Normal Saline

[Psai]

Why do IM docs swear by it? If it were up to me, everyone who needed fluids would get lactated ringers. Or maybe plasmalyte if they're rich. If you have a patient with slightly elevated potassium or renal failure and you suggest LR they look at you like you're insane even though there are data from multiple trials that show that in patients undergoing renal transplant, normal saline increases k and lactated ringers decreases it. But nah let's put in a bunch of hypertonic acid into our patients' veins.

If your blood k is 5 meq/L and you're giving fluid that has 4 meq/L then the potassium should go down. When you put an acid (normal saline which has 154 meq/L of chloride vs 110 in your blod) intravenously, the k should go up because all that acid goes intracellular and you have a ****ton more k in your cells than you do in that liter of LR. Drives me crazy.

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[Tenk]

Because it has the word normal in it.

 

[deleted763299]

I agree that, generally speaking, balanced crystalloids (LR, plasmalyte) are superior fluids.

Why do IM docs swear by it?

Many reasons that have nothing to do with the patient! They're used to it, the nurses are used to it. It's the cheapest. Nurses won't complain about NS being incompatible in the same line as blood or various other drugs like they will about LR. The fact that they're going to "bolus" a patient with 250 mL of fluid, and that amount isn't going to give the patient a hyperchloremic acidosis (that amount probably won't change much about the patient at all...).

 

[Ismet]

I have another question: why do surgeons put kids on 1/2 NS or 1/4 NS? What do they think they're fixing/doing?

 

[cbrons]

Why do IM docs swear by it? If it were up to me, everyone who needed fluids would get lactated ringers. Or maybe plasmalyte if they're rich. If you have a patient with slightly elevated potassium or renal failure and you suggest LR they look at you like you're insane even though there are data from multiple trials that show that in patients undergoing renal transplant, normal saline increases k and lactated ringers decreases it. But nah let's put in a bunch of hypertonic acid into our patients' veins.

If your blood k is 5 meq/L and you're giving fluid that has 4 meq/L then the potassium should go down. When you put an acid (normal saline which has 154 meq/L of chloride vs 110 in your blod) intravenously, the k should go up because all that acid goes intracellular and you have a ****ton more k in your cells than you do in that liter of LR. Drives me crazy.

Because as an IM intern if you put someone on LR your seniors and attendings look at you weird.

But I can't think of any situation where 0.90% NS is better than LR other than hyponatremic dehydration, in patients at risk of cerebral edema, and in the initial phase of DKA resuscitation.

 

[Raryn]

Why do IM docs swear by it? If it were up to me, everyone who needed fluids would get lactated ringers. Or maybe plasmalyte if they're rich. If you have a patient with slightly elevated potassium or renal failure and you suggest LR they look at you like you're insane even though there are data from multiple trials that show that in patients undergoing renal transplant, normal saline increases k and lactated ringers decreases it. But nah let's put in a bunch of hypertonic acid into our patients' veins.

If your blood k is 5 meq/L and you're giving fluid that has 4 meq/L then the potassium should go down. When you put an acid (normal saline which has 154 meq/L of chloride vs 110 in your blod) intravenously, the k should go up because all that acid goes intracellular and you have a ****ton more k in your cells than you do in that liter of LR. Drives me crazy.

Because great-granddaddy Osler used it. And it's a little cheaper than LR.

In addition, while I'm probably among the most liberal IM users of LR, the data comparing NS to LR is crap. There's some non-randomized trials with tons of confounders and there's some other small ones in limited populations (including the renal transplant one you reference). NS certainly causes a hyperchloremic acidosis if used to excess, but even that is more a number than anything else (and will even itself out over time). The hard outcome data is almost nonexistant and in general it almost certainly doesn't make any difference at all.

I use LR in all my pancreatitis patients (one study that shows it has a lower rate of SIRS), any of my patients with a hyperchloremic acidosis, and many of the ones with crappy kidneys, but I don't think I'm doing some kind of magic therapy. I'm pretty sure most outcomes would be damn-near identical with NS as well.

