ICU

May 9, 2018

CCUS Institute POCUS & Resuscitationist Mini-Fellowship: 2022 Update!

So over the last couple of years, the POCUS Mini-Fellowships have been slowly but steadily morphing into POCUS-Resus training.  With POCUS essentially critical in all aspects in resus, including venous congestion assessment, ventilation, diagnostics, it is a natural extension to blend the exchange into many of the other tools that we use, including discussions around fluids choices, pressor choices, monitoring using NIRS tissue oximetry, ETCO2, and overall resuscitation strategies. Of course, we will also cover VExUS as it has become an important POCUS tool, not only for the resuscitationist gauging his fluid management, but also for any clinician dealing with patients with heart failure and renal failure.

Some structured workshops can include percutaneous pigtail insertion, vascular access phantom practice and both surgical and percutaneous surgical airway manikin practice, depending on participants’ choice.

We have recently expanded with the addition of Dr. Philippe St-Arnaud, ER and CC doc and EDE (Emergency Department Echography) Instructor extraordinaire, who will increase our availability – which had been fairly limited – apologies to those whom we could not accommodate due to scheduling reasons.

This is an excellent complement to an RLA (I’m part of that faculty) or ULA fellowship, to bring a real clinical experience into the mix.

Of course, if you are a canadian trainee/resident you can get a whole month of this for free by doing an ICU elective at Santa Cabrini Hospital (foreign trainees are also welcome but more hoops to jump thru!).

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.

For more details and registration information see here.

And here is some of the most recent feedback from the fellows:

Anyway, I wanted to say thank you again. You have inspired our group to continue to move POCUS into our clinical practice; we have started a fluid management algorithm in our observation unit, and hoping that the soon-to-be-added ButterflyIQ to the unit will improve its utilization. Over the last few years, we have caught a few myocarditis cases and new CHF cases initially placed in observation as “influenza,” managed hundreds of CHF cases, and had a handful of +FAST exams in our ED that we were not quite expecting (in fact, having one that was just texted to me from a co-worker is what prompted this email!).   Our POCUS program is still in its infancy, but I think the horse is out of the barn at this point. On behalf of all of our patients that we will see, thank you.

Additionally, I have gone on to co-direct a sono-wars type event at our national physician assistant conference (AAPA), for PA students. At the inaugural event, we had free workshops and a competition that included 200 student learners, representing about 30% of PA programs from all over the country. We opened a huge door for PA programs to start implementing POCUS longitudinally within their curriculum. We received amazing feedback on the program, and are hoping to publish results soon (currently with journal editors)… 

I am excited to pay forward my debts to those that have helped me.  You not only helped me, but generations of PA’s for years to come. Thank you so much for your time and commitment to excellence. What you do matters; please keep running the mini-fellowship! Patrick Bafuma EM PA @EMinFocus, Hudson Valley, NY, USA. 2017.

        This review is for the CCUS Institute Bedside Ultrasound (US) Mini-Fellowship. I was fortunate to do the mini-fellowship after the Hospitalist & Resuscitationist conference, and I was able to put into practice various techniques that we learned. Dr. Rola was a pleasure to work with and was well-versed with the latest US and free online access meducation (FOAM). The atmosphere was conducive to learning, and we picked up an ultrasound almost immediately and used it extensively through each day. We used various US machines and were able to get a good feel for all of them. My US experience before the mini-fellowship had been a two-day introductory course with healthy medical students as volunteers. At the mini-fellowship, being able to learn on actual critically ill patients was illuminating and helped cement what I had learned. We also went over relatively new bedside techniques such as point-of-care trans-cranial doppler (TCD) and optic nerve US (ONSD). Overall, the experience was well worth the 2800 mile trip, and I would enthusiastically recommend it to anyone that is interested in learning practical applications of US. – Dr. Pranay Parikh, Los Angeles, USA. 2018.

