Most acute dysnatremias are hyponatremias with onset of symptoms <24 h before hospital arrival. Decreased consciousness and seizures are common, and women are overrepresented. In most patients serum-sodium is corrected faster than recommended for chronic dysnatremias. Acute hypernatremias have a higher mortality than acute hyponatremias.
The overrepresentation of women among patients with acute hyponatremias, including exercise-associated hyponatremia [19] and ecstacy-associated hyponatremia [11], may be caused by the fact that women in general have less body water, both because of lower body weight and higher fat percentage. The addition of the same amount of free water, or salt, will thus induce a larger change in serum-sodium. Estrogen may also contribute [21].
In patients who died of acute hypernatremia a rapid correction was attempted, but the patients died within a short period of time. Among patients excluded due to lacking information about treatment given or correction rate, the mortality was 3/12 (25%). All fatal salt intoxications (serum-sodium 175–255 mmol/L) happened within 4–36 h after hospital arrival. We also excluded several other cases due to lacking information about duration of symptoms, including several autopsy reports. Our numbers is thus not representative for the actual mortality in acute dysnatremias.
Most patients with hyponatremia, and all with hypernatremia, had faster correction rates than 10 mmol/L/24 h. A significant proportion were corrected as fast as 20–50 mmol/L/24 h. This is up to five times as fast as most guidelines recommend in chronic dysnatremias [1, 22, 23]. However some experts recommend a faster correction rate in acute and symptomatic patients; Sterns recommends up to 1 mmol/hour, with no upper 24-h limit in acute hyponatremias, and that acute hypernatremia with known duration under 24 h is corrected as fast as possible [8]. Verbalis has no upper limit for the correction rate of acute hyponatremia [4].
Among the surviving patients with the fastest correction rate, the following are emphasized: a young man with serum-sodium 196 mmol/L received 6 l of glucose solution intravenously, within half an hour, with a documented drop in serum-sodium of 37 mmol/L [24]. A man with acute hyponatremia, 98 mmol/L, received dialysis and hypertonic saline with an increase in serum-sodium of 24 mmol/L in 5 h [25]. Considering the short survival time in the fatal cases, these rapid correction rates may have been lifesaving.
A difficult clinical challenge is to distinguish between acute and acute-on-chronic hyponatremia in patients with hyponatremic encephalopathy. It also occurs that assumed acute hyponatremia has underlying causes (such as heart-, liver-, or renal disease or the use of certain drugs) and thus also may have a chronic (and partly compensated) component. These patients may get complications if a rapid correction rate is used. Our experience is that a head CT with signs of cerebral edema supports an acute genesis (Fig. 2). Both European and American guidelines for hyponatremia [1, 4] recommend that all symptomatic patients receive intravenous bolus doses of hypertonic (3%) saline. However, we question the recommendations given in the European guidelines [1] regarding the maximum correction rate of 10 mmol/L/24 h in the treatment of acute hyponatremia with known duration <48 h and no underlying risk factors.
Limitations
Although the search resulted in 3884 articles, only 67 cases made our inclusion criteria. Many articles and cases were excluded due to unknown duration of symptoms or underlying risk factors and/or insufficient information about the treatment given, or the correction rate. For the same reason no reviews or randomized controlled studies were included. Although some larger studies have compared survival and correction rate in dysnatremias, these do not distinguish clearly between acute and chronic dysnatremias. To our knowledge no randomized controlled trial regarding the correction rate of acute dysnatremias has been published.
In this review, we did not have access to the hour-by-hour correction rate for all patients. Thus we cannot know if the patients had a rapid correction of serum-sodium which then decreased, or if they had a steady correction rate. Publication bias may have contributed to the high survival and the rapid correction rate in our material. However, we believe it is worth noticing the survival- and correction rate in context with the fact that none of the authors reported signs or symptoms consistent with osmotic demyelination syndrome. Only a small number of patients received a follow-up MRI, thus we cannot rule out that some patients may have had radiological deviations, but in our review we have not found any cases of osmotic demyelination syndrome secondary to rapid correction of acute hyponatremia.