Reactions 911 - 20 Jul 2002

SCitalopram

Hyponatraemia leading to prolonged coma: casereport

A 47-year-old woman with multiple sclerosis developedhyponatraemia which resulted in prolonged coma duringtreatment with citalopram for depression.

The woman began treatment with citalopram 10 mg/day,with the dosage increased to 20 mg/day after 1 week. Fourweeks after starting citalopram, she was found unconsciousand was hospitalised. It was estimated that she had been in acoma for approximately 24 hours before admission.Investigations revealed hyponatraemia with a serum sodiumlevel of 108 mmol/L (normal > 135) and reduced serumosmolality of 246 mOsm/kg (normal > 281). She also hadelevated serum creatine phosphokinase and myoglobin levelsof 3228 U/L (normal < 70) and 4626 ng/ml (normal < 90),respectively, indicating rhabdomyolysis.

The woman was deeply comatosed and requiredendotracheal intubation and treatment with saline infusions.She was extubated 3 days after admission. At this time, shewas conscious, but somnolent, disoriented and confused. Thefollowing day, her serum sodium level had normalised and herserum osmolality was still slightly below normal. Seven daysafter admission, she had almost completely recovered. Sheremembered the events before initially losing consciousness,but had amnesia of her first few days in hospital. She refusedany further antidepressant therapy and was discharged onhospital day 19.

Author comment: ‘Some patients with neurologicaldisorders of the central nervous system seem to have aparticular risk of developing a sodium deficit when taking SSRI[selective serotonin reuptake inhibitor], and physicians shouldbe aware of this possibility.’Hull M, et al. Prolonged coma caused by low sodium and hypo-osmolarity duringtreatment with citalopram. Journal of Clinical Psychopharmacology 22: 337-338,Jun 2002 - Germany 800912008

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Reactions 20 Jul 2002 No. 9110114-9954/10/0911-0001/$14.95 Adis © 2010 Springer International Publishing AG. All rights reserved