Month: March 2014

March 28, 2014

Ministère et Association de Radiologues: On bloque le progrès de la médecine…triste réalité.T

C’est avec déception mais sans surprise que j’ai lu le communiqué du ministère en ce qui concerne l’acquisition d’appareils d’échographie pour les institutions hospitalières du Quebec. Le voici:

Acquisition échographes compacts

En effet, le développement de l’échographie au chevet dans les deux dernières décennies est certainement la plus grande avance de la médecine des derniers 25 ans, et ceci ne fait que prendre son essor, et les applications cliniques ne font que s’accroître.

Il est donc triste de voir que le Ministère – en espérant probablement économiser-  à du se laisser convaincre par certains membres de l’association des radiologues du Quebec qu’il est critique de limiter le potentiel d’améliorer la rapidité du diagnostique, la précision des interventions et la santé de nos patients.

Il est triste de voir que cette réaction est en fait relié a l’éléphant dans la pièce (celui avec le gros signe du dollar) et vient de ceux parmi les (sinon les) mieux rémunérés de notre profession. Je suis certain que ce n’est pas le cas le cas de tous, mais au moins d’une majorité de leur association. Certainement il y a l’expression superficielle de l’inquiétude de la qualité de l’acte, mais c’est une intéressante coïncidence que cette inquiétude fasse surface alors que certains groupes viennent justement d’obtenir le droit de facturer pour des examens limités. De toute façon, la qualité de l’acte s’assure via l’éducation et la vérification, pas avec l’interdiction d’obtention de matériel.

Il est aussi triste de voir le manque de compréhension du sujet par ces groupes. Pour chaque demande d’examen complet qui est peut-être évitée, il y en a au moins une sinon plus qui est nouvellement faite comme nous (échographes au chevet) trouvons de la pathologie qui n’était pas suspectée, et que nous voulons avoir un examen complet et formel.

Ca fait au delà de 13 ans que je fais de l’échographie au chevet, et maintenant 7 ans que je l’enseigne dans divers environnements, autant au chevet avec résidents, étudiants ou collègues que sous le chapiteau de formations officielles (ICCU, CAE, CCUS). La pratique de l’échographie au chevet  me ralentit un peu, mais résulte en une évaluation du patient beaucoup plus robuste et précise. Il a été clairement démontré que des étudiants en médecine avec une semaine d’enseignement sont nettement meilleurs que des cardiologues munis de stéthoscopes seuls. Les résidents et étudiants font maintenant la file pour faire un stage à l’USI chez nous parce qu’ils savent que c’est un des seuls endroits ou ils auront l’occasion de faire de l’écho au chevet à Montréal.

Et jusqu’à maintenant, je n’ai pas facturé une “cenne noire.” Aujourd’hui, en tant qu’interniste, je peux facturer un examen limité pour – asseillez-vous – 10$, à un maximum de 5 (total, non pas par patient) par semaine. Un gros 50$. Honnêtement, ca ne vaux pas le temps qu’il me faudrait pour faire les rapports officiels – chaqun de mes patients est examiné avec échographie. Heureusement, les omnipracticiens ont réussi à obtenir un forfait un peu plus raisonnable (20$ par examen, max de 2 par jour, si je ne me trompe pas). Pas la “mer à boire.”

Ce que le ministère espère economiser, il le paie bien plus en délai et erreur de diagnostique et en durée de séjour, pour ne pas mentionner le prix que les patients paient, eux.

C’est tout a fait déplorable que les cliniciens de première ligne – ainsi que la médecine en tant que science – se fasse mettre les batons dans les roues de telle facon, surtout sous la guise de qualité de l’acte. Ne soyons pas naïfs.

D’autant plus que le Quebec, ayant beneficié de quelques pionniers dans le domaine ainsi qu’une attitude plus progressive que le reste de l’amérique du nord, est certainement aujourd’hui parmi les endroits au monde ou l’échographie au chevet est la plus utilisée. Rembrouons-nous plutôt parmi les masses.

Quoi faire?

En fait, c’est assez simple.  Ceux dont les hopitaux n’ont pas encore munis d’appareils dédiés devraient commencer a demander des échographies formelles a chaque fois que l’on a besoin d’une réponse simple. Si il faut trois examens pulmonaires pour s’assurer de voir la disparition des lignes B avec la diurèse, ou bien quatre examens de la veine cave pour assurer la qualité de la reanimation liquidienne, faisons les radiologues venir au chevet. STAT. Le cout? Aucune inquiétude, il s’agit ici de la qualité de l’acte.  Euh…y-a-t’il une limite aux examens sur le meme patient? Peu importe, si c’est nécessaire, qu’il les fassent gratuitement, ou bien qu’ils renégocient avec le ministère. Trois heures du matin? STAT: Peu importe, c’est la qualité de l’acte qui compte, non? Quoi, le département ne peux plus fournir? Allons voir le DSP et le CMDP, il nous faut plus de radiologues, et probablement une liste de garde en établissement. Désolé, ministère, ca va côuter un peu plus qu’une ou deux machines d’echographie par hôpital…

Dans quelques semaines, on devrait voir alors l’envers du décor.

