Genomics & Preventive Medicine: The Next Level. #FOAMed

So, on a totally different note that has little to do with my usual rants about bedside ultrasound, resuscitation and critical care, I wanted to share with everyone an interesting project I’m involved in which really applies not only to prevention and early diagnosis, but even to the care of the acutely ill, and this is genomics.

To us physicians in the trenches, mutations are generally clinically relevant in certain limited settings, such as thrombosis (factor V et al, ), cancers (BRCA1, etc), but not really in our day-to-day. However, in the next decade, this will probably change quite a bit. The human genome project not turbocharged by crisper technology has resulted in an exponential increase in research and discovery of genetic mutations, disorders and, around the corner, gene therapy.

 

So in the last year we’ve put together a team, developed and designed a process by which an individual can get his entire genome sequenced, then ran against the current crop of known and significant mutations. We have a team of genetic counselors that will ensure follow-up of anything found. Additionally, genomes will be re-run on a yearly basis against any newly discovered significances.

So, what does this mean clinically? Well, I won’t bore everyone with a mutation-by-mutation breakdown of what could be done, but I think everyone understands the advantage of knowing specific disease propensity and having a heads-up for the development of certain associated pathologies. If I had factor V leiden, I might be tempted to take a couple aspirins before boarding and make sure I walk the aisles regularly in my trans-pacific flight, or if I have the philadelphia chromosome, I might get a cbc when my cold/flu lasts more than a couple days…

To get a little more perspective, here is a recent article by the American College of Medical Genetics that may help see the possibilities:

ACMG Article

So I’m really quite excited by this development, and I think it can have quite an impact. For the moment, there are costs involved, but as we are clinician group and not a corporate machine, we are keeping these as low as possible. For anyone interested, for themselves, their practice or their patients, or just have some questions, please get in touch! We have just opened up the “door” in Montreal and are starting up in Toronto shortly.

The real value to this organization is a turn-key solution to genetic testing and follow-up, unlike any other out there, none of which are MD-run nor involve genetic counselors and association to specific clinics and medical follow-up, in addition to the updating of the patient’s variants against new discoveries and treatments.

This is the cutting edge. That’s why I like it!

See below for some more details:

cheers

 

Philippe

Great things to come at TheRounds! Webminar Series 2017

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Just to let everyone out there know about a cool thing coming up on TheRounds (www.therounds.ca), which is a professional network for medical students and physicians, permitting an exchange of ideas and knowledge between peers in a secure network (verifiable credentials needed, but free to join).

So we are starting up what should be a pretty cool series of webminars in the next couple of months, and I’ve been asked to chair the scientific committee, so we’ll be drawing up the programme in the next month or so, so needless to say we should have some familiar FOAMed names in the fields of ED/CC and probably hospital medicine contributing.

We’ll be sure to cover interesting topics, controversial ideas, groundbreaking studies and set it all in  physiology, with the philosophy of individualized care. I’m happy to entertain ideas and requests from the FOAMed world, and highly encourage everyone to join and contribute. You won’t find any “industry” talks here, I guarantee it.

So great topics and speakers aside, this will be a great CME opportunity, as the formula will include the faculty remaining active answering questions for a couple of weeks after each webminar, which will likely feature 2-3 talks on a given topic. Even better, TheRounds also has a system that keeps a log of your CME (including browsing time) so it will be really simple to tally every year.

So looking forward to this new venture, and hope to see a slew of the FOAMers join in!

 

cheers

 

Philippe

 

 

Hepatic Portal Venous Gas (HPVG): a Less Ominous Sign than We Thought? A Case of HPVG associated with massive PE… #FOAMed, #FOAMcc

So a few years ago I had a patient in the ICU, post op for some abdominal surgery, and, using POCUS, I detected a hyper echoic area in the liver, in a wedge shape.  I scanned the patient and, lo and behold, there was a matching area of air-filled hepatic venous sinuses on CT scan. Well, my surgical colleague and I were very concerned and proceeded to inform the patient he would be needing exploratory surgery for what was likely ischémie bowel. He essentially – though in more polite words – told us we were idiots and that his belly felt fine and he didn’t think surgery would be needed at all.