Recently I went and studied with Philippe in Montreal. I was really impressed with how seamlessly ultrasound was used in the physical exam for each one of his patients without any loss in time and often a gain in clinical information that I doubt we would have had without the ultrasound. Philippe’s ability to teach was also amazing as we worked on some very interesting concepts like portal vein pulsatility, hepatic vein and renal doppler for fluid stop points. He definitely exemplified how facile one could become with ultrasound with dedicated practice. I very much enjoyed my time and believe I learned a lot that could be used immediately at the bedside. Thanks! Dr. Joe Quinn, EM/IM/CC, Vidant Medical Center, East Carolina University, 2018.

So join us for a few days of intense, real clinical learning.

cheers,

Philippe

December 14, 2017

The Hospitalist & The Resuscitationist. Montreal, April 18th & 19th, 2018. #Hres2018

NOTE: THIS WAS THE H&R2018 PAGE, SO IF YOU ARE LOOKING FOR H&R2019, CLICK HERE!

So for this winter, we’ve put together a little gem of a conference which will be a mix of hospitalist and critical care medicine, both with a dash of POCUS for good measure. Our focus here will be short, to the point, highly relevant and highly physiological talks on key topics, in short, 15 minute talks.

What are we going to talk about?

Day 1: The Hospitalist

 

Day 2: The Resuscitationist

 

 

You can figure there will also be late-breakers, “ask the crowd” talks and more.

Workshops? Sure:

Yup. You can ask for a workshop. Enough similar requests will probably make it happen. A few have already asked for Neuro-POCUS, so that is a likely addition.

 

So, who will be talking?  The lineup already includes Andre Denault, Josh Farkas (@Pulmcrit), Jon-Emile Kenny (@heart_lung), Rory Spiegel (@EMnerd), Hussein Fadlallah, Peter Barriga, Daniel Kaud, Davide Maggio, Michael Palumbo, William Beaubien-Souligny, and a few more to confirm. And who knows who might do an impromptu drop-in…

 

The short answer is yes. Of course, it does depend on what you do. If you are a hospitalist, involved in critical care or acute care of any kinds, you will find something here for you. Totally awesome for IM residents/FM residents planning on doing some hospital medicine or ICU coverage. Who will get the most bang for his or her buck here? Real docs training or working in the trenches. This isn’t a cutting edge research conference, but a cutting edge clinical application conference.

 

Oh yes, and the CME, of course:

 

This will be a small, fun conference. Space is purposely limited, for an intimate feel and to encourage discussion between peers. No need for these exclusive “meet-the-professor lunch” or anything like that: that’s what the whole event is like!

 

Registration is open! Print, fill, write a cheque and send the form below:

RegistrationV2

If you’re crazy busy, or have any questions, feel free to email hospresusconference@gmail.com or tweet (@ThinkingCC) to reserve a spot! 

Download the brochure here:

H&R2018 Brochure – Participants

 

cheers!

 

The H&R 2018 Scientific & Organizing Committee:

Dr. Philippe St-Arnaud – ER and Critical Care doc, POCUS instructor and constantly pushing the clinical envelope.

Dr. Carola Zambrana – our Hospitalist on the panel, constantly seeking excellence in care and working on bringing POCUS to the wards.

Dr. Mario Rizzi – our friendly neighborhood respirologist and educator.

Dr. Philippe Rola – Critical Care doc, long time POCUS aficionado and instructor, working at bringing POCUS into the everyday physical exam.

 

December 6, 2017

Jon-Emile (@heart_lung) chimes in on the whole portal vein POCUS! #FOAMcc, #FOAMed

When it comes to physiology, there`s no doubt that Jon is the man, so I was really curious about his take on all this, which, no surprise, is definitely worth sharing, just in case everyone doesn`t go read the comments.

 

Jon:

Wow; there is a lot to unpack here.

My first comment is that intra-renal venous flow [*not renal vein flow], hepatic vein flow, portal vein flow, etc, etc, etc [as well as IVC size and respiratory variation] are all ultrasonographic transductions of the central venous pressure …so I’ll give my boxed disclaimer that volume status and volume responsiveness cannot definitively and reliably obtained from this marker because the CVP is too complicated to make these physiological leaps.