Quand au radiologues, ne faites pas partie de cet obstacle honteux au progrès de la médecine, de façon voulue ou non. Parlez a votre association, et aidez-nous plûtot à établir des normes et à entrainer les étudiants et résidents, peu importe leur spécialité.

 

Philippe Rola

Interniste et Chef de Service, Soins Intensifs

Hôpital Santa Cabrini

March 26, 2014

Bedside Ultrasound Clip Quiz: What’s the Rhythm? #FOAMed, #FOAMcc, #FOAMer

Just a clip.

What’s the dx?

 

scroll below!

 

 

 

 

 

 

 

 

 

 

 

 

 

 

sinus tachycardia with 3rd degree HB – taken on a call on the ward before the tech brought the EKG machine.

thought it was neat.

 

Philippe

March 21, 2014

CCUS Annual Symposium 2014 – only a few spots left! Take your ultrasound game to a whole new level!

May 10th and 11th (pre-congress courses on may 9th), Montreal.

Great speakers, great topics, great city, great weather (well…hopefully no snow!).

Do you know how to use ultrasound to help you diagnose or manage coma, bowel obstruction, CHF, dyspnea, swollen joints and renal failure, among other things?  No matter how good you are at the bedside, you’re not as good as you + ultrasound. None of us are. And if you take care of patients where time is of the essence, then you need to make sure your game is as good as it gets.

Mike Stone, Vicki Noble, Haney Mallemat, JF Lanctot, Michael Woo, Catherine Nix, Max Valois, Rob Chen, Edgar Hockmann, Massimiliano Meineiri, Sarah Sebbag, Alessandra Bruns, Alberto Goffi, Ashraf Fayad and Andre Denault have put together some great talks about how to add ultrasound to your approach of common clinical scenarios.

We’ve got the #FOAMed spirit, too. If you really can’t make it, all the lectures will be freely available on our website in the weeks following the symposium.

The workshops will be awesome, faculty-led and will also feature the use of simulators.

The best part is the atmosphere. It’s a great exchange among like-minded people, eager to learn form each other. I know I always come out of that weekend with my head buzzing and brimming with ideas and things I need to learn and others to put into practice.

…and if you’re an educator, then there is a pre-course you will find extremely interesting, as Catherine Nix has put together an educator’s half-day to help overcome the common hurdles faced by budding ultrasound programs at the undergraduate or post-graduate level:

CCUS US Educator May 9th program

We’re not in a huge venue, so if you’re thinking of coming, register now, there are only a handful of spots left.

http://ccusinstitute.org/Symposium6.html

looking forward to meeting you!

Philippe

March 19, 2014

NEJM: The Septic Shock Issue…groundbreaking or same old same old? #FOAMed, #FOAMcc

Ok, so it was pretty cool to see an NEJM issue basically dedicated to septic shock management, I must admit. But let’s dig a little deeper, shall we?

So here is where they are: http://www.nejm.org, and fully available for now.

I won’t go through all the details and numbers, after all they are in the papers, so let’s just analyze them from two principles:

a. the N=1 principle – how was therapy individualized?

and

b. was there any integrated monitoring of the therapeutic goals?

…and we’ll conclude by looking at the potential practice-changing potential of each of these studies.

So first of all,

High vs Low BP Target in Septic Shock, by Asfar et al.

So basically a negative study except for two findings, the increased incidence of afib in the high target group and the decreased need for renal replacement therapy among chronic hypertensives in the high target group.

so N=1 is not really revealed:

“Refractoriness to fluid resuscitation was defined as a lack of response to the administration of 30 ml of normal saline per kilogram of body weight or of colloids or was determined according to a clinician’s assessment of inadequate hemodynamic results on the basis of values obtained during right-heart catheterization, pulse-pressure measurement, stroke-volume measurement, or echocardiography (although study investigators did not record the values for these variables).”

So lets just hope that the variability evens itself out between the groups, since we don’t really know. The numbers don’t really tell the tale, because the average fluids received (10 liters over 5 days) could mean one patient got 15 and one got 5 – although let’s trust they followed the French Fluid Resus protocol…

So the atrial fibrillation makes total sense – more B agonism should result in that, and the decreased renal failure also does.

