TB meningitis in children

Dr. Abdulkadir Keynaan

Banadir Hospital
Pediatric department
Keynan1443@gmail.com

 19 September 2018
OUTLINE
 Introduction

 Classification of Neuro-tuberculosis

 Epidemiology

 Pathophysiology

 Risk factors for TB

 Clinical features

 Criteria for Diagnosing TBM

 Approach to the pt with TBM

 COMPLICATIONS
 PROGNOSIS
introduction
 TB is a contagious air borne disease that typically effects the lungs
particularly the alveoli, its caused by a mycobacterium tuberculosis, a long
slender straight curved acid fast bacilli, slow growing , obligate aerobes
intracellular bacteria which has mycollic acid, overall if the TB infection is
not treated quickly the bacteria can travel through the blood stream to infect
other organs and tissues like meninges, thus the infected meninges results a,
life threatening condition known as TB meningitis

 So TB meningitis is one of usual infections that if you do not treat it, its
very fatal, if you delay treatment or we do not give treatment at all, a
100 % die,
 A number of people is reduced according to how early you get
the treatment of the disease

 Ultimatley TBM is a universally fatal condtion with high

morbidity and mortality
Classification of Neuro-tuberculosis
 Intracranial TB

1: Tubercular meningitis and meninoenchalatis

2: Space occupying lesions (Tuberculomas, Tubercular abscess)

3: Tubercular encephalopathy
4: Tubercular vasculopathy
 Spinal TB

1: pots spine
2: Tubercular arachnoiditis
3: Spinal tuberculoma
4: Spinal meningitis and radculomyelitis
Epidemiology
 TB is the seventh leading cause of death and disability worldwide. In TBM
is more common in children then adult.
 75-85% below age 5 years , uncommon below 6m and rere below 3m .
 Peak incidence is 3m-5yrs.
 TBM account 1-2% of the cases with TB and 9.1% of extra-pulmonary TB
.
 In 1997, TBM was the fifth most common form of extrapulmoinary TB.
 In subsahara africa b/c of affect of HIV become high endemic, and 75% of
HIV pts developed TB and 1% of them developed TBM .
Pathophysiology
 Droplet infection

Primary focus Bacteremia

Meninges and brain

parenchyma

Rich Focus
 Rupture in
Subarachnoid
space

ADHENSION
Vasculitis Encephalitis

BASAL Stroke
Inter Cerebral
CISTERN
A pedencular Edema
fossa

Hydrocephalu Paralysis and

s abnormal
Cranial nerve
palsies and movements Raised ICT
carotid stenosis
 Pathophiology
 Generally any infection to the lungs, the primary site is the alveoli, and alveolar
macrophage plays role in engulfing the foreign body to the inside making
encapsulated vesicles containing the pathogen and that is known as phagosome,
to eradicate the pathogen , alveolar macrophage has a hydrolytic enzyme called
lysosome which fuses the vesicle and that process is called phagolysosome, and
finally its eliminated from the body

 in case of TB infection lysosome is inhibited , phagolysosome is not formed ,

Mycobacterium TB is protected inside the macrophage getting access to replicate
in side in, initial infection gets started and that is known as primary infection
 3 weeks after cell mediated immunity and other cells surrounds the site of
infection forming granuloma, due to the inflammatory process, necrosis at
the site of the infection develops creating what is known as ghon focus, and
ultimately ghon focus effects the nearby lymph nodes at the site of the
inflammation and that is called ghon complex, fibrosis and calcification of
the lymph nodes creates ranke focus.

 Ultimately since MTB gets access to proliferate it starts to disseminated in

to the blood stream going to another organs and tissues
 In case of TB meningitis the mycobacterium tuberculosis follows
the choroid plexus and cerebral blood vessels bind the choroid
cells, in persons who develop TBM ,tubercle bacilli seed to the
meninges especially the arachnoid matter in enlarges there
increasing the size resulting the formation of arachnoid
metastatic caseous lesions termed rich focus until it ruptures into
the subarachnoid space , tubercles rupturing into the subarachnoid
space causes TB meningitis
 After that cerebral blood flow increases – endothelium shrinks
– capillary permeability increases enhancing protein,
macrophages, complement proteins permeability and
chemoattractans attracts the neutrophils, then accumulation of
these proteins cause s exudate more and more exudate
obstructing both the brain blood vessels and ventricles forming
low blood flow the the bran and hydrocephalus
Risk factors for TB
 Age less than 5 years
 HIV infection
 Severe malnutrition
 Recent episode of measles
 Other immune suppressive conditions e.g.
diabetes, children on chemotherapy
 Not BCG vaccinated (risk for disseminated TB
disease)
Clinical features
 Clinical manifestations are grouped into three stages

 stage 1 ( early or ) : -

 prodromal stage lasts 2 -3 weeks and characterized by : -

low grade fever ,

anorexia, vomiting

headache , irritability

sleep disturbance

conscious level is normal.