His belly did feel fine. So were his labs. So we worried, but, given this whole thing about free will and consent, etc, couldn’t very well force him into what we felt was necessary surgery.

The next day he was fine. On POCUS, the area of air had shrunk. The next day, it was gone altogether.

We thanked him for his keen clinical acumen and for teaching us a good lesson.

However, we were a bit perplexed, because traditional teaching equated portal venous air with a severe bowel disorder, usually ischemic or inflammatory, with exceedingly high mortality. At least that is what we had been fed. We are both grads of 1999. Hmmm…

So over the next few years we saw a few of these cases, sometimes bad, sometimes not, and a review of the literature (see below)  showed an interesting evolution of the disease. Described in the 1950’s on plain films, hepatic air was a bad omen indeed, with mortality in the 75-90% range. In the CT era, the mortality started to “drop” to the 35-60% range. Now you can find quite a few reports of “surprisingly” good outcomes with conservative management. So this evolution doesn’t represent a change in severity so much as the technological capability to detect smaller and smaller amounts of air in the venous system – just increased sensitivity. And now, with POCUS – ultrasound is the most sensitive detector of air in a vascular tree – the associated mortality is likely to take another drop, not only because of our ability to detect very small amounts of air, but also because we are actually looking at the area, and also in a wider range of patient’ pathologies that those commonly associated with HPVG.

 

Clinical Case: HPVG and PE!

So a couple weeks ago I saw a patient in the ED who’d recently broken an ankle, had her foot put in a boot and managed conservatively and came back dyspneic and tachycardic. Here are a couple of clips:

As always, I start with the IVC:

Big & fixed.

Hepatic veins:

Biphasic flow.

Femoral veins:

So here the source of the problem is pretty clear, a large common femoral DVT.

She wasn’t very echogenic so I don’t have great clips of the heart but she had a dilated and hypocontractile RV with a McConnell’s sign (preserved apical contraction), small and hyper dynamic LV with septal flattening.

Now here is where it gets interesting, the portal vein:

You can clearly see bubbles traveling up the portal vein. Ominous, or not?

So clinically, her abdomen was normal, she had no abdominal symptomatology at all…

 

Pathophysiological musings:

So the severe RV obstruction resulted in significant venous congestion. Additionally, the decreased cardiac output – as manifested by a lactate of 4 and mild tachycardia/hypotension (110 HR, BP sys 90’s) was clear.

The etiology of HPVG in the literature isn’t clear – mucosal disruption, bacterial gas are all mentioned but as far as I could find, no definitive answer.

Is it possible that there is a “normal” inward leak of mucosal gas that is normally fully dissolved in the venous bloodstream, but that, in cases of low flow and/or venous congestion, the dissolution capacity (per unit time) decreases, and that gas comes out of solution?  Alternately, those who have increased intraluminal pressure (gastric distension, etc), the increased transmembrane gas driving pressure may overload an adequate blood flow…

This would explain the benign course of many patients, particularily those with gastric dilation.

 

Clinical course:

Based on hemodynamics, tachypnea and, to some degree, venous congestion, I decided to thrombolyse her using 1/2 dose lytics. Within a couple of hours her HR decreased to the 90’s and BP rose to 110 systolic.  Echographically, however, the IVC/RV findings remained similar, but the HPVG decreased. By the next day, HPVG was altogether gone, lactate had resolved and dyspnea was significantly better.

 

Take Home Message:

HPVG, although not quite as poor a prognostic sign as once thought, nonetheless warrants concern and investigation, even if the abdominal exam is entirely normal and without symptomatology, as correction of an underlying cause of “benign” HPVG (whether low-flow or bowel distension) would still need to be addressed.

