medical education

November 22, 2014

A Bedside Ultrasound Case & Poll: All Infiltrates Are Not Created Equal. #FOAMed, #FOAMcc, #FOAMus

So I get an early morning call from a really good ER guy informing me of a likely ICU admission: a young guy (30’s) with a bilateral pneumonia and fever whom he suspected might get worse before he got better. He’s given him some fluids and started ceftriaxone and azithromycin. Sounds good to me. Sold. I tell him I’ll come take a look as soon as I roll into work (we do home call).

An hour or so later I head to the ED and see a him, in bed at 30 degrees or so with nasal prongs, maybe a little tachypneic but certainly not in severe distress and not particularly toxic. The nurse informs me that his temperature was apparently 40 degrees. The CXR (I’ll try to put it up soon) shows bilateral infiltrates, more predominant in the lower two thirds of the lung fields. WBC is 14, lactate 2.3.

So this guy had been short of breath for about 2 weeks, having some cough and localized left sided pain associated with movement, cough and pressure. The cough was non-productive.  As I was getting this history (yup, generally bedside ultrasound is simultaneous with history-taking for me), this is what I see:

(parasternal long axis)

(parasternal short axis)

(right lower costal margin)

(you can see this in most of the lung fields)

He has no past medical history or notable family history, drinks occasional wine, has not traveled of late and works as an electrician. He is active and played soccer – the last time a few weeks ago. He came to the ED for dyspnea, but had still been able to go up several flights of stairs, albeit with more dyspnea than he normally would have.

 

 

 

check back tomorrow and let’s see what happens!

 

cheers!

 

Philippe

October 8, 2014

Bedside ultrasound for Hospitalists: A Must! #Hospitalist, #FOAMed, #FOAMus

Hi, so here is a quick little overview on why anyone taking care of hospitalized patients unequivocally need to use bedside ultrasound in a daily, integrated fashion, even if they don’t realize it yet.

It isn’t just for the flashy spot diagnoses in the ICU or the ER, but really for daily rounds, assessing common cardiac, respiratory, renal, gastrointestinal and even neurological syndromes.

Love to hear from any hospitalists or medical consultants out there about their use of bedside ultrasound!

Cheers

Philippe

October 6, 2014

Fluid Responsiveness: Getting the right answer to the wrong question. #FOAMed, #FOAMcc, #FOAMus

Let me start with a clinical scenario: you have a 68 year old male in front of you who is intubated, has bilateral pleural effusions, pulmonary edema, a bit of ascites, significant peripheral edema, elevated CVP/JVP/large IVC, and a moderately depressed cardiac function.  What is the diagnosis?

If you said CHF, you might be right. If you said post-resuscitation state in a septic patient, you might equally be right. Hmmm….

So as any self-respecting FOAMite knows, there is an ongoing and endless debate about fluid responsiveness, how best to detect it, what exact percentage of some variation represents it – is it 9% or 13% – and everyone has the way they swear by.

Well, I think the entire premise behind this is essentially flawed.

The fact that this is the first question implies that the answer should radically change management (eg giving or not giving fluids “generously” – yes, the quotes imply facetiousness).  Basically, that you should stop giving fluids when your patient is no longer fluid-responsive. The implication is that fluids is a better, safer, healthier, more naturopathic, eco-friendly and politically correct therapy than any other option.

I think we should reflect on that a little.

If you put some faith into normal physiology, you have to acknowledge that the only situations in which our cardiopulmonary system finds itself nearly or no longer fluid responsive are pathological: CHF, renal failure, etc. None of those are healthy. None of those are a bridge to healing.

What do we do when we are hypovolemic?  We vasoconstrict, stop peeing, try to drink a bit (if at all possible) and slowly replete our intravascular space via the portal system. We might build up a little lactic acid (helps feed the heart and brain – yup, nothing toxic about it), but we get over it.  Of course, if we lose too much, the system fails and we head to meet our maker.

Now, having remembered that, why do we feel (and I say feel because the evidence isn’t there to back it up) like we have to get to pathological levels of intravascular venous pressure to fix the problem?  Especially when the problem at hand isn’t primarily hypovolemia, but mostly vasodilation, with possibly a relative hypovolemia in part related to increased venous capacitance.

The real question is: does my patient really, truly need a lot of fluid?

And here is the catch: just because someone is fluid responsive doesn’t mean that they need any, or that it is the best thing for them. Whoa… Heretic… I thought “aggressive fluid resuscitation is the cornerstone of resuscitation in sepsis.”

