intensive care

November 29, 2019

H&R2019 Lecture Series: Denault on POCUS and Delirium! #FOAMed, #FOAMcc

So the pundits still try to claim the lack of evidence for the use of POCUS, bla, bla bla. Just wait till they get a load of this: POCUS in delirium? Master Andre Denault introduces us here to a completely new way of assessing a little known potential aetiology of acute delirium.

 

Here it is, certainly one of the most interesting and forward-thinking lectures of H&R2019:

Denault on POCUS and Delirium.

 

 

 

Don’t forget The Hospitalist & The Resuscitationist H&R2020 is happening May 20-22 and registration is open! Seating is limited…

cheers!

Philippe

July 31, 2019

Exploring the Pulmonary Vasculature with Korbin Haycock: RVOT Doppler. #FOAMed, #FOAMcc, #POCUS

So some recent twitter discussions, particularly involving my friend Korbin (@khaycock2) and Lars (@LMSaxhaug) – whom I am trying to get on the podcast soon – were really fascinating in regards to RV and pulmonary hypertension assessment. So time to dig into this a little.
The basic POCUS RV assessment is RV:LV ratio and TAPSE, along with RV free wall thickness (should be below 5mm) and the D sign in parasternal SAX. This is a solid start to screen for significant RV dysfunction.
The next level should be to measure PAP using TR Vmax, in order to assess the degree of pulmonary hypertension. Thats pretty much where I’ve been at for the last few years and wasn’t sure there was really a lot more that was necessary from an acute care standpoint where your immediate questions are fluids/pressors/inotropes and some inhalational pulmonary dilators. I wasn’t convinced I needed more.
But of course Korbin and Lars are on another level, and started to talk about doing RVOT doppler and looking at TR Vmax to RVOT VTI ratios to estimate pulmonary vascular resistance. Is there any difference there? Is my PAP not enough? Well, turns out there may be some useful information there, so I will let Korbin do the talking, and my apologies for my dumb questions during this discussion!
So I will be toying with RVOT doppler and trying to see if this is something that warrants a place in acute care management. I suspect it may be something that may tip towards earlier inhaled vasodilator therapy, or else make not using them a more confident choice. I do like the waveform analysis. I think we generally overlook a lot of good info by focusing on numbers over morphology!
So far, images using the PS SAX view have been quite good:
Additionally, RVOT notching could be suggestive of an acute PE – makes sense (study link here!)
Here are a couple of excellent references:
So thanks to Korbin and Lars for forcing me to up my doppler game some more!
cheers
Philippe
Formula Fun:
Tricuspid regurgitation pressure gradient for sPAP:
sPAP=4*(TRvelocity^2) + RAP or
sPAP=TRpg +RAP
mPAP=(sPAP)*0.61 + 1.9
Acceleration time equations for sPAP and mPAP:
sPAPlog= -0.004(AT) + 2.1
mPAP=90 – (0.62*AT)
Pulmonary Regurgitation pressure gradient:
mPAP=4*(Peak initial velocity^2) +RAP
dPAP=4*(End velocity^2) + RAP
dPAP-PCWP should be about <6mmHg or else PVR is likely, see PCWP equations below
PVR equation to screen for increased PVR, or if PVR < 3 WU:
PVR=10*(TRvelocity/RVOT VTI) + 0.16. TR velocity is in m/sec, if <2 WU, no increased PVR.  This equation is accurate up to 3 WU
PVR equations for increased PVR > 3 WU.  These equations less accurate if PVR < 3 WU:
PVR=5.19*(TRvelocity^2) – 0.4, or more simplified: 5 * (TRvelocity^2). Note that the 5 * (TRvelocity^2 is almost sPAP equation (4 * TRvelocity^2)=sPAP
PVR=sPAP/RVOT VTI if no RVOT notch present
PVR=(sPAP/RVOT VTI) + 3 if RVOT notch is present
PCWP equations (for detection of group 2 pHTN to elevated sPAP), as you know, this is a whole other area, and gets a quite a bit more complicated, but to summarize:
PCWP likely elevated if E/e’>15, unlikely if E/e'<8
In NSR, PCWP=1.24 * (E/lateral e’) + 1.9
In ST, PCWP=1.5 * (E/lateral e’) + 1.5
In atrial fibrillation averaged over 5 beats, PCWP=0.8 * (E/lateral e’) +6
Using color M-mode and propagation velocity: PCWP=5.27 * (E/Vp) + 4.6
February 19, 2019

