Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2007) 13 P43

Halton General Hospital, Runcorn, Merseyside, United Kingdom.


A 64 year old man presented with confusion and agitation following diarrhoea for 48 hours. He had a background history of hypertension, type 2 diabetes, depression and had a normal sodium concentration of 135 mmol/L a year prior to admission. His medications included bendroflumethiazide and sertraline in addition to metformin, diclofenac sodium, aspirin, simvastatin, nifedipine and enalapril. On examination he was conscious but confused. He was afebrile with a blood pressure of 140/70 mmof Hg, with no pedal oedema and remaining systemic examination was normal. His biochemistry on admission revealed sodium of 99 mmol/L with a potassium of 3.9 mmol/L, urea of 5.3 mmol/L and creatinine of 76 μmol/L. His liver transaminases were mildly elevated. The lipid profile revealed no abnormality and his random blood glucose was 8.9 mmol/L. Haematology was normal but he had evidence of a urinary tract infection. The plasma osmolality was 207 mmol/L (288–298 mmol/L), urine osmolality of 507 mmol/L (250–750 mmol/L) urinary sodium of 67 mmol/L with a normal serum cortisol, normal thyroid function test, and a normal chest X-ray. The hyponatraemia was attributed to syndrome of inappropriate anti-diuretic hormone (SIADH) secondary to bendroflumethiazide and sertraline. These were discontinued and his fluid intake was restricted. He made a gradual and full recovery with a gradual increase in his sodium concentration reaching 127 mmol/L over a period of ten days following which he was discharged. We believe that 99 mmol/l is the lowest recorded sodium in the literature. Despite, a dramatically low sodium concentration our patient did not present with convulsions, coma or severe neurological impairment. The clinical presentation of hyponatraemia is probably influenced by the aetiology as well as the rate of decline of sodium concentration. Severe hyponatraemia with an extremely low sodium concentration can with appropriate management and monitored gradual increase in sodium concentration, make a complete recovery without residual neurological sequelae.

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