Bedside ultrasound for Hospitalists: A Must! #Hospitalist, #FOAMed, #FOAMus

Hi, so here is a quick little overview on why anyone taking care of hospitalized patients unequivocally need to use bedside ultrasound in a daily, integrated fashion, even if they don’t realize it yet.

It isn’t just for the flashy spot diagnoses in the ICU or the ER, but really for daily rounds, assessing common cardiac, respiratory, renal, gastrointestinal and even neurological syndromes.

Love to hear from any hospitalists or medical consultants out there about their use of bedside ultrasound!



Transfusion and the Glycocalyx: John strikes again! #FOAMed, #FOAMcc

A great surprise this morning:  a comment from John. Yup, THE John. So taking a page out of Scott’s book, I thought it would be worth sharing with everyone as its own post, as opposed to just a comment. I think this is must-read material for everyone.

So without any further adue:

“I thought I might add some quirky ideas to your discussion.

We are now getting familiar with the concept of endothelial cells covered by a surface glycocalyx layer, that forms part of the barrier and mechano-sensing functions of the blood-tissue interface. We have discussed in some detail, the role of the glycocalyx in preserving endothelial integrity. I am gonna try and add a bit more spice into the whole transfusion drama.

In recent times, we have started talking a lot about a bioactive phospholipid called sphingosine-1-phosphate (S1P), as a crucial element in preserving vascular barrier integrity by ‘protecting’ the Glycolcalyx. (Most geeky papers on TRALI and other transfusion related complications do mention it).

Because albumin is one of the primary carriers of sphingosine-1-phosphate (S1P), it is possible that S1P, acting via S1P1 receptors, plays the primary role in stabilizing the endothelial glycocalyx. Infact, antagonism of S1P1 receptors have been shown to cause widespread shedding of the glycocalyx, as evidenced by increased serum concentrations of Heparan sulphate and Chondroitin sulphate. (This might probably be one of the mechanisms how albumin is glycocalyx friendly).

RBC transfusions are a double edged sword…..especially in situations of acute anemia as in post hemorrhagic situations ( major GI bleed or trauma.)….I totally agree with you in that the two are conceptually very similar.

Erythrocytes have been identified as an important buffer for sphingosine-1-phosphate . In mice, depletion of plasma S1P by genetic inactivation of S1P synthesizing enzymes (sphingosine kinases 1 and 2) elicits profound pulmonary vascular leak, which can be reversed by restoring circulating S1P via RBC transfusion.

In humans, hematocrit (Hct) predicts plasma S1P levels. There also seems to be a dynamic equlibrium between SIP levels of the plasma, and the circulating RBCs. It has been demonstrated that in anemic individuals, plasma S1P levels are not uniformly restored by RBC transfusion. Rather, the age of the RBC unit at the time of transfusion tended to negatively correlate with the ability of RBC transfusion to replenish plasma S1P. During storage, the S1P content of human RBC markedly declines, likely due to enzymatic degradation. Because erythrocytes serve as a buffer for circulating S1P, aged RBC with low S1P content may be incapable of restoring plasma S1P levels and may actually remove S1P from plasma, which in turn could contribute to increased endothelial permeability, capillary leak, and infiltration of inflammatory cells.

I hope this partly answers your question as to how the glycocalyx may be impacted by inappropriate and irresponsible transfusion triggers. I agree that these are all very novel ideas and as such, exist in the realm of experimental clinical physiology, but my gut tells me that the delicate Glycocalyx may hold the clue to a lot of answers to questions that have plagued us for a long long time!

John from India…”

So first of all, thank you very, very much for reading and taking the time to comment and enlighten us.

As John says, this is still in the realm of experimental physiology, but I think there are a lot of situations we are faced with, perhaps grey zone areas where we debate two potential therapeutic avenues, where we can use some of this data. We might debate giving that extra bit of fluid, or debate crystalloid vs albumin, or blood or no blood with an Hb of exactly 70, and I think we have to start weighing in some of this physiological data, even if it isn’t “evidence-based-by-RTC” to help guide these decisions.

