H&R2018 Keynote Lecture: Re-Defining Sepsis by Lawrence Lynn. #FOAMed, #FOAMcc

Lawrence’s work on sepsis analysis is truly groundbreaking. To put this in perspective, one has to recognize that sepsis is an exceedingly heterogeneous disease that, once upon a time, and for good reasons, an arbitrary definition was formulated. This, however, does not reflect sepsis adequately, and needs to change with observational data, as this has tremendous implications in therapeutics research.

Lawrence’s efforts have resulted in data systems revealing a number of different patterns of sepsis, with clear differences in physiologic effects or responses. This may explain why so many failed therapies for sepsis have occurred. It is entirely plausible that some of these therapies may have effects in some of these phenotypes of sepsis but get lost in the statistical mix.

Love to answer any questions anyone may have, and Lawrence will certainly chime in on the discussion!

cheers

Philippe

 

 

 

Renovascular #POCUS: Technique with Korbin Haycock. #FOAMed, #FOAMcc, #FOAMus

Korbin Haycock, ER doc extraordinaire.

 

So a few months ago I got to talking with Korbin about POCUS, fluids and resuscitation, only to find out this guy is doing all sorts of awesome stuff in his ED in sunny California.  Got to meet him at H&R2018 and he had even more tricks up his sleeve he was telling me about. He will definitely be back for H&R2019 on the faculty side of things.

In the meantime, let’s review renovascular ultrasound with him:

And here is our discussion that took place at TheRounds Backstage during #HR2018.

Interesting stuff. It isn’t always so easy to get a nice renal view in ICU patients, but with some perseverance you often can. I’ve been toying with it and tying it in with the hepatic and portal flow patterns, but I have to admit I had sort of dismissed renal resistive index based on what I could find in the literature, that is until I got to chat with Korbin, who made me see there are some interesting avenues, especially the example he states on seeing it improve with vasopressin use in shock patients, which correlates with some of the data out there suggesting decreased need for RRT and better outputs with vasopressin on board.

I have a feeling there is relevance to this in acute care, and that the next couple of years will reveal some usefulness. The glitch had always been in not knowing what the baseline RRI is, and that it can be abnormal in chronic RF. There are, however, many patients who were perfectly well previously and where the assumption that their baseline is normal is probably safe.

Love to hear comments from anyone using this!

 

cheers

 

Philippe

Kylie & Korbin chime in to the Venous Congestion Issue. #FOAMed, #FOAMcc, #FOAMus

So I think much of the awesomeness of #FOAMed is sparking discussion and exchange, and the many little steps in clinical management besides the initial prescriptions. So I thought I would highlight and exploit a couple of really interesting reader comments:

So first, Kylie (@kyliebaker888):

Great to listen guys, thanks, and very timely. I had just read Tremblay’s paper after coming across a very pulsatile PV in a relatively well elderly patient with bad TR. Two questions – which PV are more likely pulsatile in the first place….Tremblay mentions RVF/TR and very thin folk. What is your experience?
Second Question – what did the GB wall/GB fossa look like after the initial very positive fluid balance? Does everyone blow out their GB wall with fluids, or only some?

It is always important to isolate the patients’ whose physiology may change the clinical signs (in this case PV pulsatility) and make their interpretation different. I agree that massive TR, especially chronic, would likely account for pulsatility. I am not certain about the physiology for the very thin patient, but I have heard the same thing from Andre.  So my personal take on a patient with severe TR and a pulsatile PV would be to look at the IVC variation, TR notwithstanding, if it is fixed and plethoric I would diurese – the organs don’t care what the cause of the congestion is.  

As for the GB, I have also seen edema, and then try to correlate with cholestatic enzyme changes that would be out of proportion to the hepatocellular enzymes if there is a primary GB process. This is certainly an imperfect science. In a critically ill septic patient, I have a low threshold to drain the GB if in doubt.

Then Korbin gives his two cents, and then some! 

Great case, loved it. Thoughtful management, brilliant!