I think that answer is relatively simple.

No matter which method you are using (mine is IVC ultrasound: -http://thinkingcriticalcare.com/2014/04/01/the-ivc-assessment-by-bedside-ultrasound-lets-apply-some-common-sense-foamed-foamcc/), if you are deciding based on a millimetre of diameter, or a couple of percentage points of variation whether or not to give liters of crystalloids to your patient, there is no truth to that in the individual patient. Trying to figure out the tiniest of differences to decide our therapeutic options is, in my opinion, a huge waste of time with no scientific basis in the one single patient you are treating.   It’s like haggling for a dollar on a hundred dollar item in a flea market: you’re missing the boat.

“85% of patients with a IVC/SVV/SPV/PLR of …. are volume responsive” or something of the sort does NOT apply to the one patient you have in front of you as a recommendation for fluids. You have to make a complete clinical picture of it – feel the belly, look at the inspiratory effort, examine the tissues for edema, etc.

Grey zone it. The best we can do is a gross categorization of truly hypovolemic (need a lot), full (please don’t give me any), and “normal” which may need maybe a little, but probably not “generous” amounts. You’ll end up generously feeding the interstitial space and making things worse – and later maybe saying “oh well, I guess he/she was just so sick…”

Even if my patient is fluid-tolerant, why to we want to push him into near-pathological states? Is it just the old adage of “You have to swell to get well?”  In the light of much of our literature, I’m not sure that old wives’ tale holds a lot of water.

Are vasopressors that bad?  Not according to what we know…

At least, avoid actually reaching the point of no longer being fluid responsive. You can’t tell me you think that CHF is actually a good thing, can you?

 

Love to hear your thoughts!

 

Philippe

PS, if you like to think out of the box and rather be on the cutting edge, make sure to mark your calendar for the coolest conference in Canada: #CCUS2015….http://wp.me/p1avUV-bh

 

 

COMMENTS

SQS Replies:

Philippe,
I think your logic is sound enough, but the moat that makes it currently unassailable is that you are working in an area with no or very little data. There is clearly a reasonably well developed and continuing to develop literature around the mortality effects of excess volume. There is an older literature that suggests that our vasopressors are actually having their effect on the more normally functioning arterioles and may shunt well oxygenated blood from the well functioning cells of a tissue and to the ones that are shocked and can’t use the oxygen, anyway. At this juncture, your guess is as good as mine, as to which of these is the greater evil. Ergo, your argument is as good as any.

One thing I will say is that the patients who concern us are those in whom endotoxin, blood loss, or other factors have resulted in a shock state wherein cells and even large parts of tissues have both inadequate oxygen supply and inadequate ability to use whatever oxygen is supplied them. Any tool we have to alter this pathological state is blunt. Blood pressure? CVP? IVC size and behavior? SVI? What do any of these say about how well we are doing at the tissue and cellular level? Even the interesting markers of lactate, ScvO2, CV CO2, etc. are blunt instruments. As is our bag of fluid and as are our vasopressors. And think about our end result – “hemodynamic stability”, “better mental functioning”, “good urine output”, “feeling better”, “walking around”, “able to go back to work”. Things that are important to us and to our patient, but barely even measurable. How blunt are they?

My own approach, which I suspect to be yours, too, is to recognize that the new onset shock patient is momentarily different from the chronic CHF patient/”chronic” shock patient you describe above. We know there is an oxygen deficit, and it behooves us to correctly that as quickly as we can. We believe, with some data to back us up, that rapid correction of that deficit, to the extent that we can, can prevent the ugly chronic state. I use the blunt measures of fluid responsiveness in the first hour or two of resuscitation to ensure that the CO component of oxygen delivery is not deficient, and then I stop giving fluid. Early in the course, I am prone to rechecking “volume responsiveness” in some hours, because I know that fluid is leaching out of the vascular space and the patient has not stabilized, yet. All the while, I am highly aware that I am hoping this makes a difference, not knowing that it does. I am aware that it is rather circular to check SVI or IVC, give fluid, see a change and say, “See? Volume responsive.” And all the while knowing that every patient has his or her own line, beyond which more fluid will not be helpful but harmful. And all the while knowing that I can’t see that line, nor measure it with any tool that currently exists.

I think perhaps that we are like Phoenicians, navigating our way across the ocean by the North Star and trying to keep land in sight. We do a pretty good job of getting where we’re going a lot of the time. But won’t it be nice when we come up with GPS? Or even the astrolabe?

