Medicine

January 22, 2014

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

http://www.hindawi.com/journals/ah/2012/924042/

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.

cheers!

Philippe

January 10, 2014

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!

Cheers,
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…

thanks!

Philippe

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,

Derek

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 http://dx.doi.org/10.1155/2012/924042).

Hope this helps……

John.

Here is the article:

924042

P

January 8, 2014

“But doctor, he’s vomiting blood!!!” – The NEJM GI Bleed article by Villanueva: Yup, time to reassess transfusion in GI bleed! @FOAMed, @FOAMcc

Screen Shot 2014-01-08 at 3.13.37 PM

Last january a highly anticipated paper came out in the NEJM (http://www.nejm.org/doi/pdf/10.1056/NEJMoa1211801), which should be a game changer, given a few provisos.  Villanueva et al reported on their large (almost 1,000 patients) randomized study on liberal (<90 mg/dl) vs restrictive (<70 mg/dl) strategy.  Interestingly but no longer surprisingly, the patients in the restrictive strategy did better.

Hmmm…sound familiar?  By now everyone  accepts the TRICC trial threshold of 70 in ICU patients, but when it first came out, there were a fair bit of disbelievers and concerned health care workers.  At the time, they excluded GI bleeds and acute coronary syndromes, understandably,

So what do the numbers say?  First lets see if there was any difference in the actual treatment. Definitely. In the restrictive group, 51% of patients required transfusion, vs 86% in the liberal group.  Sizeable difference. Now in terms of outcomes:

a. rebleeding decreased: 10% vs 16%

b. 6 week survival was better: 95% vs 91%

c. less adverse events: 40% vs 48%

But you know what, even if we throw out all the above, the absence of any difference would result in the same conclusion: there is no advantage to a higher hemoglobin goal in GI bleed.

…except for this important proviso: in their institution, UGI endoscopy was performed within the first 6 hours.  Now I’m not necessarily suggesting that the results would have been any different with a real-life, “random” timing of endoscopy, but in the spirit of scientific rigour, it is important to note.

Now there are a few important points to make that are highly relevant in the whole transfusion issue.

Why is transfusion bad? For those who may not be aware, here are a couple of reasons why transfusion looks good on paper but not necessarily so good for the patients: (a) due to stored red cell loss of deformability, the capillary bed can suffer micro-occlusion, and (b) there seems to be some immune suppression related to receiving transfusion. And I don’t (yet) have a clue what it might do to the glycocalyx…

So this is the sort of situation (not uncommon even in other clinical scenarios) where the physicians and nurses breathe a sigh of relief when seeing a nice number on a paper or a screen following transfusion, but the patient’s microcirculation is actually worse off than it was.

How valid is a hemoglobin value in GI bleed?  The answer to this is why we have MD’s after our names, and hopefully live up to that. Let me give you a quick anecdote: sometime in the past year I was called on to help a sick patient in the OR, a young woman with some post-partum bleeding who remained unstable. So the anaesthetists are concerned, the OB’s are trying to fix things, and she’s pretty unstable. A quick CUSE (critical ultrasound examination) shows she has a tiny IVC (almost virtual) and a hyperdynamic LV/RV with a near-100% EFs.  They were concerned because they had already given her fluid, etc…might she have suffered an amniotic embolism? So we were reassured that her RV was fine but clearly she needed more fluid of some sort (SBP 60’s, HR 140’s).  Just at that moment a call comes thru and the OB resident declares with a smile “its ok, her hemoglobin is 105!” and for a split second, there seems to be a sense of relief in the room, which worries me even more. I remind the resident that if he bleeds fast enough, the very last drop of his blood will have a very similar hemoglobin to the one he had while quietly sipping coffee at starbucks… So although we tend to use hemoglobin as an answer to “how much blood does my patient have,” what it really says is what the concentration of red cells is in the blood that my patient has – hence a clinical assessment (preferably with ultrasound) is required to at least determine in our minds whether our patient is empty or full, and only then can a hemoglobin value be properly interpreted. I doubt I would treat the same was someone with only 2 liters of blood going around with a hemoglobin of 75 versus someone with 4 liters of that same blood going around.  In that exact moment their hemoglobins are the same, but in all likelihood, in the ensuing hours, the first will continue to drop as the intravascular volume seeks to replete itself from the interstitial space and from possible GI intake or IV fluids.  So consideration has to be given to what fluids the patient has been or is receiving.  This is why we have MDs. If it was just about using a number, the clerk could manage our patient off the computer census and consult GI. Yep, its the N=1 concept again.

