Hey everyone, I'm Brandon Odo.
And I'm Brian Bulling.
And this is Critical Care Scenarios, the podcast where we use clinical cases, narrative storytelling,
and expert guests to impact how critical care is practiced in the real world.
Alright everybody, welcome back.
I am back of course with Brian Bulling, the man himself.
And we've been, you know, sinking into some pretty interesting, I think, medicine kind
of topics recently, much to probably Brian's chagrin.
But I think we have to deal with some of these things because, you know, no matter what
kind of patients you're taking care of, they all have bodies.
And they definitely all have kidneys.
And that's what we're going to explore today.
The perennial question of hyponatremia, a big category of disease, a lot of causes, probably
a lot of pitfalls, and something that I think we all have to understand at least a little,
no matter what we're doing.
So Brian's going to walk us through a little bit of this topic with, I think, the perfect
guest we have here, Dr. Paula Adams, who is down at the University of Kentucky with Brian,
and is dual trained in both nephrology and critical care.
He did a combined fellowship down that way.
And now splits his time between both arenas.
So no better person to explore the topic of hyponatremia in the ICU.
Brian, you're going to give us a little bit of a case?
Yeah, so I will confess right off the bat, I'm way out of my depth here.
Paul works upstairs in the smart ICU, the Mikyu, I work downstairs in the dumb guy, surgical
ICU.
And what I know of sodium tends to come from the neuro ICU where we consider you hyponatremia
if your sodium is less than 145.
So we're going to do our best to feel through this.
But I do think this is something that is probably one of the more common electrolyte
balances that we encounter in the ICU, even in the surgical ICU in the neuro ICU, where
we maybe try to ignore it a little bit more.
But it's certainly one that comes up a lot.
And one that I feel is potentially kind of confusing for students especially.
I have students who seem to struggle with hyponatremia.
So I thought this would be a good thing to talk about it.
Maybe we can all learn something together.
So Paul, you are on shift and you get a call from the ED about a new patient.
And this patient is a 65-year-old gentleman who comes in with some ultra-mental status,
a couple of days history of fever, just malaise.
This just isn't looking very good.
The ED has sort of worked him up.
Initially, consults in hospital medicine, they came down and saw him and said, this guy
does, he looks too sick for us.
I think he needs to go to the ICU.
So they call you to come down and see him.
And you find, as advertised, a 65-year-old guy who's not looking like he's in the best
of health, probably at baseline.
He is altered, but he's protecting his airway.
He is able to converse with you.
He's very confused.
At times, he is not just confused, but you can't even care in a conversation with the
guy.
His wife sits at the bedside and says, this has been going on for about two days, but
it got significantly worse this morning.
The ED has started some work up on him.
He's a little febrile.
He's a little tachycardic.
You notice he has a little bit of a distended abdomen.
And he got some lab work back.
His CBC is significant for a little leukocytosis to 13.
His H&H and platelet counter are all okay.
His electrolytes are not bad, except for his sodium.
His sodium is 128.
So start with, where do you go from here?
How do you approach this patient?
I think there's two things that you look at somewhat simultaneously.
One is, you decide on how much is this, how significant is this type of trampia?
Is 128 bad enough to be causing this guy to be altered and psychopathic, confused, definitely
different from his baseline?
Is that something that we need to correct quickly or do we have time to take your time and play
it safe?
The other thing that you're going to want to consider is, why is this happening?
Why is this sodium low?
Because that's going to change your management and what's going to happen down the road,
depending on what is driving his hyphenatremia.
So the intensivist in me wants to think, first, do I need to solve this problem?
Like right now, right?
To be honest with you, I don't think this is a right now issue.
There may be some sources that would argue with me on that, especially some of the more
critical care and ER-driven guidelines, recommendations, test prep courses, things like that.
If you see somebody with a low sodium and they're altered, confused, like some people
want you to say, you know, a hypertonic solution is something that we should be considering.
I will tell you that I feel like that gets you in the hot water down the road, right?
Like you fixed it now, great.
You know, you change that number by six mil quillabits or something.
But 12, 18, 24 hours on the line, it really puts your wrist over correct if you don't
know the underlying mechanism, which we don't know yet, right?
So for this guy, I would just put the brakes on that and say, let's just not worry about
this.
His sodium is low, but it's not terribly low.
He's in cephalopathic, but it sounds like he's protecting his airway, right?
He's not seizing.
He's not have tunded, right?
So we have time here to figure it out, which then kind of moves me on to the second point,
which is let's figure it out.
Most from your history, right, like I know this is probably like a, we'll just say we're
going to develop a pretest probability here, right?
Like I don't want to anchor on this, but just from the history, you know, this is a guy
that has developed something out in the community, probably hasn't been feeling well for a
few days before he presented, right?
And usually when people don't feel well, right, from a viral illness or bacterial pneumonia
or whatever, right, they're stuck being weak and sore and feeling terrible on their couch,
right?
And you don't really want to eat anything.
Speaking from like recent experience here this time of year, you don't really want to
eat anything.
It's a chore to even like drink some water.
And whatever you take in is probably not going to be a lot of solute, right?
Everybody pushes water and that's a good thing.
We don't want to dehydrate with our excess insensible loss with fever and things like
that, right?
And so you end up taking in a lot of hypotonic solution and you end up excreting a bunch
of isotonic solution in your urine and your stool and sweat, things like that.
And so as you see the balance there is you end up diluting yourself because you're not
taking in solid, you're not eating anything and just drinking water.
And so that's how you end up with this hypovolemic to uvolemic hyponatremia, which if you want
to put it into these traditional buckets would be a hypotonic hyponatremia, right?
So you literally just deluded out the sodium in your body by drinking water instead of
water plus your usual solute intake.
So I would put him into that bucket.
That makes sense and can certainly expand upon that decision from there.
Now, you make it sound like if you're taking in fluid and solute at a rate that's not exactly
equal to what you're losing you're going to end up changing your sodium.
But isn't it true that the kidneys are going to try to maintain a normal serum sodium,
regardless of if I'm drinking water or salt water or whatever else?
