Hyponatremia is the most frequent electrolyte disorder, affecting 15–28% of hospitalized subjects. Hyponatremia increases hospital stay and appears to be an independent risk factor for increased mortality, probably due to organic dysfunction produced even in mild hyponatremia.1, 2, 3

Approximately one-third of cases are due to the syndrome of inappropriate antidiuretic hormone secretion (SIADH). The other major cause of hyponatremia is that associated with thiazide use, which vies for the top spot depending on the series studied and can affect up to 5–10% of hospitalized patients. The remaining causes of hyponatremia (hypocortisolism, hypothyroidism, diarrhea, vomiting, and hypervolemia, among others) are much less common.1

The clinical signs of hyponatremia are predominantly neurological and resolve upon correction of the hyponatremia. Cerebral edema, induced by the movement of water into the intracellular space, is the primary reason for these clinical signs. Symptoms can range in severity from headache, instability with increased falls, memory loss, confusion, cognitive impairment, lethargy, coma, and seizures to death. More severe clinical presentations are more frequent with a more acute and pronounced decrease in serum sodium levels.4, 5, 6, 7, 8, 9, 10 A rapid decrease (in less than 24−48 h) and of moderate degree (approximately 10 mEq/L of sodium) could already cause such cerebral edema with an increase in neuronal cell volume and risk of herniation and death.7, 10, 11

It is important to differentiate between chronic and acute hyponatremia. The former usually presents with more nonspecific symptoms, although patients are rarely asymptomatic. In cases of mild/moderate hyponatremia, greater cognitive impairment and an increase in bone catabolism leading to a decrease in bone mineral density have been demonstrated when compared with individuals with eunatremia. Consequently, there is a greater risk of gait disturbance, falls, and an increased prevalence of fractures.2, 7, 12, 13

It is essential to correct hyponatremia with appropriate treatment even before knowing its etiology. However, the rate of increase in natremia is fundamental to avoid overcorrection within the first 24−48 h and thus prevent the risk of osmotic demyelination syndrome (ODS). There are factors that can increase the risk of overcorrection such as severe hyponatremia, hypokalemia, malnutrition, and liver disease. The target increase will be between 4–6 mEq/L within the first 6 h and should not exceed 8 or 10 mEq/L within the first 24 h and 16 and 18 mEq/L at 48 h depending on whether or not there is a risk of ODS.10

In this study, we analyzed the evolution of natremia during hospitalization in a tertiary referral center in patients who were admitted with hyponatremia or developed it during the episode.