22/F High grade fever since 7 days with vomiting Irritable behaviour s

22/F High grade fever since 7 days with vomiting Irritable behaviour since 2 days Csf protein 300 Csf glucose -12 Ada-15

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Clinical Assessment: Tuberculous Meningitis (TBM)

Diagnosis: Tuberculous Meningitis - strongly supported by all three clinical and lab parameters.

CSF Analysis - Interpretation

Parameter	This Patient	Typical TBM Range	Interpretation
Protein	300 mg/dL	100-500 mg/dL (often >200)	Markedly elevated - hallmark of TBM
Glucose	12 mg/dL	<40 mg/dL (reduced, but rarely as low as pyogenic)	Significantly low - supports TBM
ADA	15 U/L	Elevated above normal in TBM	Elevated; supports mycobacterial/lymphocytic etiology

Key point on glucose: A CSF glucose of 12 mg/dL is markedly low, but TBM characteristically does NOT produce the near-zero glucose levels seen in pyogenic bacterial meningitis. The glucose falls slowly in TBM and may become very low as disease progresses. Always compare with simultaneous serum glucose - CSF:serum glucose ratio <0.5 is the defining criterion.

Key point on ADA: ADA is elevated in TBM because it is abundant in T-lymphocytes, which are the dominant cell type in the tuberculous inflammatory response. According to Henry's Clinical Diagnosis and Management by Laboratory Methods, "ADA levels are significantly higher in tuberculous meningitis than in other types of meningitis and CNS disorders." A CSF ADA of 15 U/L, while seemingly modest, should be interpreted with the assay-specific cutoff - values >10 U/L in CSF are generally considered elevated and supportive of TBM.

Why This Case Points to TBM and Not Other Causes

Clinical clues supporting TBM over pyogenic meningitis:

Subacute onset - 7 days of fever is characteristic; pyogenic meningitis typically presents more acutely (hours to 1-2 days)
Irritability at day 2 of a 7-day illness - gradual neurological deterioration is the TBM pattern
CSF glucose 12 - very low but not "zero" - fits TBM better than viral (viral rarely drops glucose this severely)
Protein 300 - markedly elevated, consistent with TBM where thick basal exudate forms

Why not viral (aseptic) meningitis?

Viral meningitis rarely drops CSF glucose this low (usually normal or mildly reduced)
Protein of 300 is too high for most viral causes
ADA elevation points away from viral etiology

Why not pyogenic bacterial meningitis?

Pyogenic meningitis has a more acute/fulminant onset
CSF glucose is usually near-zero in pyogenic; here it is 12 (very low but not zero)
ADA is elevated in both TBM and bacterial meningitis, but the subacute course strongly favors TB

Pathogenesis

M. tuberculosis reaches the CNS via hematogenous spread (often after primary pulmonary TB or miliary dissemination). It forms cortical/meningeal tubercles; when these rupture into the subarachnoid space, an intense basal meningitis develops. A thick gelatinous exudate accumulates around the basal cisterns, obliterating the pontine and interpeduncular cisterns. This causes:

Cranial nerve palsies (especially CN III, VI, VII)
Communicating or obstructive hydrocephalus
Vasculitis leading to cerebral infarction
Progressive stupor and coma if untreated

MRI in TBM - gadolinium enhancement of the basal meninges, with multiple abscesses and hydrocephalus:

MRI in tuberculous meningitis showing gadolinium enhancement of the basal meninges, reflecting multiple abscesses, accompanied by hydrocephalus and cranial nerve palsies

MRI (gadolinium-enhanced) in TBM - note the intense basal meningeal enhancement. From Adams and Victor's Principles of Neurology, 12th Edition.

Staging (British Medical Research Council)

Stage	Features
Stage I	Conscious, no focal deficits, no hydrocephalus
Stage II	Confusion OR focal deficit
Stage III	Stupor, coma, or severe neurological deficit

This patient with irritability and a 7-day fever is likely Stage I-II - early intervention is critical.

Investigations to Order

CSF AFB smear and culture - sensitivity is low (10-50%) but specificity is high; repeat LPs increase yield
CSF PCR for M. tuberculosis - sensitivity ~80%; rapid result; preferred over culture alone
Chest X-ray / HRCT chest - look for primary pulmonary focus, miliary pattern
Tuberculin skin test / IGRA (QuantiFERON-TB Gold) - positive in ~40-60% of adults with TBM
MRI brain with gadolinium - basal meningeal enhancement, hydrocephalus, tuberculomas, infarcts
Serum sodium - hyponatremia is common (SIADH or Addisonian state)
HIV serology - mandatory; HIV dramatically increases TBM risk and alters outcomes
Fundoscopy - for choroidal tubercles (pathognomonic if present), papilledema
CSF adenosine deaminase - already done; supportive

Treatment

Anti-tubercular Therapy (ATT)

Intensive phase (2 months) - 4-drug regimen:

Drug	Adult Dose	Key Toxicity
Isoniazid (H)	5 mg/kg/day (max 300 mg)	Hepatitis, peripheral neuropathy
Rifampicin (R)	10 mg/kg/day (max 600 mg)	Hepatitis, drug interactions, orange discoloration of secretions
Pyrazinamide (Z)	25 mg/kg/day	Hepatotoxicity, hyperuricemia
Ethambutol (E)	15 mg/kg/day	Optic neuritis (check visual acuity/color vision regularly)

Continuation phase (10 months) - 2-drug regimen:

Isoniazid + Rifampicin
Total duration for TBM: 12 months (longer than pulmonary TB due to poor CNS penetration)

Add Pyridoxine (Vitamin B6) 25-50 mg/day to prevent INH-induced neuropathy.

Corticosteroids (Adjunctive - Mandatory in TBM)

Dexamethasone IV: 0.4 mg/kg/day for 1 week, then tapering doses over 3-6 weeks
Evidence: A landmark randomized trial (Thwaites et al., Vietnam) showed dexamethasone reduced mortality from 41% to 32% without increasing residual disability
A 2024 meta-analysis (PMID: 38858618) further supports intrathecal dexamethasone + isoniazid as beneficial in select cases
A 2026 network meta-analysis (PMID: 42112729) evaluates comparative efficacy of drug therapies in TBM

Supportive Care

Monitor for hydrocephalus - may require ventriculoperitoneal shunting (needed in ~25% of cases)
Treat hyponatremia cautiously (fluid restrict if SIADH; replace if Addisonian)
Seizure management if needed
Nutritional support

Prognosis

Overall mortality with treatment: ~10% in HIV-negative patients; up to 21% in HIV-positive
If untreated: fatal within 4-8 weeks
20-30% of survivors have residual neurological deficits: cognitive impairment, seizures, hemiparesis, cranial nerve palsies, deafness
Early diagnosis and treatment are the strongest determinants of outcome

Sources:

Adams and Victor's Principles of Neurology, 12th Edition
Henry's Clinical Diagnosis and Management by Laboratory Methods
Tintinalli's Emergency Medicine - A Comprehensive Study
ROSEN's Emergency Medicine: Concepts and Clinical Practice
Recent evidence: PMID 38858618 (2024 meta-analysis on intrathecal dexamethasone in TBM); PMID 42112729 (2026 network meta-analysis on TBM drug therapies)

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