They will and this is where, you know, this is probably more of a nephrology centered
question now to where you say, well, why don't your kidneys regulate?
Well, the guy's sick, right?
Number one.
So maybe he's got to be of an AKI, right?
Maybe he doesn't quite, he's able to regulate that as well.
He can't really reclaim all of that sodium that he's losing.
Maybe he's spilling some of that in the urine because it's proximal tubules are injured,
right?
That's about half a percent of all sodium reabsorption is proximal tubule.
It's also the most energy dependent one, right?
So when your blood pressure starts getting low, you start looking kind of bad.
It's the first thing to go.
The other thing to consider is he's 60 something years old.
Yeah, we lose the ability to concentrate our urine as we get older.
So a young person can concentrate their urine down, you know, down the 1200 milli-osms,
super super concentrated.
You know, some frail elderly person, 80, 90 years old, might only be able to get it down
to 300 or 400 milli-osms, which is basically serum, right?
I saw some uric.
And so this guy may be somewhere in the middle.
And solute clearance is going to be related to what how concentrated he can make his urine.
And so if he can't reclaim all of that sodium because he's just peeing it out because he's
just being out the lute urine because he can't concentrate it anymore, right?
That's going to be an issue.
That makes sense.
So on one hand, kidneys will try to normalize your, you know, serum osmolality.
But on the other hand, all kidneys are not created equal in age and other disease, AKI
might affect that.
Exactly.
There's limits to that, right?
Diabetes, hypertension, you know, it will impair these things over the years.
So.
Okay, let's back up real quick if we can to this idea of is this a problem we have to
deal with now, right?
You had said that certain things may take issue with your statement that it isn't an
emergency.
What in your mind constitutes, because let's be honest, right?
There's some things in critical care that we address, even though we know it's a band-aid,
we're not addressing the problem, but, you know, I've got a guy that's got a K of one.
I got to give him K.
It doesn't really matter at that point why his K is one.
He's going to arrest if I don't give him some K.
So at what point do you look at this guy and go, it really doesn't matter right now why
his sodium is low.
I just have to fix it.
In my mind, probably seizure, that's the real big one.
If somebody's a ton did and they can't protect their airway, we can insulate them, right?
Like, I don't really think you're going to give them, you know, 30 mils of hot salt and
they're going to just like wake up, right?
To me, then it goes back to ABCs and you're like, well, airway is first, right?
Like, take care of that.
Seizures, we can't just let that go on.
And you, you know, somebody's sodium is 110 and they're seizing.
You're not going to kept reload them.
That's, you know, that's not going to fix it.
It's just like you're not going to give, it's like alcohol withdrawal seizure, right?
You're not going to give, kept right as somebody who's withdrawing.
It's not going to work.
You're going to use benzo.
It's the same thing here.
In my mind, that's the one thing we should do is seizures.
And again, it's like other things in critical care.
You can do things simultaneously, right?
So if somebody is a ton did and you're worried that they can't protect their airway and their
sodium is 110, you can, you know, hang the hypertonic and you can innovate them at the
same time, right?
Like, why would you not do that?
It just, when it comes down to these things, it's like test questions and board answers
and, you know, where you have to pick like the A, B, or C choice, people like to push
correcting hypernatremia or hyponatremia when, you know, you have things like altered mental
status even at a confusion, you know, I'm just a little off.
I can't remember the day of the week level.
And usually they'll give that with you with a much lower sodium, you know, 115, 118, something
less than 120 usually.
So that's why I say with this guy, especially 128 or whatever, we'll figure that out later.
Okay.
All right.
So now you're moving on to this, why is the hyponatremic?
And your theory is that this is probably imbalance between solute and isotonic fluid intake from
illness, maybe combined with some AKI or.
Okay.
Yeah.
So back in your mind, right?
Could this be chronic?
Maybe.
I don't know.
I mean, states of chronic hyponatremia, heart failure, cirrhosis, you know, is, you
know, thighs, eyes, something like that.
I mean, you know, you're going to look into these things as part of trying to come up
with the etiology.
So do you approach a hyponatremia then by sort of trying to differentiate volume status
or what kind of what's your first?
I feel like the volume status thing is a trap.
I think the first thing to ask yourself is, is ADH active or not?
Volume status, right?
Like I feel like it's been beaten in the submission that none of us can determine a
volume status from just like looking at the patient, right?
Unless they're on like an extreme end of the spectrum, we, it's basically just a coin toss,
right?
And when you're looking at three categories of like hypovolemic, uvolemic, hyper, you
know, hyper, like there's so much gray area there centering around that, like uvolemic
that I don't think it's worth trying to, trying to look at it that way.
I like I said, ADH being active or not is the, the defining factor for me.
So you get asked yourself, well, what does ADH do?
Anti-diarratic hormone, right?
So it reclaims free water from your tubules and the distal tubule there.
And it's controllable, right?
It's an aquaporn that's inserted into the, into the tubule under influence of the hormone
of ADH.
And so if you have a need to retain more water, which is usually a high plasma awesome, so
right?
Your blood is very, very concentrated for whatever reason.
You take in more water, ADH gets turned on, right?
There are certain things that trick that, right?
So if you have heart failure or cirrhosis and you have very poor circulation and perfusion
to your kidneys, your kidneys are going to make rather concentrated urine.
They're going to have a lot of time to suck up all that sodium, you know, that travels
through the tubules because it's moving at a slow rate.
And the kidneys are going to interpret that as, oh, wow, I'm very volume down, right?
I'm very concentrated.
I need to suck up more water to compensate for that.
And that's when ADH is then present.
Same thing with maybe the picture I'm painting on this guy, right?
Is he did eat and drink for a little while?
Yeah, he took him some water, but honestly, he's probably a little on the dry side, you
know, he's, he's, you know, didn't take any solute.
And he's in his ADH.
He's sick in other ways, right?
His ADH is going to be probably pretty active in trying to reclaim water and put it back
into him.
