MOPOCUS: A great synopsis by Ha & Toh. #FOAMed, #FOAMcc, #FOAMus

Just came across this review and figured I should share. The authors make a great synopsis and review of POCUS in acute illness:

MOPOCUS Review by Ha &To

The only thing I would add to this is a more physiological way to assess the IVC, which I’ve blogged about here.  Sadly, I’ve heard a few people stating how they didn’t want to get into the dogma of IVC ultrasound, that it wasn’t reliable, etc.  The IVC doesn’t lie. It’s just not a recipe. The IVC findings have to be integrated into the rest of the echo graphic and clinical examination.  Trying to use it as a single value is akin to using serum Na+ as a diagnostic test for volume. It works only sometimes.

Please spread among the POCUS non-believers. We’ll convert them, slowly but surely. But the sooner, the better for the patients. Again, there’s no excuse to practice acute care without ultrasound. It’s not right. I’m not saying every probe-toting MD is better than one without, but everyone would up their game by adding POCUS, once past the learning curve!

cheers!

 

Philippe

The NYC Tracks with Jon-Emile: The Glycocalyx – The Next Frontier. #FOAMed, #FOAMcc

I was really psyched when Jon-Emile mentioned he would like to talk about the glycocalyx.  I first blogged about it here, basically when I stumbled on the extensive literature on this huge organ we have been completely ignoring in terms of physiology and therapeutics. It lines our entire endothelium, which is where most of our therapeutic interventions go, and we only heard of it in passing, possibly in histology class as med 1’s.   Hmmm.  Anyhow, here, Jon-Emile and I talk about it a little, discuss possible clinical implications, but more importantly Jon mentions the relatively new blog of Dr. Thomas Woodcock (@thomaswoodcock), http://www.fluidtherapy.org, who is one of the pioneer clinicians who have studied the glycocalyx, and who is now trying to bridge the bench to the bedside.

I’ve been fortunate enough to get in touch with him and we’re planning to record some discussions soon.

So, in my view, the glycocalyx is a formidable force we have been ignoring, and have been damaging often with our interventions. I’m hoping to see some developments allowing glycocalyx assessment outside of the labs in order to give us the tools to reassess every fluid in terms of the relative damage it does to what is essentially the gatekeeper between the blood and the tissues.

Love to hear some comments!

Here is the chat with Jon:

 

cheers

 

Philippe

The NYC Tracks with Jon-Emile: Paracentesis and Volume Status. #FOAMed, #FOAMcc, #FOAMus

So I was in NYC last week and met up with my buddy Jon-Emile Kenny, (@heart_lung), intensivist-physiologist extraordinaire, and we recorded a few discussions on practical matters.

I always love to debunk myths and avoid dogmatic guesswork, and, more often than not, Jon, with his encyclopedic knowledge of the physiology literature, but more importantly a cutting edge understanding of it, can back up my vague ideas and empirically derived ideas, so that the next time someone asks me why this is so, I can have a semi-enlightened answer!

So here is the first, where we discuss the common question about the need (or not) of intravascular volume repletion during or following large volume paracentesis. Yes, there are some formulas out there as to how much albumin or crystalloid one should give, due to the worry of subsequent hypovolemia. Note how those formulas use no data about your patient’s volume status at the time of paracentesis, so as far as I’m concerned, they have no value whatsoever in an era where we can assess this. Yes, ultrasound is the base as far as I’m concerned.

Here we go:

Please share your thoughts!

cheers

 

Philippe

Wicked bedside US case from a CCUS Fellow! #FOAMed, #FOAMus

So a few weeks ago I was glad to meet the latest of the CCUS Fellows, Dr. Mathieu Brunet. This guy practices in the Magdalen Islands, and came to spend 3 days with me in the ICU to sharpen his bedside ultrasound skills. In fact, his technicals skills were already very good, so we spent most of the time reviewing how one integrates the bedside ultrasound data into clinical practice. We overlapped a fair bit into critical care management and resuscitation, naturally.

