Severe hyponatremia

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lymphocyte

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I got reamed on morning handover today.

55F binge EtOH on HCTZ brought in by family with worsening confusion and nausea. Na 106 (and K 2.3 with ECG changes). Transferred to our ED, and by the time I see her, she's gotten 100mls 3%, 2L N/S and a bunch of K. Her serum sodium is 118 at 9 hours. Symptoms had long since resolved. Urine output is starting to pick up over 400 mls in 30 minutes. 2mcgs DDAVP and admit.

Morning rolls around, Na stable at around 115 and K replaced to 3.5 by titrating sterile water. ECG changes gone. Patient is lethargic but no nausea or headache. Seems like a safe correction. 9 at 24.

But then on handover, the attending keeps shaking his head and says he can't understand why I gave DDAVP. "That doesn't make any sense, just run some slow saline next time." I literally don't understand how that would have helped -- the lady seemed like she was going to correct very, very quickly with more solute.

What did I do wrong? What would you have done? I felt pretty dejected on my way home.

How do you manage severe hyponatremia? DDAVP up-front or do you wait?

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I got reamed on morning handover today.

55F binge EtOH on HCTZ brought in by family with worsening confusion and nausea. Na 106 (and K 2.3 with ECG changes). Transferred to our ED, and by the time I see her, she's gotten 100mls 3%, 2L N/S and a bunch of K. Her serum sodium is 118 at 9 hours. Symptoms had long since resolved. Urine output is starting to pick up over 400 mls in 30 minutes. 2mcgs DDAVP and admit.

Morning rolls around, Na stable at around 115 and K replaced to 3.5 by titrating sterile water. ECG changes gone. Patient is lethargic but no nausea or headache. Seems like a safe correction. 9 at 24.

But then on handover, the attending keeps shaking his head and says he can't understand why I gave DDAVP. "That doesn't make any sense, just run some slow saline next time." I literally don't understand how that would have helped -- the lady seemed like she was going to correct very, very quickly with more solute.

What did I do wrong? What would you have done? I felt pretty dejected on my way home.

How do you manage severe hyponatremia? DDAVP up-front or do you wait?

The DDAVP is somewhat counterintuitive and some docs have a hard time wrapping their minds around it. It might be the only thing I’ve even seen almost cause a fist fight at a docs only meeting of intensivist where I work!! Lol. I give it up front. If you don’t shut off the the dump of urine free water you spend more time chasing the sodium and have less control over the situation. And when the potential complication can be catastrophic I like as much control as possible. I’m a DDAVP and 3% drip guy. Though I’ve found the European guidelines helpful. And do employ a lot of 150cc 3% boluses for symptomatic patients. I put in arterial lines and use POC blood gas sodiums every two hours because I can’t get my lab to draw every two.

I tell the ED to STOP putting any fluid in the patient unless they are absolutely certain of hypovolemia. These days with patients on so many meds and so many chronic problems urine lytes are often not super helpful but I grab them and an initial serum osm just because.

I wouldn’t have chewed you out.
 
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I agree with JDH-- your management was good. You could argue to try a smaller bolus of 3% and then maint NS first (sometimes even a small saline load precipitates the free water dump in the patient you describe), as long as you are checking Na and K q 2 hours and go to more 3% if you aren't making headway in 2-4 hours (symptom resolution). Also, instead of DDAVP you can you a vasopressin drip at .01 U/hour-- works same as DDAVP but you can easily titrate it on and off.
All said, though, you took a perfectly acceptable approach.
 
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Also, instead of DDAVP you can you a vasopressin drip at .01 U/hour-- works same as DDAVP but you can easily titrate it on and off.
All said, though, you took a perfectly acceptable approach.

This is something I don't know about/haven't used in this context. I assume it works like very weak DDAVP?

How do you titrate it?

HH
 
We have some health system wide data (the system I work in) that indicates that the alcoholics seem to be more sensitive to shifts in Na and more vulnerable to PML which is why we have implemented some of the current aggressive (in ICU with arterial line) and cautious very slow correction under the most strictly controlled (as possible) conditions.

What to do with the liver-bomb alcoholic in septic shock with a presenting sodium <110?? No good answers. But we've decided you simply inform the decision makers that things are dicey and that we have to do what we have to to save life and limb first ala the sepsis (and fluid *IF* indicated), and the low sodium will be dealt with after stabilization of cardio-pulmonary issues.
 
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I’m pretty simple with hypoNa. 3% up front if indicated, then fluid restrict and monitor closely. If that doesn’t work for 24 hours, then I’ll get fancy.
 
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Thank you for the support guys. It was just a crummy night in general. I think I was harder on myself than anything else.

I caught up with the attending, and he told me not to worry about it, and "it seemed to work okay." To each their own.
 
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Thank you for the support guys. It was just a crummy night in general. I think I was harder on myself than anything else.

I caught up with the attending, and he told me not to worry about it, and "it seemed to work okay." To each their own.

The proof is in the pudding. What matters is you don’t have wild swings and they correct.
 
