Affection of central nervous system -
Affection ofperipheral nervous system -
Spinal meningeal TB
TYPES OF MENINGEAL TUBERCULOSIS -
Rich's classification -
Acute inflammatory caseous meningitis - Commonest form of neurotuberculosis, Characterized by gelatinous exudate
Disseminated miliary tubercks - Miliary tubercles over meninges in 75-80% cases of miliary tuberculosis.
Focal caseous plaques - Solitary tuberculomas of meninges
Proliferative meningitis - Rare form of neurotuberculosis characterized by excessive fibroblastic reaction.
IBM constitutes 50-80% of all bacterial meningitis in developing countries.
7-12% of tuberculosis patients are affected by TBM.
Inspite of good BCG coverage & effective treatment incidence of TBM has increased probably because of better diagnostic modalities (apparent increase), overcrowding, defaults in AKT, etc.
Focus of infection -
In children primary infection of lungs.
In adults reactivation of quiescent metastatic foci established during a primary illness, usually in the extrapulmonary location like skeletal & urogenital systems.
Spread of infection -
Its mainly haematogenous spread from primary focus to the CNS. Infrequently direct spread from nearby focus e.g. otitis media, spinal TB.
Once the tubercle bacilli reaches the CNS, it establishes a focus, known as Rich's focus (similar to Ghon's focus in lungs). These foci are mainly subependymal & remain quiescent for years or increase gradually in size.
Due to some precipitating factor like change in ICT, the Rich's focus ruptures and liberates its caseous material, along with tubercle bacilli into the subarachnoid space. From the subarachnoid space, dissemination of bacilli occurs to involve the meninges and thus results into meningitis.
The nature of the pathological response to the subarachnoid spillage of tubercle bacilli depends upon Number of bacilli ,Virulence of organism & Immunity of host
If the number of bacilli is small & resistance good, the result is an acute inflammatory caseous meningitis of localized variety.
In an individual with a high degree of resistance, diffuse proliferative meningitis occurs.
Diffuse inflammatory caseous meningitis represents a severe hypersensitivity reaction.
Exudation, CSF flow affection, vascular involvement and microangiopathy are responsible for clinical manifestations and complications of TBM.
A) Exudation -
In acute stage thin, whitish exudate containing more cells than necrotic material is found all over the subarachnoid space.
In subacute stage, grayish gelatinous exudate is found in the base of brain.
In chronic stage, gelatinous exudate is replaced by thick gray mass representing connective tissue.
Organization of exudate results into entrapment of various cranial nerves, obliteration of subarachnoid space & obstruction of blood vessels.
B) CSF flow affiction -
Hydrocephalus is nearly always present if the patient survives for more than 4-6 weeks.
Blockage of basal cisterns with the exudate in the acute phase.
Adhesive leptomeningitis in chronic phase resulting into communicating hydrocephalus.
Obstruction or narrowing of aqueduct or outlet of the fourth ventricle.
Destruction of arachnoid granulation affecting CSF absorption.
C) Vascular involvement -
Large vessels - Varying degrees of involvement & occlusion of large vessels in the circle of Willis & that of middle cerebral artery in the Sylvian fissure by the exudate leads-to ischaemic foci in the brain.
Small vessels - Involvement of small vessels particularly lenticulostriate vessels lead to focal lacunar infarcts with edema around them which clinically may present with localized encephalopathy.
D) Microangiopathy -
Without any infarction, tuberculoma or other naked eye lesions, generalized edema due to microangiopathy can produce severe brain damage. Edema & microscopic hemorrhage due to capillary damage is the most important mechanism in tuberculous encephalopathy.
CLINICAL FEATURES -
Age - most frequent between 6 months - 2 years
Sex - equal incidence in the two sexes
H/O - Contact with tuberculous adult
Preceding illness like measles or whooping cough, which may predispose to TBM by lowering the general resistance.
Clinical stages -
A) Prodromcd phase -
Onset is insidious
Duration 1-3 weeks
Features - Non specific symptoms like fever, anorexia, vomiting, constipation, headache change in temperament apathy/irritability/photophobia, acute fall in body weight, etc.
B) Phase of meningitis/transitional phase -
Stage last for 2-3 weeks
Features of raised intracranial pressure & meningeal irritation are seen
Headache, vomiting, increased irritability, photophobia
Focal neurological deficit
Bulging anterior fontanelle
Neck rigidity, Kernig sign positive
Brisk ankle jerks, patellar clonus
Increased muscle tone
Neurological deficit- cranial nerve palsy, mono/hemiplegia,
Strabismus, nystagmus, constricted pupils
C) Phase of coma/terminal phase -
Loss of consciousness
Respiration - irregular, Cheyne-Stokes or Biot type.