 

[masaraksh]

Thank the lord for Radiology and Orthopedics.

 

[failedatlife]

LR

 

[caffeinemia]

Why do IM docs swear by it? If it were up to me, everyone who needed fluids would get lactated ringers. Or maybe plasmalyte if they're rich. If you have a patient with slightly elevated potassium or renal failure and you suggest LR they look at you like you're insane even though there are data from multiple trials that show that in patients undergoing renal transplant, normal saline increases k and lactated ringers decreases it. But nah let's put in a bunch of hypertonic acid into our patients' veins.

If your blood k is 5 meq/L and you're giving fluid that has 4 meq/L then the potassium should go down. When you put an acid (normal saline which has 154 meq/L of chloride vs 110 in your blod) intravenously, the k should go up because all that acid goes intracellular and you have a ****ton more k in your cells than you do in that liter of LR. Drives me crazy.

You're aboslutely right. Now go back to your ICU cave! Cuz it hardly matters ever anyway. And if my patient's K is such a frickn problem that I have to be arsed to switch between two non-sugared crystalloids, they're going on dialysis or I'm running insulin drip with D50

 

[WheezyBaby]

Because great-granddaddy Osler used it. And it's a little cheaper than LR.

In addition, while I'm probably among the most liberal IM users of LR, the data comparing NS to LR is crap. There's some non-randomized trials with tons of confounders and there's some other small ones in limited populations (including the renal transplant one you reference). NS certainly causes a hyperchloremic acidosis if used to excess, but even that is more a number than anything else (and will even itself out over time). The hard outcome data is almost nonexistant and in general it almost certainly doesn't make any difference at all.

I use LR in all my pancreatitis patients (one study that shows it has a lower rate of SIRS), any of my patients with a hyperchloremic acidosis, and many of the ones with crappy kidneys, but I don't think I'm doing some kind of magic therapy. I'm pretty sure most outcomes would be damn-near identical with NS as well.

Fall into this camp

 

[TwoStep2021]

.

 

[WheezyBaby]

Lactate Ringer is composed of K(CH3CH2[OH]COOH) which dissociates into a weak acid with pKa of 3.8 and it allows its conjugate base to be present in concentrations required to buffer acidotic conditions like burn victims which are probably the type of patients you see as a trauma surgeon. Lactated Ringers are contraindicated in most liver disease because of a subclinical Cori Cycle defect which prevents metabolism of lactate. They are also contraindicated in all alkalotic states. For example, in acute volume loss states, the kidneys choose to retain bicarbonate ions or if you OD on aspirin you can cause the respiratory system to go into overdrive and blow off CO2. Lastly, they are contraindicated in hyperkalemic states due to K+ dissociation.


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No

 

[TwoStep2021]

No

Yes. These are basic concepts. Just because you're further along in training doesn't mean you can flip Year 1 science upside down. This is what we learned in our renal unit. Please, I challenge you explain me why I'm wrong.


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[neusu]

Neurosurgery (adults anyway) is always NS @ 80. We want excess Na most of the time, or at least not hyponatremia, so NaCl is our go to. For induced hypernatremia 3% gtt or 23% NaCl bolus is the routine.

 

[tymont12]

Yes. These are basic concepts. Just because you're further along in training doesn't mean you can flip Year 1 science upside down. This is what we learned in our renal unit. Please, I challenge you explain me why I'm wrong.


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I thought you were the C/O 2021 who already went thru Pathoma before starting med school? Now you are a student?

 

[TwoStep2021]

I thought you were the C/O 2021 who already went thru Pathoma before starting med school? Now you are a student?

I already had the equivalent of a first year.


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[SpacemanSpifff]

Yes. These are basic concepts. Just because you're further along in training doesn't mean you can flip Year 1 science upside down. This is what we learned in our renal unit. Please, I challenge you explain me why I'm wrong.

You're not technically wrong, but blanket statements (i.e. LR is contraindicated in x condition) are not terribly useful in clinical medicine. You'll find that much of what you learn in basic science units does not translate verbatim to the clinical realm, so be ready to constantly reevaluate your knowledge.

