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EUNATRAEMIC HYPOKALAEMIC CENTRAL PONTINE MYELINOLYSIS IN AN ALCOHOLIC LADY WITH BULIMIA
  1. Emily Pegg,
  2. Rebecca Exley,
  3. Shuja Punekar,
  4. Hedley Emsley
  1. Royal Blackburn Hospital; The Royal London Hospital; Royal Preston Hospital

    Abstract

    A 42 year old lady with bulimia and alcoholism, suffered a cardiac arrest at home. She was successfully resuscitated and admitted to the intensive care unit of our hospital. Hypokalaemia (3.1 mmol/l) was present, and corrected, but serum sodium concentration was persistently normal. She was extubated within 48h, but a subsequent drop in her level of consciousness prompted brain imaging. Neurological examination was normal 5 weeks after admission when seen in the neurology clinic.

    Several months earlier she had presented with vomiting. Marked ECG changes of deep T wave inversion in anterior leads and prolonged QTc (528 ms) normalised after correction of initial hypokalaemia (2.6 mmol/l).

    Appearances on MRI brain imaging were consistent with central pontine myelinolysis. Whilst eating disorders and alcoholism are well established risk factors, eunatraemic, hypokalaemic CPM is a rarely reported entity. One previously reported case1 lacked diffusion–weighted imaging (DWI), prompting subsequent correspondence around the possibility of posterior reversible encephalopathy syndrome (PRES) being responsible for the pontine MRI changes in that case, rather than CPM.2 The T2 bright pontine lesion in our patient showed increased signal on DWI, consistent with acute myelinolysis, its symmetrical nature around the midline not being in keeping with ischaemia.

    We presume our patient's cardiac arrest was also due to hypokalaemia, especially in view of the previously documented ECG changes. The most commonly reported cause of CPM, relates to hyponatraemia.3 Concomitant hypokalaemia and sodium abnormalities have been reported in 89% of cases of CPM4 and it has been suggested that hypokalaemia may predispose to CPM in the presence of sodium abnormalities. Reports of CPM occurring with hypokalaemia in the absence of sodium abnormalities are however scarce, with only 3 cases being described since 1990.5–7

    This case reports describes a rare example of CPM occurring with hypokalaemia and eunatraemia thus supporting the suggestion that there are factors other than abnormalities in sodium that are associated with the development of CPM.

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