The authors reply
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.