SQS

 

Fantastic points!

I can’t agree more. I do check for fluid responsiveness, and I do believe in rapid intervention – just perhaps not quite a vigorous and generous as medical marketing would have us buy. There isn’t more data for that than for a somewhat more conservative approach, in my opinion. Even the rate of administration is rarely looked at, just the totals. There is good animal data showing that, for instance, a more rapid rate of albumin infusion results in greater leak and less intravascular albumin at 6, 12 and 24 hours.  Little reason to think it would be any different in humans.  There is also data showing that the oxygen deficit in sepsis is not as ubiquitous as we think.

Our understanding of the septic disease state is minimal at best, and our tools exceedingly blunt, as you point out.  

GPS or astrolabe would be amazing. I’ve had a few discussions with people working on cytochrome spectroscopy – a possibility to assess mitochondrial “happiness,” which could give us an oxygenation endpoint. Then we could have a trial that might end up showing which degree of mitochondrial oxygenation is optimal, if any.

I know I am playing a bit of a devil’s advocate and that, in strict numbers, I probably don’t give a lot less fluid or a lot slower than most, but I think it is important to keep our minds open to change rather than keep a clenched fist around the ideas we have. 

When we have two docs debating whether IVC, SVV, carotid flow time (I do like Vicki’s stuff a lot) or something else, I think we are mostly in the grey zone, and the good thing is that either way, we are dealing with two docs who are aware and conscientious and doing the rest of the right things. But keep in mind there are a lot of docs out there who are in the acute care front lines who believe that bicarb “buffers” lactate. And by buffers they understand “neutralizes.”

I just hope that when the GPS comes along, we don’t lose ten years of knowledge translation time because we are still clinging to (at that point) outdated ideas like the IVC ultrasound… 😉

cheers and thanks so much for contributing fantastic material!

Philippe

Marco says:

Philippe, I really feel like being on your same wavelength when I read your posts about fluid responsiveness. I think it’s obviously easy to agree that a bleeding hypovolemic patient is fluid responsive AND needs fluids, but the more accurately I think about the physiology of fluid resuscitation when a nurse is asking me “should we give him some fluids?” the more I realise that the “grey zone” is large and its upper limit is not easily detectable. Probably if you fill your patients to the point where they are no more fluid responsive, you are sure that no more fluid is needed, but you should be able to stop a bit earlier.
Blunt instruments and measures are an issue, and integration of the data is a possible solution (at least until a GPS comes along), but critical thinking is always a valuable resource.
The more I grow old the more I become minimalist in my approach to the “chronic acute ill” patient (90% of the patients on an ordinary day in my ICU). If a patient is in the grey zone, with a reasonably good hemodynamic stability, some vasopressor support, low dose diuretics and his urine output decreases, probably the decision of giving him fluids OR diuretics would be equally harmful. When a patient is in the grey zone and your instruments are not so accurate, it’s better to keep him safely in the grey zone. When you are in the mountains, you are caught in a snowstorm and cannot find your tracks, the safest decision is to stop and wait.. or follow your GPS 😉

Marco

thanks!

You hit the nail on the head with “integration is key.”

Philippe

September 20, 2014

Fluids and Vasopressors in Sepsis, Wechter et al, CCM Journal: Anything Useful? #FOAMed, #FOAMcc

A couple of articles on fluid resuscitation worth mentioning. Not necessarily for their quality, but because they will be quoted and used, and critical appraisal of the content and conclusion is, without a doubt, necessary to us soldiers in the trenches.

The first one, Interaction between fluids and vasoactive agents on mortality in septic shock: a multi-center, observational study, from the october issue of the CCM Journal (2014) by Wechter et al, for the Cooperative Antimicrobial Therapy of Septic Shock Database Research Group, is a large scale effort do shed some light on one of the finer points of resuscitation, which is when to initiate vasopressors in relation to fluids in the face of ongoing shock/hypotension.

So they reviewed 2,849 patients in septic shock between 1989 and 2007, trying to note the patterns of fluid and vasopressor therapy which were associated with the best survival.  They found that survival was best when combining an early fluid loading, with pressors started somewhere in the 1-6 hour range.  I do invite you to read it for yourself, it is quite a complex analysis with a lot of permutations.