Quick example for LR in hyperK: https://emcrit.org/pulmcrit/myth-bu...s-safe-in-hyperkalemia-and-is-superior-to-ns/

 

[TwoStep2021]

You're not technically wrong, but blanket statements (i.e. LR is contraindicated in x condition) are not terribly useful in clinical medicine. You'll find that much of what you learn in basic science units does not translate verbatim to the clinical realm, so be ready to constantly reevaluate your knowledge.

Quick example for LR in hyperK: https://emcrit.org/pulmcrit/myth-bu...s-safe-in-hyperkalemia-and-is-superior-to-ns/

Edit: NVM

Point taken regarding evidence.


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[WheezyBaby]

Yes. These are basic concepts. Just because you're further along in training doesn't mean you can flip Year 1 science upside down. This is what we learned in our renal unit. Please, I challenge you explain me why I'm wrong.


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Lactate Ringer is composed of K(CH3CH2[OH]COOH) which dissociates into a weak acid with pKa of 3.8

The compound you listed does not exist, you either have an extra K or an extra proton, and I'm not sure which you meant. Regardless, if its dissociating, then it's dissociating into a weak base (the lactate anion)

Lactated Ringers are contraindicated in most liver disease because of a subclinical Cori Cycle defect which prevents metabolism of lactate.

LR is not contraindicated in liver disease. You may have impaired lactate clearance. And? Who cares. You even mention it as "subclinical". Well, that isn't entirely true because it can alter your measured lactate if you're following that, but regardless.

They are also contraindicated in all alkalotic states.

Again, not true. Just likely normal saline isn't contraindicated in acidosis.

Lastly, they are contraindicated in hyperkalemic states due to K+ dissociation.

This is again just not true. As has already been replied to. There's even evidence in certain situations it's superior to saline

 

[TwoStep2021]

The compound you listed does not exist, you either have an extra K or an extra proton, and I'm not sure which you meant. Regardless, if its dissociating, then it's dissociating into a weak base (the lactate anion)



LR is not contraindicated in liver disease. You may have impaired lactate clearance. And? Who cares. You even mention it as "subclinical". Well, that isn't entirely true because it can alter your measured lactate if you're following that, but regardless.



Again, not true. Just likely normal saline isn't contraindicated in acidosis.



This is again just not true. As has already been replied to. There's even evidence in certain situations it's superior to saline

I meant K[lactate] which will occur when KCl dissociates but that was irrelevant because I just wanted to say K+ and Lactate were in the solution. Then you will have lactate and its conjugate base in equilibrium. I was taught the impaired hepatic clearance would giving lactate dangerous in cirrhotic patients. I believed lactated ringer shouldn't be given because it would create a buffer region, but now I realize that range would be at 4.8 so it would be fine in alkalotic conditions, but now just confused myself.

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[WheezyBaby]

I meant K[lactate] which will occur when KCl dissociates but that was irrelevant because I just wanted to say K+ and Lactate were in the solution. Then you will have lactate and its conjugate base in equilibrium. I was taught the impaired hepatic clearance would giving lactate dangerous in cirrhotic patients. I believed lactated ringer shouldn't be given because it would create a buffer region, but now I realize that range would be at 4.8 so it would be fine in alkalotic conditions, but now just confused myself.

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In LR you have lactic acid and it's conjugate base, salt cation (mostly sodium) lactate, in solution. At a pH of 6-7 (ballpark ph of LR), that's predominantly sodium lactate. You do have impaired lactate clearance in hepatic dysfunction but lactate isn't particularly harmful, it's just a biomarker of anaerobic metabolism and by proxy cellular hypoxia. With regard to the alkalizing effect of LR, it's via hepatic conversion of lactate to bicarb

 

[Psai]

Lactate itself isn't harmful. It's used by the heart and the brain for energy. It just happens to be associated with worse morbidity and mortality. The stupidity of trending lactates is another one of my pet peeves. If you don't get a repeat lactate on someone IM docs act like you murdered someone but they just don't understand the literature.