Well, a couple of weeks later, he tells me about a great case he’d had where he was already able to apply some of the skills he’s sharpened:

Hi Philippe,

I had this trauma case this week that I think highlights once again the usefullness of POCUS in making meaningful and timely bedside clinical decisions. Unfortunately, I didn’t save the images…

A 50 year old man was brought in by EMS after a 4 meter fall. He had isolated TBI and presented with a glascow of 5 (decorticating). An obvious right temporal deformity and a right fixed mydriasis were noted in the primary survey. My initial thoughts in the context of TBI was ongoing uncal engagement…a poor prognosis sign to say the least. However I noticed in the secondary survey a significant right periorbital ecchymosis with what seems to be a stint of exophtalmia. Was the bleeding solely preseptal, or could a retrobulbar hematoma explains the mydriasis? I reached for the ultrasound while anesthesia was intubating and was able to visualise black hypoechoic fluid in the retroorbital area. I promptly proceded to do a lateral canthotomy and a few minutes later both pupils were equal and reactive! This completly changed the momentum of the rescucitation since we were now looking at a patient with a much better prognosis then an actively herniating one! POCUS also resulted in a much shorter occular ischemia time since there would have been a significant delay if discovered only by the radiologist on CT scan.

Also, I was able to record a baseline internal carotid doppler waveform in the first minutes of rescucitation showing a markedly reduced diastolic flow (wasn’t able to find a vessel by TCD). I subsequently noticed improvement of the waveform following administration of mannitol which prompted me to be more agressive on the hyperosmolar therapy (started an hypertonic saline drip) despite the absence of clinical improvement at that time. In the next few hours, the patient waveforms further improved and the patient started withdrawing to pain.

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The patient eventually transfered to the level one trauma center and unfortunately passed away a few days later in the neuro-ICU.

I thought that the case illustrates interesting applications of POCUS in the management of TBI and facial trauma:

1) Quick confirmation of orbital compression which can be mistaken for a third cranial nerve compression. This can be sight saving since irreversible damage occurs after 60 minutes of ischemia.
2) Assessment of the response to hyperosmolar therapy before clinical response is apparent, or in the paralysed patient.

Please share your thoughts!

Mathieu

 

Great job Mathieu, even if all can’t be saved. Tough case. Never having done a canthotomy, lateral or otherwise, I’m glad it was you and not me! One a serious note, I wonder if this patient had a decompressive craniotomy, which seems the only physiological therapy for the “brain compartment syndrome”  we too often seem to try to treat medically.

I completely agree with your POCUS points. Too often naysayers (always those who can’t do POCUS) say “well, we would have found it on the CT, so this ultrasound stuff really isn’t necessary.”  That is fine when time is not of the essence. In acute care, it is.

Another key point is the even greater utility of POCUS in remote areas of practice such as yours, where resources are limited, and the decision to transfer must be done rapidly and accurately.

But great use of CNS POCUS indeed. Next time save the pics and clips!!!

 

cheers

 

Philippe

CCUS Institute Bedside Ultrasound Mini-Fellowships. #POCUS #CME

The personalized CCUS Institute’s Mini-Fellowships (CME-eligible) are focused on bedside ultrasound and designed to take clinicians with some degree of proficiency in basic ultrasound to a whole other level. The opportunity to follow a seasoned clinical ER/ICU sonographer and see actual cases, learn the clinical integration of ultrasound data into decision-making is a unique one, outside of a handful of residency programs whose faculty includes experienced bedside sonographers. Basic how-to courses are great, and certainly the first step for those clinicians adding ultrasound to their armamentarium, but what we have seen, sadly, is after initial enthusiasm, many don’t really pick up the probe because the confidence to “make the call” simply isn’t there. Yet.

In a sense, it’s almost as if, as medical students, we’d read Bates, practiced physical exam on each (more or less normal ) other, and were then set out to make diagnoses and treat without having residents and attendings around to confirm our findings a few times, until we got the hang of it. Hmm. That would be rough.

Some physicians are fortunate enough to practice in a center where there are a few “veterans” of bedside ultrasound and can gain some acumen that way, but others may be the ones spearheading their institution into the 21st century, and it is from the comments of several of those, attending the CCUS Symposium (2008-2014 – perhaps a return in 2017) asking for the possibility of shadowing some of us, that the Mini-Fellowships came to be.

Mini-Fellowship Structure

Montreal Mini-Fellowship: Participants shadow one of our instructors (ICU attending) during the regular working days and discuss the cases and ultrasound-relevant aspect of each case (more often than not the case in entirety), and are able to practice their ultrasound skills. The duration is flexible although we generally suggest a minimum of two or three days. Each day would usually be about 6-8 hours, some may be more.

