Tuesday, November 18, 2014

SEVERE CHRONIC HYPONATREMIA: A Pathophysiological Rumination.

[This is the final post in the five-part series covering some important and often overlooked (and under-published) issues and concepts in the management of severe hyponatremia. While this is not, by any means, an exhaustive discussion of the topic, I hope that these posts will not only help the readers enhance their understanding of the pathophysiology of severe hyponatremia but also help them manage it more effectively with a lot less stress and mental anguish.]

In this video post, I discuss --- what I find to be --- an extremely useful method of calculating the dose of sodium chloride based infusions and predicting response to therapy while treating chronic severe hyponatremia.

Posted by Hashim Mohmand


Eoin said...

excellent video, thanks Hashim. Looking forward to trying it out and seeing how accurate it proves.

Anonymous said...

Wonderful explanation, thanks!
Very interested in how was managed the diuresing, sodium rising patient?

Dr. Helbert Rondon said...

Nice video. One interesting teaching point is that serum sodium concentration does not rise because of the "hypertonicity" of hypertonic saline compared to plasma but because the salt load forces renal water excretion (electrolyte diuresis).

Gearoid McMahon said...

Hi Helbert,

In the medium term you are correct but there are two scenarios in which this may not necessarily be entirely true. The newer recommendations are to give a bolus of 3% saline in individuals who are symptomatic. This bolus will acutely increase the sodium concentration even in the absence of a large urine output.

The second potential scenario is individuals with hypovolemic hyponatremia who you clamp with DDAVP. In that scenario, the urine output can fall to less than 30mls/hr (I had one recently) and the correction that occurs is a combination of the addition of solute and relative free water excretion.

Of course, in both of these scenarios, the excess solute will eventually be excreted with free water which accentuates the Na-increasing effect of the hypertonic saline.

Dr. Helbert Rondon said...


Thanks for your comments. However, the elevation of serum sodium concentration with hypertonic saline bolus in the case of symptomatic hyponatremia is only of 2 mEq/L or so, which is mild ,but enough to relieve cerebral edema. The major and permanent effect of hypertonic saline on sodium elevation is by increasing free water excretion. Finally, even patients with type A SIADH who receive normal saline can increase their serum sodium concentration by a few points just by the physicochemical effect of saline "being hypertonic" compared to hyponatremic plasma sodium concentration. Of course, this improvement in serum sodium concentration is very transient and, as we all know, end up becoming much worse.