Also lactate production isn't from anaerobic metabolism nor is it from cellular hypoxia. It's from beta agonism and overstimulation of aerobic metabolism such that you have way more glycolysis than pyruvate going through the tca cycle. Put someone in septic shock on an epi drip and their lactate will go up but they will clinically improve.

Lactate is only trended because of a ****ty study that showed that trending lactate clearance of 10% in 2 hours is noninferior to measuring scvo2 but if you're still putting in central lines and doing goal directed therapy in 2017 you need to start reading some Marik and reevaluate your care.

 

[WheezyBaby]

Lactate itself isn't harmful. It's used by the heart and the brain for energy. It just happens to be associated with worse morbidity and mortality. The stupidity of trending lactates is another one of my pet peeves. If you don't get a repeat lactate on someone IM docs act like you murdered someone but they just don't understand the literature.

Also lactate production isn't from anaerobic metabolism nor is it from cellular hypoxia. It's from beta agonism and overstimulation of aerobic metabolism such that you have way more glycolysis than pyruvate going through the tca cycle. Put someone in septic shock on an epi drip and their lactate will go up but they will clinically improve.

Lactate is only trended because of a ****ty study that showed that trending lactate clearance of 10% in 2 hours is noninferior to measuring scvo2 but if you're still putting in central lines and doing goal directed therapy in 2017 you need to start reading some Marik and reevaluate your care.

I'm not going to claim to be on top of the latest literature here and marik is still on my to read list, but (1) I'm not sure I see the logic in overstimulation of aerobic metabolism alone (which would shunt pyruvate away from lactate production) leading to lactate production, (2) initial lactate and lactate clearance are meaningful from a prognostic perspective, separate from EGDT, (3) worsening lactate with vasopressors can be explained by localized hypoperfusion. I believe these things are debated, but if there's widely accepted evidence conclusively demonstrating them to be false I'd be interested in reading it

 

[SurfingDoctor]

Why Normal Saline versus Lactated Ringers generally speaking (as neursu said, some instances require NS over LR):
1) It's cheaper, though not terribly so
2) It comes in multiple other volumes (ie 125 mL)
3) It is customizable
4) You can use for it things besides IV fluids

But the chloride concentration is clearly not physiologic and thus can have consequences. However, these consequences don't really harm patients so from a hospital purchasing perspective, cost + customization >>>>>> anything else.

There is a trial ongoing...
https://clinicaltrials.gov/ct2/show/NCT02565420

 

[Psai]

I'm not going to claim to be on top of the latest literature here and marik is still on my to read list, but (1) I'm not sure I see the logic in overstimulation of aerobic metabolism alone (which would shunt pyruvate away from lactate production) leading to lactate production, (2) initial lactate and lactate clearance are meaningful from a prognostic perspective, separate from EGDT, (3) worsening lactate with vasopressors can be explained by localized hypoperfusion. I believe these things are debated, but if there's widely accepted evidence conclusively demonstrating them to be false I'd be interested in reading it

http://www.oapublishinglondon.com/article/431

Enlighten yourself my son

 

[WheezyBaby]

http://www.oapublishinglondon.com/article/431

Enlighten yourself my son

That article was interesting, and I need to read on the biochem more because I'm not quite alert enough to read the cited biochem articles. In particular, just to clarify, they're arguing against tissue hypoxia as being an element of shock, correct? I've read previously on lactate not being the causative mechanism of acidosis in shock, but I have not read that tissue hypoxia is not the underlying central theme of shock states. What do they propose is the underlying pathology in shock if not tissue hypoxia, and what do they alternatively propose as the mechanism of acidosis? As far as the prognostic value of lactate / lactate clearance though, that article didn't offer a whole lot of argument

 

[SpacemanSpifff]

That article was interesting, and I need to read on the biochem more because I'm not quite alert enough to read the cited biochem articles. In particular, just to clarify, they're arguing against tissue hypoxia as being an element of shock, correct? I've read previously on lactate not being the causative mechanism of acidosis in shock, but I have not read that tissue hypoxia is not the underlying central theme of shock states. What do they propose is the underlying pathology in shock if not tissue hypoxia, and what do they alternatively propose as the mechanism of acidosis? As far as the prognostic value of lactate / lactate clearance though, that article didn't offer a whole lot of argument