As the authors note, the actual BP averages were higher than planned. For those of us practicing critical care, we know most nurses titrating prefer having a little bit of extra BP – even when I prescribe MAP 65, I usually see the 70 or so unless I make a point to tell them. Understandable. They also note the underpowered-ness of their own study, but I think it is still worth looking at their results.

So…bottom line?  I think it’s a great study for a couple of reasons.

The first is to remind us to pay a little more N=1 attention to the chronic hypertensives, and that it is probably worth aiming for slightly higher MAPs.

The second, debunking the myth of “levophed, leave’em dead” (which I heard throughout residency at McGill), and the concept of doing everything (ie juicing patient into a michelin man) in order to avoid the “dreaded and dangerous” vasopressors. So really I think an alternative way to conclude this study is that it isn’t harmful to have higher doses of vasopressors. I think this is actually a really good study on which to base assessment of more aggressive vasopressor support vs fluid resuscitation, in the right patients.

It would have been interesting to have echo data on those who developed a fib – were they patients who had normal to hyperdynamic LVs who in truth did not need B agonism at all and would have been fine with phenylephrine?  Perhaps…

Cool. I like it.

Next:

Albumin Replacement in Patients with Severe Sepsis or Septic Shock, by Caironi et al. The ALBIOS study (a Gattinoni crew)

So basically showed no difference, so pretty much a solid italian remake of the SAFE study in a sense, confirming that albumin is indeed safe overall, and may be better in those with shock.  As the authors note, mortality was low, organ failure was low, so study power a little low as well. Note the mean lactates in the 2’s at baseline. The albumin levels of the crytalloid only gorup were also not that low, low to mid 20’s, whereas I often see 15-20 range in my patients, especially if I inherit them after a few days, as I do use albumin myself a fair bit. They also used a target albumin level, not albumin as a resuscitation fluid purely.

In my mind the benefit of albumin would be greatest in those with significant capillary leak, particularly those with intra-abdominal and pulmonary pathology. It would have been nice to see a subgroup analysis where extravascular lung water was looked at (especially coming from a Gattinoni crew!).

Another interesting thing would have been to know the infusion time of the albumin, since animal data tells us that a 3hr infusion decreases extravasation and improves vascular filling vs shorter infusion times. I routinely insist on 3hr infusion per unit, which sometimes results in 9-12hr infusions, almost albumin drips!

Bottom line?

I like it. Reinforces that albumin is safe, so makes me even more comfortable in using it in the patients where my N=1 analysis tells me to be wary of third-spacing. Also the fact that they used 20% – in Canada we have 100cc bottles of 25% for the most part – is nice, since the SAFE data used 4%.

Next!

A Randomized Trial of Protocol-Based Care for Early Septic Shock – The ProCESS Trial.

So right off that bat my allergy to protocols flares up, so I’ll try to remain impartial. It just goes against the N=1 principle. The absolutely awesome thing about protocols is that it primes the team/system to react – so clearly protocols are better than no-protocol-at-all, but strict adherence would clearly not fit everyone, so that some built-in flexibility should be present.

This being said, the ProCESS study is really interesting, for a number of reasons. They have three groups, and compare basically (1) Rivers’ EGDT to (2) their own protocol (see the S2 appendix online) which gives a little more flexibility and (3) “usual care”.  Net result is that all are pretty equal, no change in mortality. As the authors note, their mortality was low, so again may not have been able to detect a difference.

So, what does this mean. To me it’s a little worrisome because I doubt that the “usual care” represents the true usual care found in EDs/ICUs all over the world, so I am concerned that many docs will use this as a reason to justify not changing their practice, similarly to many I’ve heard say they don’t need to cool anymore after the TTM trial. Human nature for some I guess.

Bottom line? You don’t have to follow EGDT if you’re conscientious and reassessing your patient frequently and have done all the other good things (abx, source control, etc). I think that’s really important because giving blood (see my post about S1P) to those with hb > 70 and giving dobutamine to patients with potentially normal or hyper dynamic LVs never made physiological sense to me, and the problem with a multi intervention study such as EGDT is that you can’t tease out the good from the bad or the neutral. Again, studies such as EGDT are pivotal in changing practice and raising awareness, so this is not a knock against a necessary study, just to highlight the point that each study is a step along the way of refining our resuscitation, and the important thing is to move on. In fact, the reason that this is a negative study is probably due to the improvement in “usual care” that EGDT brought along.

Conclusion: No new ground broken, but these studies do make me feel more confident and validated in continuing to not do certain things (strict EGDT) and  doing others (albumin and earlier use of vasopressors).