So I kind of say do a little thought experiment and say, would you expect ADH to be active
in this person or not?
So this is a conceptual framework.
It's not like you're going to look at a patient and know they're ADH, but from their history,
you might be able to.
Yeah, from the history and kind of what you're making up.
And you know, you can test it.
You're an awesome, greater than 300 slam dunk that ADH is working, right?
300 is kind of the cutoff, right?
If it's less than that, you don't have ADH present, right?
So, and then you have to entertain other ideas.
But if you got this on this guy and it was high, then you say, okay, well, you are trying
to concentrate your urine, you know.
So would that be the next step in someone like this?
You would, you would check on some of these urins, but you would have a thought going
into it what you think is going on.
Yes.
All right.
So let's say you do get a urinasm and it's 400.
400, yeah.
So you're right on the cusp there, right?
Yeah.
You're like, well, I think you got some ADH active, but it's not, it's not whopping, right?
And you could say, well, is this, is this just the best you can do?
You know, because you're a little older and maybe you got some kidney disease and whatever.
But it's there, right?
You would kind of say, well, he, he may be a little dry.
It would certainly fit the picture, right?
That his, his kidneys were trying to, to retain some water in order to bump up his blood pressure,
right?
To kind of fluid resuscitate itself.
But it would fit the picture.
And I would say, you know, in this situation, it would still fit the picture of just, you
know, hypotonic, hyponatremia.
Okay, so at this, at this point then, are you less concerned with the hyponatremia and
more concerned with just the whole picture of why is he sick and to begin with and sort
of going down that route then?
Yeah, probably.
Like let's figure out why are sick to begin with.
I would say, you know, in these people that are somewhat hypovolemic, definitely hypotonic,
you know, and trying to conserve water, fluid resuscitation is going to fix it.
They're going to get some salt, some saline in there.
They're going to get, you know, re-expanded.
Their kidneys are going to start working properly again.
And they're going to dump that excess water that they've been taking in over the course
of a few days, right?
And that, that presents a danger for over-correction because the kidney is just going to dump water.
Your urinosum is going to go from 400 to 100, right?
And that's, that represents free water leaving the body.
And you've just everything that we give.
I feel like comes in some kind of saline product around here, right?
So you're just going to give them solute and not a whole lot of other free water.
And that sodium is going to correct pretty quickly.
So that's, that's where you get into danger.
That would be my, my kind of only caveat to say, well, we can focus on more, what's wrong
with this guy rather than a hyponatremia at this point.
Okay.
So you're going to start kind of fluid resuscitating him and he's a little tacky-cardic.
His blood pressure is, we'll say soft, right?
I don't know, like, I don't really like the word soft, but we'll just say it's soft.
He's not really hypotensive, but, so you're going to give him some fluid.
Are you going to give him normal saline then to give him some sodium?
Or are you less concerned about that and just going to do something balanced?
I'll probably give him some balanced.
I mean, I think, I feel like there's enough evidence now that says, you know, balance
is better.
And there's really not going to be a whole lot of difference, right?
You know, you're talking 134 in LR versus 154, you know, milla-osms of sodium, right?
So you're, it's really hard to over-correct somebody with normal saline from a, from
a sodium standpoint, if you do the math on it, and even more so with LR.
So I'll just pick the kidney safe option and just choose LR.
All right.
So are you going to bowl us in?
Or are you going to put him on some fluid, maintenance fluid, both?
I'd probably just bowl with some so you would happen, you know, I mean, in this case, it's
just like, hey, septic, just give him this 30 mils per kg, follow the, follow the guideline
there and, you know, reassess, right?
It's your three hour window or whatever the, and just to be clear, you are approaching
this not as a replacement of their sodium.
Oh, you are, but your volume resuscitating them.
Exactly.
The type of olemic, so you're giving them that back and then their body will kind of
fix themselves.
Yeah.
Because as you alluded to earlier, the kidney will figure it out.
We just need to kind of give the kidney a better environment to work in.
Does that make sense?
Once you kind of allow them to release that ADH tone, then they can start doing their
regular things.
Yeah.
Yeah.
Because they're, they're just trying to suck up extra water at this point.
They're trying to give themselves a blood pressure and make sure that they're well-perfused.
And once you kind of reassure the body that, hey, here's three liters of fluid, you don't
have to hold on all this water anymore.
It's going to start to dump that water.
The ADH is going to be suppressed and you're going to pee out all that extra water and your
sodium will rise because now you're less dilute, if that makes sense.
Other than the urine osmolality, is there any other testing or workup or avenues you
feel like you would need to pursue before you could start treating this presumed diagnosis
or in this case, you feel pretty good about it?
For this guy, I would, I don't think I would need much more.
If you're questioning it, right, like, why would you question it?
You know, are there other reasons for hypoditremia?
You know, certainly, a urine sodium may help you with some of that, right?
If it's high, your kidney is not reclaiming sodium, you know, and those two things are
handled separately, water and sodium reclamation.
So if it's a high urine sodium, you have to wonder, well, why?
And that's, is that an ATM process, right?
Are we damaging the kidney physically?
Or are you on a diuretic, right?
Like I mentioned Thizads earlier, you know, that would help you clear sodium in that way.
If it's low, it's really not terribly helpful because that could go with heart failure,
cirrhosis, and sepsis, right?
If you're just like kind of pre-renal and kind of dry, your, your kidney is doing what
it's supposed to be doing and it's sucking up sodium to help, you know, bump up your
blood pressure.
So at this point, I wouldn't be too, too much more worried.
I think if it was a more severe hyponatremia, you know, another one 10s, one teens, I would
say we need to figure this out a little, you know, a little bit more rather than just saying
fluid or a cystate suit happens.
Is that perhaps also impatient where you might have multiple processes?
They seem hypovolemic and they're on a thiazide and they have an AKI and who knows what else?
Yeah, yeah, yeah, exactly.
I will tell you that most of the severe hyponatremia is that come in in this setting are going
to be exactly what this guy is, right?
