CCUS 2014: Taking your Ultrasound Game to another level! Montreal may 9-11, 2014!

Registration is open!

For the 7th edition of our Annual Symposium, we’ve assembled a great cast of characters to bring your bedside ultrasound game to a whole new level! Whether you’re a novice or have some experience in bedside ultrasound, we’re sure you’ll find our program very interesting, as the perspective we have chosen to take is patient-based, with each lecture explaining how ultrasound findings are integrated into clinical decision-making.

First of all, it’s in Montreal, May 10th and 11th, 2014. If you’re from out of town, its an awesome city to visit, and if you’re a Montrealer, well, it’s an awesome conference at home!

Indeed, this isn’t “just” a “how-to” course – although that is what we’ll be covering in the workshops which will follow each lecture – but a “how to integrate ultrasound into your daily practice” course, so no matter what your level is, you’ll find something suited for you. The workshops will be divided into novice and experienced and with a low participant to faculty ratio, will ensure a great experience.

So what are we going to be talking about?

In the CC/ED/hospital scene:

–       the patient with chest pain, by Max Meineiri

–       the patient with CHF, by Mike Stone

–       the patient with renal failure, by Sara Sebbag

–       the patient with a swollenleg, by Michael Woo

–       what’s my patient’s volume status? By Ashraf Fayad

–       the patient with a decreased level of consciousness, by Robert Chen

–       the patient in shock, by JF Lanctot and Max Valois

–       the patient with abdominal pain, by Haney Mallemat

–       the patient with a bowel obstruction

–       the patient with broken bones: finding and freezing, by Catherine Nix

–       the patient with dyspnea, by Alberto Goffi and Edgar Hockmann (KEYNOTE)

–       the hemodynamically unstable patient: multi-modality assessment, by Andre Denault (KEYNOTE)

In the office scene:

–       the patient with a neck mass, by Sarah Sebbag

–       the patient with arthritis, by Alessandra Bruns

Here is the program:

CCUS 2014 Master Programme

Who made this up?  Our scientific committee is made up of Michael Woo, Catherine Nix, Edgar Hockmann, Alberto Goffi and Andre Denault, who is also the co-chair – with myself – of this year’s symposium.

For those of you part of the twitterverse and #FOAMed movement, you’ll get a chance to meet @criticalcarenow (Haney), @bedsidesono (Mike), @nobleultrasound (Vicki), @EGLS_JFandMax (JF and Max) and @ThinkingCC (yours truly)…and Matt ( will be there to chronicle the event and bring the highlights to the #FOAMed world.

So who should come?  Anyone taking care of sick patients.  If you’re an ED doc, ICU doc, hospitalist, anaesthetist, surgeon, student or resident, this stuff is gold. Even if most of your practice is office-based, precise assessment of dyspnea, volume status and cardiac function is highly practical.

Additionally, there are several very interesting pre-congress courses taking place on May 9th, particularly the Echo-Guided Life Support course (JF Lanctot and Max Valois), a Bedside Ultrasound Course for Nurses, an Acute Care Procedures Course and a Symposium for Ultrasound Educators on how to set up training programs. All in all, a lot of great stuff.

For more details and registration, please go to  And yes, of course there are CME credits by the University of Montreal.

As I said a few months ago – well, tweeted, to be exact – if you’re an acute care MD and NOT using bedside point-of-care ultrasound, you’re stuck in the 20th century… rude, but true.

Hope to see you there!

Philippe Rola

President, CCUS Institute

Pleural effusion in the sick patient (Part 1of 3): Don’t miss it!!! #FOAMed, #FOAMcc

This, in my opinion, is an under-recognized problem when bedside ultrasound is NOT a routine part of examination of critically ill patients. I’m happy to say that as many of my colleagues have been picking up probes, it is somewhat less of an issue now, whereas a couple of years ago I’d often put in 4 or 5 pigtail catheters on day 1 of taking over the ICU.

The first and foremost reason for this is that the portable supine ICU CXR sucks at picking up the small to moderate to, yes, even the large pleural effusion.  Largely owing to the fact that many of our patients have some lung parenchymal abnormalities and to the recumbent position that causes a layering of the effusion, it is often difficult to properly assess the size of a pleural effusion.  Radiologists will usually report the presence of a probable effusion, but quantification is difficult, and physicians not performing routing bedside sonography will often realize the presence of a submassive effusion only on CT scan – after all it isn’t like you can turn and rotate your patient to percuss the shifting dullness, can you?  Not very practical.

So the following can often be seen:

pleural effusion

this is fairly large, or you might see:

pleural effusion and pneumonia

So the obvious and critical question is: when is it necessary to drain?

