Long Case with chronic Hyponatremia

[coprolalia]

Advertisement - Members don't see this ad

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.

No way, doc. This is a good discussion. Whatever hijack or derailment occurs, it's still important. This is how we learn. By disagreeing and discussing things. The whole SIADH, DI (central or nephrogenic) and shift of osmolality are important concepts. Just gotta keep it polite. So, discuss away!

-copro

 

[militarymd]

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?

Once again...what are you talking about?

How can sodium concentration (expressed in meq/liter) be equated with sodium intake (expressed in grams)...

Ur sodium can be high or low in SIADH...it is dependent on total sodium intake.

You are WAY out of your league here.

 

[SexPanther]

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.

Mil,

I don't like to argue electrolytes and fluids with a CCM stud like yourself as I am just an intern, but what I said in my quote is absolutely true. I am not talking about the urine concentration of sodium. This is determined by the patients diet in this disease. SIADH is all about the inability to dilute the urine and excrete free water. By definition, it has a low serum osm, inappropriately elevated urine osm and Una > 20 with normal renal, liver, adrenal and thyroid function.

Human beings have to have solute load in order to excrete free water. Normal subjects will consume at least 10 mmol/kg/day of solute; and excrete whatever they consume to preserve steady state. A 60 kg subject will consume 600 mmol/day and needs to excrete the same amount. In a normal kidney, the maximum urine concentration is 1200 mOSm (mmol)/L and the minimal (most dilute) concentration is ~60 mOSm (mmol)/L. Thus that 60 kg subject could excrete as little as 0.5L (600/1200) of urine or as much as 10L (600/60) of urine based on physiologic need to retain free water. This is why beer potomania has hyponatremia. Those pts. only take in ~3 mmol/kg/day for a total of 180 mmol and can thus only excrete 3L of free water at maximal dilution. If they drink more than 3L they will be hyponatremic. If a pt. has difficulty suppressing ADH then he will not be able to dilute his urine and his ability to excrete free water will significantly decrease.

Hence the example I used in my previous post; it assumes that there is no sodium deficit as SIADH has normal total body salt concentrations. The NS provides an ~300 mOsm solute load in 1 liter in a pt. without any problems with sodium handling. The pt. has a urine osm of 600 mOsm, thus 500 cc of the liter bolus is used to achieve equal concentration with that of his urine. The remainder is reabsorbed as free water and can worsen hyponatremia. This is an example straight from one of my mentors who is a nephrologist. I'm actually skiing right now, I you need me to give some direct quotes from papers or books I will when I get home.

You are correct in that CSW mimics SIADH. It often also has low serum osm, inappropriately high Uosm, and Una >20. The kicker with it is that these pts. are almost always hypovolemic, not euvolemic such as in SIADH. In our neuro ICU, any and all hyponatremia is treated 1st and foremost as CSW b/c as you alluded to the treatment is much different. These patients get enteral salt and often 3%NaCl, while SIADH will get only fluid restriction.

Great discussion fellas.

 

[militarymd]

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.

As I said....you are out of your league here

 

[militarymd]

Mil,

I don't like to argue electrolytes and fluids with a CCM stud like yourself as I am just an intern, but what I said in my quote is absolutely true. I am not talking about the urine concentration of sodium. This is determined by the patients diet in this disease. SIADH is all about the inability to dilute the urine and excrete free water. By definition, it has a low serum osm, inappropriately elevated urine osm and Una > 20 with normal renal, liver, adrenal and thyroid function.

Human beings have to have solute load in order to excrete free water. Normal subjects will consume at least 10 mmol/kg/day of solute; and excrete whatever they consume to preserve steady state. A 60 kg subject will consume 600 mmol/day and needs to excrete the same amount. In a normal kidney, the maximum urine concentration is 1200 mOSm (mmol)/L and the minimal (most dilute) concentration is ~60 mOSm (mmol)/L. Thus that 60 kg subject could excrete as little as 0.5L (600/1200) of urine or as much as 10L (600/60) of urine based on physiologic need to retain free water. This is why beer potomania has hyponatremia. Those pts. only take in ~3 mmol/kg/day for a total of 180 mmol and can thus only excrete 3L of free water at maximal dilution. If they drink more than 3L they will be hyponatremic. If a pt. has difficulty suppressing ADH then he will not be able to dilute his urine and his ability to excrete free water will significantly decrease.

Hence the example I used in my previous post; it assumes that there is no sodium deficit as SIADH has normal total body salt concentrations. The NS provides an ~300 mOsm solute load in 1 liter in a pt. without any problems with sodium handling. The pt. has a urine osm of 600 mOsm, thus 500 cc of the liter bolus is used to achieve equal concentration with that of his urine. The remainder is reabsorbed as free water and can worsen hyponatremia. This is an example straight from one of my mentors who is a nephrologist. I'm actually skiing right now, I you need me to give some direct quotes from papers or books I will when I get home.

You are correct in that CSW mimics SIADH. It often also has low serum osm, inappropriately high Uosm, and Una >20. The kicker with it is that these pts. are almost always hypovolemic, not euvolemic such as in SIADH. In our neuro ICU, any and all hyponatremia is treated 1st and foremost as CSW b/c as you alluded to the treatment is much different. These patients get enteral salt and often 3%NaCl, while SIADH will get only fluid restriction.