Another viewpoint: https://emcrit.org/pulmcrit/understanding-lactate-in-sepsis-using-it-to-our-advantage/

 

[PL198]

you guys are talking so much biochem I don't remember.

were you guys chem majors or something? Idk I feel like dissociation and pkas and all that stuff isn't stuff a resident is commonly thinking about

 

[WheezyBaby]

Another viewpoint: https://emcrit.org/pulmcrit/understanding-lactate-in-sepsis-using-it-to-our-advantage/

It puts some of the marik article in different context but at the same time is largely rehashing the same information. How is shock being defined? Inadequate perfusion to meet cellular needs? And those needs are specifically not oxygen supply? But we don't specify what those cellular needs are? Or propose the alternative mechanism of acidosis in shock?

 

[ortnakas]

I already had the equivalent of a first year.


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It's probably unwise to argue clinical science with residents and attendings as an almost-first-year.

(As a third year, though, I'm still fuzzy on when to order which fluid exactly, so this has actually been an educational argument to read through)

 

[SurfingDoctor]

Generally speaking, asking Lactated Ringers versus Normal Saline in septic shock, is asking the wrong physiologic question.

 

[Raryn]

It's all a pendulum swinging back and forth.

Prior to Rivers and the advent of EGDT, people were dying of underresuscitation. After Rivers, people took the entire bundle as gospel and went nuts, with some morbidity (and likely some mortality) from overresuscitation. Now the pendulum is swinging the other way.

The rhetoric surrounding the appropriate treatment of sepsis these days is over the top and you really have to be careful interpreting the trials... The control, "standard care" is worlds different than it was 15 years ago. In a positive way... that only happened *because* of the emphasis on adequate resuscitation.

We are in the process of unbundling and re-evaluating which components are vital and to what extent, but the overall care of a septic patient and death rates thereof have only gotten better overtime. Marik is a great writer in general, but it doesn't mean that he's absolutely right on every point and that the majority of other intensivists in this country are bumbling fools.

 

[CaliforniaDreamer]

I already had the equivalent of a first year.

I am interested in what this means.

 

[Raryn]

Oh, and I'll point out again: Almost all the data comparing balanced to hyperchloremic fluids is crap. If there's an effect (which I will admit that it's very possible there is) on something other than making the chloride # on the next days chem panel a little worse, its a subtle one. Theoretically there's a difference in AKI, but I have yet to see anything convincing to support that. The only large RCT that I can think of that actually compared saline to a balanced fluid showed no difference (SPLIT), the rest were either retrospective, non-blinded analyses with a million confounders or a very limited patient population that probably doesn't apply to your typical ICU patient. Even with SPLIT, septic patients weren't a very big proportion of the cohort.

I will admit that I didn't go into critical care (though I thought about it) and at this point the only time I'm admitting to the ICU is when I'm moonlighting as a hospitalist (not that often) so there could be new data out in the last 7 months, but it would certainly be news to me.

I am interested in what this means.

From his posts, looks like he did an SMP that was the equivalent of a regular M1 year.

 

[TooMuchResearch]

Oh, and I'll point out again: Almost all the data comparing balanced to hyperchloremic fluids is crap. If there's an effect (which I will admit that it's very possible there is) on something other than making the chloride # on the next days chem panel a little worse, its a subtle one. Theoretically there's a difference in AKI, but I have yet to see anything convincing to support that. The only large RCT that I can think of that actually compared saline to a balanced fluid showed no difference (SPLIT), the rest were either retrospective, non-blinded analyses with a million confounders or a very limited patient population that probably doesn't apply to your typical ICU patient. Even with SPLIT, septic patients weren't a very big proportion of the cohort.

I will admit that I didn't go into critical care (though I thought about it) and at this point the only time I'm admitting to the ICU is when I'm moonlighting as a hospitalist (not that often) so there could be new data out in the last 7 months, but it would certainly be news to me.