There are two elements to this question:

a) for diagnostic purposes: unless the diagnosis is clear (eg CHF, post-resuscitation “michelin man” patient, etc) a new effusion should be tapped.  Panapneumonic effusions, in particular, warrant ruling out empyema unless there is a compelling reason not to.  For diagnostic purposes a 22g needle usually does the trick unless you have frank pus – which generally shows up differently on ultrasound.

b) for therapeutic purposes: effusions are space occupying lesions which compress the lung and result in a variable degree of respiratory compromise, depending on chest wall and diaphragmatic compliance, as well as effusion volume.  The clinical effect is highly variable due to the above as well as the degree of parenchymal lung disease and the degree of PEEP.  In the ICU or ED, a simple way to think about it is that if your patient is in respiratory failure and has a large effusion, chances are that draining it will improve things.  It gets a little more controversial and complicated if you have a patient who is mildly dyspneic with a moderate sized effusion.

Here are a few clinical scenarios I like:

Mr. A is a 65 year old man with CHF, intubated, with large bilateral effusions. He has been aggressively diuresed to the point of his IVC being less than 5mm in diameter.  He has not been able to wean in the last 48 h.

Yes, I definitely drain this fellow. Been there and done that time and time again.  The pleural effusions are essentially the last to resolve (being the most “distal” to the circulation – vs the alveolar tissue itself) and hence can lag and cost a few more days or more of ventilation).

Mr. B is a 47 year old man with pneumonia, breathing spontaneously with a moderate (maybe 500ml) effusion. It appears free flowing and clear, he is afebrile with an improving white count, and mildly dyspneic.

Nah, I skip on this one.  If fever and WBC recur, I do a diagnostic tap to r/o empyema.

Mrs. C is intubated on PEEP 18 FiO2 85% for ARDS due to pancreatitis. She has some degree of intraabdominal hypertension (IAP 18) and has bilateral moderate pleural effusions, maybe 400-500ml.

Yup. She can physiologically benefit from decreased intra-thoracic pressure, both from the ventilatory and the intra-abdominal pressure standpoint (Remember the diaphragm is not a rigid structure so that IAP and ITP are very similar in most cases).

So is there any evidence for this?  Some. And that’s for part 2, coming within the next days. Part three will explain and show my procedure of choice for drainage.


love to hear what other guys’ practices are!   Apparently only about 15% of ICU guys “routinely” drain effusions.



Hi Philippe,
I am very happy to read your post tonight, bacause I am part of that 15% and luckily most of my colleagues are in the same group. I agree in particular when you say that pleural effusions are the last to resolve, being the most “distal” to the circulation. I often find patients, at a certain point during their ICU stay, be not only like a “michelin man” but also (and at the same time!) hypovolemic. I call this situation, when I try to explain it to residents, “empty in full” (maybe in english it doesn’t sound as good as in italian): we are trying with diuretics and some fluid restriction to manage those extravascular fluids that prevent weaning from mechanical ventilation, but often we get the only effect of causing renal failure rather than eliminating pleural effusions. In this case the only way is to drain.
Another important point is that bedside chest x-ray is absolutely useless when you have to discriminate between pleural effusion and parenchimal consolidation, both of them often coexisting in ICU patients.
In our routine we use 14-gauge single lumen CVCs, inserted with Seldinger technique and ultrasound assisted procedure, effective in 95% of the effusions and less invasive than a pleurocath (that we use most of the times for pneumothorax) or a real chest tube, which I keep for blood or traumatic pneumothorax.
Greetings from Italy,


Glad to hear it Marco!  I started with CVCs as well before we were able to find inexpensive pigtails – email me for info if you want I don’t want to “brand” these things!  They are actually really good because I found CVCs would often occlude. Patient comfort with either is so much more than chest tubes. 

Great point about the “michelin man” who is very “wet” but intravascularly dry, which we see commonly post acute phase of critical illness, especially when physicians are so keen to use crystalloids.

thanks for reading!



The Rage is all the rage! #FOAMed, #FOAMcc

So I just finished listening to the second podcast of The Resuscitationists’ Awesome Guide to Everything (, and as advertised, it is totally awesome.  It’s really cool to have the point of view of several bright acute care clinicians whose field of expertise obviously overlaps but have different perspective in terms of experience and setting.

In episode 2, they do a great review of the MOPETT trial and thrombolysis in PE in general, and really work at distilling clinical information from academic literature, which is ultimately what has to be done. The hashing out of the finer points by using specific clinical scenarios is really, really good.

I have personally applied the MOPETT half dose TPA twice with good success, both in young patients and after explaining the risks and benefits. As in full dose thrombolysis, the clinical improvements in minutes to hours of massive/submassive PEs are quite remarkable.

So much kudos and everyone interested enough to read this should most definitely be checking them out, I know I’ll be!



Blood transfusion and serum S1P levels in Sepsis: a leaky proposition? (Protecting the Glycocalyx Part1) #FOAMed, #FOAMcc

So in my ongoing quest to reframe my resuscitation step-by-step, I’ve been following up on a number of leads regarding the glycocalyx, as previously stated, and John’s reference to this article in a previous comment I feel is highly relevant. So this is it:

Synergistic Effect of Anemia and Red Blood Cells Transfusion on Inflammation and Lung Injury,  Anping Dong, Manjula Sunkara, Manikandan Panchatcharam, Abdel Salous, Samy Selim, Andrew J.Morris, and Susan S. Smyth

Advances in Hematology, Volume 2012, Article ID 924042, 8 pages

S1P (sphingosine-1-phosphate) is a regulator of endothelial permeability and immune function.  Uh-oh, why had I not heard of it? Hmmm…I don’t think it was in Guyton’s or in Harrison’s…and there hasn’t been an RCT about it… Ok, that about explains it.