In the meantime, I suspect that, reported or not, this has been noted by other POCUS enthusiasts, since we are now looking more frequently at this area, and are dealing with patients with low-flow states, congestion, bowel obstruction/ileus or more than one of these.

Hopefully some investigators will take a look at this phenomenon and delineate the pathophysiological mechanism!

Love to hear of your experience with this.

cheers!

 

Philippe

For those interested in POCUS, see here for a quick read primer on clinical applications of POCUS.

 

HPVG Review article 2009:

wjg-15-3585

 

Wicked Clinical Case: POCUS & Prone save the day! #FOAMed, #FOAMcc, #FOAMer

So I get a call from a colleague in the ED at about 2am, telling me about a 39 yr old woman post-arrest. So I start putting on my boots and warming up the car (it’s January in Montreal folks).  Apparently she had presented earlier in severe acidosis, the diagnosis is unclear, but she apparently got 2 units for an Hb of 49, then went into respiratory failure and got intubated. She arrested about 30 minutes later, cause unknown.

I tell the ICU to prepare a bed but I want to see her in the ED first. Twenty minutes later I put probe to patient and see a full IVC with spontaneous echo contrast. On that I tell the nurse to hold the fluids – there was a bag and tubing and a pump with 100ml/hr on it – and turn into a subxiphoid view to see a normal RV and a hypokinetic LV with some WMAs. She has marked consolidations  in both posterior lung fields and B lines laterally, with small effusions and dynamic air bronchograms (indicating patent airways). At this point she has a HR of about 120, but there is neither perceptible BP (by NIBP) nor saturation. She’s on levophed at 20mcg. She’s about an hour post arrest which was witnessed and brief (<10min to ROSC).

The theories about the arrest are possible hyperkalemia: she was intubated with succinylcholine before the K of 6.1 was back from the lab, and her pre-intubation pH was 7.0, and post-intubation she was only ventilated at 400 x 18, possibly precipitating a drop in pH and a rise in K. Her EKG had some nonspecific signs at this point, but also a poor anterior R wave.

So we head to the ICU, as instrumentation was needed. Cerebral saturation (SctO2) is 42% and ETCO2 is 20mmhg, which reassures me that the BP is probably in the measurable range (normal SctO2 is >60% and varies, but 47% is certainly viable)…  A jugular CVC with continuous ScVo2 and a femoral arterial line goes in:

screen-shot-2017-01-05-at-10-44-50-pm

So with a BP of 59/44 (ignore the 100/46, not sure whose arm that was on!) I start epinephrine, as the POCUS is similar, as I want some added beta-agonism. ScVO2 matches SctO2 in the 40’s. We get the BP up the the 90-1oo range, the ETCO2 goes to 30, the SctO2 and ScVo2 go up into the high 40’s, which is very reassuring, because with this I know that my epi drip is improving perfusion and NOT over-vasoconstricting. Without looking at a real-time tissue perfusion index of some sort or other, it is nearly impossible to know rapidly whether your therapy is helping or harming (will discuss tissue saturation & resuscitation monitoring in more detail in another post sometime soon).

screen-shot-2017-01-05-at-10-46-31-pm

So now the sat finally starts to record in the low 60’s. We have a PEEP of 5, so start bringing it up. We hit 16 before the BP starts to drop, and that only gets us to the mid 70’s sat%. She actually squeezes my hand to command.

screen-shot-2017-01-05-at-10-45-21-pm

At this point I take a few seconds to recap in my mind. I’d spoken to the husband briefly and she had had recurrent episodes of feeling unwell with headache, nausea and diaphoresis, and that had been out for dinner earlier and she felt fine until later in the evening when this came on and eventually brought her to hospital. There was also a notion of hypertension at an ER visit a couple of weeks ago. Her history was otherwise not significant. Nonsmoker.

