Long Case with chronic Hyponatremia

This forum made possible through the generous support of SDN members, donors, and sponsors. Thank you.

Noyac

Full Member
15+ Year Member
Joined
Jun 20, 2005
Messages
8,022
Reaction score
2,815
67 yo female for Anterior and Posterior Spinal fusion level L2 - S1. H/0 HTN, poor exercise tolerance due to back pain but no cardiac symptoms. ECG WNL. Labs normal x Na 128. On BP meds and HCTZ. Past labs show hyponatremia for greater than 6 mon. Long case with fluid shifts, blood loss anywhere from 500 to 2000 cc.

Do you do the case?

What fluids do you use?

What lines, monitors?

Members don't see this ad.
 
What fluids do you use?

What lines, monitors?

Lactated Ringers (Na+ = 130), standard monitors + a-line, and two large bore IVs. Type and cross for four units.

Done this particular case NUMEROUS times in this same exact patient.

-copro
 
Members don't see this ad :)
67 yo female for Anterior and Posterior Spinal fusion level L2 - S1. H/0 HTN, poor exercise tolerance due to back pain but no cardiac symptoms. ECG WNL. Labs normal x Na 128. On BP meds and HCTZ. Past labs show hyponatremia for greater than 6 mon. Long case with fluid shifts, blood loss anywhere from 500 to 2000 cc.

Do you do the case?

What fluids do you use?

What lines, monitors?

Agree with dhb and cop.

Wouldnt put a central line in if I had 2 good peripherals.
 
cancel the case....the sodium is not normal...

patient needs to see a nephrologist, internist , & a cardiologist.....probably a neurologist too....because you can get central pontine myelinlysis with hyponatremia....

elective case....a stable back does you no good if your pons is lysed.

once all the consults are in, everyone can get together to have a multidisciplinary conference before proceeding....that ways everyone gets sued...and not just you.
 
get an oncologist onboard too because occult malignancies can present with hyponatremia...and maybe the mets are causing the back problems.
 
cancel the case....the sodium is not normal...

patient needs to see a nephrologist, internist , & a cardiologist.....probably a neurologist too....because you can get central pontine myelinlysis with hyponatremia....

elective case....a stable back does you no good if your pons is lysed.

once all the consults are in, everyone can get together to have a multidisciplinary conference before proceeding....that ways everyone gets sued...and not just you.
Exactly,
I also think that you need to check the literature to see if there is any case reports of weird things happening to such patient and include them in your discussions with all these consultants.
Good job MMD :)
 
cancel the case....the sodium is not normal...

patient needs to see a nephrologist, internist , & a cardiologist.....probably a neurologist too....because you can get central pontine myelinlysis with hyponatremia....

elective case....a stable back does you no good if your pons is lysed.

once all the consults are in, everyone can get together to have a multidisciplinary conference before proceeding....that ways everyone gets sued...and not just you.

uhhhhhhhhhhhhhhhhhhhhhhhhhhhhhh

HAHAHAHAHAHAHAHAHAHAHA

your wifey is a flea, mil......just consult her while you two are sippin' Gray Goose in bed.
 
cancel the case....the sodium is not normal...

patient needs to see a nephrologist, internist , & a cardiologist.....probably a neurologist too....because you can get central pontine myelinlysis with hyponatremia....

elective case....a stable back does you no good if your pons is lysed.

once all the consults are in, everyone can get together to have a multidisciplinary conference before proceeding....that ways everyone gets sued...and not just you.

Ya know, we laugh at this, but this is academia at it's finest. :barf::barf:
 
OK, those of you that want to do the case.

The case is going fine but the Na keeps dropping. 126, then 125 next 124. What now? Blood loss is getting up there, about 1500 ml.
 
OK, those of you that want to do the case.

The case is going fine but the Na keeps dropping. 126, then 125 next 124. What now? Blood loss is getting up there, about 1500 ml.

now why would it do that unless you are giving free water or you're peeing hypertonic saline?
 
Was the hctz continued?
As i see it you have blood loss, kidneys are seeing less volume retaining water in excess of Na due to the hctz.
Keep up with the blood loss since starting Hb was fairly low and give more Na eg plasmalyte.