From his posts, looks like he did an SMP that was the equivalent of a regular M1 year.

I don't think there's anything new and earth shattering in the past 7 months.

 

[Crayola227]

Why do IM docs swear by it? If it were up to me, everyone who needed fluids would get lactated ringers. Or maybe plasmalyte if they're rich. If you have a patient with slightly elevated potassium or renal failure and you suggest LR they look at you like you're insane even though there are data from multiple trials that show that in patients undergoing renal transplant, normal saline increases k and lactated ringers decreases it. But nah let's put in a bunch of hypertonic acid into our patients' veins.

If your blood k is 5 meq/L and you're giving fluid that has 4 meq/L then the potassium should go down. When you put an acid (normal saline which has 154 meq/L of chloride vs 110 in your blod) intravenously, the k should go up because all that acid goes intracellular and you have a ****ton more k in your cells than you do in that liter of LR. Drives me crazy.

The question.

Because as an IM intern if you put someone on LR your seniors and attendings look at you weird.

Most basic and universal answer for all intents and purposes.

But I can't think of any situation where 0.90% NS is better than LR other than hyponatremic dehydration, in patients at risk of cerebral edema, and in the initial phase of DKA resuscitation.

I have always said that I typically represent the view of the "idiot clueless intern," and I couldn't have told you more than this before reading the thread. I don't know how representative that is of the typical IM doc. Practice location matters a lot for general fields.

Why Normal Saline versus Lactated Ringers generally speaking (as neursu said, some instances require NS over LR):
1) It's cheaper, though not terribly so
2) It comes in multiple other volumes (ie 125 mL)
3) It is customizable
4) You can use for it things besides IV fluids

But the chloride concentration is clearly not physiologic and thus can have consequences. However, these consequences don't really harm patients so from a hospital purchasing perspective, cost + customization >>>>>> anything else.

There is a trial ongoing...
https://clinicaltrials.gov/ct2/show/NCT02565420

Yep, more of the what I think most will tell you. @SurfingDoctor is cool enough to have looked at some stuff, and I love the answers that aren't studies or physiology but has more to do with the practical realities of money and carrying out orders in a hospital, because that stuff typically trumps any study and can't be found in any study.

you guys are talking so much biochem I don't remember.

were you guys chem majors or something? Idk I feel like dissociation and pkas and all that stuff isn't stuff a resident is commonly thinking about

Seems to me the number of IM docs that have no fellowship, are not in training, not academic, not hanging out on SDN, likely aren't biting their nails to keep current on LR vs NS knowledge base except for where I quoted.

One, it's time consuming, and two, I can tell from this thread even if I bothered to read everything you all just cited and know what you all know, I likely would either just come upon what I felt was my own personal brand of EBM that I believe in (a laudable goal) but just as likely I'm not sure the knowledge I would think I would gain would affect management in any way I could have confidence in. I think being that up on your physiology is more useful to those that aren't gen IM.

I represent the view of, "let the smarties do the studies, read the studies, debate, if anyone comes up with something definite or makes sense to me on a first pass, I'll just do what sounds good or I saw someone smarter than me do." Bad medicine? Sure. Just another answer to the question.

 

[Lawpy]

we should have more medical education threads like this one. thanks for this @Psai

 

[Raryn]

The question.



Most basic and universal answer for all intents and purposes.



I have always said that I typically represent the view of the "idiot clueless intern," and I couldn't have told you more than this before reading the thread. I don't know how representative that is of the typical IM doc. Practice location matters a lot for general fields.



Yep, more of the what I think most will tell you. @SurfingDoctor is cool enough to have looked at some stuff, and I love the answers that aren't studies or physiology but has more to do with the practical realities of money and carrying out orders in a hospital, because that stuff typically trumps any study and can't be found in any study.



Seems to me the number of IM docs that have no fellowship, are not in training, not academic, not hanging out on SDN, likely aren't biting their nails to keep current on LR vs NS knowledge base except for where I quoted.