The Andromeda-SHOCK study. A physiological breakdown with Rory Spiegel (@EMnerd). #FOAMed, #FOAMcc, #FOAMer

So recently published was the Andromeda SHOCK trial (jama_hernndez_2019_oi_190001) in JAMA this month.

Definitely interesting stuff, and have to commend the authors on a complex resuscitation strategy that had some real-world flexibility built in in terms of later generalizability and applicability for real-world cases. However there are some fundamentals I have concerns about. Let’s see what Rory thinks:

Yeah. I think the bottom line of opening resuscitationists’ eyes to NOT apply monosynaptic reflexes of giving fluids to elevated lactate is good. In that sense, definitely a step forward.

However, the insistence on maximizing CO under the illusion of optimizing perfusion remains problematic and leads to a congested state unless only a small or perhaps moderate amount of fluid is required to achieve non-volume responsiveness. I think it’s important to realize that the most rapid correction of hemodynamics is a surrogate marker and has not been definitively associated with survival across the board (eg the FEAST study and others), and it’s only proven clinical impact may be on health care workers’ level of anxiety.

Tune in soon for some other smart docs’ take on this!

 

cheers

 

Philippe

 

oh yes and don’t forget The Hospitalist & The Resuscitationist 2019:

 

February 12, 2019

Is POCUS the new PAC??? A Chat with Jon-Emile Kenny (@heart_lung) #FOAMed, #FOAMcc

So here is what Jon tweeted a couple weeks ago:

Yikes! Does that spell doom for POCUS???

So clearly we had to get to the bottom of this statement…So a google hangout was in order.

 

Part 1 my intro:

and Part 2 our discussion:

 

So the bottom line is that we agree that there is a risk that POCUS may partly head the way of the PAC, or at least be challenged in a similar fashion. Hopefully the wiser physicians will see the inherently flawed logic that would push the field in that direction. Alternately, we could all get our minds and efforts together and try to do a triangulation of data to really pinpoint hemodynamics.

Love to hear comments!

For more of Jon’s physiology awesomeness, visit http://www.heart-lung.org.

Cheers

 

Philippe

 

 

PS for cutting-edge and bleeding edge discussions, including Jon-Emile and a lot more, don’t miss H&R2019 this may in Montreal…

January 26, 2019

Volume status, CHAISE study and other silly questions. #FOAMed, #FOAMcc, #FOAMer

So I just finished reading the CHAISE study, which compared Parm as a surrogate for Pmsf as a surrogate for “volume status.”

It is a really cool study for anyone who loves physiology, which I definitely do, and there may be some interesting elements that can be clinically used.

But let’s first set the record straight. I do not believe that “volume status” is a medical and especially not a scientific term. It is a vague reference to intravascular fluid and can be interpreted in a lot of different ways, making it essentially useless. There is such a thing as the status of your flight (on time, delayed, cancelled), your reservation (confirmed, cancelled), your postal delivery (returned, delivered, in-transit), etc.  But there are no such clear strata for “volume status.”

So what are the true scientific terms that can be measured? Blood volume. So if we had a bedside radiolabelled substance test that could give us our true blood volume, that could give us a real measure of “volume status.”

On the other hand, that would be of marginal use clinically, in all likelihood.

Why? Because there are only three questions that the savvy clinician is trying to answer, in order of importance:

1. Does my patient need fluid?

2. Is my patient volume tolerant?

3. Is my patient volume responsive?

The answer to the first question is mysterious, outside of the obvious extremes, and in my opinion, anyone who feels they can clearly answer correctly is deluding themselves.