Why was the Hb low to start with? any history of kidney disease?
 
now why would it do that unless you are giving free water or you're peeing hypertonic saline?

I can think of a couple of reasons.
1) glucocorticoid def. from epidural steroid injections.
2) Kidney disease leading to Na dumping/wasting
 
Members don't see this ad :)
Does anyone want to examine the pt? Will this help you make the call?

What if I said she had bibasilar rales and 2+ pitting edema?
 
What if she becomes acidotic from blood loss (unlikely if we are doing our job) are you going to give bicarb?
 
Bicarb will mask the pb not fix it so no: blood and fluids.

Correct, and it also carries a large Na load as well.

Can you think of a better alternative assuming your blood replacement isn't doing the trick and she is needing chemical support?
 
I can think of a couple of reasons.
1) glucocorticoid def. from epidural steroid injections.
2) Kidney disease leading to Na dumping/wasting

doesn't work that way.

1 & 2 will do what you say, but the patient must have access to free water....meaning not in surgery and able to drink.
 
Does anyone want to examine the pt? Will this help you make the call?

What if I said she had bibasilar rales and 2+ pitting edema?

then it doesn't matter what the sodium is.
 
Correct, and it also carries a large Na load as well.

Can you think of a better alternative assuming your blood replacement isn't doing the trick and she is needing chemical support?

Hyperventilate... stop the ringer's lactate which can falsely elevate your lactate level... uhh ... enhance perfusion, dobutamine?
 
SIADH crossed my mind. However from history there no good reason for her having it. UA would be useful if she wasn't on diuretics already.

I'm also considering it might be diuretic induced. I wonder how her K is. If they are both low I'll be more inclined to blame diuretics.

In absence of any real dx I would probably use normal saline and chase it with lasix as necessary.
 
doesn't work that way.

1 & 2 will do what you say, but the patient must have access to free water....meaning not in surgery and able to drink.

Are you sure about that?

I know how you will answer but I have seen steroid dependent pts have a fall in serum Na after surgery albeit rare, because we supplement them. I've also seen it after etomidate. Not sure of the cause at the time but worth noting.

Enough of this hyponatremia intraop, it was a hypothetical. Are you going to do the case? Was your answer sarcastic or real? We have a few that will do it and a few that want more info.
 
Hyperventilate... stop the ringer's lactate which can falsely elevate your lactate level... uhh ... enhance perfusion, dobutamine?

coco.gif
 
Are you sure about that?

I know how you will answer but I have seen steroid dependent pts have a fall in serum Na after surgery albeit rare, because we supplement them. I've also seen it after etomidate. Not sure of the cause at the time but worth noting.

Enough of this hyponatremia intraop, it was a hypothetical. Are you going to do the case? Was your answer sarcastic or real? We have a few that will do it and a few that want more info.


I'm sure..

Yes most patients will be slightly hyponatremic when they hit the ICU on post-op day 1....usually around 130...sometimes lower if they receive 1/2 ns over night...nature of stress hormones...but without access to free water, or have some intrinsic sodium wasting nephropathy, they just don't go much lower..

For a serum sodium to go lower, you have to lose more Na in your urine than your serum....urine sodium is rarely greater than 80 meq/liter,,,if that high

How low did your cases of hyponatremia go? Problem with some of the labs from the OR is that they are run on different machines than regular labs...although they are supposed to be the same, they frequently are not.

I'd do the case.
 
I'm sure..

Yes most patients will be slightly hyponatremic when they hit the ICU on post-op day 1....usually around 130...sometimes lower if they receive 1/2 ns over night...nature of stress hormones...but without access to free water, they just don't go much lower

How low did your cases of hyponatremia go? Problem with some of the labs from the OR is that they are run on different machines than regular labs...although they are supposed to be the same, they frequently are not.

I'd do the case.

Fair Enough. That 130 you stated comes from someone that was normal pre-op, this pt is 128. A 5 pt drop from 128 is significant. Ok Ok enough.