Great discussion fellas.

I understand what you are saying there, but that is under several assumptions:

1) that the ONLY solutes in the urine is Sodium
2) that Urine osm cannot go lower than 600mOsm/liter in SIADH...it can
3) free water is not lost anywhere else...respiration, sweat, etc.

Under those strict "assumptions, then yes , your serum sodium can go down more with Normal saline...but ask yourself this....have you EVER seen a measured Ur sodium of 600!!!

But I have personally never seen this happen....have you?

You've got the book stuff pretty down pat....especially for Vanderbilt guy🙂

 

[Planktonmd]

Once again...what are you talking about?

How can sodium concentration (expressed in meq/liter) be equated with sodium intake (expressed in grams)...

Ur sodium can be high or low in SIADH...it is dependent on total sodium intake.

You are WAY out of your league here.

I meant that: sodium concentration X urine output = sodium intake.
Why do I have to spell everything for you?
I thought you understood what I was saying but you as usual try to divert the discussion into minute details to confuse the whole picture.
And what league is that you are talking about?
I would say you are out of your league because you claim to be an intensivist and you seem to have issues with very basic concepts.
By accusing me of being out of my league it doesn't make you right.
I am not going to get dragged into an endless exchange with you this time because you will always try to turn it personal when you have nothing to say so keep on the good work.

 

[militarymd]

I meant that: sodium concentration X urine output = sodium intake.
Why do I have to spell everything for you?
I thought you understood what I was saying but you as usual try to divert the discussion into minute details to confuse the whole picture.
And what league is that you are talking about?
I would say you are out of your league because you claim to be an intensivist and you seem to have issues with very basic concepts.
By accusing me of being out of my league it doesn't make you right.
I am not going to get dragged into an endless exchange with you this time because you will always try to turn it personal when you have nothing to say so keep on the good work.

Allow me to clarify then.

When there's a bunch of doctors discussing a complicated patient, sometimes there is one doctor, usually a primary care MD, or an intern, who doesn't know what's going on, but will enter into the conversation as if he/she knows what's going on.

That doctor..."is out of the league"

In this case, Sexpanther (an intern with a possible Vanderbilt sydrome handicap) is NOT the person who's "out of the league".

I'll leave it at that.




On a serious note though...you really don't know what you're talking about.

 

[Planktonmd]

Allow me to clarify then.

When there's a bunch of doctors discussing a complicated patient, sometimes there is one doctor, usually a primary care MD, or an intern, who doesn't know what's going on, but will enter into the conversation as if he/she knows what's going on.

That doctor..."is out of the league"

In this case, Sexpanther (an intern with a possible Vanderbilt sydrome handicap) is NOT the person who's "out of the league".

I'll leave it at that.




On a serious note though...you really don't know what you're talking about.

🙂
Allow me to clarify then:
I actually think that you are extremely dangerous because the way you present yourself on the internet might convince some of the young guys that you know what you are talking about and they might actually follow your teachings.
So here it comes:
A word of caution to the residents:
MMD is a controversial and amusing guy, the kind of guy you want to have on an internet forum but please verify everything he says.
One last note about the subject of this discussion:
The simple and practical conclusion is that in a patient with SIADH when you are replacing fluids intravenously, initially the serum sodium is not going to change because you will simply be replacing loss, once that is achieved giving more NS will decrease serum NA because the kidney will retain water and excrete sodium until you reach a point where the kidney is not going to concentrate the urine any further and this is when giving more saline will actually increase serum sodium.

 

[urge]

Damn!! I mentioned SIADH and suddenly all hell broke loose! I didn't know I could have that effect.

 

[VentdependenT]

Noy, you're a smart dude. Whatever you did worked.

I friggen detest discussing hypo/hypernatremia. Dialysis dude. Dialysis. It fixes everything.

As for the ONC consult, hell yah. I'm gonna get one on everyone with myofascial/musculoskeletal pain! Screw it, I'm getting pre-op bone scans for everyone. Crap, next time somebody sweats I'll order 123MIBG and octreotide scans along with Urine 5HIAA test to R/O carcinoid. Fuggit everyone gets an MRI and an ECT!

ECT's should lower MAC right? Less agent equals less mycardial depression!

 

[bne_12mne]

It's rather ironic that this discussion about hyponatremia and urine sodium has ultimately become a pissing match...

Anyway, I don't know how to resolve the dilemma that Mil has proposed, but it would seem to me that if you continue to give normal saline, an isotonic solution, and you continue to create a concentrated urine due to SIADH, you will eventually drive down the plasma tonicity regardless of whether the actual sodium concentration changes. I guess your BUN will go down?! Fortunately BUN is not an effective osmole, so it don't know that this means much clinically. You will also end up creating a patient who was once euvolemic with SIADH into one who is now hypervolemic with SIADH, and though the sodium concentration may stay unchanged or even rise, you have not really solved the problem. So it becomes, cough, cough, academic.

Good discussion, although I don't have any more to add now that I've become out of my league.

BNE