Indeed. It is important to realize that, as Jon states below, that the angle for looking at the PV in this case is to assess congestion, rather than responsiveness or the ever-so-nebulous ‘status.’

Wait for it … volume tolerance and the CVP, is a bit more nuanced, i think.  with a high CVP, you really have to ask yourself – **why** is the CVP elevated and go from there.  if the CVP is elevated because of tamponade, its very different management from a high CVP from a massive PE or air-trapping versus a high CVP from volume overload.

Absolutely. Diuresing a pre- or full-fledged tamponade, PE or air-trapping could have disastrous consequences, i.e. PEA arrest!

There seems to be some confusion about *the renal vein* versus *intra-renal vein*.  the lida trial is clear that it is intra-renal vein flow.  i am not terribly familiar with *the renal vein flow, however, my hunch is that renal vein flow should always be biphasic [just as the jugular venous flow, SVC flow, IVC flow and hepatic vein flow are always biphasic] – that is a normal pattern close to the right atrium.  normally the systolic inflow velocity is greater than the diastolic inflow velocity and there is fairly good data correlating reversal of systolic to diastolic venous flow ration to right atrial pressure [in the IVC and SVC].

Definitely the intra-renal vein should be the target here – not always easy in some patients, because the renal vein itself, especially the right (no crossover) really has an IVC pattern and won`t necessarily reflect the effect of intra-renal hypertension.

The pulsatility that evolves in the intra-renal vein as the CVP rises is beyond me, but the authors postulate that it has to do with the compliance of the vein at higher CVP and intra-renal interstitial pressure which makes some sense.  But it is important to note that the compliance curves of an intra-renal vein and *the* renal vein are probably quite different.

Secondly, the pulsatility of the PV is a neat idea because of its relative ease of assessment.  However, the pulsatility, presumably, is due to the PV encroaching the limits of its compliance curve – the PV, like the CVP – has an inflow and outflow pressure.  It is highly likely that a pulsatile PV in a post-operative cardiac patient relates to an angry RV – but is this always true?  What about the cirrhotic?  What about differential partitioning of fluid into the splanchnic bed versus the lower body?  What about differential expression of adreno-receptors between splanchnic arteries [beta and alpha] and splanchnic veins [mostly alpha].  My point is that there could be *other* inflow and outflow differentials that are affecting PV volume, compliance and therefore pulsatility that are not yet recognized.  A cirrhotic on bomb dose phenylephrine/vasopressin may have their splanchnic venous volume recruited with blood expelled towards the liver, an engorged PV that is pulsatile – but is that RV failure?  Is that a patient who needs to be decongested?  I don’t know.

Thirdly, there are complex cardiac contributions to venous flow phase and vein pulsatility such as arrythmia – atrial compliance, etc.  As the comment above notes – how might afib contribute to SVC or IVC venous inflow?  It’s hard to know, but my hunch would be that afib itself would tend to reverse the normal S wave: D wave supremacy … that is, decrease the normal systolic inflow velocity relative to the diastolic inflow velocity.  if the atrium is not emptied fully then its pressure with rise.  if atrial pressure rises, when the atrium is pulled downward during ventricular systole, the S wave will be diminished.  additionally, the more chronically dilated and poorly compliant the right atrium, the greater its pressure will be with the loss of atrial kick.

Fantastic points. Again, looking at POCUS metrics CANNOT BE DONE IN ISOLATION, from the rest of the POCUS and clinical data.

Lastly, the venous inflow pattern analysis approach to CVP estimation – i think – is better than IVC size and collapse because of how IVC size and collapse can also be affected by IAP, ITP/PEEP, etc.  Because ITP affects systolic and diastolic inflow patterns similarly, that confound should be lessened.  Nevertheless, as Dr. Denault mentions in the cases above – you have to treat the patient!  This means integrating what the data is telling you in the patient in front of you.  If in a certain clinical context the test results do not make sense, it’s probably a false positive or false negative test.