The more I look into it the more it seems that our interventions – particularly fluid resuscitation, needs to be reassessed from the ground up both in nature, quantity and rate of infusion while measuring glycocalyx damage – e.g. biomarkers such as S1P, heparan or chondroitin sulfate, etc…

I’ve previously posted and podcasted about my general strategy for fluid resuscitation, and I am definitely in the process of revising it, still unsure what is best. I’d love to hear how John resuscitates his patients…



Other Comments:

Mystery John has an uncanny ability to describe complex physiology in the simplest way possible. I am very interested in digging more into his predictions of the possibility of aged erythrocytes removing S1P from circulating plasma.

Dr. John, if you’re out there, could you point us all to some of these studies you’ve mentioned? Any good S1P review papers you’d recommend to those, like me, who are S1P novices?

Thanks for your input! It was a pleasure.

Warm regards,


Thank you Derek, for the kind comments…. I think the concept of S1P is still in the process of evolving and assuming a definitive shape, so a good review might be hard to stumble across.

A good research article which cites some excellent references might be —

Synergistic Effect of Anemia and Red Blood Cells Transfusion on Inflammation and Lung Injury
— Anping Dong et al. (It is open access at

Hope this helps……


Here is the article:



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

Enough with the “Normal” Saline!
So its been about a year since a JAMA article ( 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.
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).

CCUS Annual Symposium 2014 – The Ultrasound-Assisted Physical Exam! stay tuned!

This year, we’re putting together a really, really interesting event.  Bedside ultrasound being a hot topic and at the brink of revolutionizing clinical examination and practice, we figured that this year, we’d go back to basics to some degree with a general ultrasound approach, but also a step further in looking at it from an integration perspective, meaning how to approach clinical problems with ultrasound as an added tool.

Talks will be clinical problem-based – e.g. the patient with dyspnea, the patient with renal failure, etc, essentially showing participants how to integrate their growing ultrasound skills into routine use.  There will be a ton of faculty led workshops to review all the basic ultrasound skills (lung, cardiac, abdominal, vascular) on live models and on advanced CAE simulators, both adult and pediatric.

Our faculty will be fantastic, including Andre Denault, Haney Mallemat (@criticalcarenow), JF and Max (@EGLS_JFandMax), Edgar Hockmann, Catherine Nix, Alberto Goffi, Massimiliano Meineri, Matt Hoffmann (, Jeff Burzynski, Jason Fisher, Alyssa Abo and many more…

The two day core event will take place in Montreal, on may 10th and 11th, and, equally interesting will be a pre-congress set of courses on may 9th, including:

EGLS (echo-guided life support)

Focused TEE

Bedside ultrasound for nurses (vascular access, IVC volume status assessment)

Critical Care Procedures (drains, tracheostomy, central lines)


Registration is not yet open but will be in the next few weeks, so for anyone interested please visit and join (it’s free!) and we’ll email you when its up and running.

Please forward/link this to all your forward-thinking colleagues~




Bedside Ultrasound & the patient with Acute Renal Failure – an N=1 Podcast #3, #FOAMed, #FOAMcc


So here is a quick and dirty approach to the patient with ARF using bedside ultrasound, which enables the rapid diagnosis or ruling out of two important and time-dependant conditions with significant clinical impact: hypovolemic and post-renal/obstructive renal failure.

Let me know what you think!

Philippe Rola

Bedside Ultrasound Picture Quiz 4 – #FOAMed, #FOAMcc

75 year old patient on the wards with poor urine output. Got a bolus, got some lasix. Still nothing.


what do you see?

Full bladder despite foley copy



…scroll down for an answer!















…that’s a full bladder with a correctly positioned but blocked foley. Change it!

CHF-associated Renal Failure: Low-Flow…or not??? #FOAMed, #FOAMcc

So here’s a common enough clinical scenario:  An elderly patient with CHF presents in exacerbation, requiring significant oxygen and eventual NIPPV. He is admitted to a critical care bed.  The next day, it’s noted that his creatinine has almost doubled. He remains on NIPPV. The intensivist is hesitant about how aggressively to pursue diuresis: he’s worried about worsening the “low-flow state” and the renal function.

I know I grew up hearing that as a resident, and never questioned it. On the surface, it makes plenty of sense. Someone with CHF has a “bad heart”, pre-renal failure is a definite entity, so why not?

