LR vs NS

[miacomet]

Have you folks switched to LR for most patients? I'm trying, but our pre made order sets are all NS, and changing that enterprise-wide will be a huge endeavor. I realize the data is not definitive, but it's compelling.

What are you folks (and academia) doing clinically, and are you addressing your order sets system-wide?

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[WilcoWorld]

Have you folks switched to LR for most patients? I'm trying, but our pre made order sets are all NS, and changing that enterprise-wide will be a huge endeavor. I realize the data is not definitive, but it's compelling.

What are you folks (and academia) doing clinically, and are you addressing your order sets system-wide?

I've switched to LR for those who I expect to require large volumes (>2L).

I'm still using NS when I'm only expecting to give a liter or so, because our hospital is concerned that we'll run out of LR if we start using it on every patient.

 

[Psai]

I've switched to LR for those who I expect to require large volumes (>2L).

I'm still using NS when I'm only expecting to give a liter or so, because our hospital is concerned that we'll run out of LR if we start using it on every patient.

Agree. Even for neurosurgical cases we try to avoid more than 2 L NS. Anecdotally, that seems to be the point where you start seeing changes on the abg electrolyte panel.

 

[miacomet]

No studies in kiddos as far as I can see. Any thoughts?

 

[TooMuchResearch]

Have you folks switched to LR for most patients? I'm trying, but our pre made order sets are all NS, and changing that enterprise-wide will be a huge endeavor. I realize the data is not definitive, but it's compelling.

What are you folks (and academia) doing clinically, and are you addressing your order sets system-wide?

No.

 

[southerndoc]

I've always used LR since residency because of a SICU attending that preached on hyperchloremic metabolic acidosis. However, our order sets default to NS and don't allow a change. If I'm ordering via an order set, they get NS because I'm too lazy to go back and change it. If I'm order it off my preference list, then they get LR always.

The studies aren't the best supporting LR over NS. However, I've always gone with it since my SICU rotation. Lew Kaplan was big on the strong ions.

 

[RPedigo]

I've always used LR since residency because of a SICU attending that preached on hyperchloremic metabolic acidosis. However, our order sets default to NS and don't allow a change. If I'm ordering via an order set, they get NS because I'm too lazy to go back and change it. If I'm order it off my preference list, then they get LR always.

The studies aren't the best supporting LR over NS. However, I've always gone with it since my SICU rotation. Lew Kaplan was big on the strong ions.

There's a couple of new studies published last month in the NEJM that were large randomized (single center, but multiple ICU for the critically ill) trials that showed a benefit over "balanced crystalloid" (either Plasmalyte or LR) over NS. The absolute benefit was small, but we give so many people fluids that maybe it will make a difference?

Balanced Crystalloids versus Saline in Critically Ill Adults
Balanced Crystalloids versus Saline in Noncritically Ill Adults

For what it is worth any time I've been giving "large" amounts of fluid I have tried to use a balanced solution (burns, sepsis, etc.). I will continue to do that based on the results of these studies.

 

[southerndoc]

Those are the studies I'm referring to that are weak. The average amount of fluids was a little over 1 L, which I think is abysmal. I routinely give 2 L to dehydrated patients. Septic patients only getting 1 L? C'mon. The details of the study make it not that great.

I agree though, this is just one of many that shows a small benefit to not using NS.

 

[Psai]

There's a couple of new studies published last month in the NEJM that were large randomized (single center, but multiple ICU for the critically ill) trials that showed a benefit over "balanced crystalloid" (either Plasmalyte or LR) over NS. The absolute benefit was small, but we give so many people fluids that maybe it will make a difference?

Balanced Crystalloids versus Saline in Critically Ill Adults
Balanced Crystalloids versus Saline in Noncritically Ill Adults

For what it is worth any time I've been giving "large" amounts of fluid I have tried to use a balanced solution (burns, sepsis, etc.). I will continue to do that based on the results of these studies.

If you need a composite endpoint, your study is negative.

 

[Vigileo]

If you need a composite endpoint, your study is negative.

I think that's a tad of an overstatement. Depends on what your individual endpoints are in the composite, if they are patient-centered outcomes that are clinically relevant and assess the same disease process, etc. A lot of trials are negative if you exclude any composite end points. The reality is was that before this, there was clinical equipose between balanced crystalloids and NS. So if there is a benefit (NNT of 97 in the trial for MAKE-30 events), and they cost the same, no downside to using balanced over NS.

