Lets talk about a case of Na of 110 and seizure. Medications involved are mephobarbiturate and escitalopram( recent in last 2 years). The exam is consistent with euvolemia and you make a diagnosis of SIADH. Neuro status improves after receiving hypertonic saline and furosemide in the first 24 hours.
The Na corrects by 10Meq in the first 24 hours and another 20 meq by 36 hours. A little too rapid.
The urine output had just picked up. As a result, desmopression was administed and D5W to bring the Na down by 5Meq in 48 hours.
Discussion points..
Would you attribute SIADH to lexapro?
What do you do when there is overcorrection?
Saturday, March 13, 2010
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http://www.ncbi.nlm.nih.gov/pubmed/18235152
ReplyDeletehttp://www.ncbi.nlm.nih.gov/pubmed/17183251
The above two references are great in the over correction concept. I think that the concept of 0.5meq/ hour is now changing. If someone is symptomatic and having siezures, correct by 3-4 meq within 2 hours acutely first using 3 or2% Saline. once that has been established, then go slowly as we do 0.5Meq/ hour. BUT, we often forget the brisk diuresis sometimes we observe even with just giving them hypertonic saline or tiny amounts of lasix. a close watch on output has to be observed.
When large amount of urine output is observed,more frequent checks of Na should be done and also diagnosis might be confounded by a low "solute intake" or "beer potemenia" as well in some cases. Then, we have to apply "BRAKES" with the use of ddavp and D5W. Either one is fine but one we have control over, the other we don't. Once we give ddavp, we just hope it will do its job and once given, its out of our control.
Overcorrection is a problem, but only if someone has chronic hyponatremia, in acute setting, perhaps, some early faster correction is probably more beneficial and if you over correct, apply the brakes soon enough.
http://www.ncbi.nlm.nih.gov/pubmed/19627709
ReplyDeletehttp://www.ncbi.nlm.nih.gov/pubmed/16896026
http://www.ncbi.nlm.nih.gov/pubmed/12503252
Risk factors for the development of hyponatremia with SSRIs include older age, female gender, concomitant use of diuretics, low body weight, and lower baseline serum sodium concentration. In published reports, hyponatremia developed within the first few weeks of treatment and resolved within 2 weeks after therapy was discontinued. The mechanism by which SSRIs cause hyponatremia is thought to be secondary to development of SIADH in these reports. Its hard to make a case for SIADH after 2 years unless there was underlying SIADH from SSRI bring it down to 130s and then there was another cause leading to worsening of Na. Regardless, holding it is the best thing to do in any circumstance.