Endocrine Abstracts (2015) 38 P32 | DOI: 10.1530/endoabs.38.P32

An unusual presentation of osmotic demyelination syndrome

Vinit Kirankumar Shah & Jayadave Shakher

Birmingham Heartlands Hospital, Birmingham, UK.

Introduction: Osmotic demyelination syndrome (ODS) or commonly known as central pontine myelinolysis is commonly associated with rapid correction of hyponatraemia resulting in neurological deficits that manifests within days. The population commonly affected include alcohol dependence patients, the malnourished and liver failure patients. We describe a case of ODS developing in an alcoholic patient with symptoms developing 4 weeks after correcting hyponatraemia.

Case: A 44 year old gentleman with heavy alcohol use of up to 40 units a week presents with 1 week history of progressive left hemiplegia, dysarthria and dysphagia. Initial investigations showed he had normal serum biochemistry including serum sodium. Initially thought clinically to be stroke, MRI was done given the atypical history, which showed pontine and extrapontine myelinolysis. On further review it was noted he was admitted 4 weeks ago following alcohol intoxication during which he was hyponatraemic (125 mmol/l) and was treated with 0.9%sodium chloride with rapid correction of serum sodium to 133 mmol/l. He however did not develop any neurological symptoms at the time. Management involved multidisciplinary care with alcohol dependence, dietitian and neuro-rehabilitation team input and after a 6 month of rehabilitation he made a full recovery and returned to normal independent level of function.

Discussion: ODS is a non-inflammatory demyelination disorder in high neuron density areas of the brain resulting in the neurological sequale. This occurs as a result of rapid correction of a chronic osmolar abnormality with rapid fluid shift and osmotic stress related nerve damage. High risk patients include those that do not have adequate compensatory mechanisms for rapid osmotic changes. The neurological consequences of ODS can be significant including permanent neurological damage and even death. Management is aimed at prevention with slow correction in serum sodium of ~8 mmol/l every 24 h especially in high risk groups which should be done proactively.

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