So I love the UVM EM Update at Stowe. It’s a great little conference, run by my good friend and all around awesome guy Peter Weimersheimer (VTEMsono) ED Pocusologist, and his super team including Kyle DeWitt (@emergpharm), Meghan Groth (ENpharmgirl) and Mark Bisanzo (@mbisanzo). It’s a smooth running show with some really amazing speakers where I always learn a bunch. Had the chance to finally meet Sergey Motov (@painfreeED) and learn from an awesome opioid lecture. And it’s always great to hang with Josh (@PulmCrit) and listen to the pearls!
So here is my fluid talk. The Keynote pdf is just below. Hope there’s a useful tidbit or two in there!
So recently a colleague asked me about one of my twitter posts where I had put a clip of doing venous congestion assessment using a handheld – which is without pulsed Doppler (PW). Since VEXUS is predominantly based on Doppler findings, seems like 2D and colour might not cut it, but can it be done in a screening or “lite” fashion?
Definitely. Here is a mini-discussion about it, and some clips below to illustrate.
Clearly Pulsatile PV likely near 100%
Ascites, plethoric IVC, pulsatile PV, markedly abnormal HV with “police siren” appearance due to substantial retrograde flow – likely VExUS 3 or C.
Normal looking HV
Markedly abnormal HV
Love to hear some questions or comments!
of course, lots of VExUS discussions with William Beaubien Souligny, Andre Denault, Rory Spiegel, Korbin Haycock and myself at H&R2020!
So anyone who knows Korbin (@khaycock2) realizes he is a true trailblazer in the ED, essentially doing cutting edge critical care from the get go in his shock patients. In my mind this should be the goal for any critically ill patients, that they get the highest level care right at entry and for however long they may be staying in the ED until they get to the ICU.
So today, I was really happy to corner Korbin lounging somewhere in sunny California (as 6 inches of snow come down hard in Montreal) to tell me how he is using this technology in his resus patients.
So this has got me interested in using this technology. I see it as an early warning signal that your patient may be less fluid tolerant than you may think, and that the signs of pulmonary fluid intolerance I use (oxygen requirement, appearance of B lines (FALLS Protocol-style), etc…) have yet to manifest.
So I’m looking forward to hearing Korbin explain this further (during H&R2020!) and in actual cases where the change in management is clear.
For more lectures that will change the way you practice medicine, do try to make it to H&R2020! It is the very ethos of this small conference, to exchange with docs pushing the envelope of acute care as well as like-minded peers. This isn’t the conference to go to if you want to see what most people do and review guidelines. This is the one to go to if you want to be on the cutting edge. Only 100 spots, has sold out every year. For more info and registration click here!
So the pundits still try to claim the lack of evidence for the use of POCUS, bla, bla bla. Just wait till they get a load of this: POCUS in delirium? Master Andre Denault introduces us here to a completely new way of assessing a little known potential aetiology of acute delirium.
Here it is, certainly one of the most interesting and forward-thinking lectures of H&R2019:
So one thing we all pretty much agree on is the importance of source control. Biliary sepsis is one of the more common causes of intra-abdominal sepsis, and among those, there is a not insignificant proportion of cases where a percutaneous drainage procedure is indicated, often related to an elevated surgical risk.
This is the case of a 90 year old man with severe aortic stenosis and a perforated cholecystitis with sepsis (AKI, delirium, coagulopathy) admitted to our ICU. Due to the aortic stenosis, surgical mortality was felt to be quite elevated, hence a percutaneous procedure was done.
I am sharing this to make the case that a percutaneous cholecystostomy is not outside the reasonable skill set of a clinician who is both POCUS competent and has solid guided procedural experience (central lines, thoracic or abdominal pigtails, etc) and in my opinion falls into that same category as pericardiocentesis. All the more so for clinicians working in community hospitals without the luxury of a 24/7 IR team, because in many cases, it is simply not reasonable to wait many hours for source control – the fact that the patient may make it alive to the next morning to have a drainage procedure is not relevant, as the ongoing sepsis over several hours may be something he or she does not always recover from in the ensuing days and is not a risk worth taking unless there is no other viable option. In our center the critical care physicians perform this intervention when IR is not available.
Here, an in-plane approach was chosen with a trans-hepatic route in order to avoid potential peritoneal spillage.
(1) Always visualize the guidewire inside the intended space.
(2)When dilating, make sure the proximal part of the guidewire within the target area “disappears” ultrasonographically, confirming entry of the dilator. Why? In some cases the wall may give more resistance (particularly an inflammed pericardium) and the dilator may remain outside – cannulation with the catheter will be impossible.
So here was a late-breaker talk at H&R2019. Portal vein pulsatility and hyponatremia by a nephrologist – intensivist. Love it. Sharad, a really great guy, also recently published a case report on this topic.