Toronto Mini-Fellowship: Participants get a dedicated and highly experienced preceptor (Dr. Edgar Hockmann) who is not on clinical service but with access to the ICU patients, and will provide a structured and dynamic session adapted to the participant’s needs and abilities.

The case exposure will be mainly ICU as well as ER and ward patients. The focus will be on acute care issues. After two days, participants who had a basic ability in ultrasound should be fairly comfortable with assessing volume status, cardiac function, perform lung ultrasound, be able to identify and assess intrathoracic and intr-abdominal fluid collections, assess the kidneys, bladder and gall bladder, measure optic nerve sheath, assess carotid flow and some may have exposure to trans-cranial doppler. The focus may be shifted depending on a participant’s interest.

This takes place in Montreal, Quebec or Toronto, Ontario, Canada.

Participants will have the opportunity to work with handhelds, midrange and high-end ultrasound devices.

Space is limited as we can generally only accommodate 1-3 participants per month.

CME

So, great news, finally went thru the CME process and lo and behold, the Mini-Fellowships qualify for 25 Section 2 credits (regardless of the length) and 3 hours of Section 3 credits (per day of fellowship). For you americans:

Through an agreement between the Royal College of Physicians and Surgeons of Canada and the American Medical Association, physicians may convert Royal College MOC credits to AMA PRA Category 1 Credits™. 

Bonus!

Upcoming participants will also receive a copy of the forthcoming handbook:

covercover-back

Requirements 

Please have basic experience in bedside ultrasound. We don’t want to teach you about depth and gain. We’re happy to fine tune your views but not to introduce you to the main cardiac views. It would just be wasting your clinical time. We’re here to show you how to assess pathology and integrate your findings into clinical decision-making. Take the basic group course to learn the views, or be self-taught from youtube/iphone and practicing on your patients. You don’t have to be great, but to get the most out of this experience it shouldn’t be your first time holding a probe.

Registration

email me at philipperola@gmail.com or reach out on twitter @ThinkingCC

Tuition (Updated 2022)

Montreal Mini-Fellowships: 600$ CAN / 500$ USD per day for 1 physician, 400$ CAN / 350$ USD per person per day for additional days, and 400$ CAN / 350$ USD per person per day for a 2-3 physician group (maximum)

Toronto Mini-Fellowships: 800$ per half day (4h).

100% refundable until you start. Even if you don’t show up. Really. We’re not in it for the business. We get to go home earlier if you don’t come.

Testimonials:

« I have had the chance to participate in a shadowing experience with Dr Rola at the Scarborough General Hospital ICU during two days in 2013. As a general internist and assistant program director, this experience really opened my eyes regarding the use of bedside ultrasound in general internal medicine and for IM residents. I think I would have benefited more of this experience if I had done more training previously, and I encourage future participants to do so. However, I came back from this experience with a very clear idea of the benefit of CUSE for my patients and for our residency training program. I really saw how ultrasound was used ‘in action’, in a much more realistic way than what is usually shown in CPD meetings. I also saw its limitations and the skills I needed to develop to generate good images (not something you can learn over the weekend!). Since then, I participated in formal trainings and licensing activities (more than 250 supervised US on acute care patients) and now practice bedside ultrasound autonomously. We now offer a bedside ultrasound training for our residents with the help of the emergency medicine department and an ultrasound-guided procedural simulation lab. Nothing in CPD has improved my practice and benefited the health of my patients as much as bedside ultrasound training. »

Alexandre Lafleur, MD, MSc (Ed.), FRCPC
Spécialiste en médecine interne
CHU de Québec – CHUL
alexandre.lafleur.1@ulaval.ca

“Thank you very much for the exposure and teaching offered via the CCUS “Mini-Fellowship.”  These few days allowed me to enormously improve my mastery of bedside ultrasound in clinical decision-making in critical care. I recommend the experience to clinicians already having experience in bedside ultrasound, but who feel they could benefit from the expertise of an instructor to attain a level beyond basic courses and available textbooks.”