 

[cbrons]

I am a medicine resident and I use almost exclusively LR for the various reason cited above, the recent SALT-MED trial, etc. I also read this interesting article awhile ago about LR in severe DKA: PulmCrit - Four DKA Pearls which had me thinking about this for awhile.

 

[deleted547339]

If you need a composite endpoint, your study is negative.

So what you’re saying is that you don’t believe any cards literature published in the last 30 years?

(I’m not saying your entirely wrong, but just saying how sketchy almost all of the cards literature is)

 

[Angry Birds]

I’ve been using NS due to residency inertia. Looks like I need to switch.

Any instances in which we shouldn’t use LR?

 

[deleted547339]

I’ve been using NS due to residency inertia. Looks like I need to switch.

Any instances in which we shouldn’t use LR?

Any head patient. That’s about it as far as I can think.

 

[medic25]

I've always used LR since residency because of a SICU attending that preached on hyperchloremic metabolic acidosis.... Lew Kaplan was big on the strong ions.

Lew Kaplan..... Now that's a name I have not heard in a long time...... a long time......

 

[deleted109597]

Any head patient. That’s about it as far as I can think.

Liver failure patients can't metabolize the lactate. You'll cause acidosis.

 

[southerndoc]

Lew Kaplan..... Now that's a name I have not heard in a long time...... a long time......

I think he's at Penn now.

Any instances in which we shouldn’t use LR?

It has some potassium and calcium in it. Probably shouldn't use it if you suspect hyperkalemia. Also, it's incompatible with ceftriaxone (Rocephin). It will not end well, trust me. It crystallizes in the tube and will cause emboli in your patient. Rocephin and LR are the bad step-children that just don't get along.

 

[SpacemanSpifff]

It has some potassium and calcium in it. Probably shouldn't use it if you suspect hyperkalemia. Also, it's incompatible with ceftriaxone (Rocephin). It will not end well, trust me. It crystallizes in the tube and will cause emboli in your patient. Rocephin and LR are the bad step-children that just don't get along.

K in LR is 4mEq, I feel like that should drag your serum K back towards normal if it’s high.

Liver failure patients can't metabolize the lactate. You'll cause acidosis.

Even in folks with wicked liver disease, does the 28 mM of lactate cause any real change to their pH?

 

[Psai]

Lr is better in hyperkalemia. Been studied in esrd patients having surgery, ns causes a larger k increase. I hope that myth dies soon.

Pyruvate plus hydrogen ion and nadh equals lactate plus nad+. Lactic acidosis is another myth, especially in the tiny amounts involved. Not sure where the acid is coming from there but it ain't from lactate. And even if your liver couldn't handle it (which it can), no reason why your heart or brain can't.

And why would ceftriaxone crystalize with the calcium in the tube but not in the blood? Sounds sketchy to me.

Trials are unconvincing but I still think LR is superior and use it almost exclusively.

 

[NITRAS]

There's a couple of new studies published last month in the NEJM that were large randomized (single center, but multiple ICU for the critically ill) trials that showed a benefit over "balanced crystalloid" (either Plasmalyte or LR) over NS. The absolute benefit was small, but we give so many people fluids that maybe it will make a difference?

Balanced Crystalloids versus Saline in Critically Ill Adults
Balanced Crystalloids versus Saline in Noncritically Ill Adults

For what it is worth any time I've been giving "large" amounts of fluid I have tried to use a balanced solution (burns, sepsis, etc.). I will continue to do that based on the results of these studies.

Those articles supporting balanced fluids over NS aren’t that impressive to me. (Given I don’t practice in a critically ill setting). NS is usually a herpertonic solution and LR is usually a hypotonic solution. I admit I don’t know the point of the lactate.

I’m also curious why LR is better for hyperkalemia than a fluid without potassium.

Edit: so the acidosis causing shift of K is more important than the added K in solution. Cool.

 

[deleted547339]

Liver failure patients can't metabolize the lactate. You'll cause acidosis.

Not necessarily. Lactate is also metabolized outside of the liver.