Pheo? Maybe, but shock?  I repeat the EKG, and now, in I and AVL, there is perhaps a 1mm ST elevation. She’s 39 and essentially dying. Lactate comes back >15, pH 6.9.  I give her a few more amps of NaHCO3. You can see the BP respond to each amp. I decide we need to go to the cath lab and get the cardiologist on call to get on the horn with the interventional team at a nearby hospital with a cath lab and ECMO, which is what I think she needs. Hb comes back at 116, making that initial 49 that prompted 2 PRBCs probably a technical or lab error…very unfortunate. There are no visible signs of significant bleeding.

But back to the patient, because this isn’t really a transferrable case.

Recap: a 39yr old woman in cardiogenic shock AND in severe congestive heart failure exacerbated by fluids and packed red cells, with a PO2 in the 40’s and sat in the 70’s.

So I decide to prone her.

screen-shot-2017-01-05-at-10-47-44-pm

Along with draining tamponades, this had to be one of the most rapid and rewarding maneuvers I’ve done. There was a scry drop of sat to the 40’s for a few seconds (may have been a technical thing), but then within a few minutes: BP to the 130’s, SctO2 to 59% and sat 100%!

screen-shot-2017-01-05-at-10-46-46-pmscreen-shot-2017-01-05-at-10-47-31-pm

screen-shot-2017-01-06-at-12-08-05-am

 

We dropped the vasopressors, the FiO2, and all breathed a collective sigh of relief. Now for the novices out there, prone ventilation improves VQ mismatch by moving perfusion from diseased, posterior lung fields to now-dependant, relatively healthy, anterior lung fields.

So transfer at this point was in the works. I planned to leave her prone until the last minute. The miraculous effect started to slowly wane within about 30 minutes, with sat and BP creeping down. At the time of transfer, we were back up to 80% FiO2.

So why is this?  Simple enough, this being simple pulmonary edema – rather than consolidated pneumonia – it migrated to dependent areas  relatively quickly. This was confirmed by a quick POCUS check:screen-shot-2017-01-05-at-10-48-06-pmscreen-shot-2017-01-05-at-10-48-26-pm

So in the still shots, you see a pristine “A” profile (normal, no edema) from the patient’s back, and a severe consolidation or “C” profile with ultrasound bronchograms in the antero-lateral (now dependant) chest. Impressive. (for those wanting some POCUS pearls see other posts and here). This is the reverse of her initial POCUS exam.

So we flipped her back and transported her – lights & sirens – the the cath lab, where they were waiting with ECMO cannulae. As an aside, it was quite refreshing to speak to the ICU fellow who spoke POCUS as well as french and english – it’s not usually the case, but I’m glad to see the change. I do believe it to be a direct effect of the influence of my friend and mentor, Dr. Andre Denault, one of the POCUS deities.

So she turned out to have a normal cath and a large adrenal mass. She did well on ECMO, being weaned off it today, and is now alpha-blocked and waiting for surgery, neurologically intact for all intents and purposes. A big thanks to the interventionists and the ICU team at the Montreal Heart Institute. Puts a smile on my face.

 

Take Home Points:

  1. don’t resuscitate without POCUS. I wouldn’t want anyone guessing with my life on the line, would you?
  2. keep pheo in mind as a cause of “acute MI” and shock
  3. if you’re not using some form of realtime monitor of perfusion (continuous CO, SctO2, ETCO2, ScvO2) then all you’ve got is looking at the skin and mentation, so you are essentially flying blind. Lactate and urine output are not realtime in real life.
  4. get ECMO in the house, it’ll come in handy. I’m working on it.

 

Love to hear some comments!

cheers

 

Philippe

 

ps I’ll try to add more ultrasound clips from this case in the next few days.

N=1 Principle in ARDS and esophageal pressure directed mechanical ventilation. #FOAMed, #FOAMcc

So i recently came across a review on esophageal pressure-guided ventilation in ARDS, which is in fact a technology I’ve had in my shop since 2008, but rarely use.

