Why does Na drop in DKA?

[Boatswain2PA]

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Patient today - 21 yo type 1 diabetic train-wreck (GCS of 4). Na was 124 and I'm trying to figure out why.

Here's what I remember.

BP 50/38, P180, R30+
BS 1390 (after 20 units Insulin)
K 9.2
ABGs were horrible, only thing I remember was pH of 6.72
Urine was clean, but sweet (1000 glucose) .

Don't remember specifics of other lab values, but they all made sense and could be chalked up to sepsis/DKA.

I just can't figure out why the Na was 124. I read that Sodium drops by 1 per 62 glucose up to 400, and 1:24 for glucose over 400, but I don't understand why. Pt was incredibly dry so beans would use sodium reuptake to conserve water. Plus through hemoconcentration I would expect a higher sodium concentration.

So I can't understand why the sodium was at 124. Can anyone help out?

 

[Paseo Del Norte]

Patient today - 21 yo type 1 diabetic train-wreck (GCS of 4). Na was 124 and I'm trying to figure out why.

Here's what I remember.

BP 50/38, P180, R30+
BS 1390 (after 20 units Insulin)
K 9.2
ABGs were horrible, only thing I remember was pH of 6.72
Urine was clean, but sweet (1000 glucose) .

Don't remember specifics of other lab values, but they all made sense and could be chalked up to sepsis/DKA.

I just can't figure out why the Na was 124. I read that Sodium drops by 1 per 62 glucose up to 400, and 1:24 for glucose over 400, but I don't understand why. Pt was incredibly dry so beans would use sodium reuptake to conserve water. Plus through hemoconcentration I would expect a higher sodium concentration.

So I can't understand why the sodium was at 124. Can anyone help out?

Glucose is osmotically active and causes an intracellular to extracellular shift of water. This acts to effectively "dilute" the Sodium. However, you should run your Sodium through a correction formula in any event. If the corrected Sodium is low, you need to consider other issues such as elevated lipids.

 

[chimichanga]

Wow...I used to love ER, for that very type of pt.

Now all I can ask is, why the he!! didn't someone bring him in a couple days earlier??

That kind of pt is EXACTLY the reason why I left the damn ER for good.

That poor guy was just festering (dying) at home

FUBAR

 

[Boatswain2PA]

Glucose is osmotically active and causes an intracellular to extracellular shift of water. This acts to effectively "dilute" the Sodium. However, you should run your Sodium through a correction formula in any event. If the corrected Sodium is low, you need to consider other issues such as elevated lipids.

I've got that, but then doesn't the extracellular/intravascular water just diurese away? This kid was DRY, and the first liter of fluid we put in him went right through him.

So if it shifts, then is diuresed away, then the only thing I can think of is the active Na reuptake pumps in proximal tubules shut down due to lack of available energy.

 

[deleted6669]

for every 50 glucose over 200 add 1 to sodium

 

[Boatswain2PA]

for every 50 glucose over 200 add 1 to sodium

I read that too (with some sources saying to vary it, with a +1 per 62 for up to 400, and a +1 per 45 or so over 400)....but I'm just not getting the physiology behind it.

I'll keep digging. Thanks!

 

[Paseo Del Norte]

Remember, you can pull a hell of a lot of fluid from the intracellular space in spite of the diuresis. I imagine this patient was experiencing significant intracellular dehydration.

 

[primadonna22274]

Look at your potassium. Remember the K+-Na+ exchange?
High glucose is hyperosmotic, and drives water intracellularly. Sodium follows water. For every 3 Na+ you push into the cell, 2 K+ are forced out of the cell and into the ECF.
You are measuring serum lytes, so serum K+ is high, serum Na+ is low compensatorily.
Hyperkalemia drives acidosis.
Remember what your chloride is doing? The Na+ gradient drives Cl- intracellularly. Hence hypochloremia in serum.
Insulin drives K+ into cells. Lack of insulin causes reflux of K+ extracellularly, as does hyperosmolarity due to severe hyperglycemia. None of these electrolytes have disappeared, they have just shifted.
That's to say nothing of the complicated dance of acid-base chemistry that's going on in response to the wild electrolyte shifts.
I highly recommend Costanzo's Physiology text...makes all this so much easier. 🙂

 

[facetguy]

Not sure how closely this applies, but there's a phenomenon called natriuresis of fasting, aka natriuresis of starvation that occurs during periods of very low carbohydrate consumption. I'd think that DKA would have similar effect. In these conditions, the kidneys dump sodium. The mechanism was worked out in the '70s and is thought to relate to anion/cation balancing. Here's one reference:
http://www.jci.org/articles/view/107941

This is such a common scenario among very low carb dieters (<50 grams/day) that low carb researchers and clinicians recommend these folks drink boullion to replete with sodium.