If you want to make the argument that you should use NS to decrease the rate of cerebral edema in an acute liver failure, id go for that argument, but not for lactic acidosis.

 

[Zebra Hunter]

Those are the studies I'm referring to that are weak. The average amount of fluids was a little over 1 L, which I think is abysmal. I routinely give 2 L to dehydrated patients. Septic patients only getting 1 L? C'mon. The details of the study make it not that great.

I agree though, this is just one of many that shows a small benefit to not using NS.

I think you misread the study. Septic patients received averages of around 4L. All comers received an average of 2L, the MEDIAN was 1L, which just means there was a large proportion of critically ill patients that did not require fluid resuscitation (ICH, traumas, heart failure patients, ESRD).

 

[Psai]

Those articles supporting balanced fluids over NS aren’t that impressive to me. (Given I don’t practice in a critically ill setting). NS is usually a herpertonic solution and LR is usually a hypotonic solution. I admit I don’t know the point of the lactate.

I’m also curious why LR is better for hyperkalemia than a fluid without potassium.

Edit: so the acidosis causing shift of K is more important than the added K in solution. Cool.

Point of lactate is to be metabolized into bicarb. I think it is better than gluconate.

If you have a patient with a k for 5 and you give a fluid with a k of 4, what will happen? K should go down. LR causes a bit more diuresis than ns which also removes some k, about 300 per liter in a pig study I believe. Your body has an enormous amount of k intracellularly, adding 4 meq per liter is a drop in the bucket.

NS causes a hyperchloremic acidosis which causes increased transcellular shift of k. It has been shown to cause higher k levels in esrd patients having surgery, 3 small rcts in 2008 to 2013 or so. I will post references later if I get a chance.

 

[Groove]

I give NS and rarely give LR unless there is a sodium I don't want to correct very quickly or I anticipate a large volume resuscitation and they have already received 2L NS. Every time I have re-visited this topic over the years, the data remains the same...unconvincing. I don't like the theoretical issues with the lactate consumption (or lack thereof) in hepatopaths, trending lactate in sepsis or undeclared septic pts, remaining contraindication in sepsis (yes I know about the new studies, SPLIT, etc..but only 4% of those pts were septic and there was still no diff in mortality), K in ESRD (we have A LOT of these pts) and I can't keep straight which drugs are compatible and which aren't (There are several drugs you can't give through the same line, nor can you give blood transfusions through the line last time I checked.) NS is just easier and I can't think of a single case where my choice in fluids for resuscitation led to any issues whatsoever downstream in their management and certainly not while they were in the ED. Yes, you can cause hyperchloremic met acidosis with NS, but it's not like you can't cause any metabolic derangements with excess LR...alkalosis, hypotonicity, hyperlactatemia, etc.. How many of us are giving 4-6L NS in the ED? I continue to see a lot of people feel very impassioned about this topic though but fail to see the evidence yet. For every "AHA!" Isolated research study that looks promising, I could probably dig up 10 that would seem to contradict. I just don't think we're there yet and for most of my patients who are receiving under 2L, I doubt very strongly that it really matters in the end.

 

[Groove]

Lr is better in hyperkalemia. Been studied in esrd patients having surgery, ns causes a larger k increase. I hope that myth dies soon.

Pyruvate plus hydrogen ion and nadh equals lactate plus nad+. Lactic acidosis is another myth, especially in the tiny amounts involved. Not sure where the acid is coming from there but it ain't from lactate. And even if your liver couldn't handle it (which it can), no reason why your heart or brain can't.

And why would ceftriaxone crystalize with the calcium in the tube but not in the blood? Sounds sketchy to me.

Trials are unconvincing but I still think LR is superior and use it almost exclusively.

Send a letter to the FDA so they will remove the warning against using LR in ESRD and hyperkalemic pts so the rest of us can use it. Until then, good luck convincing anybody working outside academia in "non-sovereign immunity land" that giving our pt's with a K of 7, a fluid...with more potassium, is a good idea.

I hear you and I've read the criticisms and supportive lit, Emcrit, etc.. I’m not saying you’re wrong, but the warning is still there and it's going to be tougher than it perhaps should be convincing the lawyers that the sudden arrest in that pt wasn't due to K worsened by the fluid you were giving....with more K in it.