 Stage 2 ( intermediate)
1: Convulsion

2: signs of meningeal irritation

3: Neurological deficits

a) Cranial nerve palsy

b) Motor deficits

4: Signs of intracranial pressure

5: Impaired consciousness
Stage 3 ( advanced ) :-

1: Progressive neurological deficits with dilated pupils

2: signs of brain stem compression ( episthotonic posture , neck

retractions , decorticate, and decerebrate posture, hyperpyrexia , monoplagia ,
hemiplegia and paraplegia)

3: Movement disorders

4: Deep coma and death

 Criteria for Diagnosing TBM
 Modified AHUJA criteria for the DX of TBM in children

 A) Mandatory features

1) fever lasting more then 14 days

2) abnormal CSF findings :-

lymphocytiosis > 60%

protein > 100 mg/dl

glucose < 60 mg/dl

B) PLUS ANY TWO OF THE FOLLOWING CRITERIA : -

a) evidency of extraneural TB

b) possive family HX exposure tpo case

c) positive mantoux reaction
d) abnormal CSF findings ( 2 or more )

exudate in basal cistern

hydrocephalus

infarcts

gyral enhancement
Approach to the pt with TBM
 History taking

 Physical examination

 Investigation

 management
History taking
 Sings and symptoms of TB

 close contact pt with PTB

 Past history of TB

 History of immunosuppression( from known disease or drug therapy)

 Negative history of BCG vaccine

 Sings and symptoms of meningitis

 Poor feeding

 Immunization history for PENTA

 History of measles, checking boxes

Physical examination for TBMs
 Vital sings

 Anthropometric measurement

 Generally: Conscious level, convulsed , petechial and purpura.

 Heed: palging anterior fontanel and hydrocephalus.

 Eye: Photophobia , Lateral gaze, subconjectival hemorrhage , ptosis, Anisocoria and

papillary edema.
 Nose: Nasal bleeding , Nasal flare bc of risk of aspiration
 Mouth : Mouth deviation , spatula test negative and gagrefelax positive

 Neck : Stiff neck , unable to hold neck and brunzik sing positive

 Chest :Chest movement symmetrical, chest indrowing and wheezing or crepitation

 Heart :murmur
Investigations
 CBC
 CSF analysis
 Chest x-ray
 CT-scan
 ESR
 GASTRIC LAVAGE OR SPUTUM EXAMINATION for
tubercle bacilli.
MANAGEMENT
 Specific Treatment:

 Start treatment with 4 anti- tuberculous drugs and treatment should be

continued for 12 months.

 1.Isoniazid (INH): • It is the drug of first choice.

It is rapidly absorbed and penetrates into the CSF.

Isoniazid and rifampicin and highly bactericidal for M.tuberculosis.

• Main side effect are hepatotoxicity , peripheral neuropathy ,optic neuritis,

hypersensitivity and fever.

Neuritis is due to competitive inhibition of pyridoxine.

2. Rifampicin: • It is also a first line drug, well absorbed and penetrates CSF
well.

 It causes orange discoloration of the urine and tears , GIT disturbance and
hepato-toxicity.

 Combined use of INH and rifampicin increases the risk of hepatotoxicity ,

which can be decreases by lowering the dose of INH (10 mg/kg/day)
3. Pyrazinamide • It is bactericidal in acid medium and enters CSF readily.

 It is used as a third drugs for 2-3 months initially

 Main side effect are arthralgia ,arthritis ,hyper-uricemia (gout)

 5. Ethambutol: • It is not recommended below 6 years of age.

 Side effects are Optic neuritis ,hypersensitivity and GIT upsets.

 Weight based dosing table
Numbers of tablets
Continuation
Intensive Phase Phase
Weight RHZ E RH
bands 60/30/150 100 60/30
4-6kg 1 1 1
7-10kg 2 2 2
11-14kg 3 2 3
15-19
kg 4 3 4
20-24kg 5 4 5
Go to adult dosages and
25 kg+ preparations
Note, when new FDCs become available, WHO will revise this table

s
Dosing Chart
GENERAL MEASURES
1. Corticosteroids:
 Decrease mortality rate and long term neurologic sequelae.

 Reduce vasculitis ,inflammation , and intracranial pressure.

 Dose of prednisolone is 1-2mg/kg/day for 4-6 weeks.

 Help to reduce cerebral edema and prevents formation of adhesions .

2. Daily monitoring of complications:

 Main complications are to be monitored •

 Raised intracranial pressure •

 Drugs toxicity, etc.

3. Phenobarbitone: Dose 5 mg/kg/day to control convulsions.

4. Antipyretics: ibuprofen syrup(10—15mg/kg/dose 4-6 hourly) and fresh

water sponging to control temperature.

5. Pyridoxine: 1-2 mg/kg/day daily to prevent polyneuritis.

6. Feeding : NG tubes feeding according to requirement .

 Ideally 100 calories /kg/day are given .

 Iron and multivitamins can be added too.

7. Bed Sores : Change posture every two hours.

8. Screening: Important to screen the family members for tuberculosis and

treat infected persons.
COMPLICATIONS:
 1. Mental retardation

 2. Cranial nerve palsies (3rd , 6th and 7th )

 3. Blindness (optic atrophy)

 4. Deafness

 5. Hydrocephalus

 6. Hemiplegia, paraplegia

 7. Epilepsy

 8. Endocrine disturbances (diabetes insipidus).

 9. Tuberculoma.
PROGNOSIS:
It depends upon two factors:

 1. Age of patient

 2. Stage of disease at which treatment started.

 Without treatment it is fatal.

 In stage1, 100% cure rate is expected.

 Even with optimal therapy mortality ranges from 30-50% and incidence of
neurologic sequelae is 75-80% especially in stage 3.

 There may be blindness, deafness , paraplegia, mental retardation and diabetes

insipidus.

 Infants and young children have poor prognosis as compared to older children