 

[JoBreeze]

.

 

[bchurchmanpac]

Typically the initial sodium on lab testing is FALSELY low due to the elevated Glucose...see above post about sodium correction...due to the way the lab measures sodium....also as noted above...we often pay little initial attention to the sodium because in DKA your going to give several liters of 0.9% NS in the initial namagement therefore specific management of sodium is not needed until your in the ICU. Lastly, as noted above, due to the acidosis driving potassium out of the cell, you must pay closer attention to potassium, even if the initial potassium level is normal this would be falsely ELEVATED, so when you start treating the DKA with Insulin, the already slightly low potasium will move intracelluar and you may experience the consequences of hypokalemia.

 

[Boatswain2PA]

Look at your potassium. Remember the K+-Na+ exchange?
High glucose is hyperosmotic, and drives water intracellularly. Sodium follows water. For every 3 Na+ you push into the cell, 2 K+ are forced out of the cell and into the ECF.

I don’t think that is right. The Na+/K+ exchange is an active pump requiring ATP, not a passive osmotic pump. And water osmotically follows sodium, especially in the tubules which is why the active sodium reuptake pumps in the proximal tubule is a primary factor in water balance.

You are measuring serum lytes, so serum K+ is high, serum Na+ is low compensatorily.

I still don’t see the connection between true hyperkalemia and true hyponatremia. I don’t think it is because of the ATPase Na+/K+ pump like you proposed, especially in a kid whose metabolism was so low (core temp 85.5*).

Hyperkalemia drives acidosis.

I think you have this backwards as well….acidosis causes hyperK. HyperK secondary to renal dz can be found concomitantly with acidosis, but that is also secondary to renal dz. Acidosis, on the other hand, can push H+ ions into the cell and thus pushes K+ out of the cell….right??

Remember what your chloride is doing? The Na+ gradient drives Cl- intracellularly. Hence hypochloremia in serum.
Insulin drives K+ into cells. Lack of insulin causes reflux of K+ extracellularly, as does hyperosmolarity due to severe hyperglycemia. None of these electrolytes have disappeared, they have just shifted.
That's to say nothing of the complicated dance of acid-base chemistry that's going on in response to the wild electrolyte shifts.
I highly recommend Costanzo's Physiology text...makes all this so much easier. 🙂

I don’t remember what his Cl was so I don’t think it was wildly off. I understand K+ requires insulin/glucose to enter the cells. Just don’t understand why Na+ would be truly low. Thanks for the reference, I’ll try to find it.

Typically the initial sodium on lab testing is FALSELY low due to the elevated Glucose...see above post about sodium correction...due to the way the lab measures sodium....also as noted above...we often pay little initial attention to the sodium because in DKA your going to give several liters of 0.9% NS in the initial namagement therefore specific management of sodium is not needed until your in the ICU. Lastly, as noted above, due to the acidosis driving potassium out of the cell, you must pay closer attention to potassium, even if the initial potassium level is normal this would be falsely ELEVATED, so when you start treating the DKA with Insulin, the already slightly low potasium will move intracelluar and you may experience the consequences of hypokalemia.

So the Na+ is falsely low due to lab measurement techniques in the face of severe hyperglycemia. That is what I inferred in my reading (ie: the sodium correction formulas), but I never found a source saying that we did the correction formula because of lab technique. That makes complete sense now (ie: Sodium is there, lab magic just can’t find it amongst all the sugar).

Got the rest of it. I wasn’t worried about the sodium level, just couldn’t understand WHY it was so low (makes sense now).

Thanks for all of your help!

 

[Instatewaiter]

Wow there is a lot of wrong information on this thread.


There are 2 reasons why there is hyponatremia:
1. Glucose is osmotically active. It pulls intracellular water into the vascular space and "dilutes" the sodium. As you correct the glucose, so too corrects the sodium

2. DKA is a volume depletion state. So in addition to the main reason (#1), you also have whole body hypovolemic hyponatremia. Normally, the kidneys reabsorb all of the glucose in the proximal tubules. However, above roughly 250mg/dl, the Sodium-Glucose absorber is overwhelemed and you start dumping glucose into the urine. This glucosuria causes diuresis and volume depletion.