 

[deleted547339]

I give NS and rarely give LR unless there is a sodium I don't want to correct very quickly or I anticipate a large volume resuscitation and they have already received 2L NS. Every time I have re-visited this topic over the years, the data remains the same...unconvincing. I don't like the theoretical issues with the lactate consumption (or lack thereof) in hepatopaths, trending lactate in sepsis or undeclared septic pts, remaining contraindication in sepsis (yes I know about the new studies, SPLIT, etc..but only 4% of those pts were septic and there was still no diff in mortality), K in ESRD (we have A LOT of these pts) and I can't keep straight which drugs are compatible and which aren't (There are several drugs you can't give through the same line, nor can you give blood transfusions through the line last time I checked.) NS is just easier and I can't think of a single case where my choice in fluids for resuscitation led to any issues whatsoever downstream in their management and certainly not while they were in the ED. Yes, you can cause hyperchloremic met acidosis with NS, but it's not like you can't cause any metabolic derangements with excess LR...alkalosis, hypotonicity, hyperlactatemia, etc.. How many of us are giving 4-6L NS in the ED? I continue to see a lot of people feel very impassioned about this topic though but fail to see the evidence yet. For every "AHA!" Isolated research study that looks promising, I could probably dig up 10 that would seem to contradict. I just don't think we're there yet and for most of my patients who are receiving under 2L, I doubt very strongly that it really matters in the end.

Blood is compatible with LR....you just have to convince your nurses of this.

 

[NITRAS]

@Psai
Thank you for the explanation. Makes sense.

 

[alpinism]

Myth-busting: Lactated Ringers is safe in hyperkalemia, and is superior to NS.

 

[Psai]

Send a letter to the FDA so they will remove the warning against using LR in ESRD and hyperkalemic pts so the rest of us can use it. Until then, good luck convincing anybody working outside academia in "non-sovereign immunity land" that giving our pt's with a K of 7, a fluid...with more potassium, is a good idea.

I hear you and I've read the criticisms and supportive lit, Emcrit, etc.. I’m not saying you’re wrong, but the warning is still there and it's going to be tougher than it perhaps should be convincing the lawyers that the sudden arrest in that pt wasn't due to K worsened by the fluid you were giving....with more K in it.

Look, lactate doesn't cause a lactic acidosis. Do you expect a bolus of sodium bicarb to cause a carbonic acidosis? It makes no sense.

You can easily give blood products with LR. In fact, I use LR preferentially with an N above 20 for giving prbcs with zero adverse effects. The data that suggest that blood and LR are incompatible is from 50 year old studies that actually say that 1:1 ratio of LR to blood is okay and that you start seeing clot if you have 2:1 LR to blood ratios with the blood just sitting in the line for several minutes (somewhere from 5-15 minutes I believe but it would probably clot by itself anyway if it sits for that long.)

Your average banana has more K than a bag of LR. Your body has about 2800 meq of K. The strong ion difference in NS (40 or so) will cause an acidosis causing more potassium shift than adding a dinky little 4 meq. If you're scared of giving LR because of that, you need to revisit your chemistry and physiology classes. It is ridiculous to think that a patient with a K of 7 will have their K go anywhere but down when you give a fluid with a K of 4.

 

[deleted547339]

Look, lactate doesn't cause a lactic acidosis. Do you expect a bolus of sodium bicarb to cause a carbonic acidosis? It makes no sense.

You can easily give blood products with LR. In fact, I use LR preferentially with an N above 20 for giving prbcs with zero adverse effects. The data that suggest that blood and LR are incompatible is from 50 year old studies that actually say that 1:1 ratio of LR to blood is okay and that you start seeing clot if you have 2:1 LR to blood ratios with the blood just sitting in the line for several minutes (somewhere from 5-15 minutes I believe but it would probably clot by itself anyway if it sits for that long.)

Your average banana has more K than a bag of LR. Your body has about 2800 meq of K. The strong ion difference in NS (40 or so) will cause an acidosis causing more potassium shift than adding a dinky little 4 meq. If you're scared of giving LR because of that, you need to revisit your chemistry and physiology classes. It is ridiculous to think that a patient with a K of 7 will have their K go anywhere but down when you give a fluid with a K of 4.

What he (or she) said.