I spoke with the spine surgeon and he decided to "delay" the case 1 week and hold the HCTZ. She returned with a Na of 136 no edema or rales and stated that she felt better. Sure she felt better, she wanted to have surgery. Her case lasted about 7 hrs and we had an EBL of 3500. This is very unlikely for this surgeon but he thanked me afterwards for my insight. Did we do the right thing? Who knows, but she did fine with our approach. The funny thing is that I wouldn't have worried a bit about this Na level normally but this time I got a feeling and well the rest is history. Well she would have done fine either way, right.
 
Well she would have done fine either way, right.

Who knows? You may have gotten her out of the OR the other way, but she might have died 10 days later. And, while this may not have been attributed to you, it still might have been directly related to bringing her in early.

I still would've done the case. But, what the hell do I know. I'm just a CA-2.

-copro
 
The w/u of hyponatremia involves first determining plasma osmolality. secondly, you need to understand the pt's volume status. in this case we were not given plasma osm's. I would order that. the na, bun, glucose calcuation may or may not tell the whole story. there could be lipoproteins, paraproteins causing a normal plasma osmolality, etc. Assuming the pt.'s plasma osmolality is low, we then look at volume status. In this case, they appear to be volume overloaded, before we even start the case. By definition then, this is one of three things, nephrotic syndrome, cirrhosis, or chf. with the pulmonary findings, chf is highest on the differential. if the pt. had started euvolemic, then we have SIADH and it's mimcs (with thyroid dz, chronic HCTZ, etc, etc, in that differential). If the pt. is volume depleted, then they may simply be appropriately holding onto water.

Let's assume we have SIADH, then regardless of how the fluid is administered....be it isotonic IV fluids or worse yet, hypotonic (LR), or worst, free water by mouth or D5 etc)...they will drop their sodium. Indeed as mil points out, it's because they will create a concentrated urine given the ADH effect on the collecting duct. they key is recognizing that this can happen with our routine IVF.

Generally when pt.'s are chronically hyponatremic and symptom free, or Na >120 they do not need rapid correction. If there are symptoms (seizure, obtunation etc.) then the treatment calls for 3% saline with the goal to raise the sodium by no more than 12meq per 24 hours. This usually works out to be a 50cc bolus followed by 15cc/hr of hypertonic saline. If the potassium is also low, then you can often treat both problems simply by giving runs of K. As the K+ is taken up by the cells, water goes with it, thus dropping the serum Na. You need to then be careful you don't overshoot with the K, especially if your are also giving hot salt.

Would I do the case? No. It's elective, and I'd be concerned about my ability to monitor the electrolyte situation effectively. This is a problem that needs to be fixed slowly.

Central Pontine Myelinolysis occurs 4-5 days later, so you won't really know that you f'd up until it's well too late.

BNE
 
The w/u of hyponatremia involves first determining plasma osmolality. secondly, you need to understand the pt's volume status. in this case we were not given plasma osm's. I would order that. the na, bun, glucose calcuation may or may not tell the whole story. there could be lipoproteins, paraproteins causing a normal plasma osmolality, etc. Assuming the pt.'s plasma osmolality is low, we then look at volume status. In this case, they appear to be volume overloaded, before we even start the case. By definition then, this is one of three things, nephrotic syndrome, cirrhosis, or chf. with the pulmonary findings, chf is highest on the differential. if the pt. had started euvolemic, then we have SIADH and it's mimcs (with thyroid dz, chronic HCTZ, etc, etc, in that differential). If the pt. is volume depleted, then they may simply be appropriately holding onto water.

Let's assume we have SIADH, then regardless of how the fluid is administered....be it isotonic IV fluids or worse yet, hypotonic (LR), or worst, free water by mouth or D5 etc)...they will drop their sodium. Indeed as mil points out, it's because they will create a concentrated urine given the ADH effect on the collecting duct. they key is recognizing that this can happen with our routine IVF.

Generally when pt.'s are chronically hyponatremic and symptom free, or Na >120 they do not need rapid correction. If there are symptoms (seizure, obtunation etc.) then the treatment calls for 3% saline with the goal to raise the sodium by no more than 12meq per 24 hours. This usually works out to be a 50cc bolus followed by 15cc/hr of hypertonic saline. If the potassium is also low, then you can often treat both problems simply by giving runs of K. As the K+ is taken up by the cells, water goes with it, thus dropping the serum Na. You need to then be careful you don't overshoot with the K, especially if your are also giving hot salt.