I couldn’t help thinking as I listened, that it is so important to avoid over-resuscitation with fluids in the first place. We all know that the majority of crystalloids given will end up as interstitial edema, so any benefit from the increase in stroke volume is temporary at best (consider carefully what you gain and at what cost). Wet lungs=increased mortality, days on the vent, and ICU stays. Wet kidneys=AKI 2-3 days after initial resuscitation and potential RRT. Congested liver=gut edema and continuation of inflammatory cytokines/sepsis syndrome. Too much fluids–>BNP levels rise, high BNP levels in the presence of LPS=glycocalyx shedding, and more interstitial edema everywhere.

Cannot agree more.

I think there is some decent evidence that an early fluid liberal approach combined with a late fluid restrictive approach can potentially benefit a patient in septic shock, but its clear that an overall positive fluid balance does harm. Perhaps, even the early fluid liberal strategy (in sepsis specifically) should be tempered by a careful consideration of what is really going on.

My take here is that, by using POCUS, there is no need for a “general approach.” POCUS takes essentially no time. In about 5 seconds you can confirm a small IVC that can (initially) take fluid, a medium one (that you need to watch) or a full one (yes, it happens – that gets no fluid). So to me there is no need to have a pre-determined approach…

Sepsis is an entity characterized by venous return being limited by a decrease in mean systemic pressure (MSP) due to an increase in venous capacitance, rather than a decrease in fluids that generates the stressed volume (MSP=fluid filling/venous capacitance). The body compensates with an adrenergic response that maintains (or attempts to maintain) MAP by an increase in a catecholamine driven augmentation in cardiac output/contractility. This adrenergic response likely has more to do with the increase in lactate production observed in sepsis, rather than actual tissue hypo-perfusion and anaerobic metabolism mechanism. Increases in CVP inhibit venous return and congest the kidneys and GI tract (the left atrial pressures are the equivalent problem for the lungs, combined with the fact that pulmonary vascular permeability is increased in sepsis as well). Given this, I think in distributive shock, we should fix the lack of MSP by an earlier vasopressor therapy approach, both to supplement and decrease the crystalloid load to the patient, which is un-natural and contrary to their deranged septic physiology.

Agree.

Also, could the type of crystalloid given be important? NS gives a considerable sodium load compared to LR, and this likely promotes/sustains fluid retention that is difficult to remove during de-resuscitation. The high chloride levels of NS will promote an increase afferent arteriolar vasoconstriction and thus decrease GFR, making it more difficult to diuresis the patient later on, and contribute to AKI beyond the iatrogenic interstitial kidney edema caused by the crystalloids we gave.

Absolutely. NS is given by medical peeps only by cultural habit. Most do not know the pH (zero SID due to chloride) of  a solution they give by the buckets. RL is the best option I have available.

If you are involved in the early phase of resuscitation of a shocked patient, consider the downstream consequences of your fluid strategy that you give your patient that may give you a temporary comfort because they will look better in the short term.

Dr. Maitland and the FEAST study corroborates exactly this.

This is not to say that an aggressive and upfront resuscitation is not critical–it surely is. I’m saying resuscitate smarter, not wetter. Look for stop points for crystalloids–E/e’ ratios, consider PVPI, RV dilation/TAPSE, hepatic vein doppler, IVC dynamics, portal vein pulsatility, intra-renal venous Doppler patterns and renal resistive index. Fix the hemodynamics from an approach of the root of their problem, rather than pushing fluids for every hypotensive patient (whether you are taking care of them early, or late in the time frame of their illness). Fluids do have their place, but be careful and cognizant of their real down side. Look at your patient, think it through, and make the best actions for them.

Ok, now I don’t even get to have a punchline. Thanks Korbin!

So if this interests you, tune in to The Great Fluid Debate at H&R2018, and I look forward to meeting both Kylie and Korbin who will be in attendance and, I’m sure, putting us all on the spot!

And yes, there will be a POCUS workshop on portal and hepatic vein POCUS.

click here if you want to take part: H&R2018

cheers!

Philippe

 

POCUS & Venous Congestion – A Clinical Case Discussion with Rory Spiegel (@EMnerd_), #FOAMed, #FOAMus, #FOAMcc

Hi, so as a follow up to our earlier discussion, which can be found here, Rory and I discuss a recent case he had, which I think exemplifies well many of the clinical conundrums that are seen in fluid resuscitation, one being the general resistance of many to diurese patients who are still in shock on vasopressors, instead preferring to (hopefully) wait until shock resolution to de-resuscitate. But sometimes, it is exactly what they need, as some of this congestion may be, in fact, a cause of shock…

Here you go:

Love to hear opinions, so feel free to reach out.