The truth is that I haven’t seen much “ARDS” in the last years, and I believe quite strongly that this reflects simply our hospital’s increased awareness of the nocive effects of over-zealous fluid resuscitation. Although in the ICU we still admit patients who, in our opinion, have received a bit more fluid than they should have, we have become more aggressive with diuresis “despite” the presence of shock, and usually see “ARDS” resolve. This is a direct consequence of actually “looking” at our patients’ volume status using ultrasound (for more see, well…most other posts on this blog!).

However, what seems like genuine ARDS does come around once in a while, and we recently had severe respiratory failure develop in a morbidly obese patient, and all of a sudden, in the presence of an FiO2 of 100%, a PEEP of 14, intra-abdominal pressures between 20 and 25, and on Flo-Lan, it seemed it might be a good idea to tailor ventilation.

Current Practice:

The most common practice currently is the ARDSnet type low volume (5-7ml/kg) lung protective ventilation, using a PEEP/FiO2 scale and aiming for plateau pressures (Pplat) below 30. Generally speaking a good idea, but one has to understand that this is, once again, a one-size-fits-all (except for the per kg) approach, which isn’t ideal if you try to follow  the N=1 Principle.

Why is this?  Because, due to physical characteristics (obesity, chest wall stiffness, etc,) and pathology (increased abdominal pressure, etc), the airway pressure reflects the respiratory system pressure (Prs) rather than the transpulmonary pressure (Ptp), which is the variable most related to volutrauma (which has eclipsed barotrauma as the mechanism for most ventilator-induced lung injury (VILI).  Ptp essentially relates to overdistension, which is what results in pneumothoraces. In terms of parenchymal micro-injury, it seems to be most related to atelectrauma, in essence the opening and closing of alveoli, with the resultant shear forces disrupting surfactant and cell surface. This type of injury relates best to finding optimal PEEP to both recruit and prevent de recruitment – in effect minimizing the amount of lung tissue collapsing and reopening.

 

Esophageal pressure (Pes)-guided Practice:

So Pes is used as a measure of pleural pleural pressure, and:

Ptp = Paw – Pes

That equation is the central tenet to this, and basically, you have to reset your goals to:

a. Ptp (exp) around zero – optimal PEEP – (meaning no over distension and no de-recruitment)

b. Ptp (insp) below 25 – though this is not really individualized as a hard data point, but has been shown to be a reasonable cutoff for volutrauma.

 

How do you do this?

By slipping in a special oro/naso-gastric tube with a balloon connected to the ventilator, one is able to simultaneously measure airway pressure (as is standardly done) and esophageal pressure. This is what it looks like:

img_6207

Here we can see that this patient has a PEEP of 20 (top), a Pes of about the same, and thus a Ptp (bottom) near zero.

We’ll discuss this case hopefully tomorrow, but just to show the mechanics/technique of it.

 

Bottom Line:

So this involves tossing out the ARDSnet charts and trying to individualize and optimize Ptp (insp and exp) instead of plateau pressures and PEEP.  How may it be useful clinically? Well, you may be able to detect unsuspected states of de-recruitment/ateletasis due to excessive chest wall or abdominal pressure, and allow you to increase PEEP “safely.”

When should I use this?

I’m not sure what everyone else is doing, but we are in the process of setting up a protocol where esophageal balloons will be inserted for any patient whose ventilator settings are approaching or exceeding FiO2 70%/PEEP 15, indicative of sufficiently severe respiratory failure warranting this additional level of fine-tuning.

I tend to use it when ventilating two groups: those with (a) elevated intraabdominal pressure, and (b) the obese patients, as they often have elevated Pes (usually due to diaphragmatic displacement. Interestingly, the correlation between obesity and Pes is not very good, so one should not “blindly” feel they can crank up the PEEP to 25 and ignore plateau pressures, as some obese patients have normal Pes (likely due to compliant abdominal walls.

Would love to hear what others do.

 

Here are the relevant articles/references:

talmor-nejm-2008

ajrccm-2014-review

 

Cheers!