This is what I teach my residents as well.

 

[Groove]

Look, lactate doesn't cause a lactic acidosis. Do you expect a bolus of sodium bicarb to cause a carbonic acidosis? It makes no sense.

"Lactate levels increased significantly in patients who received Ringer's lactate (0.48 +/- 0.29 vs 1.95 +/- 0.48)."

You can easily give blood products with LR. In fact, I use LR preferentially with an N above 20 for giving prbcs with zero adverse effects. The data that suggest that blood and LR are incompatible is from 50 year old studies that actually say that 1:1 ratio of LR to blood is okay and that you start seeing clot if you have 2:1 LR to blood ratios with the blood just sitting in the line for several minutes (somewhere from 5-15 minutes I believe but it would probably clot by itself anyway if it sits for that long.)

Your average banana has more K than a bag of LR. Your body has about 2800 meq of K. The strong ion difference in NS (40 or so) will cause an acidosis causing more potassium shift than adding a dinky little 4 meq. If you're scared of giving LR because of that, you need to revisit your chemistry and physiology classes. It is ridiculous to think that a patient with a K of 7 will have their K go anywhere but down when you give a fluid with a K of 4.

You don't get it. I'm not saying you are wrong, but what I am saying is that it's a warning ON THE BAXTER FDA INSERT for crying out loud. Let me cut and paste it from the manufacture's website:

Lactated Ringer’s and 5% Dextrose Injection, USP should be administered with particular caution, if at all, to patients with hyperkalemia or conditions predisposing to hyperkalemia (such as severe renal impairment or adrenocortical insufficiency, acute dehydration, or extensive tissue injury or burns) and in patients with cardiac disease.

Get it now? If your ESRD pt with K of 7 arrests you are going to look like a gigantic dumb ass on the stand as they query a Baxter MD/PHD about whether LR is safe to use in hyperkalemia. He'll say they don't recommend it and caution strongly against it. Why? Because of the theoretical risk of hyperkalemia. You can quote academic critiques and studies all day long but essentially you are quoting studies that have yet to convince the manufacturer to change their damn insert on their warning concerning use in hyperkalemia...or it WOULDN'T BE ON THERE.

Ultimately, this is one of those ridiculous topics that nobody cares about outside of an academic morning rounds or an attending's opportunity to pimp an unsuspecting intern during morning report. I mean c'mon...How many lives have you really saved from your choice in LR vs NS? Be honest... Probably about as many pt's I've harmed by giving them NS. So, why are we even still talking about this? Quit trying to shame the rest of us who prefer NS as our initial fluid for resuscitation.

I practice evidence based defensive medicine at its finest.

 

[Psai]

Lactate level is not lactic acid. And a lactate of 1.95 is clinically insignificant, especially in this context.

Bupi 0.5% specifically says on the bottle that it is not for spinal anesthesia. Guess what we use almost exclusively for spinal anesthesia?

I practice evidence based medicine that is consistent with basic scientific principles. The post above yours has plenty of literature that will support my view. Why use a fluid that is inconsistent with physiology? I can see why medicine takes so long to change, even in the face of mounting data.

 

[VA Hopeful Dr]

Lactate level is not lactic acid. And a lactate of 1.95 is clinically insignificant, especially in this context.

Bupi 0.5% specifically says on the bottle that it is not for spinal anesthesia. Guess what we use almost exclusively for spinal anesthesia?

I practice evidence based medicine that is consistent with basic scientific principles. The post above yours has plenty of literature that will support my view. Why use a fluid that is inconsistent with physiology? I can see why medicine takes so long to change, even in the face of mounting data.

Because we're rightfully afraid of lawsuits?

Or because we've been burned before by changing practices too quickly?

 

[Groove]

Lactate level is not lactic acid. And a lactate of 1.95 is clinically insignificant, especially in this context.

Bupi 0.5% specifically says on the bottle that it is not for spinal anesthesia. Guess what we use almost exclusively for spinal anesthesia?

I practice evidence based medicine that is consistent with basic scientific principles. The post above yours has plenty of literature that will support my view. Why use a fluid that is inconsistent with physiology? I can see why medicine takes so long to change, even in the face of mounting data.