GI bleed = Trauma?   Conceptually, GI bleed is not that different from trauma.  You have a breach in vascular integrity. What are the determinants of rate of bleeding? The size of the hole and the pressure gradient.  Our body will try to shrink the hole with a fibrin mesh and a platelet plug and some vasoconstriction, and hypotension will decrease the pressure gradient.  That’s why in major trauma we don’t want to “stay and play” but want to “scoop and run” to an OR while just maintaining life until someone can plug the hole surgically (just look up some of Karim Brohi’s great #FOAMed lectures), because all that medical resuscitation (big crystalloid boluses) will do is blow those fibrin meshes away and increase the pressure gradient!  So aggressive fluid resuscitation may not be the best idea in GI bleed either. And yes, I’ve used tranexamic acid in bad GI bleeders while waiting for intervention.

Philosophical rambling… 

I think most of us forget that phrase…what was it again? Primum…primum non nocere?  Oh yes, we all said it, know it, but do we really remember to apply it to everything we do, every day? And why not? Because, in our desire to help, we more often than not feel like we have to “do something.”  And in truth, so does staff, families and the patients themselves.

Conclusion:

So, how will this change my practice?  It will make me completely comfortable in allowing my hemodynamically stable and nearly euvolemic (IVC can be seen and LV/RV not just a tachycardic blur) GI bleeder to have a hemoglobin of 70. Will I insist on an endoscopy within 6 hours? Not necessarily, but I will be monitoring (as I usually do) for any deterioration to get on the phone and push a little or a lot.

What’s next…?   I’m thinking down the line we might just see small volume resuscitation (100 cc at a timewith a glycocalyx-friendly albumin), a bolus and infusion of tranexamic acid and a quick endoscopic intervention will be the way to go, while keeping a hemoglobin no greater than 70…cuz who knows, maybe 60 or 50 might be better…

love to hear what anyone has to say!

Philippe

Check out Ken and I discussing this on the SGEMs Podcast:

SGEM#61: Blood on Blood (Transfusion Strategies for Upper GI Bleeds)

December 18, 2013

Ultrasound MedED at CCUS 2014: for educators! #FOAMed, #FOAMcc

This year, as part of the pre-congress courses being held prior to the main symposium (may 10th and 11th), we are introducing a half-day symposium entitled: “The Educators‘ Symposium: How to integrate Bedside Ultrasound into Ungergraduate and Graduate Programs,” coordinated by Dr. Catherine Nix of the University of Toronto who has been the driving force behind U of T’s implementation of an ultrasound program for undergraduates.

Here is the preliminary programme, really good stuff for anyone involved in education, whether at the institutional level or even at the departmental level.

Screen Shot 2013-12-18 at 3.53.07 PM

program subject to (minor) changes…

Attendants may register for this independently or as part of the whole symposium. You can register at:

http://www.ccusinstitute.org/Symposium6.html

Stay tuned for more updates, and the final programme of the main conference should be out by next week.  Guess what, it’ll be a great place to meet @criticalcarenow, @bedsidesono, @EGLS_JFandMax, @nobleultrasound, and many more not yet deep into the #FOAMed or twitter-verse, but soon to be.

See you there!

Philippe

November 30, 2013

Bedside Ultrasound Clip Quiz #4 – #FOAMed, #FOAMcc

So you’ve been doing ACLS for a few minutes in the ED on an elderly male who collapsed at a bus stop and shocked out of VF on the scene by EMS, and when you do a 3 second pause to assess the heart, just after an epi got flushed, this is what you see in the subxiphoid view:

 

Is this a case of tamponade?

Scroll below!

 

 

 

 

 

 

 

 

Nope!  There’s no pericardial effusion, and the atria are huge!  What you do see is microbubbles from the flushed IV medication in the RA and RV, and severe LV dysfunction.   The severe LA dilation suggests at least a component of chronic overload (also supported by significant leg edema in this case). Note that you can have severe LV dysfunction (post-resuscitation myocardial dysfunction or PRMD) after cardiac arrest of ANY etiology and does not necessarily imply pre-existing LV dysfunction or predict eventual LV function.