So…is it a good study?  Insofar as a retrospective study on a highly heterogeneous bunch of patients, I think so. But can I take the conclusion and generalize it to the patient I have in front of me with septic shock? I don’t think so. In all fairness, in the full text conclusion the authors concede that this study, rather than a clinical game-changer, is more of a hypothesis generator and should prompt further study. That, I think, is the fair conclusion.

In the abstract, however, the conclusion is that aggressive fluid therapy should be done, withholding vasopressors until after the first hour.  This is somewhat of a concern to me, since it isn’t uncommon for some to just read that part…

So why is this not generalizable?  First of all, I think that the very concept of generalizing is flawed.  We do not treat a hundred or a thousand patients at a time, and should not be seeking a therapeutic approach that works best for most, but for the one patient we are treating. Unfortunately, this is the inherent weakness of any large RCT and even more so in meta-analyses, unless the right subgroups have been drawn up in the study design.

Let me explain.

Patient A shows up with his septic peritonitis from his perforated cholecystitis. He’s a tough guy, been sick for days, obviously poor intake and finally crawls in. If you were to examine him properly, you’d have a hard time finding his tiny IVC, his heart would be hyperdynamic, his lungs would have clear A profiles, except maybe for a few B lines at the right base. You’d give him your version of EGDT, and he’d do pretty well. A lot better than if you loaded him with vasopressors early and worsened his perfusion. Score one for the guideline therapy.

Patient B shows up with his septic pneumonia, also a tough guy, but happens to be a diabetic with a past MI. He comes is pretty quick cuz he’s short of breath.  If you examine him properly, he has a big IVC, small pleural effusions, right basal consolidation and B lines in good quantity. He gets “EGDT” with an aggressive volume load and progressively goes into respiratory failure, which is ascribed to his severe pneumonia/ARDS, but more likely represents volume overload, as he was perhaps a little volume responsive, but not volume tolerant. An example of Paul Marik’s “salt water drowning.” (http://wp.me/p1avUV-aD) Additionally he goes into acute renal failure, ascribed to severe sepsis, but certainly not helped by the venous congestion (http://wp.me/p1avUV-2J). If he doesn’t make it, the thought process will likely be that he was just so sick, but that he got “gold standard” care. Or did he?

It may very well be that the studied group may include more Patient A types, and less B types, whose worse outcome will be hidden by the “saves” of the As. If you have a therapy that saves 15/100 but kills 5/100 you still come out 10/100 ahead… Great for those 15, not so much for the 5 outliers.

We, however, as physicians, need to apply the N=1 principle as we do not treat a hundred or a thousand patients at a time. I would not hesitate to be much more conservative in fluid resuscitating a B-type patient, regardless of the evidence.

Unfortunately, until trials include a huge number of important variables (an accurate measure of volume status, cardiac function, capillary leak, extravascular lung water, etc), it will be impossible to extrapolate results  to an individual patient.  These trials will, I suppose, eventually be done, but will be huge undertakings, and I do look forward to those results.

So, bottom line?

It’s as good a study of this type as could be done, but the inherent limitations make it of little clinical use, unless your current practice is really extreme on fluids or pressors. What it will hopefully be, however, is an onus to do the highly complex and integrative trials that need to be done to determine the right way to treat each patient we face.

 

thanks!

 

Philippe

 

COMMENTS:

Lawrence Lynn says:

Excellent post. This thoughtful quote should be read and understood by every sepsis trialists!!

“We do not treat a hundred or a thousand patients at a time, and should not be seeking a therapeutic approach that works best for most, but for the one patient we are treating.”

This single quote exposes the delay in progress caused by the ubiquitous oversimplification which defines present sepsis clinical trials. Bacteria (and viruses) generate “extended phenotypes” which are manifested in the host. These phenotypes combine with the phenotypic host response to produce the range of “dynamic relational hybrid phenotypes of bacterial and viral infection”. These hybrid phenotypes are also affected by the innoculum and/or the site of infection (vis-à-vis, your example of peritonitis).

Certainly Wechter et al and the Cooperative Antimicrobial Therapy of Septic Shock Database Research Group should be commended for beginning the process of moving toward the study of the dynamic relational patterns of complex rapidly evolving disease and treatment.

We are excited to see the beginning of the move of trialists toward the study of dynamic state of disease and treatment. However, before they can help us with meaningful results, trialists will need to study and define the range of “the dynamic relational phenotypes of severe infection” and then study the treatment actual phenotypes. This will not be easy as these organisms have had hundreds of thousands of years of evolution writing the complex genotypes which code for the extended of human infection. Sepsis trailists need to be encouraged by clinicians to rise to the task.

