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We thank Decaux et al (1) for their interest in our article (2), recently published in Critical Care Medicine. We are happy that they endorse our approach of active therapy for hyponatremic encephalopathy with the use of hypertonic saline. However, we take exception when they suggest that our approach differs from recent European guidelines (3). It is important to note that we were the first to introduce the concept of the use of intermittent boluses for the treatment of hyponatremic encephalopathy in marathon runners (4) with hyponatremia. We have continued to advance this concept since that time (5). It is this original research upon which the European guidelines are now based. There is no discrepancy in the approach other than 150 mL of 3% saline as a bolus rather than 100 mL as we have advocated. Please refer to Figure 4 of our article (2) as our approach to hyponatremic encephalopathy is detailed there.
Furthermore, we are a bit confused when Decaux el al (1) suggest that 10 mL/kg of free water be given during the treatment of hyponatremic encephalopathy as this would be counterproductive. Likely, they are referring to actively relowering the sodium if an overcorrection has occurred, in which case we would agree with such. We also present in our article (2) a detailed description of the use of desmopressin for the prevention of overcorrection of the serum sodium on pages 1769–1770.
Finally, we take exception with the suggestion that enteral urea given through a nasogastric tube is a viable alternative to hypertonic saline in the treatment of hyponatremic encephalopathy. We feel that enteral urea given to a patient who may be obtunded or at high risk for seizures is a dangerous therapeutic maneuver due to the risk of aspiration and should never be done. Hypertonic saline has been shown to be safe and effective in the management of hyponatremic encephalopathy in multiple series (6–8) and as recently demonstrated can be safely administered through a peripheral IV catheter (8). Oral urea lacks this evidence base; therefore, we assert that oral urea has no role for acute management of this condition.
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