 

Philippe

 

Bedside Ultrasound Case: Control the source. #POCUS #FOAMed, #FOAMcc, #FOAMus

So this morning a 65yr old man with shock and respiratory failure was admitted to the ICU, hypotensive on levophed and vasopressin, with a lactate over 10.

So, as usual, my first reflex was to reach for the probe to assess hemodynamics. He had been well resuscitated by a colleague, and the IVC was essentially normal, somewhere around 15 mm and still with some respiratory variation. However, scanning thru the liver, my colleague had noted a large hepatic lesion, which on CT scan (non-infused since patient had acute renal failure) the two radiologists argued whether it was solid, vascular or fluid filled.

image

Having the advantage of dynamic ultrasound, you can tell that there is some fluid motion within the structure, very suggestive of an abcess, especially in the context of severe septic shock:

So the next step was source control:

 

Pretty nasty. Pardon my french!

We got over 1.5 L of exceedingly foul pus.

imageimage

Within a couple of hours the lactate dropped to 3 and the levophed was down by more than half.

I think this case illustrates once again, the power of POCUS in the hands of clinicians.  While I am certain that the diagnosis would have been made without POCUS, it probably would have taken additional time as the radiologists themselves were debating its nature, and without POCUS, bedside drainage in the ICU would have been out of the question. That liter might still be in there tonight…

For those interested in how to integrate POCUS in their daily rounds, I think I put together a fair bit of clinical know-how and tips in this little handbook.

 

Cheers!

 

Philippe

Bedside Ultrasound: a primer for clinical integration. #POCUS

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So I had a lot of people ask me over the years to put to paper (or screen) a POCUS book, but I figured there were so many good ones out there, like my original Bible, General Ultrasound in the Critically Ill by my good friend Daniel Lichtenstein, or Vicky & Bret’s book, Emergency and Critical Care Ultrasound, that I would be trying to re-invent the wheel, and probably not doing as good a job.

But then I remembered Dubin’s EKG book, the kind of book you could almost read in a single sitting, and certainly over a few days, and get a decent grasp of the concepts and actually have some skill at the end of it.  So I figured maybe I could put together something like that for POCUS from the standpoint of clinical integration. Not so much a protocol, but how you fit your findings together in clinical syndromes, and inserting as many tips and pearls as possible.

It’s a light read, it’s irreverent, it’s kinda like #FOAM. So I hope I did a decent enough job, and I was pretty happy with the comments from a couple of respected colleagues:

Philippe has created a fantastic real-time reference for the busy practicing clinician who wishes to adopt point of care ultrasound into their working cinical armamentarium. The strength of this work is it’s immediate applicability to the clinical scenario. Dr. Rola’s extensive experience in clinical practice and teaching shines through with a concise and clinically minded approach to each scanning modality. The work is greatly enriched by many practical tips and tricks and that are often missing from larger, more formal texts. The sum of these “truths” is an important part of what transforms a clinician to an expert in the field. A final unique feature of this resource is it’s focus on integration. In Philippe’s mind, findings of differing ultrasound modalities are blended together with the patient’s clinical picture to derive a true ultrasound enhanced understanding of the patient’s pathophysiology. With characteristic plain language and descriptions, the book succeeds in taking the reader closer to that vision.

Dr. Edgar Hockmann, MD, FRCP

Dr. Rola has created the ideal compendium for contemporary healthcare professionals. Bedside Ultrasound: a primer for clinical integration concisely and intuitively describes the essentials of examining a patient in the 21st century. The guide is both unique and useful because it speaks to all levels of training for all professionals caring for patients within multiple hospital environments – the emergency department, general medical ward, operating room and intensive care unit. Dr. Rola’s succinct account of ultrasound examination leads the reader through a patient’s anatomical and physiological underpinnings using the ultrasound probe as his guide; it is a resource to be found in the pocket – virtual or otherwise – of all those interested in the future of the physical exam.