For a CA-3 anesthesia resident with their profile clamped down, you feel awfully strong about what fluids we should or should not give in the ER. Any Baxter stock in your portfolio?

 

[EMhawkeye]

I think he's at Penn now.



It has some potassium and calcium in it. Probably shouldn't use it if you suspect hyperkalemia. Also, it's incompatible with ceftriaxone (Rocephin). It will not end well, trust me. It crystallizes in the tube and will cause emboli in your patient. Rocephin and LR are the bad step-children that just don't get along.

Yep he's at Penn now. He's chief of surgery at the Philly VA now.

 

[WheezyBaby]

Liver failure patients can't metabolize the lactate. You'll cause acidosis.

Do you actually mean acute liver failure or just the NASH / cirrhotics / etc? Liver isn't the only site of lactate metabolism and regardless lactate anion doesn't cause acidosis. I'll use LR in cirrhotics. If you mean ALF, I will use NS, but my concern is more avoiding worsening cerebral edema

 

[BoardingDoc]

regardless lactate anion doesn't cause acidosis.

Agree. This seems to be a common misconception both in general and in this forum. Lactate != lactic acid. Lactate isn't an acid. It's an acid anion (e.g. can accept a hydrogen ion... e.g. a BASE). Adding lactate to a system doesn't increase acidosis, if anything, it decreases it (assuming the liver is working. If not, it still doesn't make things more acidic).

Lactate is associated with acidosis because of the fact that it is produced by anaerobic metabolism which is itself a situation which tends to create an acidosis (generally through large scale ATP metabolism). That said, the lactate itself isn't creating the acidosis. This may seem like a small distinction but it is an important one and without it, people can easily assume that lactate itself is causing an acidosis which is patently false.

 

[SpacemanSpifff]

Agree. This seems to be a common misconception both in general and in this forum. Lactate != lactic acid. Lactate isn't an acid. It's an acid anion (e.g. can accept a hydrogen ion... e.g. a BASE). Adding lactate to a system doesn't increase acidosis, if anything, it decreases it (assuming the liver is working. If not, it still doesn't make things more acidic).

Lactate is associated with acidosis because of the fact that it is produced by anaerobic metabolism which is itself a situation which tends to create an acidosis (generally through large scale ATP metabolism). That said, the lactate itself isn't creating the acidosis. This may seem like a small distinction but it is an important one and without it, people can easily assume that lactate itself is causing an acidosis which is patently false.

Not exclusively, and honestly probably not primarily in most of the pathophysiology we see. Bench investigations suggest that lactate production in shock is not entirely anaerobic. This is a more common thought in the clinical realm as well (see this month's EMRAP piece, any of Paul Marik's numerous publications on the topic, or this Josh Farkas post). Basically, lactate is a nonspecific indicator of physiologic stress NOS, assuming an intact response to catecholamines.

 

[BoardingDoc]

Not exclusively, and honestly probably not primarily in most of the pathophysiology we see. Bench investigations suggest that lactate production in shock is not entirely anaerobic. This is a more common thought in the clinical realm as well (see this month's EMRAP piece, any of Paul Marik's numerous publications on the topic, or this Josh Farkas post). Basically, lactate is a nonspecific indicator of physiologic stress NOS, assuming an intact response to catecholamines.

Thanks for the links. Both are interesting reads, however, they both agree completely with what I said above. They say that lactate is due to B2 receptor activation which activates glycolysis to produce ATP, which creates pyruvate... but then the mitochondria can't keep up with the rapid rate of glycolysis and so pyruvate is converted into lactate ....... which is by definition anaerobic respiration. While anaerobic respiration obviously occurs in oxygen poor environments, it can occur at any time. It by definition simply means "it doesn't require oxygen." I feel like we jumped from one intrinsically easy to misunderstand term (lactic acidosis, where lactate is NOT an acid) to another (anaerobic metabolism, where oxygen isn't required, but can absolutely be present).

 

[deleted547339]

"Lactate levels increased significantly in patients who received Ringer's lactate (0.48 +/- 0.29 vs 1.95 +/- 0.48)."