The clinicians must actively teach the trialists, (as you have in your post) that we expect trails which help to identity the therapeutic approach that works best in response to the dynamic hybrid phenotype “we are treating”.

The two linked articles below explain the present oversimplified state of the science of sepsis trails and why we clinicians must teach the trailists not to oversimplify and assure that they move quickly toward the study of the actual dynamic phenotypes of severe infection.

http://www.ncbi.nlm.nih.gov/pubmed/24834126

http://www.ncbi.nlm.nih.gov/pubmed/24383420

This is a paradigm shift so we, as clincians, must act to teach trailists this move is necessary. Otherwise we will continue to be left with hypotheses, which, while nice, are not useful at the bedside.

Lawrence Lynn

 

 

September 1, 2014

The Clinical Revolution of Bedside Ultrasound: Not Bloodless! #FOAMed, #FOAMus, #FOAMcc

Thanks to @icerman_ex’s sharp eye, just finished reading @EMNerd’s awesome post on bedside ultrasound (http://t.co/y1B5G9RBIv).   I think it casts the right light on bedside ultrasound, and as usual in spectacular prose that is the only #FOAM I know that discusses science so artfully.

There are a couple of things I’d like to add, for those who may be interested.  And, as a disclaimer, I am heavily, heavily biased towards the widespread use of bedside ultrasound. It is a revolution in medicine, undoubtedly the biggest one of the last decades, but, as with any revolution, blood will be shed, and it’s only when the dust settles that our science will be better.

First of all, everyone should understand that due to bedside ultrasound coming into its own in the era of evidence-based medicine, it is being asked to jump through hoops like no other tool has been. Try looking for a randomized trial on the use of the stethoscope… So it is important to keep this in mind as the fine tuning takes place, rather than try to blindly adopt it or toss it out with every new study that comes out.

As Rory points out, the issue isn’t one of accuracy per se, rather than the clinical interpretation of that accuracy – that is, the clinician being able to tune out the noise, just like one would parts of the history or physical that are irrelevant or misleading. The failure to do so will lead to unnecessary interventions or testing.

Another point is that the second generation of bedside sonographers are not inherently the same as the first, who took up the probes to answer clinical questions and created the protocols and algorithms – as always, much kudos to Daniel Lichtenstein, “le premier des pioneers” – whereas the second generation will be a very mixed bag, many of which will carry bedside ultrasound and push it farther, but also many others who will apply what they have learnt without necessarily the same framework.  If you look at the history of medical developments, initial wonders often have subsequent setbacks, until training and practice are fine tuned – take the history of laparoscopic surgery, for instance.

The key point in all this is that proper clinical integration is necessary, and that trainees have to be well mentored by those who do use the tool in a daily fashion, and finally – as always – some good studies in a number of clinical scenarios, so as not to have (only) a pixelated view of the patient.

 

cheers!

 

Philippe

 

Jon-Emile says…

Wonderful post:

You know my position on inspiratory IVC collapse [http://pulmccm.org/main/2014/critical-care-review/inspiratory-collapse-inferior-vena-cava-telling-us/]

My problem with the Kenji trial is that is certainly does not [and cannot] tell us if seeing IVC collapse means that a patient will augment their cardiac output in response to a fluid bolus. What their trial tells us is that using less fluids and more pressors in shocked patients probably improves outcomes … but i think few of us doubt that currently [especially in light of the PROCESS trial last spring]. Instead [and i say this facetiously of course] they could have used a random number generator that was weighted to giving less fluids and more pressors instead of bedside ultrasound … and they probably would have received similar results.

It is hard for me to imagine a physiological scenario whereby a patient has a fixed and dilated IVC on ultrasound with respiration [spontaneous, triggered, or passive] but could still be fluid responsive. So when I see a fixed, dilated IVC, I feel fairly confident that fluids should stop [again this does not tell me about the patient’s volume status, as a patient could have a very plump IVC and be volume deplete].

But this physiology is not new and was published by Magder in the early 90s [invariant right atrial pressures with respiration predicted fluid non-responsiveness very well] and also by Pinsky in the early 90s when he found that in post surgical patients that right atrial distending pressure is dissociated from right ventricular end-diastolic volume. Which means that when you see right heart congestion, you have probably already reached cor pulmonale.

