Osmotic demyelination syndrome
BMJ 2005; 331 doi: https://doi.org/10.1136/bmj.331.7520.829 (Published 06 October 2005) Cite this as: BMJ 2005;331:829
- Rachel Abbott (rachel.abbott@nhs.net), senior house officer1,
- Eli Silber, consultant neurologist1,
- Joerg Felber, senior house officer1,
- Enefiok Ekpo, care of the elderly consultant1
- 1Queen Elizabeth Hospital, Woolwich, London SE18 4QH
- Correspondence to: R Abbott
- Accepted 8 June 2005
Introduction
Patients with chronic alcoholism are commonly admitted to hospital and given intravenous fluids as part of the treatment of alcohol withdrawal. These patients are predisposed to chronic severe hyponatraemia because of a variety of mechanisms including psuedohyponatraemia, hypovolaemia, “beer” potomania syndrome, cerebral salt wasting syndrome, and reset osmostat syndrome.1 If hyponatraemia (serum sodium concentration < 136 mmol/l) is present it is important to correct this slowly, at a rate of less than 8 mmol/l/day to minimise the risk of developing osmotic demyelination syndrome, the general term for central pontine and extrapontine myelinolysis.2
Case report
A 42 year old man with chronic alcoholism presented with confusion. He had no significant medical history and was not taking any regular medications. On the day of admission his serum sodium concentration was 105 mmol/l at 5 pm. His serum was hypo-osmolar at 212 mmol/kg and his urine sodium concentration was 22 mmol/l, suggesting hypovolaemia. Over the next 11 hours he was given 1 litre of intravenous 0.9% saline with 40 mmol potassium chloride, followed by another litre over the subsequent 24 hours, as well as intravenous multivitamins (Pabrinex) and oral chlordiazepoxide. His …
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