So let’s examine those assumptions. First of all, not all patients who present with CHF actually have a bad ventricle, some may have valvular heart disease, hypertension with elevated filling pressures, etc… Secondly, few of our CHF patients are really in a severe “low-flow state”, since that would essentially be cardiogenic shock, a very different entity, even if along the same spectrum. More importantly, however, the renal autoregulation curve is actually broader that most of the rest of our tissues and organs. That makes it unlikely that, in someone normotensive (as most patients in CHF tend to be), worsening renal failure is attributable to a “low-flow state”.  The ARF attributable to a low-flow state – which we see often enough – is the organ failure resulting from shock: shock liver, shock kidneys, etc…

So…what could it be?  Let’s continue to apply basic physiological principles. What is the pathognomonic feature of CHF?

Congestion: pedal edema, ascites, effusions, anasarca, etc…

What if we had…congestive renal failure?

I have to credit a bright colleague of mine, Dr. Jason Fung (, for putting me on that track. As a bedside sonographer, what I could see in most of these patients is that their IVCs were still really full, and that most didn’t have other clinical signs of poor flow such as cool extremities and decreased mentation. And given that they were still in significant respiratory failure, I felt they needed diuresis. Also, the full IVCs suggest that these patients are on the flat part of the Starling curve (after all, that’s what the fluid retention causing CHF is trying to do!) and that they should not suffer a drastic drop in cardiac output with ongoing diuresis.

Well, Jason was the first to point out to me that the elevated IVC pressure (CVP) is directly downstream from the kidney! And directly by a couple of inches, the length of the renal veins! I have to say that was an embarrassing lightbulb moment, but a lightbulb moment nonetheless.

So let’s review renal blood supply and flow physiology. As is the case for any organ, the following applies:

Q = (P art – P ven) / R

where Q is renal blood flow (RBF), P art is MAP and P ven is CVP, and R is the renal vascular resistance.

Let’s keep that in mind.

Uniquely, the kidney has two set of arterioles which modulate the GFR and allow for the celebrated autoregulation curve. The resistance of each is controlled by the number of factors, hormones and drugs.

The reason P ven is CVP is that the renal vein drains directly into the IVC, which drains in turn into the RA, the pressure is the same. Now some of you may have read my rants against CVP in some of my posts (see, but that is in reference to its use as a marker of preload and volume responsiveness. When the answer one is seeking is the downstream venous pressure, barring some pathological venous obstruction, CVP is it.

Hence, the higher the CVP, the lower the RBF.

This makes complete sense, but how often has anyone heard this mentioned in the management of renal dysfunction in CHF patients?  As in the case for many things in medicine, we often forget (or are not taught to) link basic physiology (all that medical school stuff…) with clinical pathophysiology (…the “real” world).

Well, it turns out that fortunately, a bunch of smart people have been looking into this matter, and the best study in my opinion is by Mullens et al (JACC vol 53, n 7, 2009), which reveals a clear increase in prevalence of worsening renal failure with increasing CVP, but more interestingly, the lack of significant association between cardiac index and worsening renal failure, which is the “low-flow” traditional hypothesis.  The most clinically important finding in this study, however, is their finding that failing to reduce the CVP to below 8 resulted in a 51% incidence of renal failure (vs 18% for those patients who were reduced to a CVP < 8mmhg).

An excellent review for this was recently published by Gnanaraj et al (Kidney International 83, 384-391, mar 2013), which reveals a fairly strong association between an elevated CVP and renal dysfunction.

So it seems fair to conclude that congestive renal failure is an under-recognized clinical entity that is commonly untreated (or even improperly treated) due to unfounded and unphysiological concerns.

Now something our group will be focusing on is a study on the use of IVC sonography in the assessment of CHF-associated renal failure. We believe that IVC ultrasound will provide a better, simpler and less invasive method to assess renal congestion.

The use of IVC ultrasound in CHF would not be new:  Goonewardena et al (JACC Cardiovasc Imaging 2008; 1, 595-601, or found that IVC size at discharge was the best predictor of readmission. In other words, if someone didn’t get your IVC down below 20 mm, you were much more likely to be readmitted.

As an ICU physician, I rarely discharge patients home.  But I do make sure I get IVCs into a normal range (below 15mm generally) before my CHF patients leave my unit, and, especially recently, I do make sure to continue diuresis when faced with a distended IVC with little variation and worsening renal failure.

This is certainly a topic that merits further study, but I think there is enough good evidence and physiological rationale to hang up those old beliefs in a dark closet and start treating congestive renal failure.

Please let me know what you think, what your practice experience is, and if you have anything else to add!

thank you,

Philippe Rola