Somewhat hypovolemic, hypotonic hypovolemic or hyponatremia where it was just, it was
poor soil you didn't take and hypotonic water intake and kind of soft blood pressure, you
know, nausea, vomiting, diarrhea, right, respiratory illness, whatever that may be.
That's kind of how they tend to act.
The majority of them.
Tell me, you know, in my mind, the patient who is hyponatremic from hypovolemia and the
patient who is hyponatremic from inadequate solute intake, you know, they're malnourished
or they're alcoholic or something.
They seem like different mechanisms, but they often end up overlapping.
Can we just kind of think of them as the same patient or are there any important differences?
They're different because the person that is malnourished, right, your alcoholic, your
teen toast, whatever, they're not going to get better if you get fluid, right?
That is a long, long standing process where the hypovolemic, you know, kind of sick person
is a probably days to weeks process.
And you can differentiate them based on what their urine, your urine ausum does.
And this is where we leave the ADH world a bit to where if you compare them, both of
the urine sodiums are going to be low.
And the sick kind of hypovolemic guy, his urine sodium is going to be low because he's
trying to reclaim all of that because he's poorly perfused.
And that's a signal for the kidney to reclaim sodium.
And the malnourished person, they just don't have any sodium to reclaim, right?
Like they don't take any in because they just, you know, drink a 30 rack of bush every
day and there's no sodium in that, you know?
So they're, they're urine ausum will also be low because ausum output at some point equals
ausum input, right?
So if they don't take any ausums in, normally it's, you know, 1,200 plus ausum intake per
day for a normal person.
If they're only taking in 300, right, and they make two liters of urine, right, their
ausum is going to be pretty low.
It's going to be below 300, you know?
They can have all the 8H action in the world and it's not going to go up because there's
nothing there versus the sick person where their ausum should be, should be higher than
300.
Does that make sense?
In both cases though, isn't it true that we're probably going to give them some sort
of IV crystalloid, which will give them fluid and solute.
And in both cases, they'll start to, or it may even overcorrect and they'll sort of
behave similar clinically.
Yeah.
The sick person's going to overcorrect more.
When you're talking about giving crystalloid, you know, you can do the math.
There's like equations out there that can tell you how much someone's serum sodium
arise based on how much you give them, right?
So if you give them a liter of normal saline, you know, and they're a usual 70 kilo person
with 42 liters of body water, it's going to go up by barely a point, right?
So that's assuming they're a closed box and they don't have any other intake, but it's
just not going to be a lot because you're one liter and 42 liters of body water is just
not a lot.
So.
I see.
So the sort of ADHD problem can fluctuate very quickly, but if it's due to just not having
enough solute to, you know, concentrate your urine, then that'll take a little while to
build that solute backup.
Exactly.
There's also kind of a concept of like medullary wash out to where the medulla of the kidney
is usually where there's a lot of very, very concentrated solute within the tissue.
And that helps concentrate your urine, right?
Because as the tubule moves through there, water can enter or leave, right, through osmosis.
It wants to go to a place of how you're solute.
And that's how you can concentrate your urine, right?
That's how you would claim a lot of water.
Well, if you don't have solute to put there over time, it washes out and then you really
can't even concentrate because there's not a gradient there anymore.
So that can happen.
All right.
So you're resuscitating this guy, you presume sepsis, you know, kind of guideline based stuff
and you get him upstairs.
He starts to look better.
Our rates coming down, blood pressure is still a little soft, but you know, stable,
stable.
At what point do you or do you even recheck that sodium?
Are you worried about watching it or do you just sort of get flabs daily like you would
on any other person and say, I expect it's going to be a little low.
I'd probably get another BNP after I gave him his initial resuscitation bolus, right?
If I wanted to give him two liters, I'd give him two liters.
I'd say recheck a BNP.
Yeah, because it's probably going to be two, three hours after, you know, the initial one.
And if it's relatively stable, I'd probably check another one in four to six hours.
Because we don't know if this is acute or chronic at this point, right?
If it's chronic, we want to be much more cautious if this is acute, which is usually considered
anything over two days or two weeks, two weeks.
Yeah, the rate of correction doesn't matter so much in an acute scenario, but you don't
know, so you play it safe.
Okay, and so in this case, we're not really trying to correct him, but you're saying
he's going to correct himself.
Yeah, if I'm right, he's going to correct himself.
We don't want to make sure he doesn't correct himself too quickly if this is...
Exactly.
Okay.
Now, if this is a chronic problem, is he likely to correct himself too fast or...
You know, and that's why I kind of get into, well, what is the etiology, right?
Because if this is a hypovoleum, a cup of tonic scenario where he's just sick and he's not
taking in solute, he's drinking water, that's probably acute.
But you don't know how long that's been going on, right?
This guy can kind of linger in for a month, or has this just been a week because his kid
gave him the flu, right?
You don't know.
And so you just have to play it safe and say, I'm going to stick to the six to eight mill
equivalents per day, right, for 24 hours.
The chronic guy, you know, how could you...
There's not really a scenario that I can think of that you would be chronically hypovolemia,
hypovolemia, cup of metremia, right?
Like all the time, that kind of transports you more into the world of this like tea and
toast area.
And by just by giving them fluid, like I said before, you're probably not going to correct
them very quickly.
Hypovolemia correction is one of those things where it's like, you don't see a lot of case
reports about it, probably, and the rumor is that it's probably because it's all litigated.
So I'm not a big fan of like, you know, CYA medicine, but this is a scenario where you
probably just want to be pretty cautious and just recheck, right?
It's...
You probably don't need to do it, you know, sodiums at more than every three or four hours.
I'm not really sure what the utility is of every hour, right?
Because like by the time you get the result back, like it's different.
So...
In a case like this, what over correction is mostly going to be due to, you know, dilute
urine.
Do you think it's reasonable to just monitor the urine if they start having a lot of watery
polyurea than you worry about it?
Yeah, I really like doing that.
And just...
I just get cereal, urine, awesomes.
And when that starts dropping, right?
Let's say you started at 5,600, you start seeing coming down, you know, definitely below
that 300 mark, right?
