Abstract
Aripiprazole-precipitated hyponatraemia is rare. We could find only two cases of aripiprazole-induced hyponatraemia in the current literature [1,2]. The use of aripiprazole has gained popularity recently due to its comparatively benign adverse effect profile. Whilst the precise mechanisms of how aripiprazole may cause hyponatraemia are unknown, it has been postulated that it may cause the syndrome of inappropriate antidiuretic hormone secretion (SIADH) [1]. We report a third case of a patient developing hyponatraemia that can be attributed to the use of aripiprazole.
A 56 year old lady with a long history of schizoaffective disorder and intellectual disability presented to hospital with a worsening of her mental state that had been characterized by disorganization, disinhibition and perceptual abnormalities. Collateral history suggested that she had had a fluctuating course since her last admission to hospital eight months ago characterized by periods of relative mental state stability interspersed with periods of disorganization and confusion. Her past history suggested a treatment-resistant psychosis requiring a combination of sodium valproate 1 g BD, depot flupenthixol decanoate 40 mg fortnightly, and olanzapine for management of symptoms. The atypical antipsychotic had been converted to aripiprazole 30 mg/day due to significant weight gain. Her current lack of improvement had been in the context of the ongoing, albeit, erratic use of aripiprazole. Detailed investigations during the current admission revealed hyponatraemia with serum sodium concentration of 128 mmol/L. Thyroid, renal and liver function tests and serum cortisol were unremarkable. Serum osmolality was reduced at 258 mosmol/kg. Clinical examination revealed no evidence of hyper/hypovolaemia and no neurological deficits. Although a urine osmolality would have been desirable this was precluded by the significant agitation of the patient and difficulty in obtaining a urine sample. Rectifying her hyponatraemia was first attempted with a combination of fluid restriction (1.5 L/24 h) and sodium chloride tablets (1.2 g/day). Her serum sodium levels continued to decline despite these interventions and her serum sodium level was 124 mmol/L 5 days later. Aripiprazole was discontinued at this point of time, with an increase in serum sodium levels to 134 and 136 mmol/L, respectively, 4 and 10 days later. She continued to maintain these levels despite the cessation of sodium chloride tablets a week later. Chlorpromazine 300 mg was added in lieu of aripiprazole. There was a concomitant improvement in mental state along with the normalization of sodium levels.
Both sodium valproate [3] and antipsychotic medication [4] in general have been implicated in the causation of hyponatraemia. The patient had, however, been on a combination of both sodium valproate and flupenthixol in addition to olanzapine without event for several years. She was concomitantly prescribed a thiazide diuretic, indapamide, for the management of her hypertension. Indapamide is known to cause electrolyte abnormalities but largely related to potassium levels rather than sodium. Her potassium levels remained normal at all times. Additionally, the removal of aripiprazole appeared to correlate closely with the sodium levels returning to baseline levels; an improvement she continued to maintain during the next three weeks in hospital. It is possible that aripiprazole prescription along with three other agents with the potential to cause hyponatraemia may have precipitated this crisis.
Our patient is representative of clients with chronic psychosis in several respects: multiple medications, metabolic complications and the inability to give a clear account of symptoms. While not common, hyponatraemia-related deteriorations in mental state could easily be confused for a worsening of psychosis. Medical practitioners need to be aware of this uncommon complication that may potentially result in a fatality.