Mathieu Brunet, MD, GP/ER/ICU, Magdalen Islands, Quebec, Canada

“The CCUS Mini Fellowship In House training is very essential in to experience the echo skills that we get from the courses,being supervised in ICU will offer the chance to be corrected and get real live practice/exposure by being at the bedside and learn what is priority in echo for the best of patient care. The in-house experience is very helpful, practical, I recommend this training to any physician involved in ER, ICU, CCU, Anesthesia and rapid response team.”

Joe Choufani, MD, Internal Medicine/Cardiology, St-Lawrence Health Association, NY

“Thanks for everything. I really appreciate you sharing your vast fund of knowledge with me.”

Sean Sue, MD, ER, Philadelphia

CME

So, great news, finally went thru the CME process and lo and behold, the Mini-Fellowships qualify for 25 Section 2 credits (regardless of the length) and 3 hours of Section 3 credits (per day of fellowship). For you americans:

Through an agreement between the Royal College of Physicians and Surgeons of Canada and the American Medical Association, physicians may convert Royal College MOC credits to AMA PRA Category 1 Credits™., #CME

Bedside US Procedure: Pericardial drainage – Pearls! #FOAMed, #FOAMcc, #FOAMus

So here is a video of a pericardial drain placement for pre-tamponade in a 33 yr old man, presumptively for a viral pericarditis (cultures and cytology pending).  In this case, the approach was subxiphoid, because this offered a large pocket of fluid with little or no risk of hitting the RV. The apical approach would have been more risky. Due to technical issues, the video only starts once the guide wire is already in place, but there are a couple of teaching points worth sharing nonetheless.

First, it is useful to confirm guide wire placement prior to dilating. Secondly, in cases such as this where the distance to the pericardium is more than a couple of centimetres (it was about 6 cm here), it is nice to be able to confirm under real-time that the dilator is indeed in the intended area. Because the guide wire is highly echogenic, and the dilator is not, one can see the proximal part of the guide wire “disappear” which indicates that the dilator has covered it, now visibly in the effusion. Once the pigtail is  inserted over the guide wire, final confirmation can be obtained by injecting back thru the pigtail and seeing echogenic material (due to minute amounts of air) appear in the pericardium. This is known as the Ajmo sign.

Cheers!

 

Philippe

Cerebral & Somatic NIRS (Near InfraRed Spectroscopy) in shock states: tailoring therapy. (PART 1) #FOAMed, #FOAMcc

So I’d mentioned using NIRS to monitor and tailor therapy a few months ago, and promised a more in-depth discussion to come, so here we go.

For this not familiar with the technology or the concept, NIRS measures tissue saturation, predominantly venous. Hence physiologically it is akin to central/mixed venous gases, but localized. Cerebral NIRS found its foothold in the OR with carotid and cardiac surgery, but its use is now expanding. Given typical knowledge translation time of a decade, it should end up joining ETCO2 as a routine vital in monitored units, but probably not soon enough.

So in our unit at Santa Cabrini Hospital in Montreal, we’ve had this technology for about a year (the INVOS system), and have been studying its uses. In this time, three applications have stood out:

  1. Finding the “Sweet Spot” for vasopressors.
  2. Confirmation that therapeutic interventions are hemodynamically appropriate.
  3. Cardiac arrest: CPR adequacy, prognostication and detecting ROSC.

 