Where ADHD is no longer acting.
That's when you start to say, well, this person's probably at risk for over-correction.
Because that's like right there in front of you and you don't have to stick anybody,
they probably have a fully in, then theirs can just collect it, like it's easy.
But I would kind of do that in conjunction with checking the serum, right?
Like it's reassuring to see that the two, you know, kind of things going together, urine
awesomes dropping, serum sodium is rising.
You said, oh, this is the issue.
Because then you have an avenue to fix it, which is some DDAVP, right?
Just give them a dozen press in, which will act as ADHD stimulus, and you put the clamps
on so to speak, right?
And they will start reclaiming some more water in their tubules, and that will just slow
that process.
How do you feel about giving them DDAVP ahead of time, just avoiding the issue?
Yeah, I like it.
I think if you're worried about over-correction, especially in a scenario of hypovolemia like
this guy, I think it's a good idea.
128, I'm not terribly worried about, but certainly lower numbers.
I would probably be using it.
There's also a bit of like, who's at risk, you know, for bad outcomes during over-correction.
And it basically is a longer duration of hypovolemia is at higher risk.
People with low solute intake, you know, malnourished alcoholics, right?
People with, you know, these more chronic issues.
And then severity, right?
So if you're a sodium is 105 versus 125, like the 105 person is way more at risk, right?
So I just tend to be more cautious when those things are at play.
And there's really not a big downside to DDAVP.
So it's kind of one of those things where it's like, well, if you're concerned and you
don't want to worry about it, you should just give it and, you know, see what happens.
So let's talk about correction.
You know, so we decided in this guy, we didn't need to really worry about it.
We're just going to rehydrate him and volume or so that's a take him.
But let's say instead of 128, he's 110, or he's starting to show worse neurological
signs.
And he's saying seizures is your, I need to deal with this right now trigger, but maybe
something short of that, but something that makes you think that, you know, it's not necessarily
life and death emergency.
I drop everything, but we need to really kind of start getting things corrected.
What are your triggers for being a, I guess, more aggressive with correction?
And then how are you doing correction?
So there's probably debate on who you want to look at for this.
If you're going to correct, right?
Like correction is probably like a situational decision.
And let's say like for me, it's going to be, we're losing his mental status.
It's getting worse, right?
Like this is a guy that was like conversing.
He's not really oriented, but he's at least alert enough to talk to you.
Right.
Now if, you know, an hour later, he's like not doing it anymore.
I don't know, you know, maybe he's sort of got lower for some reason.
I don't know.
You just make it up, right?
But he's just looking worse and you're concerned for hyponatrenia.
I would say, yeah, it's probably reasonable to go ahead and treat that.
Or again, seizure is my big one.
These other things we can manage, right?
Like we can fix that issue and kind of correct when it's convenient, but seizure, right?
You can't just let somebody seize.
So if I were, if I were going to correct, like I said, it, it depends on what guidelines
you look at.
The American guidelines are, I don't want to say not great because there, there were
not a lot of people who came up with them.
So the quality of that recommendation is not terribly high.
The European ones are excellent.
It seems like they got everybody in Europe who knew anything about sodium to talk about
this.
So I would, if you're looking for a resource, I'd go to them over the American ones.
And they basically say give a somewhat of a bolus of, you know, a hypertonic 3% saline.
I think it's like 100 or 150 mils over 15 or 20 minutes.
And then check a serum sodium and then don't, don't stop.
Like give it again until, don't wait for your sodium to come back, right?
Give it, check it, give it some more until symptoms resolve or you be corrected by five
mil equivalents.
And there's a little drought there that says that, you know, most of these cases of true
symptomatic hyponatremia where we're trying to correct the problem such as, you know,
changes in severe changes in mental status or seizures.
They, they usually acquire about 500 mils of 3% given in somewhat bolus fashion.
You're not bolusing 500 mils, but you're giving it at 100, 150 mil aliquots until you
get a result that you like.
So, or you corrected by five or six mil equivalents.
At that point, you're kind of like, well, I'm not really sure this is hyponatremia.
Maybe there's something else to play.
Okay.
So, and you're using 3% for that?
3%.
Yeah.
Is there a role for more concentrated?
Um, could be like your 23 that you have in the neuro ICU stuff like that.
You know, at that point, you're just playing a volume gain, you know, so with 3% or there's
500 roughly five, you know, 513 mil equivalents per per liter.
Um, with 23, I think it's four mil equivalents per mil, right?
So you just can give less, you know what I mean?
Mm hmm.
Um, I can't do the math up top of my head to tell you how much how many mil equivalents
sodium is in, uh, you know, 150 mils of 3%, but you wouldn't have to get a whole lot of
23% to catch up with that.
Um, speaking from experience, good luck trying to get a hold of 23% anywhere outside of an
neuro ICU.
But, you know, while we're, uh, while we bring up the topic of neurocritical care, sometimes
when those patients, a question arises, you have a patient who is initially not hyponatremic.
Maybe they're completely normal, but you have acutely increased their sodium by the
same amount that you might worry about correcting them from hypo to, you know, closer to normal.
Like maybe they went from 140 to 155 in eight hours or something like that because you're
trying to treat, you know, their brain problems.
Do you think there is risk in those people of osmotic demyelination or it's really the
load of normal you worry about?
I think it's probably the load of normal.
Um, yeah, I mean, like theoretically, right?
That's there, uh, because your body is adapted to run it, you know, a certain osm load,
right?
Um, and if you change that acutely, something's going to happen.
Uh, but, you know, there's not mountains of literature out there that says, you know,
you have to worry about these, uh, cerebral edema patients, right?
Or somebody with a stroke or whoever that you raise their sodium 10 points and, you
know, they don't, they don't divine one eight.
Like I almost never heard of that.
So.
Sure.
I can't explain why that happens, but it's out there.
Yeah, I was going to say anecdotally, we do that a lot in the neuro ICU.
Yeah.
The drive people, people will come in with essentially normal sodium.
