# LR and DKA



## usalsfyre (Jun 16, 2011)

Has anyone heard that using LR for fluid replacement in DKA is suboptimal? The only thing I've found so far is that it "may" be metabolized into glucose, nothing else.


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## MrBrown (Jun 16, 2011)

Brown has not heard anything, and given that Ringers only contains small quantities of ionic compounds (K, Na, Cl etc) Brown is unsure how those get metabolised into glucose.

If we gave the patient a bag of free fatty acids or something then perhaps


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## usalsfyre (Jun 16, 2011)

That was my thought, and considering LR is a far better resuscitation fluid than NS in the acidotic patient I figured the ED would continue that path. However, the ED physician ordered the LR stopped, a second liter of NS started, and gave explicit instructions not to give anymore LR. Asked him about it, he said LR had dextrose in it (which it doesn't) and he only uses NS for DKA until it's time to switch to D5.

Weird, I was just wondering if I had missed a subtlety.


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## MrBrown (Jun 16, 2011)

usalsfyre said:


> ...considering LR is a far better resuscitation fluid than NS in the acidotic patient I figured the ED would continue that path.



Do you have some sources for this?


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## fast65 (Jun 16, 2011)

Yeah, I've heard of this as well, however, I've never been able to figure out why :/


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## J. Burdett (Jun 16, 2011)

usalsfyre said:


> Has anyone heard that using LR for fluid replacement in DKA is suboptimal? The only thing I've found so far is that it "may" be metabolized into glucose, nothing else.



Lactate is metabolized into glucose and glycogen during anaerobic metabolism. I believe it's called the Cori cycle. Maybe there is a correlation?


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## Smash (Jun 16, 2011)

MrBrown said:


> Do you have some sources for this?



Normal saline in large volumes can lead to hyperchloraemic acidosis, which contributes to organ failure.  Specifically in DKA I believe it causes renal arteriole constriction, decreased urine output and increased acidosis.  LR would be my fluid of choice for DKA (if I had it)



Usalsfyre, where and what have you heard about ringers?


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## Akulahawk (Jun 16, 2011)

J. Burdett said:


> *Lactate is metabolized into glucose and glycogen during anaerobic metabolism.* I believe it's called the Cori cycle. Maybe there is a correlation?


That's what I'm thinking as well. LR, while it doesn't actually have dextrose in it, the lactate is metabolized into glucose/glycogen. Ringer's or NS would probably be better. The only thing I can "see" for LR being a better fluid for resus of acidotic patients is that the lactate may also function as a buffer agent and therefore help keep the acidosis from getting worse.


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## MrBrown (Jun 16, 2011)

Ah yes of course, that good ole metabolism of lactate into glucose during anaerobic glycolosis ... how could Brown have not known that?


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## usalsfyre (Jun 16, 2011)

I can't find the stuff I'm looking for, I researched it extensively about three or four years ago when I was first dipping a toe into critical care. I seem to remember three or four studies indicating that hyperchloremic acidosis was a predictable, preventable outcome from resus with large volumes of NS. However, a brief search on the subject today revealed no study with an outcome difference, so perhaps "far supperior" is a bit of a stretch.

That said, throwing a non-gap acidosis on someone who already has a strong gap acidosis and can expected to be acidotic for a few days is not going to be helpful. Hard on your kidneys (and DKA is hard enough on those already) and although it can be fairly easily corrected with bicarbonate, overshoot your target with bicarbonate and you've just upped your patients chance for cerebral edema. As it's seemingly easily avoided, I don't see what the advantage of NS is.

Lactate is metabolized by the liver into glucose, I don't know if there's enough of it in LR to be a factor. Straight Ringer's is probably a better choice, but not available commonly on EMS units or from what I've seen, in EDs.

One more, slightly off topic, item to remember about fluid resus in DKA patients for any newer medics out there. Watch your volumes, or you risk hypoosmolar cerebral edema. Unless you've got an exceptionally large or small patient a two liter initial resuscitation is usually adequate, then get some labs to start guiding your administration rate.


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## 18G (Jun 17, 2011)

NSS is used pretty must exclusively around here. Had a DKA patient not to long ago and 3L of NSS were given... no LR. 

My only thinking with the LR is too that the lactate gets converted to glucose. How much I would be curious to know. With current insulin therapy would the amount even be clinically significant?