So here are some factoids about S1P:

–       serum levels correlate with HCT as RBCs serve as an S1P reservoir.

–       anemic patients’ S1P levels are NOT fully replenished by transfusion, especially the older the transfused blood is.

–       In fact, older RBCs may actually remove plasma S1P.

The study:

They basically took mice, and in the first group, bled them (by 20ml/kg) and looked at inflammatory markers, lung permeability and also S1P levels. That’s basically the control group, and they noted that hemorrhage significantly increased inflammatory markers (interesting in and of itself) . They then transfused these mice using wither fresh, S1P-loaded RBCs, or 14-day old RBCs, and, lo and behold, the fresh blood resulted in less inflammation, increased S1P, but most importantly, markedly decreased lung permeability. So clearly, S1P attenuates transfusion associated lung permeability.

In the next group, they injected the mice with LPS following hemorrhage, and found a synergistic effect of blood loss and LPS on inflammation and lung permeability, as could be imagined. Following the LPS, they were transfused with one of four strategies: fresh blood, old blood, fresh blood + S1P or old blood + S1P.  Well, lung permeability still increased in all groups, but least in the fresh blood + S1P, and the old blood + S1P a close second.

Note, interestingly enough, that saline alone (the “control”) also increased lung permeability, highlighting yet again that NS (and probably any crystalloid) is not innocuous…

So here we’re looking at the finer effects of transfusion, and why, against “common-sense” correcting a patient’s hemoglobin level does not seem to help in all situations.  We have understood the aging issue and loss of deformability, but it is time to take a finer look.  We are familiar – at least in concept – with transfusion-associated lung injury or TRALI, but the mechanism remains unclear.

Summary and Take-Home message:

S1P infusions in sepsis?  Maybe someday…

Yes, this is an animal study, and the results cannot be extrapolated directly to humans, but it is food for thought, as John had mentioned.  Certainly at least this should tell us to keep and ear/eye out for human work with S1P, but personally, it will make me even more comfortable in not transfusing my septic patients with hb’s in the low 70’s and maybe even high 60’s (try repeating the cbc, more often than not comes back a couple points higher and you can avoid transfusion), and for those who are a little more aggressive with transfusion, maybe this should make them think twice…

I’ll add what I can dig up on human S1P studies soon.



Bedside Ultrasound Clip Quiz #7: Discussion #FOAMed, #FOAMcc

So here is the clip again.  This is a transverse epigastric view with the IVC in short axis and the hepatic veins (bunny ears) draining into it.  We can see bright hyperechoic material moving up and down, which are air bubbles.  Note that this is air in the hepatic veins and NOT the portal veins, which can be “relatively” common due to ischemic bowel and a few unusual causes.

Air in the systemic hepatic circulation is quite unusual.  Obviously, air anywhere in the circulation implies a breach of vascular integrity somewhere – in the case of portal venous air, the breach is in the bowel microvasculature as the bowel breaks down. In the case of air in the hepatic veins, we are looking at air coming from (a) the lower body vasculature, so in the absence of trauma the most likely cause is iatrogenic from a femoral line, or (b) the upper body vasculature if associated with tricuspid regurgitation (iatrogenic or lung vascular injury coupled with positive pressure ventilation).

Here is an article discussing hepatic vein air.


Their clinical point is important to note – you have to investigate to get an idea of the amount of air and the possible source.

So this patient was transferred to my ICU from a smaller centre for more aggressive care. He was in profound septic shock felt to be pulmonary in aetiology, on levo/vaso/epi and dobutamine, ventilated on 100% with PEEP 16. My basic CUSE (critical ultrasound examination) done on essentially every critical care patient revealed this rapidly and, concerned that air embolism had occurred (femoral line was in situ at arrival), I scanned him.

Here is the CT:

photo-8 copy


photo-7 copy

You can see a small sliver of air in the IVC, and none was noted in the liver or in the heart (which was what I wanted to r/o). Now of course ultrasound is much more sensitive than CT for identifying small air bubbles (a CT image is a composite of several slices so a small bubble is lost) but when he returned form CT and I scanned him again, the hepatic veins no longer had air, but the IVC was full of air below the liver (as in the CT), so I think moving the patient had relocated the air.

More to come on the clinical story and investigations of this particular case, which is still ongoing.

thanks for looking!



Bedside Ultrasound Clip Quiz #7: What is it? #FOAMed, #FOAMcc

Ok, so no history for you. Say you’re doing a general bedside ultrasound exam on someone in shock and you see this:

What am I looking at?  (HINT we’re in the RUQ)

What should I be thinking of?

Answers tomorrow.  Lets see what you guys come up with!


rubbadoc says:  What’s air doing there?

…and indeed he is right, it is air where there should not be. Now where is it exactly? (experts, refrain from answering…)

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: