Tuberculous Meningitis Presenting as Cerebral Salt Wasting Syndrome

Abstract

Hyponatremia in the neurocritical care patients is commonly encountered in the setting of either syndrome of inappropriate ADH secretion or cerebral salt wasting. However, differentiation of SIADH and CSW is paramount in view of their divergent treatment strategies.

Hyponatremia in Tuberculosis Meningitis: Navigating the Diagnostic Challenges of Cerebral Salt Wasting – A Case Report

“…CSW, a hypovolemic hyponatremia, triggered by brain natriuretic peptide, increases water and Na+ release, resulting in elevated urinary Na+. 4,8 As the case unfolds with the classic presentation of tuberculous meningitis, it emphasizes the importance of thorough investigation even in the absence of typical imaging abnormalities. The identification of rifampicin resistance highlights the evolving challenges in tuberculosis management.…”

Cerebral Salt-Wasting Syndrome in a Patient With Active Pulmonary Tuberculosis

“…Previously reported cases of CSW in the setting of TB meningitis initially considered SIADH as the main cause for hyponatremia, but patients did not correct with fluid restriction and 3% hypertonic saline, leading to further loss of sodium in the urine [ 13 , 14 ]. The fractional excretion of uric acid (FEUA) is also used as a marker to distinguish CSW as increased levels of FEUA persist after correction of hyponatremia by water restriction and salt supplementation [ 15 ].…”

Targeted Therapy of Tuberculous Meningitis in Rats with Methylprednisolone Composite Nanoparticles

“…MPS diffuses through the cell membrane and binds to specific receptors in the cytoplasm. The resulting conjugates enter the nucleus and bind to DNA to initiate the transcription of mRNAs, followed by the production of various enzyme proteins, which exert their strong anti-allergic effects and inhibit the migration and activation of inflammatory cells and the release of inflammatory mediators (19). Beardsley et al (2019) (20) explored the use of MPS in the treatment of viral meningitis, which can not only reduce the inflammatory response and protect the blood-brain barrier, but also reduce intracranial pressure, reduce neuron-specific enolase content, facilitate the recovery of brain injury, and avoid or reduce the occurrence of neurological sequelae, which is similar to the results of this experiment.…”