Jon-Emile Kenny M.D.

The first print run just got off the press, is on Amazon here, as is our casebook, and on our website http://www.ccusinstitute.org. The iPad version is available on iTunes here! Please give me feedback as it is important, so that the second edition just gets better!

cheers!

Philippe

The NYC Tracks with Jon-Emile part 2: a discussion on congestion, pulmonary and otherwise. #FOAMed, #FOAMcc, #FOAMus

So here is our second discussion, where we delve a bit into diuretic physiology, the issue of organ congestion, the myth of the “low-flow” acute renal failure associated with CHF (see earlier post), and a couple other things including a great way to determine if a patient isn’t respecting the low salt diet prescription!

I meant to, but forgot to discuss with Jon what I think is an important end-point in CHF management: the IVC. Yes, it is useful not just to make the diagnosis of congestion, but also target normalization of IVC physiology prior to discharge. It just makes common sense. If you decongest a patient just enough to get them off O2 and send them home, they bounce back a lot quicker than if you make sure you’re given them some intravascular leeway.  How do you determine this? Simple enough, make sure your IVC is down at least to below 20mm, and has recovered the classic acxvy and respiratory variation. I personally try to get into the 8-12 mm range, but that’s arbitrary. Here is some good data for 20mm:

06005

Without further due, here is the NYS Track 2:

 

Please share your thoughts!

 

cheers

 

Philippe

Fluids in Sepsis: An EmCrit Webinar! #FOAMed, #FOAMcc

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Screen Shot 2016-04-27 at 1.43.23 PM

So a few weeks ago Scott (@EmCrit) asked me to be part of a pretty cool webinar organized by the Greater New York Hospital Association about fluids in sepsis. The gang consisted of David Gaiesky, Emmanuel Rivers and moderated by Scott himself. And for some obscure reason, he asked me to be part of it – much to my honour (terror, also), naturally.  It was only afterwards that he told me it was to help stir the pot and be controversial, challenge the “old school” etc… He seemed to have overlooked that I am Canadian, and inherently and perhaps overly polite and considerate – at least live and in “person”!

We talk about a bunch of stuff around fluids, which, how much, how to assess, etc.

Anyhow, I hope I got a few ideas across, but it was really cool to hear that these gurus do use ultrasound – don’t necessarily strictly adhere to, for instance, EGDT, and also advocate that guidelines are guidelines and not necessarily gold standards.

Here is the link to the webinar for those interested:

 

https://t.co/dbL03Vuqlj

 

And here is the figure for the section where I refer to fluid responsiveness/tolerance:

Screen Shot 2016-02-21 at 9.25.50 AM

I further talk about this in a previous post here.

Scott and I also recorded a debrief which should be coming up in the next weeks on EmCrit – link to follow!

cheers!

 

Philippe

Bedside US Procedure: Pericardial drainage – Pearls! #FOAMed, #FOAMcc, #FOAMus

So here is a video of a pericardial drain placement for pre-tamponade in a 33 yr old man, presumptively for a viral pericarditis (cultures and cytology pending).  In this case, the approach was subxiphoid, because this offered a large pocket of fluid with little or no risk of hitting the RV. The apical approach would have been more risky. Due to technical issues, the video only starts once the guide wire is already in place, but there are a couple of teaching points worth sharing nonetheless.

First, it is useful to confirm guide wire placement prior to dilating. Secondly, in cases such as this where the distance to the pericardium is more than a couple of centimetres (it was about 6 cm here), it is nice to be able to confirm under real-time that the dilator is indeed in the intended area. Because the guide wire is highly echogenic, and the dilator is not, one can see the proximal part of the guide wire “disappear” which indicates that the dilator has covered it, now visibly in the effusion. Once the pigtail is  inserted over the guide wire, final confirmation can be obtained by injecting back thru the pigtail and seeing echogenic material (due to minute amounts of air) appear in the pericardium. This is known as the Ajmo sign.

Cheers!

 

Philippe