The true challenge is IVC collapse … it is affected by many conflicting variables [as you know]; there is probably a good portion of patients who have IVC collapse [especially those on PEEP, triggering the ventilator] who are actually fluid non-responders, yet we push them closer and closer to cor pulmonale needlessly … so until someone finds a better non-invasive physiological solution …

as EM Nerd, so aptly puts it …

“In medicine we frequently propagate half-truths and unsubstantiated certainties.”

Thanks for the post space,
Jon-Emile

 

Excellent points!

Thanks!

 

Philippe

July 18, 2014

Bedside Ultrasound Clip Quiz: The Incidentaloma! #FOAMed, #FOAMcc, #FOAMus

Ok, so in the process of doing a little bedside ultrasound teaching, I was scanning this lady in the ER who was being worked up for urosepsis. She had been previously a little hypotensive, apparently, and had gotten some fluid boluses, but was not looking quite comfortable with a BP of about 90 systolic.

So her IVC was pretty normal, about 10-12 mm with visible respiratory variation.

Then I saw something funny in the parasternal views (short axis at the level of the aortic valve)…

 

 

 

Any takers?

Hint:  as I scanned around the patient for the possible cause of this, I noted a pressure bag hanging with an empty bag of NS (argh! NS!)… Really empty. I mean, not a drop left in the tubing…

 

Scroll below.

 

 

 

 

 

This is iatrogenic air embolism.  You can see the bulk of the air is in the RA (left side of the screen), and air bubbles make it into the RV (inflow-outflow) at the top, and some into the PA (curving to the bottom right).

This is not elegant. There is always some air in the drip chamber, so, especially on a pressure bag, an IV bag can’t be allowed to be totally empty…

When we agitate saline to do a bubble study, you get a few seconds of bubble persistence. In this case, two separated examinations about 10 minutes apart revealed little or no change.

Fortunately for the patient, the amount if air is not really enough to cause pulmonary vascular obstruction, as you generally need upwards of 150cc to cause an arrest, and, as we can see by the normal IVC/RV, there was no evidence of even pulmonary hypertension.  I left her in the left lateral decubitus position and she remained monitored, recovering uneventfully. I’ll review the management of venous air embolism in the next post!

Here is another clip, a bit of a reverse and hybrid parasternal short axis view but for some reason gave me the best images:

 

cheers

 

Philippe

June 2, 2014

Bedside Ultrasound Clip Quiz: Abdominal pain and fever! #FOAMed, #FOAMcc, #FOAMus

Saw this poor fellow recently who presented to the ED with fever and abdominal pain. 73 years young. He came to my attention because of borderline BP (95 systolic) and a lactate of 4.5 mmol.

Here is a transverse scan at his lower right costal margin:

 

What do you think?

Turns out he had been having pain for about two weeks, and it had intensified about two days ago. His wife dragged him in.

What would you do?

 

 

 

 

 

 

 

 

 

 

 

This is septated fluid collection around the liver.  With the fever and history, sounds pretty suspicious for a septic source. After carefully scanning in all angles and watching for a while to make sure this wasn’t a strangely placed loop of bowel, a 22g needle aspiration showed cloudy bilious fluid and a trip to the OR a couple of hours later revealed a perforated duodenal ulcer.

He made it ok.

 

cheers

 

Philippe

May 18, 2014

What’s this sign? Bedside Ultrasound Picture Quiz! #FOAMed, #FOAMcc, #FOAMus

Here is a one of the “classic” and physiologically important echocardiographic signs:

 

Screen Shot 2014-05-18 at 11.34.10 PM

 

What do you see in this parasternal short axis view, and what are the physiological implications?

Scroll below for the answer!

 

 

 

 

 

 

 

 

 

 

This is the “D” sign, aptly named for the D-shape taken by the LV (normally circular) when RV overload occurs and there is paradoxical septal motion and flattening, as early diastolic RV pressure exceeds early diastolic LV pressure.  This is NOT a good thing and points to a very strained hemodynamic pattern.

Note the RV is huge in this cut, bigger than the LV (remember that in all views, the RV should be about 60% of the LV size – this is simply due to the semi-lunar shape the RV takes as it “wraps” around the LV – they both have the same stroke volume). Also note the small posterior pericardial effusion.

So what is the diagnosis here?  Well there isn’t enough information to say with just this image.  This happens to be a case of worsening ARDS, but all you can tell is that there is acute right ventricular failure due to pressure overload, so that the diagnosis includes (a) PE, (b) acute pulmonary hypertension due to some kind of pulmonary disease – ARDS, pneumonia, etc…  Obviously, in the absence of significant parenchymal abnormalities on CXR or B lines/effusions/consolidations on lung ultrasound, PE should be strongly considered.