I dug up this gem from 30+ years ago. Excellent paper [https://www.ncbi.nlm.nih.gov/pubmed/3907280 – “Ultrasonic assessment of abdominal venous return. I. Effect of cardiac action and respiration on mean velocity pattern, cross-sectional area and flow in the inferior vena cava and portal vein”].

Ok that’s on my short reading list for the next 48h!

They show the venous inflow waveform for the IVC [presumably very similar to *the renal vein]; Afib *does* cause the S wave to become attenuated – so it would change the normal biphasic form to more of a monophasic form. In theory, giving a calcium channel blocker and slowing the patient down should improve this somewhat. They even have a brief discussion on portal vein pulsatility.

This venous inflow stuff is very interesting and potentially very applicable. @iceman tweeted out wave velocity patterns in the MCA during high ICP – indeed – an increase in ICP renders the flow more pulsatile and then there is loss of diastolic flow. Probably similar physiology for an intra-renal vein as intra-renal capsular pressure rises. A good sign that the kidney is under pressure!

Thank you Jon for some really excellent physiological points and the reminder that, in POCUS just as in clinical medicine, we cannot rely on one assessment, and that measure must be considered in the context of the factors affecting it. Otherwise, we are not truly tailoring our therapy to the patient, but only pretending to.

Don’t miss Jon and the POCUS workshops at  next april!

December 3, 2017

Portal Vein POCUS: A Reader’s Case and a Follow-Up to the Denault Discussion

So I’ve been meaning to post a follow up and discussion about portal vein POCUS and how I am integrating it so far, and a few days ago I got a really interesting comment from Dr. Korbin Haycock, and I think it’s got some awesome elements to discuss.

Before we get into it, I would invite anyone reading this to go listen to the original Denault Track here, without which this discussion would be missing some elements.

What we are looking at here is the physiological assessment of venous congestion, and how doppler interrogation of the portal vein may help us. So here is Korbin’s case, and I will interject (in bold) where I think a point can be made, or at least my thoughts on it.

“Awesome post. Awesome website. I had never heard about portal vein pulsatility until reading your blog. I have previously been looking at the renal resistive index and renal vein Doppler pattern in my hypotensive/shock patients (along with doing a bedside ECHO and POCUS pulmonary exam) to guide when to stop fluid resuscitiation.

Very impressive. I have only ever heard of a handful of resuscitationists looking at this (including Andre, and consequently myself) so I’m gonna have to have a chat with this fellow soon! For those who have not tried or are not familiar, some basic info can be found here. I’ll have to review this, but I think one issue with RI is that there is an associated ddx, so that without knowledge of baseline, I would not be certain how to use it. Renal vein doppler seems very interesting to me, as that venous path is the one of the cardiorenal syndrome (forget about all that “low flow” nonsense in CHF – not in shock – patients), and there is clearly bad prognosis associated with abnormal (discontinuous) flow patterns. Here is a really good study (Iida et al)  and its editorial (Tang).

Iida Doppler_CHF Heart Failure JACCHF 2016

Tang Editorial JACCHF 2016

I had a case last night that I think illustrates that fluid administration can be the wrong thing to do in some septic shock patients. Plus, I got to try something new and look at the portal vein for pulsatility.

My case was a gentleman in his late 60’s with a history of HTN, atrial fibrillation and HFrEF who presented with three days for a productive cough and fever. POC lactate was 2.7. His HR was 130-140’s, in atrial fibrillation, febrile, MAP was 50, and he looked a bit shocky and was diaphoretic. The resident had started antibiotics and a fluid bolus of LR, of which not much had gone in (maybe 200cc) when I came to start a night shift and evaluated the patient. I asked that the fluids be stopped until we could have a look at him.

His IVC was about 1.5-2 cm with >50% collapsibility.

