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Central pontine myelinolysis temporally related to hypophosphataemia
  1. A W Michell,
  2. D J Burn,
  3. P J Reading
  1. Regional Neurosciences Centre, Newcastle-upon-Tyne, UK
  1. Correspondence to:
 Dr Michell; 
 awmichell{at}hotmail.com

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Central pontine myelinolysis (CPM) is known to be associated with the rapid correction of severe hyponatraemia. However, there have been case reports of CPM occurring in normonatraemic patients.1 Here we describe two patients in whom chronic alcohol abuse led to profound hypophosphataemia that was closely temporally related to the development of CPM.

Case 1

A 29 year old woman was admitted for investigation of painless jaundice of 10 days’ duration. She had consumed 100–140 units of alcohol a week for the preceding 18 months and had been noted to have mildly deranged serum transaminase levels one year previously.

On admission she was fully oriented with normal speech and gait. She had a mild postural tremor but no asterixis. A plasma biochemical profile showed her sodium to be 122 mmol/l, potassium 2.1 mmol/l, and urea 5.9 mmol/l. Serum creatinine was 182 μmol/l, phosphate 0.65 mmol/l, magnesium 0.59 mmol/l, and total corrected calcium 2.18 mmol/l. She was immediately given potassium and magnesium supplements, chlordiazepoxide, and intravenous vitamins including vitamin K and thiamine.

Three days after admission she developed a Staph aureus septicaemia secondary to a peripheral venous cannula infection. This required treatment with intravenous cefuroxime and …

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