One, it's time consuming, and two, I can tell from this thread even if I bothered to read everything you all just cited and know what you all know, I likely would either just come upon what I felt was my own personal brand of EBM that I believe in (a laudable goal) but just as likely I'm not sure the knowledge I would think I would gain would affect management in any way I could have confidence in. I think being that up on your physiology is more useful to those that aren't gen IM.

I represent the view of, "let the smarties do the studies, read the studies, debate, if anyone comes up with something definite or makes sense to me on a first pass, I'll just do what sounds good or I saw someone smarter than me do." Bad medicine? Sure. Just another answer to the question.

Last I understood, you were still a resident. Fluids, along with oxygen, are among the most commonly ordered medications you will see on an inpatient. There's not really an excuse to not do your best to understand the reasoning for how you're using them.

 

[cbrons]

lactate isn't particularly harmful, it's just a biomarker of anaerobic metabolism and by proxy cellular hypoxia.

I've read recently that this is actually a myth, and lactate is actually a marker of physiologic stress, having next to nothing to do with hypoperfusion/anaerobic metabolism.

Here is one such article/podcast I've heard this:

https://emcrit.org/pulmcrit/understanding-lactate-in-sepsis-using-it-to-our-advantage/

 

[OnePunchBiopsy]

Also lactate production isn't from anaerobic metabolism nor is it from cellular hypoxia. It's from beta agonism and overstimulation of aerobic metabolism such that you have way more glycolysis than pyruvate going through the tca cycle. Put someone in septic shock on an epi drip and their lactate will go up but they will clinically improve.

Lactate actually comes from both of these things. Lactate rises from the anaerobic metabolism of dead bowel all the time.

Great that you pointed out the beta agonism though! That is often overlooked.

 

[SpacemanSpifff]

I've read recently that this is actually a myth, and lactate is actually a marker of physiologic stress, having next to nothing to do with hypoperfusion/anaerobic metabolism.

Here is one such article/podcast I've heard this:

https://emcrit.org/pulmcrit/understanding-lactate-in-sepsis-using-it-to-our-advantage/

... see above, post 28.

 

[SpacemanSpifff]

Lactate actually comes from both of these things. Lactate rises from the anaerobic metabolism of dead bowel all the time.

Great that you pointed out the beta agonism though! That is often overlooked.

True. Different pathophysiology.

 

[mimelim]

When the 30 or so Nephrologists that make up my referral base tell me to use LR instead of NS in their patients, I'll switch. Until then, I'll stick with what they tell me to use. At least half of them are as academic as they come and despite bringing up these papers and others, they all universally tell me to keep using NS in our ESRD patients. Admittedly, I have not investigated this in exquisite detail, but given that these guys do this day in, day out and half of them read a heck of a lot more journals about electrolytes than I do, I'll defer.

 

[Psai]

When the 30 or so Nephrologists that make up my referral base tell me to use LR instead of NS in their patients, I'll switch. Until then, I'll stick with what they tell me to use. At least half of them are as academic as they come and despite bringing up these papers and others, they all universally tell me to keep using NS in our ESRD patients. Admittedly, I have not investigated this in exquisite detail, but given that these guys do this day in, day out and half of them read a heck of a lot more journals about electrolytes than I do, I'll defer.

This is the mentality that keeps clinical practice 10 years behind the literature.

 

[BeddingfieldMD]

As the saying goes..."historical reasons."

That and comfort with NS vs LR/plasmalyte, RN comfort/familiarity, cost, availability, etc. Largely emotional and logistics issues that have nothing to do with patient care or medical science.

 

[VA Hopeful Dr]

This is the mentality that keeps clinical practice 10 years behind the literature.

Given how often new findings turn out to be wrong/incorrect, this isn't always a bad thing

 

[mimelim]

This is the mentality that keeps clinical practice 10 years behind the literature.

I'm not sure if you are referring to my mentality or the nephrologist's mentality. I am one of the biggest pushers of independent thought and practice, but overstepping the experts in the field on something like this is an easy way to hurt patients, hurt relationships with consultants and end up with law suits. I'm not going to name names to keep myself anonymous, but when faculty from 3 different nephrology fellowships, including one considered to be one of the best in the country all tell you the same thing, you generally take their word for it. These are among the best published in this area and are at the forefront of resuscitation in ESRD patients. When they say that the data is crap and to use something in particular in your mutual patients, you would be a fool to disregard them.