We'll drive them up to 145, 150, 155, even, uh, intentionally.
And I'm like, you have never heard of, um, demyelination occurring with that.
I've never seen the load church on that.
And, and like, I don't know why.
Yeah.
I mean, it's, I know this is different physiology here, but it's like the same principle of
like a hypoglycemia versus hyper, right?
Like for whatever reason, we just tend to not like the low range.
Can tolerate the high range a lot better.
So what about drugs?
Do you, are you ever employing specific medication agents to correct folks?
Or are you just predominantly just giving themselves?
Um, you know, like for SIIDH, um, we're, somebody's producing ADH and they really
shouldn't be, um, a loop diuretic, uh, can help.
Um, because believe it or not, they actually contribute to free water clearance.
Um, a thiazide will actually clear more sodium than, than, you know, a loop does, uh,
which is helpful in hypermetering.
Yeah.
But if you give them a little bit of lysics, they should clear a little bit of free water
and that should help.
But, you know, it comes down to like, why is your, why is your sodium low?
Right.
If it's just type of olemia, we'll give you fluid.
That's fluids drug, right?
In my mind, um, if it's SIIDH, like I said, maybe a little bit of lysics, but that really
comes down to fluid restriction, which can be very, very difficult, you know,
especially in some of these erotic patients where, you know, you look at their
free water clearance and they, they pee like 500 mils of free water a day.
We're like, I'm sorry, you can't drink anything.
You know, heart failure happened to me from that aspect.
It's treat the heart failure.
Right.
So whatever drug does you order that you want to recommend there?
I remember years ago when I was a nurse in the cardiac ICU, I gave a patient
told that Dan or hyponatremia.
Is that still a thing?
Do we do that?
And when's that?
I really don't know.
I mean, like I said, I don't deal with this.
I feel like that's a move with a specific goal in mind, which is usually
transplant because there's certain, you know, I think it's 125 or something that,
that they want you at or above to get a transplant.
Right.
So if this is just, you know, we're trying diuretics.
We're trying to treat your heart failure.
Nothing is working.
You know, we want you to get a heart transplant, right?
Like here we go.
Till about 10.
Right.
It's less common in the liver transplant world because
baptums have been associated with patectoxicity.
There may be some debate on how that was, how that originated, right?
They studied it in a lot of serotics and so had a lot of bad
liver outcomes.
Maybe they had liver failure for other reasons, but people tend to be
wary about giving baptans to serotics.
But, you know, it's been done.
You know, just monitoring is much more intense.
So.
So all right.
So you brought up SIEDH.
Um, let's talk about what I think are the three things that
sometimes confuse people when we're looking at hyponatremia,
SIEDH versus DI versus cerebral salt wasting.
Um, first of all, is it even necessary or even helpful to
distinguish between the three or do we just sort of treat the patient?
Sort of like we're doing with this guy, right?
We're just treating his sepsis and, or,
or is it more of an academic exercise to say this is a say to each versus
cerebral salt wasting versus DI?
Yeah, it's probably somewhere in the middle.
Um, cerebral salt wasting, right?
Like it's almost like a religion, if you believe in it or not.
Um, and there's like some evidence that says it exists.
And then like there's another camp that says like it's, it's not really there.
I'll just say I'm a, I'm agnostic on that one, right?
Because I don't really think it matters.
Just treat the patient, right?
Mm.
Um, look at the numbers and then kind of respond to that physiology, right?
If, if, if your and awesoms are high, like think about that and saying, what does that mean?
Right?
If you're, there's a bunch of sodium in your urine, right?
Think about that and say, well, what does that mean?
You know, this is maybe ATM, you know, they can't concentrate here.
I don't know.
Um, but, uh, and then SADH is also a little bit voodoo because I feel like if you
spend enough time, you could find a case report for a, for SADH that is due to
literally any cause you could think of, right?
Like, uh, from, you know, pain, the, the phase of the moon, like whatever, somebody
probably has blamed it on, you know, for SADH.
Um, so again, I, I just kind of look at the numbers and treat the, treat the
physiology there, right?
So SADH, when I said the numbers meaning low sodium, um, kind of low plasma
awesome.
So they're hypotonic, but they're relatively uvolemic, right?
They look like you and I, they're not hypotensive.
They're not orthostatic, right?
Uh, but they have, um, a high urine, awesome and a relatively normal urine
sodium.
They're not trying to hold on to fluid and have a low urine sodium, right?
Um, but if you see that person and you're like, Oh, wow, you, you just like
persistently, um, holding on to water for some reason.
Um, you can, you can, you can kind of sodium challenge them, right?
You get the leader of normal saline, which has a bunch of sodium in it and kind
of just see what happens, right?
If, uh, maybe they're just on the cusp of being dry, right?
Like they're just there and we just can't really detect that, right?
Because again, we're terrible at volume status assessments.
You give them a leader of saline.
Uh, if they're dry, their urine sodium really shouldn't change, right?
They should suck up all that urine sodium or law.
It's sodium go through the cadine.
It shouldn't really change.
If they're truly uvelemic, they'll dump that sodium because they don't want it.
Does that make sense?
So you do kind of a pre post and say, well, did this get better?
You know, did your serum sodium go up or down?
And then what happened to your urine sodium?
You know, because if you dumped it, then it's, it's SADH.
Also worth remembering that, um, if you give a leader of normal saline with a
awesome of 308, uh, to somebody whose urine, awesome is 600 because they're
80 Hs on, you know, is activated.
Uh, you're going to drop their sodium, right?
Because they will hang on to all of that water, get rid of all of that sodium.
And you'll just dilute them by, you know, a further leader.
So, um, if you're going to give something, it has to be higher than their urine
awesomes, which starts to become ridiculous.
Right.
So at that point, you just water restrict them or find a thing that's causing it.
So I think the, the upshot of all of this is if they're not seizing, then we
probably have time to think we don't need to get to bog down into numbers.
Um, if they are seizing, then that definitely needs to get corrected.
Cause like you said, all the Keprun in the world is not going to fix it.
