saline

January 1, 2014

The N=1 concept. #FOAMed, #FOAMcc

First of all, happy holidays to all and happy new year!

Following a few requests, I’m gonna put up a few words about the N=1 concept, as I think it comes up in every single therapeutic and diagnostic strategy.

We do not treat a thousand, a hundred or even ten patients at a time.  As clinicians, we deal with a single patient, with a certain pathology, and his own, unique physiological pattern of response to that pathology.

In a medical utopia, we would be able to have a precise biophysiological profile of our patient – probably including parameters that either don’t yet exist, or are on the verge of being found or invented.  We would know, for instance, the degree of glycocalyx damage, the nature of this damage, the degree of subsequent capillary leak, the specific inflammatory cytokine pattern, and thus be able to use a potential combination of agonists and antagonists to favor healing, and tailor fluid therapy to the “just right” amount, avoiding both under-resuscitation and tissue edema. This would be similar to antibiotic sensitivity testing. Who, in this century so far, would deliberately not order sensitivities, instead satisfying themselves with a positive result and happy with empiric therapy?

Just in terms of biological variability, it is impossible to believe that all patients would respond best to a single goal or therapy. How can an MAP of 65 be as good for a septic hypertensive patient as it is for a young septic woman who normally walks around with an SBP of 110? Not that I don’t use that number myself most of the time, but certainly food for thought, and something to keep in mind when treating either of those “types” of patients…

And the answer to the N=1 riddle isn’t just subgroup analysis. The questions have to be answered in prospective fashion, built into the study design. Not easy work, and especially since we don’t yet even know what the key variables/questions are… But personally, as mentioned in an earlier post, I do now suspect that the ubiquitous glycocalyx holds some of those answers.

Let’s look at the whole fluid debate through the N=1 lens: it makes no sense whatsoever to debate crystalloids versus colloids. This negates thinking and only encourages near-religious fervour amidst both camps. Rather, look at your patient. Is he truly dehydrated/volume depleted or just volume responsive on the basis of vasodilation. If we want to restore the ICF and the interstitium, then crystalloids are probably better, but if we want to restore effective circulatory volume, then some measure of colloid may help avoid excessive edema, though even this can be debated. Even more important is the composition of the resuscitation fluid. Much as we adjust our TPN, we should probably design our resuscitation fluids, rather than only using Ringer’s Lactate (I say only just to drive the point that NS should not be used as a resuscitation fluid, unless repleting chloride is specifically necessary).

Now this may sound like a rant against large trials, but it isn’t. Absolutely invaluable information can be derived from these, it is just a matter of thinking how that information can benefit the one patient you have in front of you. And this isn’t easy. You have to put together your history, physical exam, bedside ultrasound exam and labwork. You can’t just say  “sepsis? 2 litres,” or any other such recipe (aka protocols).

ok, enough for a january 1st!

 

Love to hear what anyone thinks!

 

Philippe

 

November 18, 2013

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).
September 30, 2013

Bedside Ultrasound Picture Quiz 2 #FOAMed, #FOAMcc

73 yr old woman recovering from septic shock with abdominal distension and difficulty tolerating enteral feeds…

 

what do you see?

BUPQ2

 

 

scroll below for the answer…..

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

BUPQ2 Answer

 

Extensive third spacing from resuscitation has resulted in bowel edema and ascites.  Another “benign” effect of massive crystalloid use… A bedside 22g US guided tap confirms benign transudate.

September 20, 2013

The Ideal Resuscitation Fluid – an N=1 Podcast #FOAMed, #FOAMcc

So here is the first in a series of mini-talks geared towards having us think about fluid resuscitation, which, for those in acute care of almost any type (ER, wards, ICU, anasthesia, surgery, etc…) is part of our daily routine. And that’s exactly what it shouldn’t be, routine. It should be carefully thought out and adapted to each individual clinical situation we’re facing.

So I’ve decided to approach this from a completely different angle, not looking at what we do, what’s available, and see what has been stacked up against what, etc, etc… Instead, I’ve decided to start the discussion from a completely theoretical standpoint and talking about something that doesn’t exist:  The Ideal Resuscitation Fluid.

Please, let me know your thoughts!

Philippe

http://www.ccusinstitute.org

(sorry the last 40 seconds were cut – now the “full” 5 minutes are up!  apologies, I am techno-challenged!)

September 18, 2013

Why do we bother checking CVP? #FOAMed, #FOAMcc

I was recently scanning the literature in preparation for our symposium, and came across what should have been a 2003 instead of a 2013 publication in the March issue of the CCM Journal, entitled “Point-of-Care Ultrasound to estimate Central Venous Pressure:  A Comparison of Three Techniques.”

I have to admit this is a pet peeve of mine, from the standpoint of a clinical physiologist, which is, as far as I’m concerned, what any physician looking after critically ill patients should be, at least some of the time.

So our real question is: is my patient fluid-responsive?  And perhaps a corollary question would be: is he fluid tolerant?

As a longtime bedside sonographer, physiology, experience and slowly growing evidence all support my using IVC sonography as a tool to assess volume responsiveness.  It isn’t perfect, and personally, I find the common M-mode, two-point measurement to be inadequate compared to a global assessment of the IVC, but it certainly is far closer to “the truth” we seek than CVP.

This then begs the question: why on earth would we be seeking to correlate one type of data to another which is clearly more removed from “the truth” we seek?

The use of CVP is largely cultural and deeply ingrained. There are some limited ways and pathologies in which it can be useful, but not as a measure of preload.  My friend Paul Marik published a piece that was both enlightening and entertaining in Chest a couple of years ago which I would have thought would have been the final nail in the coffin for the use of CVP as a preload tool, but it endures…even in the latest surviving sepsis guidelines…

A testament to religion over science.

Philippe Rola

http://www.ccusinstitute.org

note that this was first posted in my buddy Matt’s awesome website pulmccmcentral (http://pulmccm.org/2013/critical-care-review/why-do-we-bother-to-check-cvp/) please check it out!