The answer to the second question is complex and multi-factorial and includes echographic findings (venous congestion/hypertension, B lines, effusions, ascites) as well as physical examination findings (tight abdomen, edema) and clinical findings (respiratory failure, intracranial pathology) and more. But this is a critical one, because if the answer is no, then you need some really compelling evidence to even consider trying to answer the third question.

The answer to the third question is, outside of the extremes, a bit of a quagmire of assessments and technology with generally poor evidence, particularly in terms of duration of effect. The most fearsome aspect of this third question is that it is usually the first question asked instead of the last, and thus has the side effect of creating volume-responsiveness terminators who, 500cc shot after 500cc shot end up satisfied that they have blasted responsiveness into oblivion.

But that’s probably bad news for the patient, that they have now pushed into venous congestion or salt-water drowning. Unless, of course, they just look for volume-responsiveness in the same way that bird-watchers do, for the sake of scientific satisfaction, and do no more than look, or maybe snap a picture at most.

So sure, echocardiographic parameters for volume status should be under fire, as all other parameters should. The authors in this paper themselves state two critical assumptions in the Parm/msf logic:

(1) that the fluid stay intravascular in the 10 minutes (ok, I’ll buy that)

and

(2) that the compliance is linear (nope, I don’t buy that, especially not in sick patients on vasopressors – as opposed to the normal cardiopulmonary and hemodynamic patients this study was done on).

Essentially, what should be under fire is the obsession with a measurable variable to assess intravascular volume. Too many factors in play, and the answer is useless clinically anyway.

On the other hand, this study is fascinating in terms of what might be done using dynamic Parm… Maybe individualizing pressor response, unstressed volume recruit-ability?  I’ll let @iceman_ex tell us about that at H&R2019!

So what is important is stop points. And reverse points. And yes, these can be looked at using POCUS, and also CVP, and CVP tracings. And yes, there is good data that venous hypertension is a bad state. And this is what you should be looking at, to make sure you have not pushed your patient into a universally pathological state of non-volume-responsiveness.

Cheers

Philippe

So Kylie (@kyliebaker888) had some comments and questions:

Hi Philippe, I just had to read the article after your blog. Most is a bit above my head (yeah right Kylie)– but I am perplexed by three things that I did understand -perhaps you can help me with….
1. Is P(arm) a useful measure? – it went up in 19 patients and down in 8 patients after a 500ml bolus yet they claim it went up (after statistical repeated measures or something)..if P(arm) is confounded by something else – I think they suggest sympathetic tone – shouldn’t we sort that before we start using P(arm) as a reference test.

I don’t think we can consider it to be a reference at all. I think it is an interesting physiological measure and that it might have some application in phenotyping vascular tone/compliance and possibly helping in vasopressor fine tuning. In my opinion for fluids it adds little to what we have.

2. What do you think of their IVC measure – 0.5cm below junction with RA?

As I do for all IVC diameter measures, I think it is inherently mathematically flawed to try to assess a volume using a diameter. Eyeball the whole IVC. A recent study finally looked at this. 3D IVC assessment and (of course) found it better.

3. What do you think of the fact that E changed, but e prime and E/e prime didn’t….That seems like there may not be enough precision in some of those measurements.

I agree.

I also have another savvy-clinician question to add to yours
Q4: Is my patient leaking?

Excellent!

Thanks!

December 27, 2018

#POCUS IVC Pitfall Twitter Poll & Discussion. #FOAMed, #FOAMer, #FOAMcc

So I ran a couple of twitter polls sets the other day. Here is the first:

(if you want the twitter videos see here)

 

 

and part 2:

And to sum it up:

So I just wanted to illustrate something I keep bringing up, essentially that the entire IVC literature based on the AP diameter measurement is physiologically and mathematically flawed. I think the poll and images above clearly support this: given a short axis view, clinicians clearly have a different opinion (and possibly intervention!) than using only a long axis view.

My take, as I’ve said and will keep saying, is that there is a lot of info in IVC POCUS, and the one I am LEAST concerned with is volume responsiveness, which sadly seems to be everyone’s only focus nowadays when it comes to the IVC.