  1. Finding the “Sweet Spot” – I think (hope) that anyone reading this with professional interest understands that pressure does not necessarily equal perfusion.  With that in mind, adjusting vasopressors to a pressure makes little sense, and represents at best a guesstimate of perfusion, which is what we really are after. We can all agree, however, that a certain minimum pressure is required, but whether that is 65, 55 or 45 MAP no one can say for sure.  So the way I like to use it is to establish a baseline and watch the direction of the tissue saturation with vasopressor therapy. If the saturation begins to drop off, we may have reached a point at which excessive vasoconstriction is worsening tissue perfusion, and that inflexion point may represent the upper beneficial limit of the vasopressor – this may happen to be under 60 or 65 of MAP.  However, it is key to understand that this inflexion point is reflective of the current state of hemodynamics, such that a change in volume status or cardiac output, in one direction or the other, would likely change the position of this physiological point.  For example,  a volume depleted patient may reach a decreasing tissue saturation point at 55 MAP, but, once volume replete, may reach a higher MAP of 65 or above before a drop in saturation is seen.  Conversely, a patient whose best tissue saturations were around 65 MAP who suffers an MI and sudden drop in cardiac output may now see his perfusion compromised at that same MAP, which would now be achieved with a greater vasoconstriction, less cardiac output and consequently, poorer flow… I posted a case discussion which illustrates this.
  2. Confirmation that therapeutic interventions are hemodynamically appropriate – I feel this is really important. When a patient’s life is literally on the line, and knowing that our interventions are seldom without potential nefarious side effects, it is poor medicine to be introducing a therapy without having some form of monitoring – preferably multiple – that we are headed in the right direction, or at least not making things worse. Of course, we already do this – with BP, sat, lactate, CCO, ultrasound, ETCO2 – but I think using a realtime measure of tissue saturation adds to this. It is also my firm opinion that integrated, multimodality monitoring is necessary – at least until someone develops some form of mitochondrial monitoring which tells us that the cytoenergetics are sufficient to survive. Until then we are stuck with surrogate markers and many of them (e.g. lactate) are the result of complex processes that preclude them being a simple indicator of perfusion adequacy. For instance, when giving a fluid bolus/infusion – after having determined that the patient is likely fluid responsive AND tolerant – one should expect to see an increase in ETCO2 (other parameters being constant), an increase in CO, an increase in NIRS values. The absence of such response should make one reconsider the intervention, because without benefit, we are left only with side effects.

Here is a patient’s cerebral (top) and and somatic (thigh – bottom) and CO values. This patient had an RV infarct and was in shock.

IMG_7948IMG_7946

 

Following initiation of dobutamine, this is what occurred:

IMG_7951IMG_7949

Given that we cannot always predict the response to an inotrope – depending on the amount of recruitable myocardium, it is reassuring to see an improving trend. This enabled us to decrease the vasopressor dose significantly.

Note that, so far, and unless some good evidence comes out, I don’t use a goal value, and so far, I have not identified a value that is predictive of prognosis. However, downward trends usually bode very poorly. For instance, I had a severe chronic cardiomyopathy patient whose cerebral saturation was 15%!!!  But more surprisingly, she was awake, alert and hemodynamically stable. Adaptation.

Part 2 and the stuff on cardiac arrest coming soon!

Please, anyone using NIRS in shock, share your experience!

 

cheers

 

Philippe

Resuscitation Leadership Academy: Check it out!

 

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Just wanted to invite everyone to take a look at the Resuscitation Leadership Academy (www.resuscitationleadership academy), brainchild of Haney Mallemat (@criticalcarenow) and Scott Weingart (@emcrit), neither of whom need an intro at this point, needless to say.  Much thanks to them for inviting me to the faculty, very honoured to be a part of the team!

Basically the RLA offers an online curriculum packed with great material, but more importantly the opportunity to do an online hangout with any faculty member and discuss cases, topics, etc, in an informal but very informative manner. I think this is a great resource for trainees as well as those who are in practice but either lack an academic environment or really just want to tap into some of these guys’ experience and knowledge.

Looking forward to meeting some of you in a hangout!

cheers

Philippe

Physician, know thy fluids! #FOAMed, #FOAMcc, #FOAMer

So I posted a quick poll on http://www.therounds.com, a really upcoming physician site, with the intent of getting an idea of what people use as fluids and what they know about them.

 

The first question was “What is your fluid of choice for resuscitation?”

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…no big surprise, 61% choose NS.  Despite the evidence of increased renal dysfunction (JAMA 2012 – I posted about this here: http://thinkingcriticalcare.com/2013/11/18/enough-with-the-normal-saline-foamed-foamcc/)

Well, at least this is chosen with good knowledge of its pharmacological properties, right?

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Hmmm… 57% peg it as physiological or basic.  Only 9% get it right. The pH is 5.6 or so.

So here we have favorite medication used by a lot of people, who use a lot of it, usually in quite ill patients, often acidotic, and who are not aware that the pH is in fact also quite acidotic.

I think it just is an important example on how we need to treat fluids as medications, and not think of them as benign interventions, and by doing so, we’d feel much more obliged to look at what we are giving in terms of composition and quantity, rather than the debonair attitude we have mostly grown up with.

 

cheers!