They just need probably 3%.
We don't need to go crazy with the hot salts and, uh, that pans, et cetera.
Just some 3% voluses to kind of get them corrected to a stable place.
Uh, and then the reason behind their hyponatremia is important in that we
were looking for the sort of root cause that we can correct, but we don't need
to get necessary bogged down in the details of is this SIDH is this DI is this
cerebral salt wasting, et cetera.
So much is just treating the physiology of the patient we see.
Is that fair?
Yeah.
Like in, in this guy, if you guessed wrong and he does have SIDH and you're giving
him three liters of LR to fix his sepsis and resuscitate him in that regard.
And then you drop him.
You're like, Oh, we guessed wrong.
This is probably SAAH, right?
You just have to kind of look at physiology and think about it.
Like this is a very, in my mind, this is a very hard thing to like make into an
algorithm, right?
Um, I say, well, why does the sodium go down?
Uh, well, probably because his ADH is never going to get turned off.
It's always on, right?
Maybe he's serotic, maybe his heart failure, right?
And we're just missing that.
Um, just kind of go back and reassess.
And, and this is, I should repeat for everyone, just to stress this is in the
sort of general presentation of hyponatremia.
Uh, certainly we, we think of, at least in neuro, I see, we think of people who
get DI for brain reasons, right?
For pituitary problems or whatever.
And that's a little bit different of an animal, right?
And that their sodium is not necessarily altered.
Yeah.
Most of the time, DI will, you know, depending on how long goes on, we'll make
you hypernaturing that.
Yeah.
Right.
Because you're peeing out just a butt, you're, you don't have any, um, adh action, right?
So that's what DI is going to be.
Um, just a bunch of the urine because you can, can suck up that water.
So.
Yeah.
And in that case, you do want to give DDAVP, right?
Yeah.
That's the preferred one.
Uh, we actually, we had a recent case, um, where somebody had like a
cellar mass or something and, you know, they were peeing out like five
liters of water a day and their sodium was like 160.
And, um, there was a thought that put them on the vasopress and it's the same thing.
Right.
Mm-hmm.
Uh, you know, but it was, you have to change the dose.
Um, I can't remember what it is.
Right.
But it's not the usual, you know, point zero or three units per kilo or whatever
that we use for sepsis and shock.
Um, it's much higher than that.
So, um, that kind of.
Didn't, didn't click an anybody's mind for a minute.
And then, you know, when they fixed it, the higher dose of vasopressin, uh, it worked.
But, you know, you get to remember that a higher
vasopressin will also be a better, a better vasopressin.
Right.
And you might not want that.
Right.
So that's why DDAVP is probably just better.
It's easier.
Um, you, you're going to get a very focused response from that.
That's going to work.
So, yeah, usually a mic or two every, you know, four to six hours.
All right.
Well, I think we could easily wander into the world of hypernatremia if we're not
careful.
So, Brandon, do you have anything else you want to add?
Yeah.
As you said, there's probably another four episodes we could do exploring
different flavors of hyponatremia.
Um, one question for you just to briefly touch on the hypervolemic hyponatremia
is which, you know, people will usually say is maybe your, your
serotic patient and your heart failure patient.
Um, is there really anything to do about the hyponatremia in these cases as
far as actually treating it?
Or, I mean, is it, is it just kind of a marker of their disease?
And if you can treat their underlying disease and maybe it'll get better.
And this is just kind of an annoying lab that you'll keep seeing or is there
anything to do about it?
I kind of follow that, that second camp of this is just a bystander, right?
You're, it's part of their pathophysiology and you're probably not really
going to make it go away.
Um, they've adapted to it, right?
Uh, this is something, you know, they didn't end up being a decompensated
serotic overnight, right?
It took years and years without development.
You know, they've adapted to running around with sodium 120.
Yeah.
Um, that being said, uh, I think it's worth trying to improve, um, because it,
it does increase their, their risk of, um, having complications.
The lower it goes, right?
So if you can get it up by better managing their disease, then you should do that.
But if you've done everything you can and you think they're on optimal therapy,
and that's about as good as you can get, I wouldn't worry about it.
Right.
Like I wouldn't go give it, um, you know, hyper tonic is, because now you're giving
hyper, you're giving it a big sodium load to somebody that doesn't need sodium.
Do you think, I mean, talking about chronic states that you adapt to, uh, you
know, some of these other flavors are also pretty chronic.
Do you think that the chronic, you know, let's say that malnourished
patient, for instance, or the alcohol or whoever, do you think their chronic
hyponatremia is causing them problems?
If they're not like really obviously acutely altered or seizing or whatever,
and that fixing it will help them in some way.
Or are they just, it's like the chronically hypercarbic patient.
And we say is it bad if their CO2 is always 80, you know, probably not.
I mean, like, like from a hospital admission standpoint, probably not from a
life standpoint, it's not good.
You know, um, we know the chronic hyponatremia is associated with, uh, you
know, osteoporosis and bone loss, right?
Um, just off the top of my head, I can give you that.
Um, there's probably some other things that are, it's related to, right?
But everybody who lives in a normal range for a reason.
Right.
So if you're lower than that, then yeah, you're not going to be
obtunded, right?
If you're adapted to that, but there's a price to be paid somewhere.
Um, and over years, that's probably a main issue, but you're two week
hospital stay probably not that big of a deal, you know, I feel like more
people are kept in the hospital because there are sodium is 122.
We want it to be 125.
Well, it's interesting for some of those patients, uh, because if it's
related to something about their lifestyle, then very possibly they're
going to go into the same state when they're discharged, right?
I mean, if they go off, don't eat or drinking or whatever, unless you
discharge them on a salt tab or something.
I mean, it's,
Oh, yeah, 100%.
You know, as you bring up salt tabs, I feel like that's, uh, I feel like
you just shoot yourself in the foot with salt tabs with these, you know,
sidagers or chronic hyponatremia just because, um, salt makes you thirsty,
right?