But here’s some food for thought, some of my clinical applications in 5 seconds of scanning:

initial shock patient: big fixed IVC -> no fluids, hurry and find the downstream problem and correct!

resp failure patient: small IVC -> it’s not a massive PE, keep looking for the cause don’t send for a STAT CT angio!

AKI patient: big IVC look at venous doppler and call for lasix, stop the fluids and albumin that were being mistakenly given!

AKI or shock patient & small IVC: sure , start with some fluids and reassess soon (that means hours not the next day)

 

etc..etc.. there’s more, and “fluid responsiveness” is only in extremes and fairly low on the list for me!

 

cheers

 

Philippe

 

ps if you like physiology, and a physiologico-clinical approach, don’t miss H&R2019!

December 23, 2018

Discussing “ARDS” (and of course fluid management and #POCUS) with @iceman_ex! #FOAMed, #FOAMcc

So sparked by some recent twitter discussions where we were talking about ARDS in a somewhat controversial fashion, I thought it may be worth expanding a bit on the topic.

Essentially my stand is that ARDS is largely an iatrogenic disease mediated by (1) overeager fluid resuscitation of various disease states that fundamentally do not require large amounts of fluids despite commonly held beliefs (sepsis, pancreatitis, etc…) and (2) the absence of frequently used “stop points” of fluid resuscitation with instead a misguided focus on detecting (and intervening upon) volume responsiveness.

In our ICU, true “ARDS” (eg not generated by salt water drowning) is a rarity. Maybe one or two a year, usually a massive primary pulmonary insult.

Anyhow, here, Segun and I discuss this:

 

Ognjen Gajic refers to this article in our discussion.

 

So it seems clear that there is much to discuss. We didn’t even really get into the juice of the stop points. Stay tuned!

 

oh yes… so if these controversial, cutting- and bleeding-edge topics, don’t neglect joining us at H&R2019. Segun and many others will be there!

https://thinkingcriticalcare.com/2018/11/04/hr2019-final-programme-register-now-montreal-may-22-24-2019-hr2019/

 

 

cheers!

 

 

November 11, 2018

POCUS, Mythology and Hemodynamic Awesomeness with Jon and Korbin! #FOAMed, #FOAMer, #FOAMus

In Greek mythology, Prometheus (/prəˈmiːθiːəs/; Greek: Προμηθεύς, pronounced [promɛːtʰeús], meaning “forethought”)[1] is a Titan, culture hero, and trickster figure who is credited with the creation of man from clay, and who defies the gods by stealing fire and giving it to humanity, an act that enabled progress and civilization. Prometheus is known for his intelligence and as a champion of mankind.[2]

So, fresh from reading Jon’s post, I felt I had to add a bit of nuance in my previous post to what I feared some might extract as a take-home message, even if in fact, we are not that differing in opinion at all – which Jon expressed here:

i agree with ultrasound for finding the uncommon causes of shock. these examples seems to permeate twitter and make ultrasound very appealing. because ultrasound is non-invasive, it makes the risk-to-benefit ratio very low for these uncommon but highly-lethal and treatable causes.

but that needs to be compared to the risk-to-benefit ratio of ultrasound for the more common causes of shock – like ‘non-cardiogenic, septic’ etiologies as seen in SHOC-ED. here, “static’ ultrasound [as per the RUSH and ACES protocols] – per SHOC-ED – appears to be neither helpful nor harmful. your read of the discussion is perfect, but i was depressed because it read as if the authors only realized this ex post facto – study of previous monitoring utensils [e.g. PAC] should have pre-warned the authors …

i will take some mild issue with markers of volume responsiveness and tolerance. you are correct on both fronts – but what the data for the IVC reveals – perhaps paradoxically – is that true fluid responders can have a very wide-range of IVC sizes from small to large and unvarying … this was born out in most of the spontaneously breathing IVC papers [airpetian and more recent corl paper] the sensitivity was rather poor.