 

 

 

 

November 27, 2013

A Paradigm shift: re-thinking sepsis, and maybe shock in general… #FOAMed, #FOAMcc

Thomas Kuhn, physicist and philosopher, in his groundbreaking and science changing text, The Structure of Scientific Revolutions, states that:

“Successive transition from one paradigm to another via revolution is the usual developmental pattern of a mature science.”

In other words, a science has growing pains and is bound to have a fair bit of debate and controversy, until a new paradigm becomes dominant.  I think that there is a current – in part prompted by the power of socio-professional media which has allowed minds to connect and knowledge to spread – that will see many of the things that are now “Standard of Care” out the door.

So first of all, the following are must-listens, the first a lecture by Paul Marik, whom I have had the chance to collaborate with in the last years and respect greatly, on knowledge, experience, and even more on his refusal to take anything for granted and being in a seemingly-constant quest for the improvement of medicine.

The second link is Scott Weingart’s take on it, which I think is equally awesome.

I think Paul is pushing the envelope in an essential way, and Scott does a fantastic job of seeing or putting it in perspective. Enjoy:

http://emcrit.org/podcasts/paul-marik-fluids-sepsis/

EMCrit 112 – A Response to the Marik Sepsis Fluids Lecture

My (very) humble opinion on this is a rather simple, almost philosophical one:  why are we seemingly obsessed with treating a predominantly vasodilatory pathology with large amounts of volume?  I’ve said this in previous posts and podcasts, but this, in my opinion, is largely cultural and dogmatic. “Levophed – Leave’em dead” is something I heard as a student and resident, and came to take for granted that I should give lots of fluid in hopes of avoiding pressors… But there’s no evidence at all to support this.  The common behavior of waiting until someone has clearly failed volume resuscitation before starting pressors befuddles me (think how long it takes to get two liters of fluid in most ERs…).  If I was in that bed, I’d much rather spend an hour a bit “hypertensive” (eg with a MAP above 70) than a bit hypotensive while awaiting final confirmation that I do, in fact, need pressors.

I strongly suspect that it’s just a matter of improving vascular tone, giving some volume (which may be that 3 liter mark), and ensuring that the microcirculation/glycocalyx is as undisturbed as possible. Now when I say it may be the 3 liters, I firmly believe this will not apply to everyone, and that it will be 1 liter in some, and 4 in others, and that a recipe approach will be better than nothing, but likely harm some.

I think that blind (eg no echo assessment) of shock is absurd, and for anyone to propose an algorithm that does not include point-of-care ultrasound is only acceptable if they are in the process of acquiring the skill with the intention of modifying their approach in the very near future.

The whole microcirculation/glycocalyx is absolutely fascinating stuff, and undoubtedly will come under scrutiny in the next few years, and it is definitely something I will focus on in upcoming posts & podcasts. Our resuscitation has been macro-focused, and certainly it is time to take a look at the little guys, who might turn out to have most of the answers. For instance, there is some remarkable data on HDAC inhibitors (common valproic acid) and their salutatory effects in a number of acute conditions such as hemorrhagic shock (Dr. Alam) which have nothing to do with macro-resuscitation, and everything to do with cell signaling and apoptosis. Hmmm…

please share your thoughts!

thanks

Philippe

November 14, 2013

Bedside Ultrasound: The Sluggish IVC – something to look for… #FOAMed, #FOAMcc

So take a look at this:

I’m sure most experienced bedside sonographers come across this all the time.  For those who are starting out, and until now have just been looking at size and variation, take a second to look at the flow.  You can actually see the flow stop and start, which tells you your cardiac output is bad.  It could be bad because of the RV, the LV, the pericardium, the tension pneumothorax, anything, but it’s bad.  So just in case you were only gonna look at the IVC, keep looking! You will find something abnormal downstream, perhaps that you can do something about (not fluids, though).

I have seen this disappear and clear up with – when possible – correction of the problem, back to the normally anechoic IVC we usually see.

thanks!

Philippe

ps note there is also a mirror artifact in the right lower portion of the field, making it look as though there are two beating hearts.

