Tuberculous meningitis (TBM) is a severe form of tuberculosis characterized by high morbidity and mortality, primarily affecting young children in areas with high TB prevalence. Diagnosis is challenging and requires a high index of suspicion, with clinical features progressing through three stages leading to neurological deficits. Management includes specific antituberculosis therapy and corticosteroids to reduce inflammation and complications, alongside supportive care and health education to prevent transmission.

1. TUBERCULOUS MENINGITIS
(TBM)
PRESENTED BY
ASHOK KUMAR
(NURSING OFFICER)

2. INTRODUCTION
• Tuberculous meningitis (TBM) is difficult to diagnose, and a high index of suspicion is needed to make an early diagnosis.
• Inquire about the patient’s medical and social history, including recent contact with patients with tuberculosis (TB). Elicit
any known history of a positive result on the purified protein derivative test, especially a recent conversion. Determine if
the patient has a history of immunosuppression from a known disease or from drug therapy.
• CNS tuberculosis is account for 1% of all cases of TB.
• Most common form is TB meningitis in Indian children.
• Almost always associated with primary tuberculosis.
• Most common route of transmission is lymphohematogenous.
• It is highly suspicious with DIAGNOSTIC DIFFICULTY and LACK OF STANDARDIZE CRITERIA.
• Morbidity and mortality are higher in TBM.

3. CONTINUED..
• Tuberculous meningitis: Meningitis due to tuberculosis. Tuberculous meningitis is the most severe form
of tuberculosis. It causes severe neurologic deficits or death in more than half of cases.
• The pattern of tuberculous meningitis in the population is different in different areas of the world.
• In areas with much tuberculosis, tuberculous meningitis usually affects young children.
• It develops typically 3 to 6 months after the primary tuberculosis infection.
• By contrast, in areas with less tuberculosis, tuberculous meningitis tends to strike adults.
• It may follow a primary infection but, more frequently, is due to reactivation of an old focus of
tuberculosis that had been dormant, sometimes for many years.

4. ETIOLOGICAL FACTORS
• The causative organism is Mycobacterium tuberculosis. Various risk factors have been identified.
• Risk factors:
1. Human migration plays a large role in the epidemiology of TB.
2. Once infected with M tuberculosis, HIV co-infection is the strongest risk factor for progression to
active TB. Although patients who have HIV infection and TB are at increased risk for TBM.
3. Other predisposing factors for the development of active TB include malnutrition, alcoholism,
substance abuse, diabetes mellitus, corticosteroid use, malignancy, and head trauma. Homeless persons,
people in correctional facilities, and residents of long-term care facilities also have a higher risk of
developing active TB compared with the general population.

5. PATHOGENESIS
 Tuberculosis meningitis is always a secondary lesion with primarily usually in lungs.
 Meningitis result from formation of metastatic caseous lesion in cerebral cortex, meninges and choroid plexus
during the process of initial occult lympho-hematogenous spread of primary infection.
 Then caseous foci form on the surface of brain ( Rich’s foci). They increase in size and discharge bacilli in CSF.
 A thick, gelatinous exudate may infiltrate the cortical or meningeal blood vessels, producing inflammation,
obstruction or infarction.
 Most commonly involved site is the brain stem causing frequent involvement 3rd, 6th and 7th cranial nerves.
 Basal cisterns obstructed causing Communicating Hydrocephalus. Accompanying inflammation may cause
cerebral edema.

6. CLINICAL FEATURES
In a classical cases, onset is insidious but may be fulminant in certain cases.
A more progression of the disease may occur in young infants in whom symptom
develop only for several days before the onset of acute hydrocephalus, brain
infarction or seizures.
Classically the onset is gradual ( over several weeks)
The clinical manifestation usually divided into 3 stages and each stage last
approximately one week.
•

7. STAGE-I ( PRODROMAL STAGE)
1. It is for last 1-2 weeks.
2. The child become listless or irritable, loss interest in play, has fever,
anorexia, vomiting, constipation and weight loss.
3. May complain of headache and drowsiness.
4. No focal neurologic signs.
5. May be loss of or stagnation of the development milestones.

8. STAGE-II
1. Onset is more abrupt.
2. Signs of meningeal irritation with increased CSF pressure.
3. Positive Kernig's and Brudzinski signs with increased tendon jerk and extensor plantar responses.
4. There may be generalized hypertonia.
5. Headache is cardinal symptoms in older children with constant fever.
6. Vomiting and constipation may become severe.
7. Abducent nerve paralysis is common. Oculomotor lesion causes internal squint. Facial palsy is also common.
8. May be disorientation and speech and movement disorders.

10. CONTINUED..
• 9. In the infants anterior fontanelle may be bulging and sutures become separated with
“crackpot” sign.
• 10. In older children papilledema develop. Head circumference start enlarging rapidly.
• 11. Choroid tubercles may be seen on fundoscopy.
• 12. Child semiconscious and develop convulsions.

11. STAGE-III
1. Rapidly develop comatose.
2. High grade irregular fever and convulsions.
3. There may be hemiplegia or paraplegia.
4. Extreme neck stiffness opisthotonus develop with the decerebrate rigidity and pupil
become dilated and fixed.
5. Deterioration of vital signs especially hypertension.
6. Death may be occur if treatment is started late during this stage.