the same *could* be true for the opposite side of the coin. a large great vein may not mean a volume intolerant patient. i tried to exemplify how that could be so in the illustrative case in my post. an elderly man, with probable pulmonary hypertension and chronic TR who probably “lives” at high right-sided pressures. nevertheless, he likely has recurrent C. diff and is presenting 1. hypovolemic and 2. fluid responsive despite his high right-sided pressures. portal vein pulsatility *could* be quite high in this patient – but he still needed some volume.

the obvious underlying issue here – which I know you are well attuned to – is that a Bayesian approach is imperative. when you PoCUS your patients, you are inherently taking this into consideration – i know that you are a sophisticated sonographer. my hidden thesis of the post is that if ultrasound findings are followed in a clinical vacuum and followed without really understanding the physiology [which can explain clinico-sonographic dissociation – like the patient in my fictitious case]… disappointment awaits.

Then Korbin Haycock chimes in and adds a level of understanding that I completely agree with but had difficulty in expressing, but which I think is key to understanding the current and future evolution of POCUS. Complex, operator-dependant medical leaps such as laparoscopic surgery suffered with similar growing pains. But I’ll let Korbin shed some light:
I think the issue of POCUS in resuscitation is somewhat analogous to Prometheus’s gift of fire to humanity.
Jon has quite aptly pointed out that if POCUS (particularly a single POCUS supplied data point such as IVC diameter), if used in isolation, without clinical context, and without comprehensive information, is not much better than using a single data point such as CVP to make complex clinical decisions. Multiple factors influence the behavior of the IVC, just as they do with the CVP. Being a dynamic entity, the IVC does have some advantages over a static number like the CVP. However, if considered by itself, the IVC POCUS evaluation will only result in the same pitfalls as using the CVP as a guide to fluid management. If POCUS is applied in such a blunt manner, we are doomed to repeat our previous folly of using the CVP as a guide to fluid resuscitation. I hope I am in the ball park of the core of Jon’s point here, if not as very eloquently stated by him.
Phil is advocating a more nuanced and sophisticated approach to POCUS than what the SHOC-ED trial investigators used to guide management in their study. Most shocked patients presenting to the ED (“Emerge!”) come with a phenotype of distributive shock. Indeed, these were the majority of the patients in the SHOC-ED trial. Any experienced clinician will recognize this syndrome virtually every time, with no more than an “eyeball and Gestalt” assessment from across the room and a set of vital signs. Current dogma is that this syndrome ought to be treated with 30 cc/kg of crystalloids and then to add a vasopressor if the patient’s blood pressure is still low. Given this, there couldn’t have been much difference as to how patients were managed in either group in this study. I however, disagree with this aggressive crystalloid administration approach, as I’m sure many readers of Phil’s blog do as well. What I gather Phil is saying here is, as he insightfully stated in the past, “IVC never lies, it’s just not telling you the whole story.” A complete POCUS gives us (OK, well almost) the whole story. The caveat here is you must know a whole lot about POCUS. Thus the Prometheus analogy. A little information is a child playing with fire.
Someone new to POCUS, with only a novice’s understanding of what an IVC POCUS evaluation means, will probably make the correct assessment of a patient’s fluid status about 60-70% of the time. This probably is only slightly better than an experienced clinician’s non-POCUS judgement. Hardly enough to translate into any meaningful clinical outcome in a trial without a ridiculously large sample size to find a pretty small benefit. But POCUS potentially offers so much more information. LV and RV systolic function, LV and RV diastolic function, SV, CO, SVR, PVR, RAP/CVP, sPAP/mPAP/dPAP, LVEDP/LAP/PAOP, valvular pathology, tamponade, fluid responsiveness (for what ever that’s worth!), RV/LV interactions (both in series and in parallel), EVLW, insight into pulmonary vascular permeability, renal resistive index/renal venous congestion, portal hypertension/congestion, gut flow resistance, and on and on. Most of this information can be more or less determined in less time that it takes to put in a central line in order to get the damned CVP (actually, I do like to know what my CVP is, for what it’s worth). The more data points you are able to collect with increased POCUS skills and experience, the more grasp you have as to what is going on with your patient and the right way to treat them. I would argue that given the information attainable with advanced POCUS skills, POCUS is a no-brainer that will enormously improve not only individual patient outcomes, but effect populations at large, if only the general hospital based practitioner can attain a more than introductory understanding of POCUS.
So, I guess the question is, “how much training is enough training?” I don’t know. Inevitably, POCUS knowledge will incur a bit of the Dunning-Kruger effect as pointed out by Jon’s example of an IVC POCUS fail. But reading Jon’s clinical case example, from the get go, I found myself asking questions that would change may management one way or another with additional information that I could get quickly and easily with additional POCUS interrogation of the patient. Jon pointed this out himself by revealing that the patient has pulmonary hypertension as manifested by the tricuspid regurgitation upon auscultation of the heart. With POCUS, I don’t need to guess what a heart murmur is or how bad it is or even if it is relevant to my patient in this case for that matter. POCUS can tell me it’s TR and it tells me what the sPAP/mPAP/dPAP and PVR is if I care to find out. So if this level of information can be gleaned, for me, no one can argue that POCUS has no merit. But, I’ve spent a lot of time striving to be good at this, just as probably a lot of people reading this have done as well. What about newbies?
Consider: At my main hospital, for a variety of sensible reasons I won’t get into, we decided to train a group of nurses in POCUS in order to evaluate septic patients. They achieve basic training in POCUS and are very competent sonographers with regard to IVC, gross LV and RV function, and pulmonary edema. They are a small group of very intelligent, skillful nurses that are excited to learn all they can. We had them evaluate every septic patient that presented to our hospital, do a POCUS exam, and discuss the findings with a physician. We established some very basic resuscitation endpoints largely based on POCUS findings applied to each individual patient and their POCUS exam. Our severe sepsis/septic shock mortality rates dropped from 35-38% to 8-10% with this program. Our hospital plans to publish this data officially soon for public analysis, but it did make a difference in our experience. That said, my nurses do frequently show me cases where I notice some small detail on their POCUS exam that propmts an additional investigation that alters the plan in management. Also, some of my very competent POCUS savvy residents make errors because they don’t have enough knowledge yet. I’m sure I can make these errors too at times as well, although hopefully less and less so with time.
Here’s my point: Heed Jon’s admonition to look at the big picture and not rely on isolated data points. Be inspired by Phil’s passion for the potential of a good POCUS evaluation. If you only get your toes wet with POCUS, you are playing with forbidden fire. But if you care to look into it further, POCUS opens up worlds to you. By all means, learn all you can about POCUS. Recognize that if you are new to POCUS techniques, there are improtant caveats to each finding, and physiology that needs to be considered with a comprehensive view, some of it may be strictly non-POCUS related information as well. Your patient is unique and only a careful comprehensive consideration of what’s going on with your patient will guide the best approach to your management of their illness. I don’t think SHOC-ED or any other trial for that matter can address the nuances of good individualized patient management. That is up to you.Jon replies:

nice analogy – i think Korbin’s response is appropriate and i look forward to speaking alongside him in May. as i chew on the SHOC-ED a little and try to distill my concerns – i think what it boils down to is this: it’s less about playing with fire – i think – and more about how this fire is brought to the community as a whole. my post on pulmccm was more of a warning to the early adopters [like us] who are planning these trials. imagine 40 years ago:

-the flotation PAC is introduced, a small group of clinical physiologists use it thoughtfully, understand the caveats, the problems of data acquisition, interpretation, implementation, the problems with heart-lung interactions, intra-thoracic pressure, etc.
-these early adopters present their results to the community as a whole
-the physiology of the PAC is simplified
-the numbers from the PAC are introduced into algorithms and protocols and **widely** adopted into clinical practice
-the PAC is studied based on the above and found to make no difference in patient outcome.
-in 2010 a venerable intensivist suggests floating a PAC in a complicated patient and the fellow on rounds chuckles and states that their is ‘no evidence of benefit’

does this sound eerily familiar? is our present rhyming with the past? if the planners of POCUS trials are not careful, i promise you that the same will happen but insert any monitoring tool into the place of PAC. i can very easily visualize a fellow on rounds in the year 2030 scoffing at the idea of PoCUS because trials [SHOC-ED, and future trials x, y and z] showed no difference in patient outcome. is it because PoCUS is unhelpful or is it because the way it was introduced and studied was unhelpful? and the three of us will sound like the defenders of the PAC from 30 years ago: “PoCUS isn’t being used correctly, it’s over-simplified, it works in my hands, etc. etc.”