Go into bag of potato chips and you're thirsty and then you drink a bunch
of water and now you're in a worse position for your sidh or your cirrhosis
or whatever you have, right?
So, um, I would tend to stay away from that.
Honestly, I don't, unless you're trying to like salt load somebody for a reason,
you know, to get them up.
Um, I probably wouldn't, wouldn't just say here, here's some salt.
So,
so even in your, your sidh patients in the hospital, you don't try to give them oral
salt.
No, cause it was just peed out, right?
Cause the sodium handling is separate, right?
It's the same thing with that example of giving the, the leader of sodium or that
leader of saline as a, as a bit of a challenge, right?
Their body's going to see that and say, I don't need it because it doesn't really
know that it's making adh when it shouldn't be.
So they'll, they'll take their three grams of salt tablets.
They'll temporarily raise their serum, which drives thirst.
They drink two liters of water.
Another sodium slower.
Well, you could fluid restrict them in the hospital.
You could.
I mean, you could, but that's a, it's probably a form of torture.
Right.
So.
So do you essentially do nothing for SIADH?
Uh, you want to try to find the underlying issue and fluid restrict.
But like I said, try to find the underlying issue some days.
It's like good luck out there.
But once where you get lucky is where there's a, you know, a well known, um,
offending agent and there's a timeline, right?
Like you look in, you know, in April, this person's sodium was normal in May,
they got started on an SSRI and in August, they came in with a sodium of 120.
You're like, Oh, okay.
Well, I bet it was the SSRI, you know, you stop it six months later.
It's normal.
You patch yourself on the back, you know, um, that's not every one of them.
But that's a good chunk, right.
Um, where you, you kind of stop a couple of agents and hope the best.
Um, but otherwise, you know, you're always pushing fluid restriction.
I had somebody who wants to tell me that fluid restriction works for all
hypodontremia, but it may not be a best idea in some cases, like we already
have a volumic.
So you, you brought up a good, an interesting point that I, that struck me
with something.
So you said, you know, you, you give these people salt and their kidneys,
don't want it.
They're just going to pee it out.
And we see that sometimes in the neuro ICU, when we, you know, attempt to sort
of empirically raise someone's sodium, because they have a lot of cerebral
demon typically young people, they don't have a lot of room to swallow their heads.
We want their sodiums high, but they also have good kidneys.
Uh, and we, let's set aside the debate of whether empirically raising
somebody's sodium to ward off cerebral edium is a good thing or not.
Cause we could, you know, I thought we were done a minute ago and we keep
going, but we'll really go for a long time if we go down that road.
But, you know, we'll, we'll give these folks.
One and a half percent, three percent.
And, and it's just not budging their, their sodium.
And sometimes we'll even pull out fludric cortisone.
What's the role of fludric cortisone in hyponatia?
Is there a role for it in treatment of hypo, true hyponatremia?
Uh, probably more from like, uh, you know, and adrenal insufficiency.
Right.
But, but then you're, you're going to usually globally adrenally insuffition,
right?
So you're not using fluidural alone, but right.
You just don't have that, a vostroin around, right?
You're trying to replace that, you know, that, that mineralic corticort activity.
Um, so it's probably more of a chronic thing, you know, acutely, I'm not really sure what it does
because it's a steroid and steroids take a long time to act, right?
They have to, it's gene transcription and protein synthesis, right?
It's probably not a thing that we're waiting around for in the ICU.
Yeah.
Um, I also kind of chucked on myself when people give flu, drug,
ESRD patients who haven't met urine in years, right?
Like, you have to make urine for it to work.
So, um, so there's that, but, uh, uh, I think, you know, your point is well taken that you're
trying to raise the sodium and people's kidneys are just peeling it out.
Um, I think one and a half percent is almost worthless, right?
Because you're just not, there's not a lot of bang for your buck there.
You would have to just give leaders and leaders and leaders, you know, to, to make a difference.
Three percent is, is more worthwhile.
Um, and I think this is where you get to your 23%.
Right.
Like if you're really in a hurry and you really feel like you need to do this, I think, you know,
some well controlled 23% is, is reasonable.
Um, especially in somebody with good kidneys because they are, they're just going to peed out.
Um, and you can, you can predict this.
You know, I think off top of my head, it's like you look at the, um, serum
sodium, I know what you're infusing minus the serum sodium divided by their total body water.
Right.
So, uh, if you're infusing 3% at 500 milligwevelins and you're trying to get them, you know,
well, you know, 140, right.
So 500 minus 140 over 42, whatever you do, the math there and you tell me how much you're going to go up.
It's, it's not by a whole lot.
Right.
Maybe one or two milligwevelins.
So you just have to give them a lot of leaders to make that change.
Um, so that's what I think something is 7th percent is kind of nice and
a mediary, right?
Uh, it's not going to be too caustic, right?
Because 23 is that that might damage themselves, you know, locally.
That's a lot.
It's an emergency use kind of situation.
Um, seven is nice and, you know, we push 7% all the time.
We're pushing by car bamps.
So, right.
That's eight, eight, four, so yeah, that's true.
Right.
So, uh, somewhere, somewhere in the middle ground is, is probably fine.
Well, like I said, I thought we were done and then we just got off on another whole thing.
And so before we get off on another whole thing and are here for another hour, I think we'll call it quits for today.
Um, thanks, Paul for coming on and talking to us about this.
Um, I think, uh, I feel better about this.
Maybe I don't know.
It seems simpler and yet at the same time more complicated because now I have to understand physiology and think about it.
The lesson I'm taking away is that you don't treat hyphenate, treat itself.
You know, most of the time it's probably true.
I want to say I feel like, uh, in the hospital, um, less is more sometimes and, you know, just, just kind of figuring out why something happens is more important than, um, you know, creating an action.
Right.
So that's spoken like a real internist.
Yeah.
Uh, thanks everybody for joining us as always.
As always, what we've said is this is just for educational purposes and hopefully you're not using us as your sole resource to treat your patients.
Uh, and our, this is our opinion, not representative of any of our respective institutions.
Thanks again and see you next time.
♪♪♪
you