Enough with the “Normal” Saline!!!!! #FOAMed, #FOAMcc

Enough with the “Normal” Saline!
So its been about a year since a JAMA article (http://jama.jamanetwork.com/article.aspx?articleid=1383234) finally showed that the downside of 0.9% saline isn’t just theoretical, but has some associated clinical morbidity (bad for the kidneys!).  Sadly enough, it still seems to be the routine fluid used for boluses. Whether the ER, hospitalist or intensivist, residents, students…it seems people are reluctant to let go.
Today, rounding in the ICU, I was changing an order for a bolus from another doc from NS to RL, and a nurse asked me why.  I gave her a capsule summary and she was in disbelief.  “Come on Phil, they wouldn’t call it normal saline if it wasn’t!”
I’m an internist by training, so naturally I grew up using NS, since that’s what all the attendings and residents used around me.  Ringer‘s was the stuff the surgeons used, so well, I guess it had to be wrong…no?
So forward to 2001 and John Kellum‘s lecture on acid-base I’ve previously mentioned, and my exploring Stewart’s Physicochemical Approach, and wait, I look at the back of a bag of NS, and find out, much to my dismay, that the stuff I’ve been using like holy water has a pH of 5.6.  And who have I been giving liters and liters of this stuff to?  Yup, mostly patients with acidosis. Hmmm. Interesting. So although I don’t necessarily advocate correcting metabolic acidosis for the sake of doing so (see my previous post on bicarb), I’m not a proponent of worsening acidosis either, even if by another mechanism.
I think there are a number of factors that have resulted in this situation.  For starters, there is the issue of false advertising – the “normal saline” monicker has been influencing subliminal thought for decades (think Malcolm Gladwell thin-slicing), making physicians feel they are giving and inherently “good” substance.  Then there’s the whole tribalism thing with the surgeons vs non-surgeons making all the non-surgeons polarize away from RL (not that RL is perfect, just a bit better, and certainly closer to “normal”). Finally, there’s this sad, sad factor that makes people, even (or maybe even more) smart people reluctant to accept that they have been doing something wrong (or, for those who are offended right now, not ideal) for a long time (I sure was) and prefer to fight it and rationalize it for a few more years until, eventually, the evidence becomes overwhelming or the changing of the guard has fully taken place.
I think what we should be hanging on to is not a drug or a fluid but rather what we learned in the first couple of years of med school: physiology.  Now mind you, at that point we (or most of us) didn’t have a clue how to use it for anything more that answering multiple choice questions, but at some point, we have to go back to it and realize that is what we should be basing our assessment of our therapeutic acts and decisions.
So…if I have a situation where I am low on chloride, I might want to use NS. But otherwise, let try to give something whose composition is a bit closer to our own than NS is.  So, for my students and residents, don’t let me see you prescribing boluses of NS.  If you really, really need to, wait until your next rotation please.
thanks!
Philippe
ps for a great review of the original aritcle, please see Matt’s on PulmCCM at :
Reply:  by Marco Vergano
Totally agree!
I have been struggling for years with the bad habit of some of my colleagues prescribing NS as the most harmless and physiologic replacement fluid. Here in Italy we don’t have such a clear separation between internists and surgeons about NS/RL choice: the bad habit of easily prescribing NS is ubiquitous.
Given the results you mentioned about the increased incidence of renal failure with NS, I am wondering if the ban on ALL starch solutions would have been necessary after the introduction of new balanced starch/electrolyte solutions.
What I really don’t like about RL is that it’s not only hypotonic, but also low in sodium. In our ICU we often have many ‘neuro’ patients (trauma or vascular) and sodium variations become a major issue. Also I prefer Ringer’s acetate over lactate on most of the patients who struggle to ‘manage’ their own lactate.
So my favorite solution remains our good old “Elettrolitica reidratante III” (very similar to Plasma-lyte).

Bicarb: Myths and Facts…

So I was in the ED a few days ago as overheard a conversation between one of the staff internists and a resident, and how they were planning to correct a lactic acidosis using some bicarb.  I cringed under the surface, because the attending was explaining how this would buffer the acidosis, and the resident was nodding. The attending then turned to me and asked me how much I would give in this case.

I had a moment of hesitation because it was a particularly busy day and I hadn’t planned on an impromptu teaching session which I knew would have to happen if I opened my mouth. On the other hand my…academic principles (? – or something like that) wouldn’t allow me to agree…

I wouldn’t give any at all.