There is a lot of stuff on venous congestion in the woodwork, some of which we are involved in, but also some springing up from different places, and this is really exciting, because POCUS gives you a non-invasive tool to assess and differentiate pathological degrees of congestion that really nothing else can with as much breadth, and as part of a comprehensive exam.
Venous POCUS is worth learning, and keep your eye on this space for how it evolves as a clinical tool. Our VEXUS classification will soon have some real substance behind it.
So last week sometime we had an interesting twitter exchange which made me realize it is important to explain how some of us are using venous POCUS in different clinical scenarios, which is key, because the development of monosynaptic clinical reflexes with POCUS findings is a rabbit hole we should try not to go down. Instead, POCUS should be about asking the right question and taking that answer as a piece of the pathophysiologic puzzle facing us, which may mean intervening sometimes, and sometimes not, for the same given finding, but with different surroundings.
Thanks to those involved in that discussion – it is how we grow!
And here are some thoughts:
For those not up to speed on venous congestion POCUS I put up the chapter that Korbin Haycock, Rory Spiegel and I worked on in this earlier post.
Here are Korbin’s thoughts on this:
I’m very glad Dr. Eduardo Argaiz pointed this case out, as it brings up considerations apropos both chronic venous congestive cases as well as management of acute illness, particularly in sepsis, where we would expect patients to most likely be fluid responsive, but fluid tolerance is largely overlooked with current management strategies by the majority of clinicians.
Phil’s above audio commentary points out the difference is these two broad categories very nicely. If you didn’t listen to it–you should.
With respect to chronic venous congestive conditions, the knowledge and application of Doppler assessment to therapy will hopefully be the next advance in management at large. Already, I think there is more than adequate research available to show the value of Doppler POCUS (D’POCUS, D/POCUS, or DPOCUS?) in managing these patients. It’s only a matter of clinicians willing to commit to learning and integrate this technology into their skill set.
With respect to resuscitation of the acutely ill patient, there is by far less data, and we are probably into the realm of N=1 here, in terms of how to manage these patients. But, I personally believe–and I understand this is my opinion–that current trends in resuscitation (especially sepsis resuscitation), largely ignores the effect of over volume resuscitation and the potential downstream damage inflicted on our patients.
This theoretical damage of over aggressive fluid resuscitation is multifactorial, including glycocalyx shedding issues/endothelial dysfunction, positive fluid balance and EVLW causing increased mortality (which there is ample evidence for, I think), venous congestion leading to perfusion injuries to encapsulated organs, such as the kidney (AKI) and brain (congestive encephalopathy), and end organ edema leading to the perpetuation of a malignant inflammatory syndrome (portal HTN and gut edema).
In the case called out by Dr. Argaiz, (which can be reviewed by the previous post on this website) my patient had an IVC that whilst not plethoric, was not an IVC that one would expect to find in a patient with a typical distributive shock pattern (i.e. increased cardiac output, decreased SVR, and decreased RAP). Firstly, the complicating factor of atrial fibrillation with RVR was central to the patient’s shock state, however this was quickly addressed with rate control. However, in addition, this particular patient did exhibit additional signs of venous congestion. The portal vein was pulsatile and the intrarenal Doppler pattern was interrupted/bi-phasic in nature. Granted, a pulsatile PV Doppler could be interpreted as related to the hyper dynamic nature of septic shock (as the esteemed Dr. Denault correctly cautioned in his comments on the original post), however a less than flat IVC and the intrarenal findings gave weight to a venous congestive hypothesis as a cause the PV findings as well as a possible cause for his AKI evident on his initial labs.
With this particular case, given my personal global POCUS/FOCUS assessment of his increased LAP (high E/e’), RV dysfunction, RAP, PV, and intrarenal Doppler venous pattern, AND that fact that the RRI was insanely high with an AKI, I elected to treat my hypothetical construct of his renosarca with furosamide and his RRI with vasopressin (as the NE infusion did increase his MAP, BUT NOT decrease his RRI–which the vasopressin infusion did decrease, or so I presume as no other therapeutic interventions were given with respect to the time frame the RRI decreased).
In the end his kidneys had recovered by the next morning, which I’m sure that any intensivist will admit is the opposite of the norm, as the kidneys usually get, at least transiently worse initially-being the delicate sissies/whimps that they are. Whether this was because of the diuretic or the vasopressin, or something else, is debatable for sure, but it sure didn’t get better by 30 cc/kg of crystalloid mandated by CMS, because he got not a drop more than what was needed to push the diltiazem, the lasix, the antibiotics, and the vasopressors.
So to summarize, in the case of chronic cardiogenic venous congestion, clinician realization and adoption of Doppler assessment of this entity will likely be the next leap in improvement in the management of these patients. In the case of acute resuscitation, venous congestion may be a bit more nuanced, and a more comprehensive evaluation is in order in a case by case fashion. However, I think recognition of the issues of over aggressive volume administration will probably be the next frontier in sepsis resuscitation.