-to-moderate hyponatremia present in roughly 45% of patients - in some cases constituting a true syndrome of inappropriate diuretic hormone secretion (SIADH). • Blood urea nitrogen (BUN) and creatinine level • Urinalysis • Tuberculin skin testing
  27. 27. • CSF Analysis -Cell counts, differential count, cytology -Glucose level, with a simultaneous blood glucose level -Protein level -Acid-fast stain, Gram stain, India ink stain -Cryptococcal antigen and herpes antigen testing
  29. 29. • Culture: (87% diagnostic) - 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. • Polymerase chain reaction: - 60% sensitive in rapid detection of M. tuberculosis in CSF. - Recommended whenever clinical suspicion is sufficiently high for empirical therapy or AFB is negative.
  30. 30. • Neuroimaging: - 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. • 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.
  31. 31. MRI showing basilar enhancement
  32. 32. • Interferon-gamma release assay (IGRA) using specific tuberculous antigens is a rapid, specific and sensitive method for the detection of tuberculous infection.
  33. 33. OTHERS • Angiography- for narrowing of the arteries especially the small vessels at the base of the brain • Electroencephalopathy-abnormal if meninigitis has progressed to advanced stage • Brainstem Auditory Evoked Response Testing- abnormal in advanced stage of meningitis
  34. 34. TREATMENT • The mainstay of treatment for TB is clinical suspicion & starting of empirical therapy. • First line drugs — Isoniazid (INH), rifampin (RIF), and pyrazinamide (PZA) are bactericidal, can be administered orally all having good meningeal penetration.
  35. 35. RECOMMENDED REGIMEN • Intensive phase (Initial 2 months) • A four drug regimen- INH, RIF, PZA, and either EMB or STM • Continuation phase (9-12 months) • INH and RIF alone if the patient makes good progress.
  36. 36. 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 with isoniazid and thiacetazone.
  37. 37. VALUE OF CORTICOSTEROIDS • has now been established by a controlled trial. • Particularly for young children and severely ill. • Begin with Prednisolone 30 mg twice daily (1mg/kg twice daily for chidren) for 4-6 weeks then decrease over several weeks as the patient improves. • For the patients on rifampicin the dose should be increased by half, i.e. 45 mg for adults and 1.5 mg/kg for children. The reason being Rifampicin antagonises the action of Prednisolone.
  38. 38. • 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.
  39. 39. SECOND LINE DRUGS • Aminoglycosides: e.g., amikacin , kanamycin • Polypeptides: e.g., capreomycin, viomycin, enviomycin; • Fluoroquinolones: e.g., ciprofloxacin , levofloxacin, moxifloxacin ; • Thioamides: e.g. ethionamide, prothionamide • Cycloserine (the only antibiotic in its class); • p-aminosalicylic acid (PAS or P).
  40. 40. OTHERS • Macrolides: e.g., clarithromycin • Linezolid (LZD) • Thioacetazone (T) • Immunomodulators- cytokine-based therapy which enhance both the mycobacterial killing activity of effector cells and the restriction of bacterial intracellular multiplication • BCG vaccination offers a protective effect (approximately 64%) against TBM.
  41. 41. SURGICAL INTERVENTION • In patients with evidence of obstructive hydrocephalus and neurological deterioration who are undergoing treatment for TBM, placement of a ventricular drain or ventriculoperitoneal or ventriculoatrial shunt should not be delayed.
  42. 42. COMPLICATIONS • Hydrocephalus • Infarctions • Coma/stupor • Motor deficits- CN palsies, hemiparesis • Seizures • Mental impairment • Abnormal behavior • Brain damage • High morbidity and mortality
  43. 43. PROGNOSIS • Very critical disease in terms of fatal outcome and permanent sequelae, requiring rapid diagnosis and treatment. • Prognosis is directly related to the clinical stage at diagnosis. • Kumar et al reported that children with TBM who have been vaccinated with BCG appear to maintain better mentation and have superior outcomes. • Coexisting HIV encephalopathy and diminished immune competence contribute to the more severe clinical and neuroradiological features.
  44. 44. TAKE HOME MESSAGE • Start ATT empirically when suspicion of TB • See for the BCG scar in suspected case • Counsel the patient for medication/side effects • Complete the course • Follow up
  45. 45. REFERENCES • Harrison’s Principle of Internal Medicine • Clinical Tuberculosis: John Crofton, Norman Horne, Fred Miller • Medscape • Uptodate