Tb meningitis

1. TUBERCULAR MENINGITIS Siddharth Ray
Intern ( Batch 2017)

2. OVERVIEW
Introduction
Epidemiology
Etiology
Pathogenesis
Clinical features
Investigation and diagnosis
Treatment
Prognosis

3. INTRODUCTION
MENINGITIS – Inflammation of leptomeninges.
TYPES-
•Bacterial meningitis
•Viral meningitis
•Fungal meningitis
•Tubercular meningitis

4. TUBERCULAR MENINGITIS
Most common form of CNS tuberculosis
If untreated, high frequency of Neurological sequelae and
Mortality
TBM complicates 0.3 %of untreated TB infections in children
Common between 6 months and 4yrs of age
Clinical progression- Rapid or Gradual
Rapid progression more often in infants and young children
Ocassionally , TBM occurs many years after the infection

5. EPIDEMIOLOGY
Comprises 1% of total TB cases
5-10% of extra pulmonary TB cases
 TBM comprises 70-80% of CNS tuberculosis
RISK FACTORS
Young age
HIV infection
Malnutrition
Immunosupression
Recent meseals/ pertusis infection

6. PATHOLOGY
primary infection
Lymphohematogenous dissemination
Metastatic caseous lesion in the cerebral cortex or meninges
Discharges few tubercule bacilli into the sub arachnoid space
Forms gelatinous exudate( sylvian fissure, basal cistern)
Infiltrates the cortico meningeal blood vessels
Inflammation, obstruction and infarction of cerebral cortex
brainstem ( commonest site ) interferes CSF flow
CN III, VI and VII dysfunction Hydrocephalus

7. CLINICAL FEATURES # MRC STAGING
First stage( prodromal stage or stage of invasion)
Lasts for 1-2 week ( Non specific symptoms)
Low grade Fever
Loss of appetite
Disturbed sleep
Drowsiness , irritability, photophobia
Malaise
Stagnation or loss of development milestones
Focal neurologic signs are absent

8. SECOND STAGE( MENINGITIS)
Begins more abruptly Some with encephalitis
 high grade fever - Disorientation
Nuchal rigidity / hypertonia - Movement disorders
Seizures - Speech impairment
Positive Kernig’s and Brudzinski signs
Cranial nerve palsies / Focal neurological signs
Hydrocephalus / Vasculitis

10. THIRD STAGE(STAGE OF COMA)
Coma
Hemi or paraplegia
Hypertension
Decerebrate posturing
Deterioration of vital signs
Death

12. DIAGNOSIS
TST – Nonreactive in up to 50 % OF cases
CXR 20-50% of children have a normal findings
HIV serology
Lumbar CSF study
Polymerase chain reaction (PCR)
Cultures of other body fluids can help confirm the diagnosis
Neuro imaging

13. CSF STUDY
CSF pressure may reach to 30-40 mmhg
CSF cells – leukocytes 10-500 cells/ microL( Lymphocytes)
CSF glucose - < 2/3rd of blood glucose
CSF protein – markedly high (400 – 5000 mg/dl)
Early stage 1 - viral aseptic meningitis then progress severly
Success of CSF study reated to its volume
5-10 ml of lumbar CSF
Acid –fast stain positive in up to 30 % of cases
Culture is positive in 50-70% of cases

15. A pellicle or coagulum ( cob web pattern) is formed by CSF on
standing in a tube.
CSF ADA levels > 8 IU/L suggestive of TBM
CSF INF-Y assay +
CSF lactate levels 5-10 mmol/litre

16. RADIOGRAPHIC CHANGES
CT or MRI – brain
Normal during early stages of the disease
As disease progresses
- basilar enhancement
- communicating hydrocephalus
- signs of cerebral edema
One or several clinical silent tuberculomas

18. TUBERCULOMA
Another manifestation of CNS tuberculosis
Tumor like mass
Formed by aggregation of caseous tubercles
Singular / multiple
Clinically manifests as a brain tumor
Account for upto 30 % of brain tumors

19. LOCATION
Supratentorial in adults
Infratentorial in children
At the base of the brain near the cerebellum
CLINICAL FEATURES
Headache
Vomiting
Fever
Focal neurological deficits
Convulsions

20. DIAGNOSIS
TST is usually reactive
Chest radiograph is usually normal
CT or MRI – brain
-Discrete lesions with surrounding edema
-Contrast medium enhancement shows ring like lesion
Surgical excision
To distinguish tuberculoma from other causes of brain tumor

21. Treatment
Corticosteroids
- alleviates severe clinical signs and symptoms
- used during 1st few weeks of treatment or
- in immediate post op period to decrease cerebral edema
 surgical removal is not necessary
- most tuberculoma subside with medical management( later)

22. DIFFERENTIALS
Acute bacterial meningitis
Encephalitis
Typhoid encephalopathy
Brain abscess
Brain tumor
Chronic subdural hematoma
Amoebic meningoencephalitis

23. COMPLICATIONS
Hydrocephalus
Stroke
Opticochiasmatic – arachnoiditis
visual loss - during treatment with ATT/ withdrawl of steroids
 Seizures

24. PROGNOSIS
Correlates most closely with
- clinical stage of illness at the time treatment is initiated and age of onset
Untreated cases die within 4-8 weeks
Most with 1st stage have an excellent outcome ( RECOVERY IS RULE)
2ND Stage mortality is 25% and 25% of the survivor suffer neurological deficits.
Most with 3rd stage , mortality is 50% and those who survive have permanent disabilities
- blindness
- deafness
- paraplegia
- diabetes insipidus
- mental retardation
Prognosis for young infants is worse than for older children

25. TREATMENT
1. Anti tubercular therapy
2. Corticosteroids
3. Symptomatic therapy
Anti Tubercular therapy
 ATT for 12 months
- intensive ( 2 months) + continuation phase ( 10 months)
i.e 2HRZE(S) + 10 HR
Children with TBM should be hospitalized
- preferably for first 2 months / until clinically stabilized
Intensive phase – HRZE/S FOR 2 MONTHS
Continuation phase- HR for 10 months

26. Corticosteroids
Parenteral dexamethasone 0.15 mg every 6 hourly IV,
Then oral prednisolone
HIV negative
- All children with TB meningitis at 2 mg / kg daily for 4 weeks
- Then gradually tapered over 1-2 weeks before stopping
HIV positive
- advised in the absence of the threatening opportunistic infections
ATT to be considered for any child who develops
- basilar meningitis
- hydrocephalus
- CN palsies , stroke with no other apparent etiology

27. SYMPTOMATIC TREATMENT
Treat seizure, raised ICP , dyselectrolytemia.
Observe for papillodema, optic atrophy, hydrocephalus.
Ventriculo caval shunt in case of increasing head circumference
and persistent decerebration.
 Often the key to the correct diagnosis
- identifying an adult with TB who is in contact with the child
 TBM has short incubation period / rapid progression
- Needs high index of suspicion

28. REFERENCES
Nelson textbook of pediatrics , 21st edition
Ghai textbook of pediatrics 9th edition
National guidelines for extra pulmonary TB
PG textbook of pediatrics by Piyush Gupta