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Initially I was confused, certainly sounded odd...but with a little further reading, it makes perfect sense in EtOH intoxicated patients, given the effects of alcohol on ADH secretion. Without taking that into consideration, it does seem totally counter-intuitive. And in hyponatremia without the EtOH effects, I would say the question becomes why do you think they are ADH deficient or resistant. If you have a reason, give it
 
Initially I was confused, certainly sounded odd...but with a little further reading, it makes perfect sense in EtOH intoxicated patients, given the effects of alcohol on ADH secretion. Without taking that into consideration, it does seem totally counter-intuitive. And in hyponatremia without the EtOH effects, I would say the question becomes why do you think they are ADH deficient or resistant. If you have a reason, give it

It's not that these folks have an "ADH problem" per se, but if you drop the DDAVP hammer on them, their kidney's stop dumping freewater. You are making them do this. It's like the difference between trying to adjust the sodium content in two aquariums with spigots, one with a spigot open and running, and the other with the spigot off (not a perfect analogy but pretty close). You are simply controlling ONE mechanism/variable to make sure the body water content is staying stable and is mostly being changed by the physcian
 
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Initially I was confused, certainly sounded odd...but with a little further reading, it makes perfect sense in EtOH intoxicated patients, given the effects of alcohol on ADH secretion. Without taking that into consideration, it does seem totally counter-intuitive. And in hyponatremia without the EtOH effects, I would say the question becomes why do you think they are ADH deficient or resistant. If you have a reason, give it

It only has to do with controlling free water clearance and nothing more. The formulas people often use to correct hyponatremia don't really work because they assume you're just mixing one salty bucket of water with another -- and hence you can predict what the final concentration of salt will be. The problem is that one of the buckets is leaking, and you don't know by how much (i.e. auto-diuresis after a solute load). So you give DDAVP to plug the leak, because the patient stops peeing. Now you can use the formulas very, very accurately.

 
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Anyone else shocked by how many people out there don't know jack about hyponatremia management?

I would expect a reaction that the OP got from their attending from a nurse or a PA student, not from an academic attending. Did these people go to a different school than the rest of us or something?
 
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Hyponatremia is very mismanaged. Even by the IM/CCM people who you would think would be the experts next to the renal folks. I did a rotation with the nephrologists in my fellowship and became really good friends with the attending.
I personally hate hyponatremia but have learned a lot about it. It can be very complicated.
I understand why the OP gave the DDAVP. In chronic ETOH abusers, and other chronic hyponatremics, too quick correction can be detrimental to their brain. So like the others have said, plug the faucet a little if you can and "go slowly my dear"
Anyway, the book "Acid base balance made ridiculously simple" is a great one.
 
Anyone else shocked by how many people out there don't know jack about hyponatremia management?

I would expect a reaction that the OP got from their attending from a nurse or a PA student, not from an academic attending. Did these people go to a different school than the rest of us or something?
I guess I should definitely throw away my board certification, because I had never heard of the DDAVP method. Oh, wait, maybe I know how to treat hyponatremia slowly, even without DDAVP. :p

I also distinctly remember a patient who almost coded from DDAVP for diabetes insipidus.
 
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I guess I should definitely throw away my board certification, because I had never heard of the DDAVP method. Oh, wait, maybe I know how to treat hyponatremia slowly, even without DDAVP. :p

I also distinctly remember a patient who almost coded from DDAVP for diabetes insipidus.
They almost coded from the treatment for DI? That's some poor management and sounds like a lawsuit waiting to happen.
 
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I guess I should definitely throw away my board certification, because I had never heard of the DDAVP method. Oh, wait, maybe I know how to treat hyponatremia slowly, even without DDAVP. :p

I also distinctly remember a patient who almost coded from DDAVP for diabetes insipidus.
Well to be fair, it wasn’t the OP who pushed/gave the 3%. He or she was just trying to slow things down.

How did the patient almost code? Severe cerebral edema? Just trying to understand.
 
Okay. This happened AGAIN with a different outcome.

Heavy EtOH and indapamide are the culprits. But this time, the patient also has profound hypovolemia with orthostatic hypotension SBP 150 -> 70 and urine Na 14. Total intraventricular obliteration on bedside TTE. Dry as a chip.

You could chase the haemodynamics with volume -- as they did in ED -- but he immediately becomes polyuric and starts correcting way too quickly for his EtOH pickled brain. On top of that, K 2.1. Easy decision. 2mcgs IV DDAVP and admit. Morning roles around, Na corrected by 4 in 10 hours and K 3.4. Symptomatology much better. Haemodynamics stable. I'm feeling pretty good. Very satisfying resuscitation.

I then get GRILLED by our very brilliant department director. He's pimping me for 30 minutes about renal physiology at the end of a long night shift. I feel gutted but I hold my ground. Once again, I go home pretty dejected.

That night when I come back on he grabs me and says he wants to have a chat. He then thanks me for showing him something new. Seems to work pretty well. He appreciates that I could reason through the physiology. Our department will now stock more DDAVP. He tells a few of the other intensivists about it. It's probably the kindest thing any boss has ever said to me. I feel like a colleague in training as opposed to a mere underling.

Why am I sharing this? Because 1) DDAVP clamping works quite well but 2) if you have fellows or trainees, please treat them like this. Give them some latitude and congratulate them when things go right -- especially if they're being safe. You'll win loyalty for the rest of your life.
 
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Visiting from pathology. Y’all might like this cute story. I’m retired so this is from long ago. With new residents, when i was a new attending, we would take a “stock” piece of autopsy brain. Specifically, a thin core of pons. We would submit it with a requisition generally stating something to the effect-“ needle biopsy of pons. hyponatremia with cns changes. r/o central pontine myelinolysis.”
Most everyone would gross it without question and one even ordered a luxol fast blue myelin stain up front!
 
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