Serum sodium disorders: safe management

Editor – I suspect that Wakil and Atkin were set an impossible task, in reviewing the aetiology, assessment and acute mangement of hyponatraemia and hypernatraemia in three pages (Clin Med February pp 79–82)! The 2007 American guidelines on hyponatraemia alone run to 21 pages, including 120 references.¹ However, the authors of the CME acute medicine review covered this complex topic in a readily accessible manner, for which they should be commended. However, I fear that a number of important and clinically relevant points were not highlighted due to space limitations. Firstly, the contribution of excessive water intake to hyponatraemia should be stressed. Although classically presented as a psychiatric condition of psychogenic polydipsia, water intoxication is an important differential diagnosis for hyponatraemia. It can also cause a diagnostic challenge and contributes to many cases of hyponatraemia. This was evident in the lesson of the month, published in the same edition of Clinical Medicine, where a young man presented with hypovolaemic hyponatraemia.² Secondly, it should be stressed that in older patients with low serum sodium levels, there are often multiple contributing factors. Diuretic therapy may promote hypovolaemia; co-morbidities such as chronic kidney disease or heart failure cause a tendency to hypervolaemia. At the same time, underlying diseases or other medicines such as tricyclic or selective serotonin-reuptake inhibitor antidepressants may cause inappropriate antidiuretic hormone (ADH) secretion. However, the authors’ advice that, where there is doubt, isotonic saline should be given is probably valid; but the response to this therapy may be unpredictable. Finally, I worry that the review lacked sufficient detail on pharmacological therapy, advocating the use of new aquaretic drugs but without mention of demeclocycline, which is still commonly prescribed. However, I would strongly counsel against the use of such agents in the acute setting and only where there is a clear diagnosis (with an underlying cause for) inappropriate ADH secretion.