Hyponatraemia, defined as a decrease in serum sodium concentration (Na) below 135 mmol/l, is the most prevalent electrolyte disorder in both outpatient and hospital settings,1 affecting 19% of hospitalised patients2 and 7% of those treated on an outpatient basis.3

Acute hyponatraemia, which by definition develops in less than 48 h, is serious in itself, capable of inducing deep cerebral oedema, cerebral herniation and, therefore, high mortality. On the other hand, while chronic hyponatraemia, which takes more than 48 h to develop or has an unknown onset time, can also be serious, it is usually mild to moderate, given its more latent development. However, it is not an indolent condition, as it is associated with gait instability and risk of falls and fractures,4, 5 as well as increased hospital stay, and both in-hospital6, 7 and outpatient mortality in the immediate period after discharge.2 Given its multiple aetiologies, hyponatraemia is often the first sign of pathologies with important prognostic repercussions. In addition, its presence notably increases the costs of healthcare,8 not only due to its direct effects, but also due to the important association with a lower functional capacity and quality of life, especially in elderly patients.

After correction of severe hyponatraemia, whether acute or chronic, or its overcorrection, complete neurological recovery may take weeks, and some patients may present permanent neurological sequelae.9 Therefore, early treatment of severe hyponatraemia, with an increase in Na of at least 4−6 mmol/l in the first 4−6 h, is essential and has been shown to improve the survival prognosis.10 Likewise, correction of chronic hyponatraemia, after reaching sustained levels of eunatraemia (>135 mmol/l), has been associated with a significant improvement in gait stability11 and very probably in mortality, as suggested by Corona et al.12 in their latest meta-analysis. However, if the increase in Na is very rapid and exceeds the established limits, it can cause the appearance of osmotic demyelination syndrome (ODS), especially in patients with chronic hyponatraemia and associated risk factors, such as alcoholism, malnutrition, prolonged use of diuretics or hypokalaemia.13, 14

Despite the aforementioned impact and the currently available therapeutic options, hyponatraemia, even severe hyponatraemia, is frequently underestimated and inadequately treated, which has highlighted the need to develop consensus statements and clinical practice guidelines aimed at improving the diagnostic and therapeutic approach to this condition in a structured way.

These documents include a consensus guide from a Spanish multidisciplinary group15 made up of two specialists in nephrology, one in hospital pharmacy, two in internal medicine and two in endocrinology, which was drawn up in 2013 with the aim of providing a specific guide and a detailed description of the treatment of hyponatraemia induced by the syndrome of inappropriate antidiuretic hormone secretion (SIADH).

With the intention of giving continuity to the aforementioned guide, the water metabolism working group (Acqua Group) of the Área de Conocimiento de Neuroendocrinología [Neuroendocrinology Knowledge Area] of the Sociedad Española de Endocrinología y Nutrición [Spanish Society of Endocrinology and Nutrition] (SEEN) has prepared this update document.