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

 

Portal Vein POCUS: A Reader’s Case and a Follow-Up to the Denault Discussion

So I’ve been meaning to post a follow up and discussion about portal vein POCUS and how I am integrating it so far, and a few days ago I got a really interesting comment from Dr. Korbin Haycock, and I think it’s got some awesome elements to discuss.

Before we get into it, I would invite anyone reading this to go listen to the original Denault Track here, without which this discussion would be missing some elements.

What we are looking at here is the physiological assessment of venous congestion, and how doppler interrogation of the portal vein may help us. So here is Korbin’s case, and I will interject (in bold) where I think a point can be made, or at least my thoughts on it.

“Awesome post. Awesome website. I had never heard about portal vein pulsatility until reading your blog. I have previously been looking at the renal resistive index and renal vein Doppler pattern in my hypotensive/shock patients (along with doing a bedside ECHO and POCUS pulmonary exam) to guide when to stop fluid resuscitiation.

Very impressive. I have only ever heard of a handful of resuscitationists looking at this (including Andre, and consequently myself) so I’m gonna have to have a chat with this fellow soon! For those who have not tried or are not familiar, some basic info can be found here. I’ll have to review this, but I think one issue with RI is that there is an associated ddx, so that without knowledge of baseline, I would not be certain how to use it. Renal vein doppler seems very interesting to me, as that venous path is the one of the cardiorenal syndrome (forget about all that “low flow” nonsense in CHF – not in shock – patients), and there is clearly bad prognosis associated with abnormal (discontinuous) flow patterns. Here is a really good study (Iida et al)  and its editorial (Tang).

Iida Doppler_CHF Heart Failure JACCHF 2016

Tang Editorial JACCHF 2016

I had a case last night that I think illustrates that fluid administration can be the wrong thing to do in some septic shock patients. Plus, I got to try something new and look at the portal vein for pulsatility.

My case was a gentleman in his late 60’s with a history of HTN, atrial fibrillation and HFrEF who presented with three days for a productive cough and fever. POC lactate was 2.7. His HR was 130-140’s, in atrial fibrillation, febrile, MAP was 50, and he looked a bit shocky and was diaphoretic. The resident had started antibiotics and a fluid bolus of LR, of which not much had gone in (maybe 200cc) when I came to start a night shift and evaluated the patient. I asked that the fluids be stopped until we could have a look at him.

His IVC was about 1.5-2 cm with >50% collapsibility.

So I’m gonna hit the pause button right there for a couple of comments. That’s not a hypovolemic IVC. The RAP may be raised by some of the  It may very well be volume responsive, but I think the first thing to go for is correcting that tachycardia. The antibiotics are definitely the right call, but the fluids should, in my opinion, be held until assessment for volume tolerance is done.

His LV looked to have some mildly decreased EF and was going very fast. RV looked normal. His average SV was 45, CO was 6.1, E/e’ ratio indicated a slightly elevated left atrial pressure. His estimated/calculated SVR by the ECHO numbers was about 550. Lungs were dry anteriorly, without B-lines, but PLAPS view was c/w bilateral lower lobe PNA. Renal vein Doppler was biphasic and the resistive index was very high. I looked at his portal vein and it was pulsatile.

Excellent. So there is pulmonary pathology, which makes fluid tolerance already of concern. The CO is certainly adequate and SVR is low, suggesting a vasodilatory shock etiology. 

In the past, based on the IVC and the way the RV looked, I would have done a straight leg raise or given a given some crystalloid to see if his SV and BP improved, and if it did, give some IVF. Instead, I told the staff to given no more fluids and I gave him 20 mg of diltiazem.

His heart rate decreased from 130-140’s to 90. His averaged SV increased to 65 (probably due to increased LV filling time and better diastolic perfusion time), CO was 5.9, estimated SVR was 570. The renal and portal vein Doppler were unchanged. The MAP didn’t bulge and stayed low at 50-55. At this point I ordered furosemide and but him on a norepinephrine infusion to increase the SVR, first at 5 mcg/min, then 7 mcg/min.

Totally awesome to see. It isn’t unusual for me to diurese patients in vasopressor-dependant shock, as more and more data is emerging on how venous congestion has deleterious effects on the gut and may even contribute to the SIRS-type state. And once a patient is in a euvolemic to hypervolemic state, the only fluid they get from me is the one containing norepinephrine. Maintenance fluid is not for critically ill patients IMO.

The NE gtt increased his MAP to 75 mmHg. His SV was 80, CO 7.1 (I was a little surprised it didn’t go down a bit), estimated SVR was 700. I had his labs back at this point and his creatinine was 1.8 and the last creatinine we had was 1.1 a few months ago. His renal vein pattern was still biphasic and his renal resistive index was also still quite high at 0.89, which would probably predict a significant kidney injury in 2-3 days.

Even though his MAP and hemodynamics looked great, I was worried about the renal resistive index. I ordered a little more furosemide and started him on a little bit of a vasopressin infusion. After things settled down, MAP was 75-80, his average SV was 80, CO 7.3, estimated SVR was about 800, and his renal resistive index (RRI) was 0.75. He looked much better too. The second lactate was 1.3.

Very interesting to see the drop in RRI.  Great case to show how you don’t need to chase lactate with fluids. That is an antiquated knee-jerk reflex hinging on the concept that hyperlactatemia is primarily due to tissue hypoperfusion, which we have learned is not the main cause. 

This morning his creatinine had improved to 1.3 and he is doing well.