November 4, 2013

NEJM Circulatory Shock Review by Vincent & DeBacker: the sweet and the not-so sweet… #FOAMed, #FOAMcc

So if anyone hasn’t read it, here it is:

Click to access Circulatory%20Shock%20-%20NEJM%202013.pdf

I read the article by critical care icons Dr. Jean-Louis Vincent and Dr. De Backer with interest  as I am always keen to find out what the cutting edge is… So here is my take on their review.

The not-so-sweet:

The inclusion of CVP in the assessment. Ouch. No evidence whatsoever. Evidence for lack of correlation to fluid responsiveness… I wonder if they themselves were cringing a little about including it, particularly form the fact that they just put high vs low rather than commit to a value, which makes me think they realize it’s a bit of a trap. (It reminds me a bit of those night-time orders I still sometimes see which say if u/o < 30 cc/hr give a bolus if CVP under 12 or lasix if over 12.  So basically depending on whether that patient’s head is elevated, or if he’s turned on one side or the other, he may go from “needing fluids” to “needing diuretics”…).

The sweet:

First of all, they obviously did an elegant job on description of shock states, and particularly of highlighting the common-ness of mixed etiology shock.

I like that they admitted that the end-point for fluid resuscitation is “difficult to define.”  Any answer other than that would really speak to non-physiological thinking, as I’ve referred to in prior posts/podcasts.

Dopamine: good job on trying to take it off the shelf for shock. As far as I’m concerned, only useful when you’ve run out of norepinephrine, although there is the odd time when you have a septic AND bradycardic patient where it could come in handy…

Bringing some focus on the microcirculation: no recommendations, but that’s appropriate since there are none to be made yet, but this is where the money is in the future, as far as I’m concerned. Once we figure out how to manage the microcirculation (we do ok with the macro circulation) we might forge ahead. But good to point the finger in that direction.

The super-sweet!

I do (not surprisingly) really, really like the fact that they included ultrasound in their assessment protocol, and emphasizing that focused echocardiography should be done as soon as possible.  Very nice. Finally.

Hopefully, this pushes mainstream ED and critical care physicians to realize they need basic bedside ultrasound skills…

 

Overall, I think it is a good review, certainly worth the read for trainees. I would like to see focus on re-examining and questioning our approach, which could spur readers to embark on research with a different angle. For instance, why do we assume that we need to fill patients to the point of no longer being fluid responsive in order to avoid vasopressors? Is there any evidence for that? Not that I know of…

But, for having put an emphasis on point-of-care ultrasound, it gets a big round of applause from me!

 

Philippe

October 28, 2013

A cautionary tale for budding bedside sonographers… #FOAMed, #FOAMcc

First of all, congratulations to all who are picking up a probe and working to add it to their diagnostic and therapeutic armamentarium. It will serve you – but more importantly, your patients – for the rest of your career.

I would like to caution you, however, in remembering that this, unlike knowledge, is a skill.  More than half the challenge is in image acquisition, and this requires practice. Practice, practice, practice. You can’t just reach for the probe in that one patient during your shift in whom you really want to have an idea of his or her cardiac function or volume status, then try to remember how to do it.  That’s a road to early discouragement and worse, never developing the skill or the necessary confidence.

Especially early on, scan everyone you can, including yourself.  You make a very patient patient.

If you’re not a fortunate medical student whose school is one of the pioneering ones with an undergraduate programme, take every course you can.  Make friends with ultrasound tech and spend some lunch hours watching some of their exams.  Pin (4 point restraints preferably) a colleague to a gurney when a machine is available.

Once you can reliably acquire images, start making clinical calls on the extremes: the tiny or the huge IVC, the hyperdynamic and the minimally moving ventricle, etc… and as your skills and experience grow, work your way towards the middle.

The last thing we need, as a bedside sonographer community, is to have the current trainees, which really represent the first generation (as most of the educators out there today are largely self-taught, or at least devised their own unique programs), misuse this amazing tool. We are under scrutiny, as it is a novel application (of an old technology), and cannot afford mistakes, lest roadblocks re-appear.

So practice, practice, practice, and if you’re not sure, get another opinion or another diagnostic modality!

happy scanning!

 

Philippe

October 23, 2013

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 (www.pulmccm.org), 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 http://www.ccusinstitute.org 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~

thanks!

 

Philippe