Would I do the case? No. It's elective, and I'd be concerned about my ability to monitor the electrolyte situation effectively. This is a problem that needs to be fixed slowly.

Central Pontine Myelinolysis occurs 4-5 days later, so you won't really know that you f'd up until it's well too late.

BNE

I disagree...I don't care how high your ADH level is..If you are receive only Normal saline...you serum sodium CANNOT drop....You have to have access to free water...and if you are NPO, and receiving IVF..you are getting no free water.

Yes...we generate water through oxidative phosphorylation...but it's not enough to drop your serum sodium while receiving normal saline.
 
I disagree...I don't care how high your ADH level is..If you are receive only Normal saline...you serum sodium CANNOT drop....You have to have access to free water...and if you are NPO, and receiving IVF..you are getting no free water.

Yes...we generate water through oxidative phosphorylation...but it's not enough to drop your serum sodium while receiving normal saline.

I agree with Mil's disagreement.

And, furthermore, when did LR start being considered a "hypotonic" solution? It is slightly hyponatremic compared to plasma, but it is not hypotonic.

Looking forward to your explanation.

-copro

P.S. Sorry, reading most of the day today (and doing housework) while the GF is on-call... Now it's time to go boozin'. I'll catch up on the conversation tomorrow.
 
I agree with Mil's disagreement.

And, furthermore, when did LR start being considered a "hypotonic" solution? It is slightly hyponatremic compared to plasma, but it is not hypotonic.

Looking forward to your explanation.

-copro

P.S. Sorry, reading most of the day today (and doing housework) while the GF is on-call... Now it's time to go boozin'. I'll catch up on the conversation tomorrow.

I disagree with your disagreements. If the kidneys are working (which they are by definition in SIADH), they will excrete any excess Na+ and retain free water due to the actions of ADH. That's why the primary treatment for SIADH is fluid restriction (not just free water restriction); some will also give NS + lasix which causes the kidney to excrete 1/2NS and serum Na+ will rise.

Since we are mentally masturbating (I am at least:laugh:), here's an example to illustrate my point:

Pt. w/SIADH has a Uosm of 600 mOsm/L, you decide to give him 1L of NS which is ~ 300 mOsm. His normal kidney will excrete that osmolar load of NS in 500 ml of urine (300 mOsm given/600 mOsm/L = 0.5L = 500 ml) which results in the generation of 500 ml of free water. This is reabsorbed and our serum Na+ is worsened.
 
If someone has SIADH and you give normal saline in amounts exceeding the total fluid loss(including blood loss), the kidney will excrete the extra sodium and retain the extra water and the result would be worsening of hyponatremia.
If you just replace fluid loss with NS, there shouldn't be significant change of sodium level because replacing the deficit only is equivalent to fluid restriction in the awake drinking patient.
 
I disagree with your disagreements. If the kidneys are working (which they are by definition in SIADH), they will excrete any excess Na+ and retain free water due to the actions of ADH. That's why the primary treatment for SIADH is fluid restriction (not just free water restriction); some will also give NS + lasix which causes the kidney to excrete 1/2NS and serum Na+ will rise.

Since we are mentally masturbating (I am at least:laugh:), here's an example to illustrate my point:

Pt. w/SIADH has a Uosm of 600 mOsm/L, you decide to give him 1L of NS which is ~ 300 mOsm. His normal kidney will excrete that osmolar load of NS in 500 ml of urine (300 mOsm given/600 mOsm/L = 0.5L = 500 ml) which results in the generation of 500 ml of free water. This is reabsorbed and our serum Na+ is worsened.

that is just plain wrong....

600 mOsm/L in the urine does not equate 600 meq /l of sodium in the urine.

go to the hospital and check ALL of the Urine sodium labs that have EVER been ordered in the computer...see if you can find one that has 600 meq/l of sodium

The body generates 10 to 15 mosm/kg/day of osmotic waste...most of which is not sodium.