 

For those who may be interested at learning some of these POCUS skills, check out H&R2018 (#Hres2018)!

 

cheers!

 

Philippe

The Hospitalist & The Resuscitationist. Montreal, April 18th & 19th, 2018. #Hres2018

So for this winter, we’ve put together a little gem of a conference which will be a mix of hospitalist and critical care medicine, both with a dash of POCUS for good measure. Our focus here will be short, to the point, highly relevant and highly physiological talks on key topics, in short, 15 minute talks.

What are we going to talk about?

Day 1: The Hospitalist

 

Day 2: The Resuscitationist

 

 

You can figure there will also be late-breakers, “ask the crowd” talks and more.

Workshops? Sure:

Yup. You can ask for a workshop. Enough similar requests will probably make it happen. A few have already asked for Neuro-POCUS, so that is a likely addition.

 

So, who will be talking?  The lineup already includes Andre Denault, Josh Farkas (@Pulmcrit), Jon-Emile Kenny (@heart_lung), Rory Spiegel (@EMnerd), Hussein Fadlallah, Peter Barriga, Daniel Kaud, Davide Maggio, Michael Palumbo, William Beaubien-Souligny, and a few more to confirm. And who knows who might do an impromptu drop-in…

 

The short answer is yes. Of course, it does depend on what you do. If you are a hospitalist, involved in critical care or acute care of any kinds, you will find something here for you. Totally awesome for IM residents/FM residents planning on doing some hospital medicine or ICU coverage. Who will get the most bang for his or her buck here? Real docs training or working in the trenches. This isn’t a cutting edge research conference, but a cutting edge clinical application conference.

 

Oh yes, and the CME, of course:

 

This will be a small, fun conference. Space is purposely limited, for an intimate feel and to encourage discussion between peers. No need for these exclusive “meet-the-professor lunch” or anything like that: that’s what the whole event is like!

 

Registration is open! Print, fill, write a cheque and send the form below:

RegistrationV2

If you’re crazy busy, or have any questions, feel free to email hospresusconference@gmail.com or tweet (@ThinkingCC) to reserve a spot! 

Download the brochure here:

H&R2018 Brochure – Participants

 

cheers!

 

The H&R 2018 Scientific & Organizing Committee:

Dr. Philippe St-Arnaud – ER and Critical Care doc, POCUS instructor and constantly pushing the clinical envelope.

Dr. Carola Zambrana – our Hospitalist on the panel, constantly seeking excellence in care and working on bringing POCUS to the wards.

Dr. Mario Rizzi – our friendly neighborhood respirologist and educator.

Dr. Philippe Rola – Critical Care doc, long time POCUS aficionado and instructor, working at bringing POCUS into the everyday physical exam.

 

Fluid Stop Points! More POCUS goodness from Korbin Haycock. #FOAMed, #FOAMcc

I am really enjoying this exchange, and I think it is in the true spirit of #FOAMed to foster these discussions, as we have the opportunity to combine and fine tune our understanding of a topic from several really bright people’s view and experience. 

Korbin:

Jon-Emile, excellent points and insight. I should clarify a couple of my comments. To be specific, by “renal vein flow” I am referring to intra-renal venous flow. Apologies for my imprecision! Thanks for pointing that out.

Yes, a lot of these renal and portal Doppler patterns are surrogates of CVP. But I don’t think any of us would use CVP in isolation these days to make any decision what-so-ever on whether fluids were indicated in our patient.

Also, to clarify, I am not using intra-renal venous flow or renal resistive index as measures of non-fluid responsiveness. Rather, I use these measures as a stop point for attempting to solve the patient’s hemodynamic dysfunction with crystalloid regardless of whether or not my straight leg test tells me the patient is still fluid responsive.

And that is a key re-iteration to me. It is important to set these stop points and not only look at whether the cardiac output can be maximized. This has been tried. And failed. Let’s remember that sepsis is not inherently a disease of low flow. It isn’t cardiogenic or hypovolemic shock at the core.