So I’m gonna hit the pause button right there for a couple of comments. That’s not a hypovolemic IVC. The RAP may be raised by some of the  It may very well be volume responsive, but I think the first thing to go for is correcting that tachycardia. The antibiotics are definitely the right call, but the fluids should, in my opinion, be held until assessment for volume tolerance is done.

His LV looked to have some mildly decreased EF and was going very fast. RV looked normal. His average SV was 45, CO was 6.1, E/e’ ratio indicated a slightly elevated left atrial pressure. His estimated/calculated SVR by the ECHO numbers was about 550. Lungs were dry anteriorly, without B-lines, but PLAPS view was c/w bilateral lower lobe PNA. Renal vein Doppler was biphasic and the resistive index was very high. I looked at his portal vein and it was pulsatile.

Excellent. So there is pulmonary pathology, which makes fluid tolerance already of concern. The CO is certainly adequate and SVR is low, suggesting a vasodilatory shock etiology. 

In the past, based on the IVC and the way the RV looked, I would have done a straight leg raise or given a given some crystalloid to see if his SV and BP improved, and if it did, give some IVF. Instead, I told the staff to given no more fluids and I gave him 20 mg of diltiazem.

His heart rate decreased from 130-140’s to 90. His averaged SV increased to 65 (probably due to increased LV filling time and better diastolic perfusion time), CO was 5.9, estimated SVR was 570. The renal and portal vein Doppler were unchanged. The MAP didn’t bulge and stayed low at 50-55. At this point I ordered furosemide and but him on a norepinephrine infusion to increase the SVR, first at 5 mcg/min, then 7 mcg/min.

Totally awesome to see. It isn’t unusual for me to diurese patients in vasopressor-dependant shock, as more and more data is emerging on how venous congestion has deleterious effects on the gut and may even contribute to the SIRS-type state. And once a patient is in a euvolemic to hypervolemic state, the only fluid they get from me is the one containing norepinephrine. Maintenance fluid is not for critically ill patients IMO.

The NE gtt increased his MAP to 75 mmHg. His SV was 80, CO 7.1 (I was a little surprised it didn’t go down a bit), estimated SVR was 700. I had his labs back at this point and his creatinine was 1.8 and the last creatinine we had was 1.1 a few months ago. His renal vein pattern was still biphasic and his renal resistive index was also still quite high at 0.89, which would probably predict a significant kidney injury in 2-3 days.

Even though his MAP and hemodynamics looked great, I was worried about the renal resistive index. I ordered a little more furosemide and started him on a little bit of a vasopressin infusion. After things settled down, MAP was 75-80, his average SV was 80, CO 7.3, estimated SVR was about 800, and his renal resistive index (RRI) was 0.75. He looked much better too. The second lactate was 1.3.

Very interesting to see the drop in RRI.  Great case to show how you don’t need to chase lactate with fluids. That is an antiquated knee-jerk reflex hinging on the concept that hyperlactatemia is primarily due to tissue hypoperfusion, which we have learned is not the main cause. 

This morning his creatinine had improved to 1.3 and he is doing well.

South of your border, CMS considers me a bad doctor for not giving 30 cc/kg crystalloid as a knee jerk reaction and instead giving a diuretic and early vasopressors as we did in this patient. Just looking at his IVC would indicate that IVF would be a reasonable strategy. If I had done a SLR or fluid challenge and found him fluid responsive, in the past, I would be temped to chase every bit of fluid response with pushing more fluids, but the renal and portal vein Doppler made me stop fluids in this patient this time. I think this example illustrates the importance of looking at each of your patients on a case by case basis and looking at the whole picture (heart, lungs, kidneys, now portal system too for me!), rather than following protocols.

Kudos. 