it’s not PoCUS that’s unhelpful, it’s how we’re implementing it – and i was most depressed when the authors of SHOC-ED appeared to stumble upon this only in the discussion of their paper – like you mentioned phil. imprecise protocols will result in equally imprecise data and the result will be nebulous trial outcomes. we should all be worried.

Korbin adds:

Excellent points Jon. The PAC example is very relevant, as on more than one occasion, I’ve had the argument put to me by some colleagues that essentially how I’m applying POCUS is really no different than the information gleaned from the PAC, and “that’s been shown to not be helpful to outcomes” etc. So, therefore, why do I bother?

Then again, I’ve seen a fair amount of phenylephrine being thrown at hypotensive cardiogenic shock patients after a 2 liter normal saline bolus didn’t do the trick.

You are absolutely spot on when you point out that seeing the big picture, knowing the physiology, and being aware of the pitfalls of isolated data points is important to making the right decisions in patient care.

Furthermore, I agree that when a clinical trial is done that doesn’t consider some of the nuances of all this, and “shows” that POCUS, or any other diagnostic modality for that matter, doesn’t contribute to better patient outcomes, it probably only serves to marginalize a potentially valuable diagnostic tool to an actually astute intelligent clinician.

I’m not meaning by saying this to bash the good intentions of the SHOC-ED trial. To be fair, it’s really hard to design a trial that can take into account all the permutations that are involved in any individual patient presents with, having their own unique clinical situations, hemodynamic profiles, co-morbidities (both known and undiagnosed), etc. POCUS, PAC, transpulmonary thermodilution, ECG, chest x-ray, CT scans, labs, physical exam–these are all merely tools that guide patient care. Albeit some are way more powerful than others. I can image various amounts of uproar if some of these traditional tools were subjected to clinical trials to prove their utility. The argument, if proven “useless” in a study for the oldest and well accepted tools would always be, “put it in the clinical context, and its value speaks for itself.” For me, I’d happily like to make clinical descisions based on information based on an advanced POCUS exam or PAC, rather than interpreting hepatojugular reflux or a supine chest x-ray.

Any diagnostic test requires that the clinician understand the limitations of that test, and understand that the whole clinical scenario must me taken into account. You’ve hit on that, I think, with your argument. This surely has implications when any technology or test is studied.

‘Nuff said.
Philippe
PS These are just the kind of discussions that can change both the way you approach medicine and manage your patients, and these are the ones you find behind the scenes and in the hallways of H&R2018. Don’t miss H&R2019 if you take care of sick patients. It’s the kind of small, chill conference where the faculty will be happy to take a few minutes and discuss cases and answer all your questions (if they can) about acute care.
November 7, 2018

The Subtleties of the SHOC-ED Trial: Don’t Just Read The Abstract! #FOAMed

So this was my comment to my friend Jon’s awesome discussion on the SHOC-ED Trial, which is certainly interesting.