 

Philippe

 

 

Enteral Fluid Resuscitation (EFR): Third-world medicine in the modern ED/ICU? (ORT part 2) – #FOAMed, #FOAMcc, #FOAMer

Screen Shot 2015-02-10 at 7.15.16 PM Enteral Fluid Resuscitation in the ER/ICU? For those who did’t come across it, part 1 of this series can be found here: http://wp.me/p1avUV-e8 So back to bringing the basics back to our ultra-tech world… Can I actually use this field technique in my bright and shiny ICU? Can I use oral hydration as a cutting edge therapy in my life-and-death patients? Sounds strange. Sounds like I should be using a precise device which lets me know exactly how much fluid has gone into my vascular space, because that’s where I want it to go, and I want to control exactly the composition of my serum electrolytes, etc, etc.  We like to control. But do we really? We actually have absolutely no idea how much of a fluid bolus remains intravascularly, in any one patient.  It will depend on his/her pre-existing venous filling, his serum protein levels, the integrity of the glycocalyx, and probably a few more things we don’t even know yet.  And as I rapidly distend atria, I release ANP which damages my glycocalyx further. Hmmm… As I mentioned in the last post, the only way fluid enters our vascular space is via the endothelial cells at the level of the GI tract for the most part. All “venous access” is iatrogenic. I do believe that the endothelial cells, by and large, will do a better job – in concert with the kidneys and rest of the blood cells – of controlling the plasma than we will, if given the chance. What logically follows is that, in the presence of a functional gut, I can consider using Enteral Fluid Resuscitation – that is, giving fluid for hemodynamic purposes, not just “maintenance,” by an enteral tube of some sort. So what could I give?   What’s in it? The current reduced osmolarity WHO/UNICEF formula contains approximately the following: Screen Shot 2015-02-10 at 7.24.28 PM So, lets take a closer look at the players: 75 mmol/l of sodium, 75 mmol/l glucose, some potassium and the rest basically to balance the electroneutrality. The whole thing hinges on the glucose-sodium cotransporter, which drags sodium and water in along with the “desired” glucose.  Optimal water absorption takes place with Na between 40-90 mmol/l, glucose 110-140 mmol/l, and an osmolality around 290.  A higher Na may cause some hypernatremia, and a higher osmolality may result in water loss. Here is our friend the enterocyte illustrating just how this kind of solution will allow sodium absorption: Screen Shot 2015-02-10 at 7.31.54 PM   Do-it-Yourself Enteral Fluid Resuscitation Solution: So I’ve got a neat DIY option if I don’t want to break out the powder and start mixing in the middle of my unit: 0.45% or 1/2 NS plus 30 ml of of D50 would give us Na 77, Cl 77 and glucose 74, with an osmolality of 228. Pretty close. That’s what I’ve been using. How much? Well, I like the slow and gradual. Some of the rehydration data out there supports some pretty huge amount of fluids, but this has been done mostly in healthy but dehydrated athletes – not the case for most of our patients. I’ve been going with 250ml every 1-2h, as – for now – an adjunct to IV fluid therapy. This is conservative and completely arbitrary, but essentially a glass every hour or two certainly doesn’t seem excessively taxing. Who can I give this to? You do need a functional gut, so for now, my criteria are (1) essentially normal abdominal exam, (2) obviously no recent bowel surgery, (3) a patent and functional gut as far as I know, (4) no ultrasound evidence of ileus or gastric distension. But how can I be sure it’s going in the right place?  I can’t. Just like I can’t be sure my IV fluids are staying in the right place. But I do check – IVC ultrasound (gross but better than skin turgor!), urine output, HR, BP, etc. None of those are perfect as they are all multifactorial, but that is the nature of the game. The other thing I check is gastric distension by bedside ultrasound every couple of hours – obviously, if I’m just getting a fluid filled stomach, there’s no point, and eventually harm may ensue. When should I stop? Whenever you clinically decide you don’t need/want any further fluid resuscitation. As far as I am concerned, might as well stop the IV infusions first and have the enteral going after – in the end, you are hoping your patient will go back to drinking and not require a PICC line for discharge, aren’t you?  So you stop when the patient does it on his or her own. I’d really like to know if anyone out there is doing something like this. It would be great to compare notes and evolution. Drop a line!   cheers, Philippe