So I’ll spare you the play by play, but here is the gist of it.

Rewind first to 2001’s SCCM in San Diego and a talk by Dr. John Kellum about acid-base, and my introduction to the Stewart or physicochemical approach to acid base.  Somewhere in that hour was one of my few genuine lightbulb moments in medicine, and a sinking realization that a lot of stuff I’d been thought wasn’t really so.

Here’s a simple equation we all know:

CO2 + H20   <-> H2CO3 <-> H+ + HCO3-       this is mediated by carbonic anhydrase.

so…

1. we have a LOT of CO2

2. we have a LOT of H2O

3. carbonic anhydrase is pretty ubiquitous…

thus…we have an (almost) endless supply of “bicarb.”    What????

Yup. I’m not particularly bright nor a chemist, and although I did read Peter Stewart’s original paper, much of it was over my head.  However smarter docs have distilled the principles (http://www.anaesthetist.com/icu/elec/ionz/Findex.htm) to make it palatable to the clinician. It does seem to make a lot of sense, and explains many clinical scenarios which didn’t seem to make physiological sense. In addition, the slow and steady growth of literature using the strong ion difference rather than traditional acid base theories is encouraging.

Most of all, being involved in education, I have had the privilege of exchanging ideas with some really bright people, and all the ones who are particularly physiological have changed their acid base understanding to the Stewart approach.

So, in super-summary, this approach tells us that the only role of HCO3 is to maintain electroneutrality, which is primarily filling the gap between sodium and chloride. Depending on what happens to sodium, chloride, or if there is another anion, HCO3 will either increase or decrease, mediated by carbonic anhydrase. We make as much or as little HCO3 depending on our needs. It is a dependant variable, and has no active role.

In fact, when we are administering “bicarb,” what we are really giving is sodium without chloride, thus increasing our strong ion difference. We can give sodium acetate or citrate and the bicarb will increase just the same – filling the gap.

So what does this mean clinically?

Well, first of all it is important to understand what we are doing if deciding to administer NaHCO3: attempting to change the pH (note that I’m not saying improve, because in varying scenarios, I’m not sure which pH is better…).

One of the common and sometimes almost subconscious beliefs is that bicarb “buffers” acids in a sense of neutralizing them. This is only true in the sense of electroneutrality, and not in a biological sense. The more important thing to realize is that none of these acids are directly “toxic” and require “buffering”…  Lactic acid isn’t toxic, it’s cellular fuel. Its the process behind it that can be and that sometimes needs to be excised!

So the question then becomes when is it truly important to increase the pH? When is there actual benefit?  I won’t argue that at some levels (<7) I get chicken too, and feel like giving some solo sodium (more commonly known as bicarb). But I think it is pretty clear (permissive hypercapnia data) that pH in the range of 7.20-7.35 is innocuous. How about 7.10-7.20?  Or 7.00 to 7.10?  I don’t know. But I do know that my DKA patients (6.85-7.20) are definitely not in cardiovascular collapse. Just a little tired from the Kussmauling…

So what am I doing with the NaHCO3?  Is increasing pH beneficial to my patient? Certainly to the one who is arresting from hyperkalemia it is, to shift the K a little, but what about my septic patient?

Well, in giving NaHCO3, I am increasing my CO2 load (equation vide supra), which my respiratory system now has to get rid of, else I am worsening my intracellular acidosis (CO2 diffuses freely).  I am also interfering with the adaptive response of the hemoglobin dissociation curve and impeding the right shift (below) which helps deliver more oxygen…hmm…and aren’t most of these patients to whom we consider giving “bicarb” having some degree or other of tissue hypoxia…? hmmm… what was the benefit again?

O2 Hb dissoc

Scott Weingart (emcrit.org) also gives a great podcast about his use of NaHCO3, especially the means (bolus vs infusion) and indications.

Personally, I think it’s reasonable to use in a mixed infusion when facing hyperchloremic acidosis, usually post-resuscitation due to overzealous use of NaCl, but never really in “treatment” of acute metabolic acidosis (especially not with the theory of “buffering”), and it is important to remember what we are trying to do, to what end and possibly at what price.

Now I know some people really, really disagree with this, so please let me know your (physiological) thoughts!

thanks!

Philippe Rola