South of your border, CMS considers me a bad doctor for not giving 30 cc/kg crystalloid as a knee jerk reaction and instead giving a diuretic and early vasopressors as we did in this patient. Just looking at his IVC would indicate that IVF would be a reasonable strategy. If I had done a SLR or fluid challenge and found him fluid responsive, in the past, I would be temped to chase every bit of fluid response with pushing more fluids, but the renal and portal vein Doppler made me stop fluids in this patient this time. I think this example illustrates the importance of looking at each of your patients on a case by case basis and looking at the whole picture (heart, lungs, kidneys, now portal system too for me!), rather than following protocols.

Kudos. 

 

So then, Andre decides to chime in as well:

Very interesting but be careful about the interpretation of portal pulsatility because it can be falsely positive particularly in hyperdynamic young patient, which was may be not the case. We published an algorithm in order to identify the true portal pulsatility associated with right heart failure and fluid overload and a normal portal vein with pulsatility:

Tremblay Portal pulsatility Flolan Mil AACR 2017

(Tremblay 2017 A&A care report) A & A Case Reports. 9(8):219–223, OCT 2017 DOI: 10.1213/XAA.0000000000000572 , PMID: 28604468)

The latter will be associated with normal RV even hyperdynamic, normal hepatic venous and renal flow, normal IVC. We still need to explore the significance of portal hypertension outside the area of cardiac surgery where we are finalizing our studies.

Always tell my residents and fellow, treat the patient and not the number or the image. That being said, the patient got better so cannot argue with success.

So I think this is a really important point, that it can become dangerous in POCUS to look for a simple, single-factor “recipe” with which to manage the patient, when in fact you can have many factors which, integrated, can give you a much better understanding about your patient’s pathophysiology.

My take on portal vein POCUS so far is that it is a marker of critical venous congestion, beyond simply a plethoric IVC. I think it is wise to stop fluids before the plethoric IVC, but a plethoric IVC with a pulsatile PV should bring fluids to a screeching halt and some decongestive therapy started. The data for this?  Andre is cooking it up, but in the meantime, there is plenty of evidence that congestion is plenty bad, and NO evidence that maximizing CO works at all, so I am very comfortable in witholding fluids and diuresing these patients. 

For fun, here is a little figure from Tang et al about the doppler patterns discussed.

Love to hear everyone’s thoughts!

and for those interested, there will be a workshop run by Andre and myself on this at :

more to come on this soon…

cheers

 

Philippe

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!

Don’t miss Andre running a POCUS workshop on PV/HV at  next april!

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.

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

MOPOCUS: A great synopsis by Ha & Toh. #FOAMed, #FOAMcc, #FOAMus

Just came across this review and figured I should share. The authors make a great synopsis and review of POCUS in acute illness:

MOPOCUS Review by Ha &To

The only thing I would add to this is a more physiological way to assess the IVC, which I’ve blogged about here.  Sadly, I’ve heard a few people stating how they didn’t want to get into the dogma of IVC ultrasound, that it wasn’t reliable, etc.  The IVC doesn’t lie. It’s just not a recipe. The IVC findings have to be integrated into the rest of the echo graphic and clinical examination.  Trying to use it as a single value is akin to using serum Na+ as a diagnostic test for volume. It works only sometimes.

Please spread among the POCUS non-believers. We’ll convert them, slowly but surely. But the sooner, the better for the patients. Again, there’s no excuse to practice acute care without ultrasound. It’s not right. I’m not saying every probe-toting MD is better than one without, but everyone would up their game by adding POCUS, once past the learning curve!

cheers!

 

Philippe

Tom Woodcock: The Revised Starling Principle and The Glycocalyx! #FOAMed, #FOAMcc

Screen Shot 2016-08-05 at 11.57.11 PM

So today, I had the chance of having a private tutorial with Dr. Thomas Woodcock (@thomaswoodcock) about the glycocalyx and the revised Starling principles.  For anyone interested in fluid resuscitation, this is an area you have to delve into. The basic principles we all learned (which are still being taught) are basically the physiological equivalent of the stick man we all started drawing as toddlers: overly simplified and far from an accurate representation of reality.

Now my first disclaimer is that I have been a colloid supporter for many years. My physiological logic for that had been to minimize the crystalloid spillover into inflamed/septic areas, particularly the lungs and abdomen, when those are the septic sources. However, I was likely misled by my education and lack of knowledge about the endothelium.

So I stumbled upon the whole glycocalyx thing a couple years ago, and this prompted me to try more enteral fluids – the only way fluids normally ever enter the vasculature – but little else. Aware that it’s there, but unsure what to do about it.

Now a year and a half ago, Andre Denault, my closest thing to a mentor, casually dropped the line to me about albumin not working. “Don’t use it. It doesn’t act the way we think it does.”  But it was a brief chat, and I didn’t get to pick his brain about it.  Just a few weeks ago, I discuss with Jon Emile (Kenny), and he’s coming to the same conclusion.  Damn. I’m finding it a bit harder to hang on to my albumin use, which is beginning to look a bit dogmatic and religious.

Here is Jon-Emile’s take on it – a must-read.

Here is Tom Woodcock’s site and article – another must-read.

And here is my discussion (in two parts) with Tom (to skip the silence, skip forward to about 30 seconds into each – sorry my editing skills are limited!)

 

Bottom line?

Probably stick to isotonic crystalloids, and some hypertonics.

 

Love to hear some thoughts!

Cheers

 

Philippe