Editor, – I have read Dr Shannon's article (Aust Prescr 2011;34:42-5) and the article in Medicines Safety Update (April 2011), both of which are excellent, simply written summaries on hyponatraemia. However, I have two objections to the traditional advice of stopping the medication that causes hyponatraemia and then giving other treatments as necessary.
Firstly, it is sometimes impossible to stop an antidepressant or antipsychotic which is necessary. Also, it is unlikely thatany other psychotropic drug will be better as they can allcause hyponatraemia due to the syndrome of inappropriateantidiuretic hormone secretion.1 Secondly, the situation can be remedied by fluid restriction, either on an inpatient or outpatient basis, provided adequate explanation is given to the patient.2
The mechanism of hyponatraemia with psychotropics is probably a combination of increased fluid intake3,4 and stimulation of central serotonergic and alpha1adrenergic receptors to release antidiuretic hormone.5
Antidepressant-induced hyponatraemia can spontaneously remit in spite of continuing treatment,6 although it is safer if there is fluid restriction of 800 ml/day with gradual liberalising of the restriction as the serum sodium rises. This approach successfully raised the serum sodium in all patients in our study, and maintained levels over a six-month follow-up period.2 It seems to re-set the hypothalamic osmostat and there is rarely need for sodium replacement.
To detect hyponatraemia, I assess urea and electrolyte concentrations three days after starting an antidepressant in all patients over 65 years old. If present, I treat with modest fluid restriction and monitor the patient.
M Roxanas
Department of Psychiatry
University of Sydney
Concord Hospital, Sydney