Why is there hyperkalemia?
- It has nothing to do with the Na-K ATPase. The ketosis causes an acidosis. Our cells have an H-K exchanger. So, the acidosis causes dumping of intracellular potassium into the extracellular space. Once you start treating with insulin the hyperkalemia goes away quickly for 2 reasons:, the acidosis goes away (causing the H-K to reverse directions) and the insulin itself causes movement of K into the cells again.

Look at your potassium. Remember the K+-Na+ exchange?
High glucose is hyperosmotic, and drives water intracellularly. Sodium follows water. For every 3 Na+ you push into the cell, 2 K+ are forced out of the cell and into the ECF.
You are measuring serum lytes, so serum K+ is high, serum Na+ is low compensatorily.
Hyperkalemia drives acidosis.
Remember what your chloride is doing? The Na+ gradient drives Cl- intracellularly. Hence hypochloremia in serum.
Insulin drives K+ into cells. Lack of insulin causes reflux of K+ extracellularly, as does hyperosmolarity due to severe hyperglycemia. None of these electrolytes have disappeared, they have just shifted.
That's to say nothing of the complicated dance of acid-base chemistry that's going on in response to the wild electrolyte shifts.
I highly recommend Costanzo's Physiology text...makes all this so much easier. 🙂

SWING AND A MISS on so many levels.

So the Na+ is falsely low due to lab measurement techniques in the face of severe hyperglycemia. That is what I inferred in my reading (ie: the sodium correction formulas), but I never found a source saying that we did the correction formula because of lab technique. That makes complete sense now (ie: Sodium is there, lab magic just can't find it amongst all the sugar).

Got the rest of it. I wasn't worried about the sodium level, just couldn't understand WHY it was so low (makes sense now).

Thanks for all of your help!

It is not so much a lab error. They are correctly measuring the sodium. It is unlike the old lab errors with severe hypertriglyceridemia (which no longer happen). The issues are glucose causing fluid shifts and whole body dehydration (not just intravascular).

 

[Instatewaiter]

Patient today - 21 yo type 1 diabetic train-wreck (GCS of 4). Na was 124 and I'm trying to figure out why.

Here's what I remember.

BP 50/38, P180, R30+
BS 1390 (after 20 units Insulin)
K 9.2
ABGs were horrible, only thing I remember was pH of 6.72
Urine was clean, but sweet (1000 glucose) .

Don't remember specifics of other lab values, but they all made sense and could be chalked up to sepsis/DKA.

I just can't figure out why the Na was 124. I read that Sodium drops by 1 per 62 glucose up to 400, and 1:24 for glucose over 400, but I don't understand why. Pt was incredibly dry so beans would use sodium reuptake to conserve water. Plus through hemoconcentration I would expect a higher sodium concentration.

So I can't understand why the sodium was at 124. Can anyone help out?

So to bring it back to the patient and take each issue one by one:
Hypotension: The hypotension was from dehydration caused by glucosuria/diuresis. As sepsis is often a cause of DKA, it could also be caused by sepsis
Tachycardia: A compensatory response to hypotension and dehydration +/- sepsis
Glucose- from lack of insulin
K- from acidosis
Acidosis- from ketosis from lack of insulin
Hyponatremia- from hyperglycemia causing fluid shifts intravascularly from the intracellular/interstitial spaces

 

[chadwickctt]

Wow there is a lot of wrong information on this thread.


There are 2 reasons why there is hyponatremia:
1. Glucose is osmotically active. It pulls intracellular water into the vascular space and "dilutes" the sodium. As you correct the glucose, so too corrects the sodium

2. DKA is a volume depletion state. So in addition to the main reason (#1), you also have whole body hypovolemic hyponatremia. Normally, the kidneys reabsorb all of the glucose in the proximal tubules. However, above roughly 250mg/dl, the Sodium-Glucose absorber is overwhelemed and you start dumping glucose into the urine. This glucosuria causes diuresis and volume depletion.

Why is there hyperkalemia?
- It has nothing to do with the Na-K ATPase. The ketosis causes an acidosis. Our cells have an H-K exchanger. So, the acidosis causes dumping of intracellular potassium into the extracellular space. Once you start treating with insulin the hyperkalemia goes away quickly for 2 reasons:, the acidosis goes away (causing the H-K to reverse directions) and the insulin itself causes movement of K into the cells again.



SWING AND A MISS on so many levels.



It is not so much a lab error. They are correctly measuring the sodium. It is unlike the old lab errors with severe hypertriglyceridemia (which no longer happen). The issues are glucose causing fluid shifts and whole body dehydration (not just intravascular).

All of this. Wow. What an awful thread... Kind of embarrassing. Haha.