Kudos to all investigators.

 

let me know what you think!

 

P

 

March 7, 2014

Bedside Ultrasound and PEA: CPR or no CPR…? #FOAMed, #FOAMcc

The usefulness of bedside ultrasound in cardiac arrest is clear, giving the clinician instant information on the hemodynamic process resulting in arrest. My arrest sequence is generally done as follows:

Step 1: IVC assessment

Step 2: Subxiphoid cardiac views

Step 3: Lung views if pneumothorax suspected.

Step 4: remaining views if possible (eg abdominal views to find source of bleeding, etc…)

The important part (as per current recommendations) is to have minimal interference on chest compressions. The IVC view, albeit jumpy, can generally be obtained during CPR.  The subxiphoid view should be “prepared” during CPR, meaning that the sonographer warns the team member doing CPR not to stop compressions until he is told to do so (unless the team are already used to ultrasound in cardiac arrest), the probe positioned optimally, then instruction given to stop for five seconds while a look +/- loop is acquired. This should be enough to look for pericardial effusion, RV/LV ratio and LV contractility. In fact, experienced sonographers can usually get this while CPR is going on in many cases. Then CPR should be restarted. Hence for now, minimal interruptions in CPR (until the concept of “stutter CPR” really emerges!!!).

Here are a couple of views with active CPR:

In this case there is  a clear RV overload with a dynamic but underfilled LV.

From the information obtained in those 5 seconds, one should be able to consider the need for volume (hypovolemia), thrombolytics  (pulmonary embolism suspected) or drainage of fluid (tamponade) or air (pneumothorax). The possibility of an acute myocardial infarction must be considered as it is one of the most common causes but is difficult to confirm by ultrasound.

Pulseless Electrical Activity

This may be the most exciting area in which ultrasound will change management.  In the absence of ultrasound, all PEA is more or less alike: there is organized electrical activity, but no pulse. Physiologically however, the range of diagnoses is very wide, with on one end, a perfectly good heart that is empty (hypovolemic shock in extremis), and on the other, cardiac standstill despite electrical activity. An astute physician does not need a randomized clinical trial to know that the management and prognoses of those two extremes are very different. Without bedside ultrasound, however, these would appear identical: “PEA.”

 The heart rate cannot be relied on since it will largely depend on the phase (both would begin as tachycardic, then eventually bradycardic until asystole occurs).

Notwithstanding guidelines,  the information obtained should be considered strongly. If we start by looking at the first end of the spectrum, there would be no physiological rationale for performing chest compressions or an empty and hyperdynamic ventricle: rapid infusers and vasopressors (to recruit venous unstressed volume) should be used instead. At the other end, the heart in standstill definitely needs compressions. Of course, there is then the whole range of varying RV and LV pathologies, tamponade, etc, all of which need to be dealt with individually. It is really a huge grey zone…

CPR or no CPR?

A very important question is whether CPR should or should not be performed in certain cases of PEA.  Certainly ACLS protocol dictates so. However, ACLS has not yet truly integrated bedside ultrasound into management, only suggests in a very loose way – understandably since the protocols must be applied by all, and still only few use it regularly.

I have to credit Dr. Sue, an ER doc from Atlanta, who asked me the question about CPR in extreme hypotension, and I had to rewind in my mind the cases in which I had used physiological information to overrule the ACLS protocol in one direction or another and try to formulate an answer.

It is an excellent question and made me realize that there is no clear answer for two reasons:

One: PEA is not a diagnosis but a clinical syndrome. It relies on manual pulse check (unless the arrest occurs in a patient with an arterial line), hence the line between severe hypotension and true PEA is difficult to determine. Technically and physiologically speaking, if the LV contraction is sufficient to open the aortic valve, there is a “pulse.” Now how far along the arterial circuit this pulse travels is not known…unless it is monitored.

Two: The key question then becomes the following: at what level of endogenous blood pressure is the perfusion better than with “good” CPR?  We do not yet have that answer. The coronary perfusion pressure (diastolic pressure – wedge pressure) data often quotes a minimal range of 15-25 mmhg, which – if we arbitrarily choose a high-ish wedge – would suggest we need a diastolic pressure in the 40’s (also note that that data is imperfect). Hence the arterial line. Perhaps there could be a role for tissue saturation/near-infrared spectroscopy or other microvascular flow indices in the future…

Now what about the huge spectrum of cases in between?  Let us exclude the cases with immediately reversible causes such as tamponade and pneumothorax, where the initial management is clear, and instead focus on differing levels of RV and LV dysfunction resulting in the absence of a palpable pulse.