SIADH does not alter the kidney's ability to handle sodium. Sodium flux in patients with SIADH is normal, meaning they take in 2 to 4 grams of sodium per day, and they excrete 2 to 4 grams of sodium per day.

Free water handling is altered....they keep in their body relatively more water than they should, leading to hyponatremia
.

What you are describing is cerebral salt wasting syndrome where you excrete more sodium than water, and the treatment for that is hypertonic saline....otherwise you get vasospasm and stroke and then die.
 
If someone has SIADH and you give normal saline in amounts exceeding the total fluid loss(including blood loss), the kidney will excrete the extra sodium and retain the extra water and the result would be worsening of hyponatremia.
If you just replace fluid loss with NS, there shouldn't be significant change of sodium level because replacing the deficit only is equivalent to fluid restriction in the awake drinking patient.


SIADH is not a disorder of sodium handling.
 

Here is how it goes:
If you give excess sodium to someone with normal kidneys (with or without SIADH) it will be eliminated by the kidneys until you reach a point where your sodium input overwhelms the ability of the kidney to eliminate it, this is when the sodium starts rising as in the case of giving hypertonic saline.
The only difference in SIADH is that the balance is shifted toward retaining water and this keeps the sodium level at a lower number than normal as long you provide fluids equal to fluid loss.
If you exceed fluid loss (Deficit + Loss) you will worsen the hyponatremia because more water will be retained.
If you restrict fluids to less than fluid loss your sodium will start rising and this is where the concept of fluid restriction to treat SIADH comes from.
 
Quote:
Originally Posted by bne_12mne
Off the top of my head...


Yeah right!
Try Tarascon pocket IM...


Urge, Well you're right, that's the source I've used a million times. But I didn't have it right in front of me.

One of the things I did many times over as a medicine intern is work-up hyponatremia, so I guess it has stuck!

I agree with Mil that SIADH (and hyponatremia in general) is a problem with water handling. Also sodium handling is normal. In SIADH, patients are euvolemic therefore they are not particularly sodium avid, because aldosterone secretion is much more responsive to ecfv than to serum osmolality. And I also still contend that a patient with SIADH can (and will) get more hyponatremic from giving normal saline. The reason is that the osmolality of their urine is fixed and high. So giving an isotonic solution to someone creating hypertonic urine will decrease the tonicity of the plasma by the addition of free water and drop their plasma sodium concentration.

BNE
 
Quote:


IAnd I also still contend that a patient with SIADH can (and will) get more hyponatremic from giving normal saline.

BNE
This will only happen if you give more normal saline than the total fluid loss.
as long as you replace the fluid loss only (Loss + Deficit) the serum sodium will not change.
 
If someone has SIADH and you give normal saline in amounts exceeding the total fluid loss(including blood loss), the kidney will excrete the extra sodium and retain the extra water and the result would be worsening of hyponatremia.
If you just replace fluid loss with NS, there shouldn't be significant change of sodium level because replacing the deficit only is equivalent to fluid restriction in the awake drinking patient.

SIADH is not a disorder of sodium handling.

:confused:
Where did I say that SIADH is a disorder of sodium handling?

right there...if you are excreting "extra sodium", then you are excreting sodium in a disordered manner like cerebral salt wasting syndrome which SIADH is not and treatment is diametrically opposite.
 
Quote:
Originally Posted by bne_12mne
Off the top of my head...


Yeah right!
Try Tarascon pocket IM...


Urge, Well you're right, that's the source I've used a million times. But I didn't have it right in front of me.

One of the things I did many times over as a medicine intern is work-up hyponatremia, so I guess it has stuck!

I agree with Mil that SIADH (and hyponatremia in general) is a problem with water handling. Also sodium handling is normal. In SIADH, patients are euvolemic therefore they are not particularly sodium avid, because aldosterone secretion is much more responsive to ecfv than to serum osmolality. And I also still contend that a patient with SIADH can (and will) get more hyponatremic from giving normal saline. The reason is that the osmolality of their urine is fixed and high. So giving an isotonic solution to someone creating hypertonic urine will decrease the tonicity of the plasma by the addition of free water and drop their plasma sodium concentration.

BNE

not only wrong, but also physiologically impossible.

tell me where the free water is coming from or where the "extra" sodium is going.