 

So then, Andre decides to chime in as well:

Very interesting but be careful about the interpretation of portal pulsatility because it can be falsely positive particularly in hyperdynamic young patient, which was may be not the case. We published an algorithm in order to identify the true portal pulsatility associated with right heart failure and fluid overload and a normal portal vein with pulsatility:

Tremblay Portal pulsatility Flolan Mil AACR 2017

(Tremblay 2017 A&A care report) A & A Case Reports. 9(8):219–223, OCT 2017 DOI: 10.1213/XAA.0000000000000572 , PMID: 28604468)

The latter will be associated with normal RV even hyperdynamic, normal hepatic venous and renal flow, normal IVC. We still need to explore the significance of portal hypertension outside the area of cardiac surgery where we are finalizing our studies.

Always tell my residents and fellow, treat the patient and not the number or the image. That being said, the patient got better so cannot argue with success.

So I think this is a really important point, that it can become dangerous in POCUS to look for a simple, single-factor “recipe” with which to manage the patient, when in fact you can have many factors which, integrated, can give you a much better understanding about your patient’s pathophysiology.

My take on portal vein POCUS so far is that it is a marker of critical venous congestion, beyond simply a plethoric IVC. I think it is wise to stop fluids before the plethoric IVC, but a plethoric IVC with a pulsatile PV should bring fluids to a screeching halt and some decongestive therapy started. The data for this?  Andre is cooking it up, but in the meantime, there is plenty of evidence that congestion is plenty bad, and NO evidence that maximizing CO works at all, so I am very comfortable in witholding fluids and diuresing these patients. 

For fun, here is a little figure from Tang et al about the doppler patterns discussed.

Love to hear everyone’s thoughts!

and for those interested, there will be a workshop run by Andre and myself on this at :

more to come on this soon…

cheers

 

Philippe

November 19, 2017

The Resuscitation Tracks 1: Portal Vein POCUS with Dr. Andre Denault. #FOAMed, #FOAMcc, #FOAMus

So this is one of the key discussions I wanted to have in my process of synthesizing my resuscitation algorithm. Dr. Denault is the one guy I’d call a mentor, and I think one of the rare and true clinician-scholar, who is just as comfortable being the anaesthetist/intensivist at the bedside of the crashing patient as he is being the keynote speaker in major conferences, or writing the textbooks that lead the field in acute care/perioperative TEE and critical care POCUS.

So to put some perspective to this discussion, back in 2014 I organized a resuscitation afternoon for internists with Andre and another awesome guy you probably all know, Haney Mallemat (@criticalcarenow). In a quick 15 minute discussion between talks, he shared with me the most recent of his discoveries, portal vein POCUS as a marker of right-sided failure/volume overload in his post-op cardiac patients, and how aggressively managing these resulted in much improved post-operative courses in terms of weaning, vasopressors and even delirium.

Interesting stuff.

So here you are:

So I’ll let you all ponder that and I would really like to hear comments and ideas. Sometime in the next few weeks I’ll be finalizing my resus algorithm – which will not be a recipe approach, as you might suspect if you have been following this blog, and will rely heavily on POCUS and the clinical exam.

cheers and thanks for reading and listening!

Don’t miss Andre running a POCUS workshop on PV/HV at  next april!

Philippe

 

October 24, 2017

Emergency Pericardiocentesis post-arrest (Part 1). #FOAMed, #FOAMus, #FOAMer

So a few nights ago I got pulled out of slumber to rush to the ER for an elderly patient who had arrested in hospital shortly after having been brought in for chest pain. The sharp ER doc had diagnosed a tamponade on a presumed aortic dissection, managed to get a needle in, aspirated some fluid and managed to get ROSC.

So when I got there we had a patient post-ROSC in rapid atrial fibrillation with a thready but palpable pulse. POCUS showed a large pericardial effusion with minimal LV filling. So here is what we did:

With the catheter in, we were able to drain. Note a couple of POCUS teaching points, always make sure to (1) visualize your guidewire in the right space, and (2) second, when using a dilator, you can note the disappearance of the proximal part of the guidewire as it is covered by the dilator. This tells you you have adequately dilated into the target structure – pericardium in this case, because it is possible (personal experience) to advance a dilator fairly deep, but not go through a perhaps fibrotic pericardium, and then result in pigtail mis-placement just outside of the target.