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## mycrofft (Jun 17, 2011)

*LR loading?*

It might be "chalkboard feasible" (in vitro or "in creta" ("in chalk), but how much LR would be needed to make a clinical difference? Another case for not indiscriminately dumping IV solutions into people.


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## cwmedic (Jun 19, 2011)

I think some people have it backward. Although this can get pretty deep, lactate is produced during anaerobic metabolism, not used during it. Lactate is the waste product. There is a lot of this subject in the fairly new sepsis studies. 

I could see that you would not want to introduce any more lactate into an already acidotic patient. That would be my answer and I am confident in it.


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## usalsfyre (Jun 19, 2011)

cwmedic said:


> I think some people have it backward. Although this can get pretty deep, lactate is produced during anaerobic metabolism, not used during it. Lactate is the waste product. There is a lot of this subject in the fairly new sepsis studies.
> 
> I could see that you would not want to introduce any more lactate into an already acidotic patient. That would be my answer and I am confident in it.



You do know the pH of NS is like 5 right? Where as the pH of LR is around 6.5 to 7?

Ringers, lactated or not, is a better resuscitation fluid. Please resus your sepsis patients with ringers. The ICU will thank you tremendously.


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## zmedic (Jun 20, 2011)

Find me some studies that support your opinion. People wax philosophical that LR should be better for this than and the other, but when they compare them head to head they don't find any difference in things that matter (mortality, morbidity) between using LR and NS. 

http://www.anesthesia-analgesia.org/content/93/4/817.short

etc


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## usalsfyre (Jun 20, 2011)

zmedic said:


> Find me some studies that support your opinion. People wax philosophical that LR should be better for this than and the other, but when they compare them head to head they don't find any difference in things that matter (mortality, morbidity) between using LR and NS.
> 
> http://www.anesthesia-analgesia.org/content/93/4/817.short
> 
> etc


Yep, I am waxing philosophic a bit, but I'm not completely talking out of a certain bodily orfice.

I looked at that exact abstract a couple of days ago before posting this. Outcomes are the same...when the pH is adjusted with additional bicarbonate. Other studies on the subject have similar results. 

I'm from the school of thought that good medicine is often less medicine, so if we can avoid dropping the patients pH, why not do it?


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## Melclin (Jun 20, 2011)

I've been interested in the difference in outcomes from NS and hartmanns for a while. LR makes good sense, but as far as I know the evidence just isn't there in most cases, regarding outcomes.

We used to carry hartmanns, but it was removed, I believe, because of a lack of evidence supporting it. 

Still, as the saying goes, the absence of evidence isn't the evidence of absence.

Does anybody know of a good article summarising the issue, a review of some sort. I'm trying to collect a series of good overview articles and I've yet to get one on fluids since my journal access was taken away.


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## J. Burdett (Jun 29, 2011)

Also, Metformin can cause lactic acidosis. So if the pt was taking it and experiencing lactic acidosis, lactated ringers could exacerbate that I would think.


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## usalsfyre (Jun 29, 2011)

J. Burdett said:


> Also, Metformin can cause lactic acidosis. So if the pt was taking it and experiencing lactic acidosis, lactated ringers could exacerbate that I would think.



Most of your DKA patients aren't going to be taking Metformin...


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## J. Burdett (Jun 29, 2011)

usalsfyre said:


> Most of your DKA patients aren't going to be taking Metformin...



Why do you say that?

I have a sneaking suspicion  I'm just wondering if it's for the same reason.


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## usalsfyre (Jun 29, 2011)

J. Burdett said:


> Why do you say that?
> 
> I have a sneaking suspicion  I'm just wondering if it's for the same reason.



Typically DKA is a complication of insulin-dependent diabetes mellitus.

If you were talking HHNK on the other hand...


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## J. Burdett (Jun 29, 2011)

usalsfyre said:


> Most of your DKA patients aren't going to be taking Metformin...



Remember that Type II diabetes can be progressive in the pt with poor eating habits. That can easily render Metformin ineffective and the pt would have to start taking insulin. Sometimes, the pt finds this out the hard way if they don't routinely check their glucose levels by experiencing HHNS. I say HHNS because that's what we encounter most of the time since DKA is more prevalent in the Type I diabetics.


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## J. Burdett (Jun 29, 2011)

usalsfyre said:


> Typically DKA is a complication of insulin-dependent diabetes mellitus.
> 
> If you were talking HHNK on the other hand...



Yes!


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