My rationale for the strategy of using intra-renal Doppler, E/e’, and Lung US (now, I can include portal vein pulsatility) as a stop point for IVF administration is that I think the patient is best served to avoid iatrogenic edema of the upstream organs, primarily the lungs and the kidneys. These are the two organs (maybe you could put the endothelium in this category as well–glycocalyx being a whole other can of worms!) most easily damaged by the chase for optimizing every bit of fluid responsiveness. We have good evidence that getting wet lungs and swollen, congested kidneys is a bad thing, and we have these tools to hopefully warn us when we are pushing things too far.

Absolutely. And the whole glycocalyx is something to keep in mind, even if only to me mindful to disrupt it as little as possible.

Of course renal resistive index, intra-renal venous flow, portal vein pulsativity, and whatever else you like will have limitations and confounders. As long as you understand what can cause abnormalities with these tools, you can make an educated guess as to what’s going on. If our creatinine is off and our RRI is high, but intra-renal venous flow and portal vein flow is normal, perhaps the RRI is caused by something other than renal congestion, like ATN. If the portal vein is pulsatile, but the Doppler patterns of the hepatic vein, kidney and the heart look ok, maybe something else is wrong with the liver. But, if all our modalities are in agreement and pointing to congestion, we should perhaps believe that it’s congestion and stop the fluids. 

That is an awesome approach to integrating RRI. I’ve been toying with it for the last couple of days, and much thanks to Korbin, I think that the limitations of RRI can be overcome by using the rest of our clinical and POCUS data.

It isn’t a hard technique, though in some patients getting a good signal can be tricky.

I think that the kidney, being an encapsulated organ, and the fact that much of our crystalloid ends up as interstitial edema, the kidney will develop sub-optimal flow patterns before CVP would cause congestion. The same is true regarding the lung, except that it’s just related to increased pulmonary permeability due to inflammation. Regardless, the idea is to save organs, and the earlier you can detect the problem, the sonner you can stop battering the more delicate organs with fluid.

As I think we have all mentioned, you really have to look at the whole picture, and put it together to tell the story of what is wrong, so we can logically and thoughtfully treat our patients.

I really appreciate this discussion. Thanks!

 

 

Thanks to Andre, Jon and Korbin for making this very educative for all!

Cheers

 

Philippe

 

ps don’t miss the POCUS Workshops on venous assessment at  !!!

Jon-Emile (@heart_lung) chimes in on the whole portal vein POCUS! #FOAMcc, #FOAMed

When it comes to physiology, there`s no doubt that Jon is the man, so I was really curious about his take on all this, which, no surprise, is definitely worth sharing, just in case everyone doesn`t go read the comments.

 

Jon:

Wow; there is a lot to unpack here.

My first comment is that intra-renal venous flow [*not renal vein flow], hepatic vein flow, portal vein flow, etc, etc, etc [as well as IVC size and respiratory variation] are all ultrasonographic transductions of the central venous pressure …so I’ll give my boxed disclaimer that volume status and volume responsiveness cannot definitively and reliably obtained from this marker because the CVP is too complicated to make these physiological leaps.

Indeed. It is important to realize that, as Jon states below, that the angle for looking at the PV in this case is to assess congestion, rather than responsiveness or the ever-so-nebulous ‘status.’

Wait for it … volume tolerance and the CVP, is a bit more nuanced, i think.  with a high CVP, you really have to ask yourself – **why** is the CVP elevated and go from there.  if the CVP is elevated because of tamponade, its very different management from a high CVP from a massive PE or air-trapping versus a high CVP from volume overload.

Absolutely. Diuresing a pre- or full-fledged tamponade, PE or air-trapping could have disastrous consequences, i.e. PEA arrest!

There seems to be some confusion about *the renal vein* versus *intra-renal vein*.  the lida trial is clear that it is intra-renal vein flow.  i am not terribly familiar with *the renal vein flow, however, my hunch is that renal vein flow should always be biphasic [just as the jugular venous flow, SVC flow, IVC flow and hepatic vein flow are always biphasic] – that is a normal pattern close to the right atrium.  normally the systolic inflow velocity is greater than the diastolic inflow velocity and there is fairly good data correlating reversal of systolic to diastolic venous flow ration to right atrial pressure [in the IVC and SVC].