Urine Osm may be high, but Urine sodium content is not....Have you EVER measured a Urine sodium that is greater than 150 meq/liter??????

I don't ever even remember EVER seeing a urine sodium content > 50 meq/liter.

You are confusing Uosm with Usodium.

There are many OTHER osmoles/osmotic waste that goes in the urine....urea being one....you think that's why it is called urine??
 
right there...if you are excreting "extra sodium", then you are excreting sodium in a disordered manner like cerebral salt wasting syndrome which SIADH is not and treatment is diametrically opposite.
No, What I am saying is that if you give more sodium than the sodium loss that extra sodium is going to be excreted by the kidney and the serum Sodium will not change unless you overwhelm the kidney's ability to excrete sodium.
The bottom line:
If you only give normal saline to cover fluid (water and sodium) loss there will be no change in serum sodium.
 
And if you give more normal saline than the fluid loss (water and salt loss) the kidney is going to excrete the extra sodium and retain the extra water and the hyponatremia will get worse.
It's a question of quantity.
 
And if you give more normal saline than the fluid loss (water and salt loss) the kidney is going to excrete the extra sodium and retain the extra water and the hyponatremia will get worse.
It's a question of quantity.

no..NO NO....your explanation of sodium/water metabolism is ALL WRONG.

Normal saline can NEVER cause hyponatremia unless patient has access to free water....or

UNLESS

Urine Sodium is GREATER than 154 meq/liter....and if ANYONE has EVER seen a measured Urine Sodium GREATER than 154 meq/liter than POST UP....I want to hear about it...

I'm willing to bet that in my years of practicing CCM, I have ordered, sent off, and evaluated more Urine Sodium concentrations than ANYONE on this board.
 
Great thread, guys. Good discussions.

And, just to reiterate, we are talking about a patient who was stable with their Na+ level over a several month period of time, not someone who got konked on the head or stroked-out recently. There's no reason to believe that the stress of surgery is going to significantly alter the serum osmolality of this patient, no matter how long or what fluid is given (unless it is excessive). I certainly would minimize the free water, though. That is what will drop the serum Na+ level more than anything during a short procedure. Post-op management may be a different story. And, listen to what Mil is saying. He's right on in this thread.

-copro
 
And if you give more normal saline than the fluid loss (water and salt loss) the kidney is going to excrete the extra sodium and retain the extra water and the hyponatremia will get worse.
It's a question of quantity.

Extra WATER????
pillepalle.gif



what are you talking about? There is no "extra water" in normal saline...by definition there is NO "extra water" in NORMAL Saline..... FREE WATER is a better term...and it exists only in hypotonic crystalloids.
 
Urine sodium concentration in SIADH is equal to sodium intake until you reach a point where the kidney can not concentrate urine any further this is when your theory works and NS actually will not decrease serum sodium.
But usually urine sodium in SIADH will be anything above 40 meq and in that range extra sodium delivered by giving extra normal saline is going to be eliminated and water will be retained.
Why are assuming that the urine sodium had already reached maximum (let's say 154) in every SIADH patient?
 
Extra WATER????
pillepalle.gif



what are you talking about? There is no "extra water" in normal saline...by definition there is "extra water" in NORMAL Saline..... FREE WATER is a better term...and it exists only in hypotonic crystalloids.
Wrong!
Saline is water and salt, Extra saline is extra water and extra salt!
Or let's say extra free water and extra salt!
By extra I mean anything more than the loss.
 
Great thread, guys. Good discussions.

And, just to reiterate, we are talking about a patient who was stable with their Na+ level over a several month period of time, not someone who got konked on the head or stroked-out recently. There's no reason to believe that the stress of surgery is going to significantly alter the serum osmolality of this patient, no matter how long or what fluid is given (unless it is excessive). I certainly would minimize the free water, though. That is what will drop the serum Na+ level more than anything during a short procedure. Post-op management may be a different story. And, listen to what Mil is saying. He's right on in this thread.

-copro
The ongoing discussion is not about the initial patient and I do apologize if you guys don't want to go any further than what MMD satated, I will not discuss it any further.
 
Top