Endocrine Abstracts

Background: Severe hyponatraemia and other electrolyte disturbances secondary to indapamide are documented in the literature. We report two cases that presented with neurological sequelae of profound hyponatraemia without seizures secondary to indapamide.

Cases: An 86-year-old female presented with a history of confusion, vomiting and frontal headache associated with lethargy and anorexia. She had been started on indapamide 1 month earlier. She was on no other medications. Her abbreviated mental test score was 2/10. She was euvolaemic and had left basal crepitations. Serum sodium was 99 mmol/l, potassium 3.5 mmol/l, and magnesium 0.58 mmol/l. Chest X-ray was consistent with infection. The patient was managed in a high dependency environment and the sodium steadily increased with slow N.Saline and cessation of the drug.

A 68-year-old male was brought to hospital by his wife because of confusion. He had been started on perindopril 1 month earlier and indapamide 3 months prior. He had presented to his GP 2 weeks before complaining of a ‘muzzy head’. Serum sodium was 100 mmol/l and potassium was 2.6 mmol/l. The patient was managed as above.

Conclusions: These cases highlight the profound hyponatraemia that can result from indapamide therapy. As the sodium loss is progressive, the hyponatraemia is chronic and therefore well tolerated. Any neurological symptoms in patients on diuretics or anti-hypertensives should have an urgent blood test to measure electrolytes. Patients with neurological sequelae secondary to hyponatraemia should be managed in a high dependency environment irrespective of serum sodium concentration.