Predominant RV failure – although PE should be strongly suspected and thrombolysis considered, the question remains about management if you see a hyperdynamic but underfilled LV.  CPR would appear reasonable in an effort to try to get some RV to LA flow. Endotracheal milrinone, sometimes used in cardiac anasthesia, can be an option as it provides inotropy and pulmonary vasodilation.

Predominant LV or biventricular failure – if cardiac activity is present, it seems imperative to start an infusion of vasopressors, and traditionally, do CPR until there is a measurable blood pressure. I have used CPR with progressing bradycardic rhythms for a few seconds to circulate the epinephrine, with at least short-term success.

Here is a typical LV “PEA” from the subxiphoid view:

Ideally, an arterial line would be very useful in these patients, and may help to decide on an individual basis when CPR should be used. Remember that CPR on a beating heart will likely worsen cardiac output as asynchronicity and increased mean intrathoracic pressure will impair filling.

Additionally, the arterial line also allows us to notice small trends during resuscitation, such as seeing that a few seconds of CPR may help circulate a bolus of vasopressor and enable it to take effect – progressive BP increase, or that the BP may be trending downwards despite vasopressor infusion – CPR may be useful until enough vasopressor/inotropes have infused.

Bottom Line:

1. if possible, put in an arterial line

2. bedside ultrasound is mandatory if you don’t want to miss anything reversible

3. if you don’t have a palpable pulse and your diastolic pressure (arterial line) is less than 40, consider some CPR until vasopressors/inotropes have had effect.

4. if you are lucky enough to have ECMO (shout out to Joe and Zack at http://www.edecmo.org)  or other mechanical support, it would be the time to consider!

I think this is actually a really interesting area to develop, and I’d really, really like to hear what other sonographer-resuscitationists are doing, or what anyone else might think!

 

Philippe

 

Joe Bellezzo – yes, THE Joe, says:

Phil, I agree with all your points here. Great post! As you know, Shinar, Weingart and I recently published a rant on PEA (over at http://www.edecmo.org/13) and Weingart threw out two possible new monikers: PRE-M (Pulseless Rythm with Echocardiographic – Motion) and PRE-S (Pulseless Rythm with Echocardiographic – Standstill). I don’t disagree with any of those concepts but I think its simpler than that.

PRE-S (standstill) = asystole and you start compressions.
PRE-M (organized cardiac activity) = profound shock. In this setting I like the recent Littmann paper that gives a simplified approach (http://edecmo.org/wp-content/uploads/2014/08/A-Simplified-and-Structured-Teaching-Tool-for-the-Evaluation-and-Management-of-Pulseless-Electrical-Activity.pdf).

As you pointed out above, the real big question is at what point do you start compressions when you have cardiac motion? Your points above are spot on. The problem with compressions on a beating heart is that you don’t know what your end-point is. You lose the ability to do minute-minute diagnostics and doing any procedures with ongoing compressions is tough. And it seems to be a knee-jerk reaction for the RN or pharmacist to have an amp of epi ready to blast away at this point. NO!

I wait. I do stuff first. Step 1 is ECHO. If PRE-M (aka profound shock): EKG and arterial line NOW. Step 2: Stop, think and decide what you think is your top probable etiology of this profound shock and fix that. Step 3: reassess = repeat echo, EKG, and see what your art line pressures are doing. I try to do all that before I start compressions.

Example: “PEA” hits your door. Echo shows a wall motion abnormality and hypokinesis. EKG suggests ischemia but is not obvious STEMI. art line goes in simultaneously. I think this is MI. This heart does NOT NEED epi 1 mg! This is cardiogenic shock and I need to fix some stuff before I start pushing on the chest and blasting superhuman doses of epi! I usually start with a push dose epi (10-20 mics or so) while a pressor drip is prepped. Calcium bolus is given. I likely start dobutamine here (or milrenone if beta blocked). If that fixes your problem, then the pt goes to the cath lab. If it doesn’t, I cannulate and put the pt on VA-ECMO.

And what if I were wrong? what if this were a big PE? massive beta blocker OD? the protocol above is works in those cases too.

An aside, since you already placed a femoral venous line….and you popped in the Art line immediately, you have nice conduits to upsize to ECMO cannulas.

Great post Phil!

 

Thanks for sharing your approach!  As you know and clearly show, a sensical physiological approach is absolutely needed in a day and age when we can (bedside ultrasound) see what’s really going on, and we can (ECMO) give these patients a fighting chance!  See you at BMBTL in a couple of weeks!

Philippe

 

PS Joe (and Zack and Scott) will be talking about all this and more at CCUS 2015! http://www.ccusinstitute.org to register soon!