 

Happy scanning!

 

Philippe

Here is an excellent review on RV dysfunction and focused bedside ultrasound assessment:

RV bedside echo

or its link:

Click to access 38TOCCMJ.pdf

April 26, 2014

Bedside Ultrasound for Internists / L’Échographie Clinique pour l’Interniste – ASMIQ/CCUS, May 23rd, 2014.

Although bedside ultrasound truly started in the emergency room and is slowly spreading to critical care, its usefulness extends to all aspects of medicine, particularily in hospitalist and consultation medicine. The CCUS Institute is proud to be involved in a forward-thinking undertaking by ASMIQ to increase bedside ultrasound use by its members.

For the second year, the Critical Care & UltraSound Institute (CCUS) is hosting ASMIQ (Association des Spécialistes en Médecine Interne du Québec / Quebec Association of Internal Medicine Specialists) members for a day of bedside ultrasound, tailored for internal medicine practice.  This year’s program will review volume status, focused cardiac and lung ultrasound as well as ultrasound-guided bedside procedures. There will be 3.5 hours of workshops in the day.

The didactic presentations will be given in french, and the workshops both in french and english.

Programme: word echo-Programme scientifique et atelier-1 – copie – copie-1

 

For participants:

Welcome to the course!  Here are a few papers which should be read in preparation and as reference, in order to enable you to get the most out of the course:

EGLS fulltext

JASE Focused echo

ICC Lung US

Thank you and looking forward to meeting you on May 23rd!

 

Philippe Rola

Course Director

 

April 13, 2014

An Update on Pulmonary Embolism: NEJM’s PIETHO Study…what’s the verdict? #FOAMed, #FOAMcc

As has been discussed in a previous post (http://wp.me/p1avUV-7T), patients with sub-massive PE (hypoxic, tachycardic, some troponin rise, etc…but no hypotension) remain in a grey zone, which is, to me , a dubious situation at best – their mortality can be up to 15%, morbidity likely more.  Everyone agrees the low-risk patients don’t need thrombolysis, and everyone pretty much agrees that the patient in shock needs it.  There is data out there suggesting that some patients clearly benefit from thrombolysis despite not being in shock, in good part relating to avoiding chronic pulmonary hypertension and its consequences.

The issue for many clinicians is that they have a “stable” patient in front of them, and they are considering giving them a drug that can potentially give them a bleed in the head and leave them dead or crippled. Many shy away from this. Part of this is cultural, because the same docs probably wouldn’t hesitate giving the drug to a lateral or posterior MI, which is not likely to kill you, or even leave you a cardiac cripple (just to be clear, I’m not advocating against thrombolysis in these cases, just trying to find a parallel), but since the AHA guidelines say to do it and everyone else does it, there’s no trepidation. It is the standard of care.  For most of us acute care clinicians who do not do outpatient medicine, if the patient survives and gets discharged home, chalk one up in the win column. But, as has become clear in recent years with the post-critical illness syndromes, morbidity can be just as important as mortality, especially in the younger patients. Kline et al (Chest, 2009) showed how almost 50% of “submassive PE” patients treated with anticoagulation alone had dyspnea or exercise intolerance at 6 months. They only had a 15% improvement in their pulmonary artery pressures (mean 45 mmhg).

What are the real risks? Pooling the data together gives a value around 2% with a spread between 0.8% and 8%, more or less. This represents each patient’s inherent risk of bleeding, as well as some of the inconsistencies with post-thrombolysis anticoagulation (safest to aim for 1.5-2 x PTT baseline in the first 48h).

The MOPETT trial which, as a #FOAMite you have certainly come across, showed that a half-dose of TPA was highly effective, and they felt it might be possible to go lower. The physiological beauty in that is that, unlike other sites we thrombolyse with full dose TPA, the lungs get 100% of the TPA (coronary artery gets maybe 5%, brain gets 15%).  Mind you, of course, the culprit clot/artery obviously doesn’t get 100%, but much, much more (if we figure that you need about 50% vascular area occlusion to cause RV dysfunction) TPA per “clot” than other pathologies. One can argue that anatomically, there is a greater clot burden than coronary or arterial thrombolysis, which may offset this somewhat. However, the date was quite clear in this trial that the therapy was effective, and the bleeding was none.

