Tuberculous Meningitis: An Endemic Cause of Intracranial Hypertension

Tuberculous meningitis (TBM) presents a complex clinical scenario, often marked by delayed recognition and high mortality. Our case involves a 27-year-old woman from Nepal with no significant medical history, presented with a two-week history of fatigue, altered consciousness, dizziness, vomiting, fever, holocranial headache, and photophobia. Initial examination revealed signs consistent with meningitis, including fever, hypertensive state, prostration, bilateral exophthalmos, sixth cranial nerve paresis, and positive Kernig/Brudzinski signs. Cerebrospinal fluid (CSF) exhibited characteristics typical of TBM: turbidity, lymphocytic-predominant pleocytosis, low glucose, and elevated protein. The patient was promptly started on meningeal doses of vancomycin, ceftriaxone, and acyclovir. However, persistent fever, neurological deterioration, and signs of increased intracranial pressure led to the decision to initiate conventional empiric treatment of tuberculosis (TB) with isoniazid, rifampicin, pyrazinamide, and ethambutol (HRZE) and dexamethasone 1 week before cultural positivity for Mycobacterium tuberculosis of CSF. The case underscores the importance of considering TBM in patients from endemic regions, interpreting CSF findings, and initiating empirical treatment in critical scenarios, contributing to a positive patient outcome despite the diagnostic challenges.