Jon, great post as always! I do agree with most of it, but would have to caution readers about reading it with the filtered glasses that make people too often take home the message that they want to – usually the path of least resistance (or change). I think your main point and most critical one is that there is no protocol or recipe that should ever be applied to resuscitation, especially single-variable-based resuscitation (eg old school orders like CVP>12 lasix and <12 bolus), and substituting the IVC for CVP won’t help. And from a standpoint of volume-responsiveness, I totally agree, with the understanding that as the IVC gets more plethoric, the percentage of responsive patients will decrease, inevitably, but one cannot predict with certainty whether that one patient will or will not. However, the parallel change is that, as the IVC gets more plethoric, the volume tolerance is likely decreasing as well, so that your benefit to risk ratio is dropping. And of course you can’t recipe that just based on IVC, but should be looking at the site of pathology (eg lung, brain abcess, pancreatitis with ACS, etc…), physical exam, to determine your patient’s volume tolerance. Because we all know that most of that miraculous fluid will end up clogging the interstitium, with consequences ranging from cosmetic to fatal (though usually blamed on the patient being “so sick” in the first place, absolving the clinician from any wrongdoing). So comments like the one previous to mine, stating “give volume and see if the response occurs” are, in my mind, a poor approach. We know from studies that you cannot simply remove the fluid you gave and go back to the start with lasix (glycocalyx damage, etc), and we also know that much of the effect of said fluid administration dissipates in minutes to hours (I’m sure Jon can quote these studies off the top of his head!).

As we have discussed in the past, I think POCUS is much underused as a fluid stop point – most of its use is on the ‘let’s find a cool reason to give.’  I would argue that you should hardly ever give fluid to a full IVC (especially if markers of pathological congestion are present – portal vein pulsatility and all), unless you are dealing with temporarily improving tamponade or tension pneumo, because even if you are volume responsive, you are likely not volume tolerant. This also goes to the point that a single, initial POCUS exam will potentially not have the same impact as a whole POCUS-based management which will use it to reassess congestion status, cardiac function, etc.

Having said all this, the most important part of the SHOC-ED article is, in my mind, their discussion, which is full of all the important reasons why the final conclusion is not `we don’t need to do POCUS in shock,’ which is what I see happening (similarly to the TTM reaction), as they outline the cognitive fallacy of putting on trial a diagnostic tool whilst the therapeutics are not yet clearly established. Those only reading the abstract or conclusion will actually miss the important points of this study which the authors clearly explain.

In particular, the ‘rare’ instances of tamponade or aortic aneurysm or PE in their series would be diluted out by the sepsis, but for those patients, it would matter. As the authors state:

‘one might argue that even a single unanticipated emergency procedure would justify the use of POCUS in critically ill patients.‘

I would have to wholeheartedly agree.

cheers

 

Philippe

November 4, 2018

H&R2019! Final Programme. Register Now! Montreal, May 22-24, 2019! #HR2019

This event is past. It was awesome. If you really wish you’d been there, you can catch most of it here!

And don’t miss H&R2020!

Click here to register!

Registration is open and we have said goodbye to the snail mail process. Fortunately, we are a lot more cutting edge in medicine than in non-medical technology.

We are really excited about this programme, and a lot of it comes from the energy and passion coming from the faculty, who are all really passionate about every topic we have come up with.

The hidden gem in this conference is the 4 x 40 minutes of meet the faculty time that is open to all. Personally I’ve always felt that I learn so much from the 5 minute discussions with these really awesome thinkers and innovators, so wanted to make it a priority that every participant should get to come up to someone and say ‘hey, I had this case, what would you have done?’   Don’t miss it!

CME Accreditation for 14 hours of Category 1.

This programme has benefitted from an unrestricted educational grant from the following sponsors (listed alphabetically):

Cook

Fisher-Paykel Healthcare

GE Healthcare

Maquet-Gettinge

Masimo

Medquest

MD Management

Medtronic

Novartis

Teleflex

 

The Accreditation is as follows:

 

Here is the Final Programme:

Final Programme

Wednesday May 22 – PreCongress course

  1. Full day Resuscitative TEE course

FOR DETAILS SEE HERE

 

    2. Full day Keynotable

    3. Half day Hospitalist POCUS (PM)

    4. Half day Critical Care Procedures (AM)

    5. Half day Brazilian Jiu-Jitsu for MDs (AM)

for more details on these pre-conference courses please see here.

 

Main Conference Programme: H&R2019 Full Pamphlet

Social Events:

Thursday May 23rd Meet the Faculty cocktail! 1900 – Location TBA – BOOKMARK THIS PAGE!

 

Register here!

FOR ANY QUESTIONS CONTACT HOSPRESUSCONFERENCE@GMAIL.COM.