In part 2 you can also see the aspiration of the effusion and improved LV filling. The patient’s BP instantly rose to 140’s systolic.

More case details and POCUS teaching points to come in part 2.

cheers,

ps – a sterile probe cover was unavailable immediately in the ER. By the time it showed up the pigtail was in. We didn’t feel we could wait. We doused it in alcohol.

Philippe

 

October 23, 2017

It’s almost here…SIG.ECG – the next generation of ECG monitors!

So our ECG pad is ready.

I’ll let the images speak for themselves.

I’ll let your imaginations tell you where it would be most useful.

But think, no leads getting in the way or falling off. Think of the time saved in echo labs and clinics.

What does it give you?

  • leads for a monitored bed (ED, ICU, CCU, stepdown, etc).
  • a continuous 9-lead ECG. Sure, “it’s not a 12 lead,” but it doesn’t stop you from ordering one. And from my understanding of ECGs (let’s check with Steve Smith maybe?), I think that if you are isoelectric (ST-wise) in 9 leads, the chances of missing a STEMI are…somewhere between slim and none.
  • no problem with a gown, extra adipose tissue or sweat – those help if anything.
  • yes, the patient can be on his or her side, no problem.
  • infection control? they’re gonna love it.
  • eco-conscious – just wipe and reuse!

Data?

Yes. For those who don’t realize that an electrical signal is an electrical signal and that the challenge is to obtain it, two studies are underway to compare it to the current gold standard traditional ECG.

Bottom line?

First deliveries anticipated mid-2018.

We’re looking at about $5K apiece. Final price TBA and will vary with bulk orders. Expected to last years – so actually cheaper than all the leads we throw away.

The first run will be limited.

When it’s officially available for pre-order, how many do you think you would want? 😉

cheers!

 

Philippe

May 6, 2017

To POCUS or not to POCUS… No, that is NOT the question! #FOAMed, #FOAMus, #FOAMer

So a few weeks ago I got into some twitter debates after I – not uncharacteristically – stated that, in my opinion, practicing acute care today without using/learning POCUS  is unethical. Now I was hasty, and, in my wording did not exclude those docs who simply do not have access to the technology, and I apologize for that. For the rest, however, I totally stand by my words.

So there was a bunch of smart people who exhibited the monosynaptic reflex of asking for the evidence, the studies, or else brandishing some that showed that some aspect or other of POCUS is flawed, or some anecdote about misdiagnoses, bla, bla, bla…

Now this time, I’m going to start the discussion with the bottom line, in a sense, and leave the nitty gritty for later (which is actually the most important part, tho). But here it is:

Unless you think that the addition of ultrasonography cannot perform more accurate and rapid diagnoses than you can with your inspection/palpation/percussion/auscultation, you cannot rule against POCUS. 

Now if you actually believe that, the corollary would be to never ask for an echocardiogram, abdo-pelvic ultrasound, etc… Not too many takers. Thats what I thought.

What you can challenge, however, is the process of POCUS, meaning how do you get Dr. John Doe competent enough to make a call of pathology X (for the diagnostic aspect) and how do we clinically integrate and act on the POCUS findings, many of them being “new” from increased sensitivity, what do they mean, what does their evolution mean? Many good questions there.

That’s why I lament the entire debate around POCUS. These smart people should focus their neurons on helping us fine-tune POCUS instead.  POCUS is a huge, exploding field. I’m pretty POCUS-comfortable, but don’t ask me to start looking at bones and tendons and ligaments and a myriad of other applications. There’s not much in the body we can’t get some ultrasound into, so all those represent areas of additional information to be assessed.

The education process is also clearly in need. I’m on a panel of the Quebec College of Physicians whose mission is to put some parameters around POCUS. There’s no holding it back, it’s just about getting it going in the right direction.

It’s like anything else in medicine. We have no perfect tools, because we are working with a hypercomplex system with many variables.