People like to tout medical literature and evidence based medicine. That is a good thing, but so is recognizing the limitations as well.

 

[GadRads]

It puts some of the marik article in different context but at the same time is largely rehashing the same information. How is shock being defined? Inadequate perfusion to meet cellular needs? And those needs are specifically not oxygen supply? But we don't specify what those cellular needs are? Or propose the alternative mechanism of acidosis in shock?

Just to add my own personal experience with lactate.

Several months back I read two case reports involving elevated lactate in a patient with cancer and another on beta-2 agonist therapy for asthma/COPD. I also quickly read about additional cases of albuterol-induced lactic acidosis including a case which showed resolution of elevated lactate once albuterol was switched to ipratroprium, further suggesting that beta-2 agonism was the mechanism for increased lactate. In these cases there was no evidence of sepsis or hypoxia.

Last month both the lab and nurse called about a patient's "lactic acid" elevated to 5. The last vitals which she obtained 30 mins earlier with O2 sats were normal. Apart from initial presentation nearly 2 days prior, she was never hypoxic. Her lactate in the ED was normal. I reviewed the patient's record briefly and noticed she was on albuterol. I went to see the young 20's student admitted for asthma exacerbation patient. I knocked, then walked in to see her having sex in her private room. She look embarrassed. No complaints. I didn't waste my time chasing additional labs or even doing a physical exam/ABG.

When I was in the ICU, we had a patient admitted for alcoholic encephalopathy with lactate at 4.5. The ED started sepsis work up with concerns for presumed aspiration, although initial chest Xray was clear. He was not hypoxic and was transferred to general med once his mental status improved. Alcohol itself can cause elevated lactate due to the generation of excess NADH by alcohol dehydrogenase. By Le Chatelier's principle, increased NADH favors lactate generation from pyruvate.

Hypoxia might independently contribute to elevated lactate, but this is likely from increased catecholamine discharge. The causes of acidosis in shock might be due in part to lactate, but the evidence strongly suggests that we start looking for other explanations for (metabolic) acidosis in shock/end-organ hypoxia.

 

[evilbooyaa]

Ironically the medicine residents at my institution are more liberal with fluids than my junior residents. The surgery interns are all terrified of boluses it seems.

If I catch one more of them giving a 250 cc bolus for patients who are clearly septic or hypovolemic I'm gonna kill them. I jokingly mocked that I'm waiting to see which of them downgrades to 125cc boluses first.

I just wanted to quote this to reinforce that in resuscitation situations, stop being a godamn ***** about it.

Unless the patient is a CHF'er (or other volume-overloaded state) or ESRD patient, you slam them with 1L off the bat, then 500cc as needed.

 

[Raryn]

I just wanted to quote this to reinforce that in resuscitation situations, stop being a godamn ***** about it.

Unless the patient is a CHF'er (or other volume-overloaded state) or ESRD patient, you slam them with 1L off the bat, then 500cc as needed.

The surviving sepsis guidelines, maligned as they are, are quite clear: You start resuscitation on a patient with a 30cc/kg bolus.

Patient weighs 100kg and is getting admitted for sepsis? You start with three liters. Not 500cc. Not one liter. Three liters. Obviously bad CHF and ESRD are exceptions, but otherwise, don't pussyfoot around. There's lots of conditions other than sepsis where that applies as well. DKAers often need 6+ liters to get close to hydrated (though if you slam it all in at once in a young patient you risk cerebral edema, better to space out a bit). Pancreatitis patients also commonly need that much or more with how much they're third-spacing due to the acute inflammation.

Of course, if you ask Marik we're committing "iatrogenic salt-water drowning". But under-resuscitation is a much worse crime than over-resuscitation IMO, and if you're paying attention to the fluid responsiveness of your patient, continuing the fluids is almost certainly more helpful than not.