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

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

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

Interesting stuff.

So here you are:

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

cheers and thanks for reading and listening!

Philippe

 

Pre-intubation #POCUS with Cian McDermott! #FOAMed, #FOAMus

So I had a fun little discussion with @cianmcdermott, a great ER doc I had the chance to meet at WCUME 2017 a few weeks ago, about the uses of POCUS prior to intubating a patient in an elective or semi-elective fashion. In fact, I think that this can also be done in a more urgent intubation if you have another set of hands helping out, the concepts still apply. I thought it might be worth sharing.

let us know your thoughts!

 

thanks,

 

philippe

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

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

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

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

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

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

cheers,

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

Philippe

 

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

So our ECG pad is ready.

I’ll let the images speak for themselves.

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

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

What does it give you?

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

Data?

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

Bottom line?

First deliveries anticipated mid-2018.

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

The first run will be limited.

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

cheers!

 

Philippe

A Discussion on Fluid Management Protocols with Rory Spiegel. #FOAMed, #FOAMcc, #POCUS

 

So Rory (@EMnerd) is in the process of working on a fluid resus protocol for Shock-Trauma, and asked me if we could have a chat about it, which I feel very honored for – and had a brief impostor syndrome crisis – but it’s always great to chat with people who are really bright, really physiological and after the same goal, to make patients better. Always a pleasure to chat with Rory, so here it is.

I really can’t wait to see their protocol, because I think this is a huge and complex endeavor, but has to be done.  I will try to put pen to paper (probably really pixels to a screen but that doesn’t sound as good) and put what I try to do for fluid resus on a diagram of sorts.

Love to hear comments and questions.

PS please skip the first 30 seconds which are a technical blank… Ièm not tech saavy so can’t trim it!

cheers!

Philippe

 

A great comment by Dr. Korbin Haycock

One issue to consider is the degree of pulmonary vascular leakage. If, as in the case of sepsis, the pulmonary vasculature is more prone to the development of lung interstitial edema, lower LVEDP’s possibly will still result in as much lung wetness as higher LVEDP’s. Therefore, reliance of E/e’ ratios may not be the best measure of a fluid resuscitative endpoint in sepsis (and aren’t we really talking about sepsis resuscitation here?). I believe that it’s relatively clear that EVLW will adversely affect outcomes, but pushing for every bit of increased stroke volume/fluid responsiveness is less clear to be beneficial, even if it makes sense from a DO2/VO2 perspective (which may not be the real issue in sepsis anyway, as mitochondrial utilization of the DO2 provided may be the real problem, rather than DO2/VO2 balance). If the assumption is that the kidneys and lungs are the most delicate organs and most at risk to over aggressive fluid administration, and will impact mortality/LOS in the ICU, perhaps a combined strategy of attention to E/e’ ratios, development of B-lines, or the renal resistive index increasing would be a signal for a different strategy rather than fluids to increase venous return (i.e. switching from crystalloids to norepinephrine or vasopressin if the CO is elevated and will tolerate a minor ding from the increase in SVR). If any of those three variables indicate a problem, stop the fluids, switch to a vasopressor. If the issue is the CO rather than the SVR, use an inotrope instead. Of course RV/LV interactions as mentioned in the comments above must be considered. No point in giving fluids to an empty LV if the RV is failing–you’ll just congest the kidneys.

Twittercase: Fouled urine and #POCUS discussion. #FOAMed, #FOAMcc, #FOAMer

So I admitted a patient to the ICU yesterday from the ED.  He’s an 80-something gentleman from a nursing home with an indwelling catheter, and presented with stupor, hypotension, fever, leukocytosis and clearly infected urine.  His labwork showed a lactate of 5.3, a double-normal creatinine and, after 3 liters or so of crystalloid, he was started on norpeinephrine and hence came to the ICU. His extremities were fairly warm, and his cerebral saturation was 62%.

Before seeing the POCUS info, however, consider a clearly septic patient with AKI and elevated lactate. He did get 3 liters of fluids, but i’ve seen these patients get more fluids, whether for hemodynamics, lactate, AKI or any combination of the aforementioned.

Below is the clip, a quick POCUS sequence going from IVC (with hepatic vein flows), subxiphoid cardiac views, both lung views.

So here, we see a plethoric and fixed IVC (sorry I didn’t include the short axis but it was round and full, so in this case the LAX is reliable) with biphasic hepatic flow. Cardiac views show normal ratios and a poor LV function. Chest views show bilateral effusions and consolidations.

So what did I do?

  1. stopped fluids (I do not believe in routine maintenance fluids any more than in maintenance antibiotics or vasopressors).
  2. gave lasix (given that he is on the flat part of FS curve, I was unconcerned with some diuresis decreasing his preload, vasopressors and lactate notwithstanding, and with the goal to decongest his kidneys, likely suffering from congestive insult on top of the septic one).
  3. did not try to chase his lactate with increasing cardiac output (lactate being a great alarm bell and prognosticator, but little else, and because he was worm and with a decent cerebral saturation, I did not feel that there was a major cardiogenic component to his shock).

So what happened?

This morning, after a negative balance of 1,500 cc in 24 hours, his levophed dose has dropped by half, his lactate is normal and his creatinine is decreasing. A decade ago, I would have chased down the last ounce of volume responsiveness with fluids, aggressively trying to drive down the lactate and creatinine, and maybe, 24 hours later, he would have developed “ARDS” because he was “so sick.”  😉

cheers

 

Philippe

 

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

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

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

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

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

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

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

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

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

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

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

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

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

 

cheers!

Philippe