Endocrine Abstracts

Severe acute hyponatremia, if untreated, can be life-threatening, leading to cerebral oedema, seizures, coma and even death. Treatment with hypertonic saline is the standard approach in acute cases, with many guidelines suggesting intravenous boluses and repeating as needed. However, no consensus exists on the use of continuous infusion of hypertonic saline for managing refractory hyponatremia, and data is limited to inform the choice between slow continuous infusion and intermittent boluses. We present a challenging case of a 61-year-old woman admitted with acute confusion, disorientation and seizures. She had past medical history of autoimmune hepatitis, hypertension and pre-diabetes. Examination revealed facial contortion. Her initial serum sodium was critically low at 115 mmol/l. Despite aggressive management with repeated hypertonic saline boluses, her hyponatremia remained refractory, necessitating continuous slow infusion of hypertonic saline in intensive care unit. Biochemical workup indicated SIADH, yet her neuropsychiatric symptoms persisted even after correction of sodium to 136 mmol/l. Further neurological evaluation revealed subtle changes in the left medial temporal lobe on MRI, suggesting limbic encephalitis. CSF analysis showed slight increase in protein (0.55 g/l) and serology later confirmed positive anti-LGI1 antibodies, leading to a diagnosis of autoimmune limbic anti-LGI1 (anti-leucine-rich glioma inactivated 1) encephalitis. Treatment with IV methylprednisolone followed by oral steroids resulted in significant neurologic improvement and normalisation of sodium. This case underscores the potential utility of continuous slow hypertonic saline infusion in managing refractory severe hyponatremia and highlights the importance of thorough investigation into the etiology of SIADH, particularly when hyponatremia is severe and resistant to standard treatment. It also suggests that the presence of autoimmune disorders should heighten suspicion for autoimmune encephalitis as a potential underlying cause of persistent encephalopathy.