Abnormal posture, clonic spasms of limbs, decorticate/decerebrate posture.
Pupils dilated & unequal
Death may occur within a week
DIFFERENTIAL DIAGNOSIS -
Hb, CBC, ESR
Family screening for tuberculosis contact
Gastric lavage for AFB
Lumbar puncture -
Typical picture of TBM -
Turbid (Cobweb formation)
At high pressure
Cells increased- 10-500/cmm, predominantly lymphocytes
Proteins raised - 80-400 mg%
Sugar low (30-50 mg%)
AFB on ZN stain
Special tests on CSF
TB antigen/antibody by ELISA
Bromide partition test (useful to differentiate from viral meningitis)
Myelin basic protein (normal levels indicate a good prognosis, persistent high levels are associated with high mortality)
Adenosine deaminase activity (can be used for early detection of TBM)
Culture/guinea pig inoculation for AFB (yield is low 10-15%)
CT Scan - basal exudates, infarcts, hydrocephalus associated tuberculomas.
X-ray skull - features of raised ICT
Supportive therapy -
Correction of dehydration, electrolyte imbalance.
Nursing care -
Monitoring & charting
Care of unconscious
Initially iv fluids
Later on RT feeds/orally
Treatment of hypotension -
Antipyretics & analgesics
Specific therapy -
Antituberculous drugs -
At least 4 drugs AKT should be given for a minimum period of 12 months (for more details of drugs & drug dosages refer to 'CHILDHOOD TUBERCULOSIS')
Role of steroids - Used for their anti-inflammatory property by which risk of arachnoiditis, fibrosis & spinal blocks is reduced. Prednisolone in a dose of 1-2 mg/kg/day for 2-3 months.
Treatment of raised ICT -
i.In acute stage - Mannitol/Dexamethasone/Acetazolamide/ Glycerol
ii.In chronic stage with hydrocephalus - A surgical intervention with ventriculoperitoneal shunt is required
Treatment of convulsions
Role of intrathecal drugs -
Intathecal hyalase (Gown Devi regimen) for arachnoiditis complicating TBM
Rehabilitation - Physiotherapy and occupational therapy COMPLICATIONS -
Neurological deficits hemi/quadri/monoplegia, cranial nerve palsies.
Side effects of drugs & surgical intervention
LONG TERM SEQUELE -
Mortality rate is high if patient presents in 3' stage.
Prognosis depends on -
Age (high risk below age of 3 years)
Stage at which diagnosis is made, with early diagnosis and prompt treatment, outcome will be better
Prior BCG vaccination
Complication like hydrocephalus
Screening for primary complex, in children who are in contact with identified tuberculosis cases.
Early diagnosis and prompt AKT
Tuberculoma is the result of local inflammatory reaction of the tissue to invasion by tubercle bacilli characterised by aggregates of small granulomatous lesions in the parenchyma of brain.
It is one of the commonest space occupying lesion in children in India.
Site - Infratentorial or supratentorial
Common sites in children - Cerebellum, around chiasma & other basal cisterns, intramedullary
Size - 3 mm to 40 mm in diameter
Number - Unlimited, may be single also.
Those over the surface of brain spread to form tuberculoma-en-plaque eliciting peculiar fibrous reaction.
Tuberculous abscess may follow caseation.
5% of tuberculomas show calcification.
Spread towards meninges can lead to granulomatous subdural cyst formation.
Small multiple tuberculomas with surrounding oedema resulting from hypersensitivity can cause diffuse brain involvement.
Pathological types - Stellate, Cold abscess type, Cystic & Granulomatous.
CLINICAL FEATURES -
Age - Common in first 3 decades of life
Sex - Commoner in male child till age of 10 years.
Fever, headache, vomiting, convulsions, signs of raised intracranial tension, localising signs of a space occupying lesion etc.
Associated meningitis will have signs of neck rigidity and disturbed sensorium.
Infratentorial tuberculomas can lead to cerebellar signs.
Hydrocephalus can be present.
Resistant, recurrent or persistent IBM also indicates presence of tuberculoma.
Hb, blood counts, ESR - TB
X-ray chest - active or healed TB
X-ray skull - sutural diastasis, calcification
CT Scan - For confirmation and accurate localisation of tuberculomas.
Small/large rings or uniformly enhancing nodular lesion
CSF may be normal or suggestive of TB meningitis.
Chemotherapy - similar to that of tuberculous meningitis
Treatment of cerebral oedema
General measures - Bed rest, high protein diet, immunisation, family screening for tuberculosis.