And speed. Anyone interested can scan thru the POCUS cases on my blog, and what you see every time is the speed and accuracy that POCUS brings. Studies are hard, and complex. POCUS is not a single intervention, so measuring impact is difficult. Let’s say we have a septic patient with an obstructed kidney. POCUS will assess the hemodynamics, guide fluid resuscitation and inotrope use, but also find the probable source quickly, then perhaps make sure there is no gastric distension prior to intubation, confirm ETT and CVC placement, and more as the evolution goes. How do you make an RCT around that?  It is, however, a good idea to validate every aspect (which has essentially been done already, but certainly there is more to do).

Sadly, most of the naysayers, in my experience, are not echo-competent and likely don’t want to feel like med students all over again, learning a complex skill from scratch, and instead are crossing their fingers hoping that somehow, ultrasonography will be discredited… Yup, it’s not just a river in Egypt.

POCUS is a work in progress. It won’t go away. Hop on and give us a hand. Your patients will benefit.

 

cheers!

Philippe

March 23, 2017

Bedside Ultrasound Quiz Part 2: A 50 yr old man with dyspnea, acidosis, hepatitis and leg edema. #FOAMed, #FOAMer, #FOAMus

So I was glad to see some great answers on twitter about this case, so let me fill you guys in on the management and the details.

So my diagnosis was of a (likely viral) myocarditis as a subacute process over the last weeks, with a superimposed pneumonia causing the acute deterioration and presentation to ED.  I didn’t think that his elevated lactate represented shock, but rather a reflection of adrenergic activation and reduced hepatic clearance due to congestive hepatitis.  He also had congestive renal failure. Of course, the LV had a 4 x 2 cm apical thrombus, which is likely secondary to the dilated cardiomyopathy.

So the management was diuretics, antibiotics, and anticoagulation, which resulted in a gradual improvement of the respiratory status and renal/hepatic dysfunction. He had a coronary angiogram the day following admission which showed two 50% stenoses deemed to be innocent bystanders.

Bottom Line:

I think the learning point in this case is that, without POCUS, this could easily have been treated as severe sepsis with multiple organ failure (potentially rationalizing away the BP of 140 as a “relatively low” BP due to untreated hypertension), and as such, may have received fluids… Especially south of the border where they are mandated to give 30 cc/kg to anything deemed “septic.”  This would have been the polar opposite of the necessary treatment.

The scarier thought is that he may have then progressed to “ARDS,” been intubated and then the debate between keeping him dry and giving fluids for the kidneys may have ensued.  Though a formal echo likely would have been done, it may not have happened in the first 24-48 hours… If MSOF progressed and he succumbed, the rational may have been that he was “so sick,” and died despite “best care…”

The reality is that he is not yet out of the woods today, with an EF of 15% and afib, but he is off O2 and sitting up in a chair. Fingers crossed he falls in the group of those with myocarditis who improve…

Love to hear anyone’s thoughts!

 

Cheers

Philippe

March 21, 2017

Bedside Ultrasound Quiz Part 1: a 50 yr old man with dyspnea, acidosis, hepatitis and leg edema. #FOAMed, #FOAMer, #FOAMus

So last night, an interesting call from the ED about a 50 year old man who presented with a 3 week history of increasing dyspnea, leg edema, temp of 39,  a lactate of 3.9, an INR of 1.7, elevated LFTs and a WBC of 18, but a BP of 130/75.

Fortunately, I was dealing with a saavy ER doc with some POCUS capabilities, so he also told me he saw a pretty big IVC and he was a bit leery about giving fluids, though this looked like pretty severe sepsis with 3 or 4 affected organ systems…

So I asked him to hold fluids until I got there. Here is what POCUS found:

He revealed a past history of untreated hypertention, and a flu-like illness 3-4weeks ago.

What’s the diagnosis (-es) and management?

Answers & Clinical evolution in part 2 tomorrow!

 

cheers

 

Philippe