Central pontine myelinolysis complicating treatment of the hyperglycaemic hyperosmolar state

Ann Clin Biochem 2008;45:440-443
doi:10.1258/acb.2008.007171
© 2008 Association for Clinical Biochemistry

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Case Reports


Grainne O’Malley1,2,
Carla Moran1,2,
Mohd Shazlie Draman1,2,
Tom King1,2,
Diarmuid Smith1,2,
Chris J Thompson1,2 and
Amar Agha1,2


1 Division of Endocrinology and Diabetes, Beaumont Hospital, Dublin, Ireland;
2 RCSI Medical School, Dublin, Ireland


Corresponding author: Dr Amar Agha. Email: amaragha{at}beaumont.ie

Central pontine myelinolysis (CPM) is well recognized to occurin a variety of clinical settings, but particularly followingrapid correction of severe hyponatraemia. The development ofCPM as a result of rapid shifts in plasma osmolality duringthe treatment of the hyperglycaemic hyperosmolar state (HHS)has hitherto been described in only one case. We report a secondcase in which this complication occurred in association withtreatment of the HHS.

The patient was a 49-year-old woman who presented to anotherhospital with drowsiness and a plasma glucose of 106 mmol/L.Her admission plasma sodium was 135 mmol/L. She received treatmentwith intravenous insulin and 0.9% normal saline, and there wasa rapid drop in plasma glucose by 60 mmol/L within 6 h, whichwas associated with a rebound rise of plasma sodium to 159 mmol/L.Her plasma glucose and sodium were later stabilized. When thepatient was transferred to our hospital a few days later, shewas noted to have flaccid quadraparesis and pseudobulbar palsy.A magnetic resonance imaging scan revealed a pontine lesionconsistent with CPM. She made a gradual recovery over severalmonths with intensive rehabilitation and eventually returnedto near normal functional capacity. This is the second casereport in the literature of CPM complicating the managementof HHS and highlights the importance of the judicious and measuredcorrection of hyperglycaemia and the appropriate managementof fluid replacement and electrolyte balance when treating thiscondition.


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