You don't get it. I'm not saying you are wrong, but what I am saying is that it's a warning ON THE BAXTER FDA INSERT for crying out loud. Let me cut and paste it from the manufacture's website:

Lactated Ringer’s and 5% Dextrose Injection, USP should be administered with particular caution, if at all, to patients with hyperkalemia or conditions predisposing to hyperkalemia (such as severe renal impairment or adrenocortical insufficiency, acute dehydration, or extensive tissue injury or burns) and in patients with cardiac disease.

Get it now? If your ESRD pt with K of 7 arrests you are going to look like a gigantic dumb ass on the stand as they query a Baxter MD/PHD about whether LR is safe to use in hyperkalemia. He'll say they don't recommend it and caution strongly against it. Why? Because of the theoretical risk of hyperkalemia. You can quote academic critiques and studies all day long but essentially you are quoting studies that have yet to convince the manufacturer to change their damn insert on their warning concerning use in hyperkalemia...or it WOULDN'T BE ON THERE.

Ultimately, this is one of those ridiculous topics that nobody cares about outside of an academic morning rounds or an attending's opportunity to pimp an unsuspecting intern during morning report. I mean c'mon...How many lives have you really saved from your choice in LR vs NS? Be honest... Probably about as many pt's I've harmed by giving them NS. So, why are we even still talking about this? Quit trying to shame the rest of us who prefer NS as our initial fluid for resuscitation.

I practice evidence based defensive medicine at its finest.

Have you ever given IV haldol?

 

[SpacemanSpifff]

Thanks for the links. Both are interesting reads, however, they both agree completely with what I said above. They say that lactate is due to B2 receptor activation which activates glycolysis to produce ATP, which creates pyruvate... but then the mitochondria can't keep up with the rapid rate of glycolysis and so pyruvate is converted into lactate ....... which is by definition anaerobic respiration. While anaerobic respiration obviously occurs in oxygen poor environments, it can occur at any time. It by definition simply means "it doesn't require oxygen." I feel like we jumped from one intrinsically easy to misunderstand term (lactic acidosis, where lactate is NOT an acid) to another (anaerobic metabolism, where oxygen isn't required, but can absolutely be present).

Correct, apologize for the poor wording - lactate production does not involve oxygen, but does not occur primarily as a result of low oxygen delivery leading to absence of oxygen. I feel like this is a distinction most people fail to make.

 

[Psai]

Correct, apologize for the poor wording - lactate production does not involve oxygen, but does not occur primarily as a result of low oxygen delivery leading to absence of oxygen. I feel like this is a distinction most people fail to make.

Correct. There are basic science studies where people measured mitochondrial oxygen levels in sepsis states induced in rat models and there was no decrease in oxygen as claimed by lactic aciders. I do believe in microcirculatory dysfunction.

 

[Groove]

Have you ever given IV haldol?

I generally don't give Haldol IV.

 

[neusu]

Agree. Even for neurosurgical cases we try to avoid more than 2 L NS. Anecdotally, that seems to be the point where you start seeing changes on the abg electrolyte panel.

We are pretty dogmatic about NS.

 

[TooMuchResearch]

I generally don't give Haldol IV.

Try it, it's awesome. Although I'm moving more towards Zyprexa in many patients.

 

[Psai]

We are pretty dogmatic about NS.

I'm cool with surgeon preference. You're the ones following up long term.

 

[Groove]

Try it, it's awesome. Although I'm moving more towards Zyprexa in many patients.

I used to give it occasionally IV on rare occasions but then thought better of it and changed practice. (Though I totally get that many docs give it this way.) It's always bugged me that it's not FDA approved IV and it seems to make sense to me that if there were going to be any QT prolongation, it would be most noticeable with a slug of it IV push but it's not something I've researched. Honestly, I don't ever really find myself wishing I could give it IV so it's not a big loss to me.

Zyprexa always seems to take too long. I also don't like that you "can't" give it IM with Ativan if needed.

Geodon 20mg IM is my general go-to for the really agitated schizos. Sometimes, I will B52 but the level of sedation just complicates dispo.

I'll give zyprexa PO for the ones that are agitated, but not tearing up the place and I don't anticipate any abrupt violent psych decompensation where I've already started fantasizing about plastic tubes and Riker sedation scores.

 

[engineeredout]

LR is more physiologic than NS - this is not a fact that can be easily debated. Therefore, the onus should be on proving that NS is superior as a justification for using it over LR, not the other way around