Endocrine Abstracts

A 41 year old gentleman presented with collapse and vomiting for one week was found to be hyponatraemic with sodium of 103. He was treated with a sodium chloride 0.9% over 100 ml/hour and once sodium was increased to 118 in less than 24 hours. He was deescalated from intensive care on day3. He had developed severe ataxia, slow speech and was highly emotional. He was previously high functioning, maintaining a job and independent. It had transpired that he had been drinking 18 cans of larger a day for the past 3 years with no contact with a physician, meaning the chronicity of hyponatraemia was unknown. The Differential for his ataxia and dysarthria was either cerebellar vermis atrophy secondary to chronic alcohol intake or central pontine myelinosis because of rapid correction of sodium. To investigate this, a brain magnetic resonance was done which revealed features of osmotic demyelination syndrome (ODS)- a life threatening demyelinating condition. ODS is classically in males between 30-50 years old predisposed by chronic alcohol use and the underlying cause of ODS is frequently rapid correction of severe hyponatraemia causing rise in tonicity. Although the symptomatology of weakness in ODS is either symmetrical limb weakness or extra pyramidal features like ataxia or dysarthria. Retrospectively, he developed permanent clinical symptoms manifesting from central pontine (dysarthria) as well as extra-pontine (ataxia, neurobehavioural symptoms- depression, emotional instability) demyelinosis. Despite careful correction of hyponatraemia, extra awareness in a patient with high risk factors of ODS (alcoholism) is needed, especially vigilance in the discordant presentations of symptoms manifesting from ODS.