13. DIAGNOSTICS TESTS
1. SUSPICION:
• A high index of clinical suspicion is important where tuberculosis contact is positive.
• Tuberculin skin test is negative in 50% of the patients.
2. BLOOD:
• ESR is high.
• TLC and DLC reveals normal counts and with predominant lymphocytosis.
3. X-ray chest:
• Chest x-ray may be normal in 20-50% the cases.
 Usually there is some evidence of tuberculosis in the lungs, hilar adenopathy, patch of pneumonia or miliary
tuberculosis.

14. CONTINUED..
• 4. LUMBAR PUNCTURE (CSF examination):
• CSF pressure increased.
• Colour is clear, hazy or straw coloured.
• Cobweb formed when left for more then 12 hours.
• Protein is markedly raised (400-5000mg/dl) because of hydrocephalus and spinal block.
• Glucose is decreased ( below 40mg/dl).
• Pleocytosis with predominant lymphocytes.
• Smear and culture: Ziehl-Nelson stain may reveal acid-fast bacilli. CSF culture confirms the diagnosis.
• Mycodot: antigen detection by PCR.

15. CONTINUED..
• 5. Gastric lavage or sputum examination for tubercle bacilli.
• 6. Lymph node biopsy in certain cases to confirm the diagnosis.
• 7. Fundoscopy for choroid tubercle, papilledema or optic atrophy.
• 8. CT Scan with contrast may help establish a diagnosis of tuberculous meningitis. Its
also aids in evaluating the success of the therapy.
• * CT SCAN may be normal during the early stage of TBM*

16. MANAGEMENT
• SPECIFIC TREATMENT:
• Start treatment with 4 antituberculosis drugs and treatment should be continued for 12 months.
1. ISONIAZID (INH):
• It is the drug of first choice.
• It is rapidly absorbed and penetrated into the CSF.
• Isoniazid and Rifampicin are highly bactericidal for M. Tuberculosis.
• Dose is 10-15mg/kg/day.
• Main side effects is hepatotoxicity, peripheral neuropathy, optic neuritis, hypersensitivity and fever. Neuritis is
due to competitive inhibition of pyridoxine.
• Transient elevation of amino-transferase may be seen at 6-12 weeks, but therapy should be continue.

17. CONTINUED..
• 2. RIFAMPICIN:
• It is also first line drug and well absorbed and penetrated into CSF well.
• Dose is 10-20mg/kg/day one half and hour before breakfast.
• It cause orange discoloration of urine and tear, GIT disturbance and hepatotoxicity.
• Combined use of INH and Rifampicin increased the risk of hepatotoxicity, which can be decreases
by the lowering the dose of INH (10mg/kg/day).

18. CONTINUED..
• 3. PYRAZINAMIDE:
• It is bactericidal in acid medium and enters CSF readily.
• It is used as a third drugs for 2-3 months initially.
• Dose is 30mg/kg/day.
• Main side effects are arthralgia, arthritis, hyperuricemia (Gout).
4. STEPTOMYCIN:
• It is bactericidal for extracellular tubercle bacilli, but its penetration into macrophages is poor.
• It penetrate into CSF through inflamed meninges is excellent but do not cross the un-inflamed meninges.
• Dose 20-40mg/kg/day given I/M for 2 months.
• Side effects is Ototoxicity (Vestibular or hearing loss), nephrotoxicity and may cause hypersensitivity reaction.

19. CONTINUED..
• 5. ETHAMBUTOL:
• It is not recommended below 6 years of age.
• Dose 15-25mg/kg/day.
• Side effects is optic neuronitis, hypersensitivity reaction and GIT upset.

20. GENERAL MEASURES:
• 1. CORTICOSTEROIDS:
• Decrease mortality rate and long term neurologic sequalae.
• Reduce vasculitis, inflammation and ICP.
• Dose of prednisolone is 1-2mg/kg/day for 6-8 weeks.
• Help to reduce cerebral oedema and prevents formation of adhesions.
2. CAREFUL RECORD OF VITAL SIGNS:
3. DAILY MONITORING OF COMPLICATION:
Main complication are to be monitored
 Raised intracranial pressure
 Drugs toxicity etc.

21. CONTINUED..
• 4. Phenobarbitone:
• Dose 5mg/kg/day to control convulsion.
• 5. Antipyretics:
• Paracetamol (10-15mg/kg/dose every 4-6 hourly) and fresh water sponging to control temperature.
• 6. Pyridoxine:
• 1mg/kg/day daily to prevent polyneuritis.
• 7. Feeding:
• NG tube feeding according to requirement.
• Ideally 100 calories/kg/day are given. Iron and multivitamin are too added.

22. CONTINUED..
• 8. Bed sores:
• Change posture every two hourly.
• 9. Care of Comatose patients.
• 10. Care of bowel and bladder.
• 11. Screening:
• Important to screen the family members for tuberculosis and treat infected persons.

23. HEALTH EDUCATION:
• Health education efforts must be directed at the patients to make them more informed and aware of all
aspects of the disease and its treatment.
• Patients must be informed of the basic rules to prevent spreading the infection to others in the family or the
community.
• Whereas one end of the spectrum of educational efforts is directed toward the health-related behavior of the
general public, the other end should be directed toward gaining the support of those who influence health
policies and funding of governments and institutions.
• To achieve this, information, education, and communication (IEC) campaigns should be designed to act as an
intermediary between the 2 groups. This strategy includes social marketing, health promotion, social
mobilization, and advocacy programs.