Definitely the intra-renal vein should be the target here – not always easy in some patients, because the renal vein itself, especially the right (no crossover) really has an IVC pattern and won`t necessarily reflect the effect of intra-renal hypertension.

The pulsatility that evolves in the intra-renal vein as the CVP rises is beyond me, but the authors postulate that it has to do with the compliance of the vein at higher CVP and intra-renal interstitial pressure which makes some sense.  But it is important to note that the compliance curves of an intra-renal vein and *the* renal vein are probably quite different.

Secondly, the pulsatility of the PV is a neat idea because of its relative ease of assessment.  However, the pulsatility, presumably, is due to the PV encroaching the limits of its compliance curve – the PV, like the CVP – has an inflow and outflow pressure.  It is highly likely that a pulsatile PV in a post-operative cardiac patient relates to an angry RV – but is this always true?  What about the cirrhotic?  What about differential partitioning of fluid into the splanchnic bed versus the lower body?  What about differential expression of adreno-receptors between splanchnic arteries [beta and alpha] and splanchnic veins [mostly alpha].  My point is that there could be *other* inflow and outflow differentials that are affecting PV volume, compliance and therefore pulsatility that are not yet recognized.  A cirrhotic on bomb dose phenylephrine/vasopressin may have their splanchnic venous volume recruited with blood expelled towards the liver, an engorged PV that is pulsatile – but is that RV failure?  Is that a patient who needs to be decongested?  I don’t know.

Thirdly, there are complex cardiac contributions to venous flow phase and vein pulsatility such as arrythmia – atrial compliance, etc.  As the comment above notes – how might afib contribute to SVC or IVC venous inflow?  It’s hard to know, but my hunch would be that afib itself would tend to reverse the normal S wave: D wave supremacy … that is, decrease the normal systolic inflow velocity relative to the diastolic inflow velocity.  if the atrium is not emptied fully then its pressure with rise.  if atrial pressure rises, when the atrium is pulled downward during ventricular systole, the S wave will be diminished.  additionally, the more chronically dilated and poorly compliant the right atrium, the greater its pressure will be with the loss of atrial kick.

Fantastic points. Again, looking at POCUS metrics CANNOT BE DONE IN ISOLATION, from the rest of the POCUS and clinical data.

Lastly, the venous inflow pattern analysis approach to CVP estimation – i think – is better than IVC size and collapse because of how IVC size and collapse can also be affected by IAP, ITP/PEEP, etc.  Because ITP affects systolic and diastolic inflow patterns similarly, that confound should be lessened.  Nevertheless, as Dr. Denault mentions in the cases above – you have to treat the patient!  This means integrating what the data is telling you in the patient in front of you.  If in a certain clinical context the test results do not make sense, it’s probably a false positive or false negative test.

I dug up this gem from 30+ years ago. Excellent paper [https://www.ncbi.nlm.nih.gov/pubmed/3907280 – “Ultrasonic assessment of abdominal venous return. I. Effect of cardiac action and respiration on mean velocity pattern, cross-sectional area and flow in the inferior vena cava and portal vein”].

Ok that’s on my short reading list for the next 48h!

They show the venous inflow waveform for the IVC [presumably very similar to *the renal vein]; Afib *does* cause the S wave to become attenuated – so it would change the normal biphasic form to more of a monophasic form. In theory, giving a calcium channel blocker and slowing the patient down should improve this somewhat. They even have a brief discussion on portal vein pulsatility.

This venous inflow stuff is very interesting and potentially very applicable. @iceman tweeted out wave velocity patterns in the MCA during high ICP – indeed – an increase in ICP renders the flow more pulsatile and then there is loss of diastolic flow. Probably similar physiology for an intra-renal vein as intra-renal capsular pressure rises. A good sign that the kidney is under pressure!

Thank you Jon for some really excellent physiological points and the reminder that, in POCUS just as in clinical medicine, we cannot rely on one assessment, and that measure must be considered in the context of the factors affecting it. Otherwise, we are not truly tailoring our therapy to the patient, but only pretending to.

Don’t miss Jon and the POCUS workshops at  next april!