Ok, so let’s get to the PIETHO. 1000 patients, TPA+heparin vs heparin alone in normotensive but intermediate risk patients. So, first question is how was that risk defined?  Patients needed to have echocardiographic/CT signs of RV dysfunction AND a positive troponin. Interestingly enough, onset of symptoms was up to 15 days before randomization…not exactly early treatment, and unfortunately there is no information about the actual time to thrombolysis or subgrouping.  The results were as one could imagine. The combined endpoint of death or hemodynamic decompensation was 2.6% in the thrombolytic group vs 5.6% in the anticoagulation.  I’m not a fan of combined endpoints. Hemorrhagic stroke was 2.0% vs 0.2%. Their conclusion? Exercise caution. Hmmm…not much of a step forward. Basically tells us what we know. It helps the hemodynamics, but you can bleed. They do re-affirm that bleeding is more likely in the over-75.

 

What do we REALLY need to figure out? 

1. echographic risk stratification – at least into moderate and severe RV dysfunction.

2. longer term outcomes (hopefully PIETHO has a follow-up study in the pipeline, since they had good numbers).

3. a point-of-care study – time is of the essence, and may have an impact on dosage. IMHO thrombolysis should be done within a few hours of presentation at most.

4. further dosage data – 1/2? 1/3? 1/4? small boluses q1h until RV function improves?

I wish I could do it, but community hospitals don’t have the ideal setup, nor do I have a research team that can handle something of this scale. But surely someone can!

 

Bottom line?

It won’t change my practice. I will continue to offer thrombolysis in select cases, especially the younger patients, who obviously have a lower risk of bleeding, and stand to benefit the most, as pulmonary hypertension  can be crippling. I know I’d take the risk of bleeding when I see 50% dyspnea/exercise intolerance two years down the road…

Finally, bedside ultrasound to anyone with dyspnea/hypoxia should be a standard of care for every acute care physician. No ifs, ands or buts, no exception. Waiting for a CT angio or formal (read daytime hours) echocardiogram is, to me, unacceptable. If you, a friend or family member were in that ER bed, would you trust a physical examination and a CXR to rule out the need for an immediate intervention? I wouldn’t, not my own, and not even Dr. Bates’, Dr. DeGowin’s or Dr. Sapira’s, or all three combined.

cheers!

 

 

 

Kline JA, Steuerwald MT, Marchick MR, Hernandez-Nino J, Rose GA. Prospective evaluation of right ventricular function and functional status 6 months after acute submassive pulmonary embolism: frequency of persistent or subsequent elevation in estimated pulmonary artery pressure. Chest 2009;136:1202e1210.

Guy Meyer, M.D., Eric Vicaut, M.D., Thierry Danays, M.D., Giancarlo Agnelli, M.D., Cecilia Becattini, M.D., Jan Beyer-Westendorf, M.D., Erich Bluhmki, M.D., Ph.D., Helene Bouvaist, M.D., Benjamin Brenner, M.D., Francis Couturaud, M.D., Ph.D., Claudia Dellas, M.D., Klaus Empen, M.D., Ana Franca, M.D., Nazzareno Galiè, M.D., Annette Geibel, M.D., Samuel Z. Goldhaber, M.D., David Jimenez, M.D., Ph.D., Matija Kozak, M.D., Christian Kupatt, M.D., Nils Kucher, M.D., Irene M. Lang, M.D., Mareike Lankeit, M.D., Nicolas Meneveau, M.D., Ph.D., Gerard Pacouret, M.D., Massimiliano Palazzini, M.D., Antoniu Petris, M.D., Ph.D., Piotr Pruszczyk, M.D., Matteo Rugolotto, M.D., Aldo Salvi, M.D., Sebastian Schellong, M.D., Mustapha Sebbane, M.D., Bozena Sobkowicz, M.D., Branislav S. Stefanovic, M.D., Ph.D., Holger Thiele, M.D., Adam Torbicki, M.D., Franck Verschuren, M.D., Ph.D., and Stavros V. Konstantinides, M.D., for the PEITHO Investigators*, Fibrinolysis for Patients with Intermediate- Risk Pulmonary Embolism, N Engl J Med 2014;370:1402-11.

Mohsen Sharifi, MDa,b,*, Curt Bay, PhDb, Laura Skrocki, DOa, Farnoosh Rahimi, MDa, and Mahshid Mehdipour, DMDa,b, “MOPETT” Investigators, Moderate Pulmonary Embolism Treated With Thrombolysis (from the “MOPETT” Trial), Am J Cardiol 2012