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 metabolic resuscitation is a topic that both Josh (@Pulmcrit) and I are really interested in. We were looking forward to the CITRUS-ALI study. The results, to me, are good. They continue to establish the fact that there are no real side effects, particularly renal, as this was a concern to some (despite the already large data sets – particularly in the Matsuda study), and in an even higher dose than the Marik study.
Of course since the study was not designed to show a mortality benefit, it wouldn’t be clean to tout their results from that angle, but it certainly should be hypothesis-generating (imagine the cheers from the pundits who would certainly have used it in reverse had the mortality been increased instead!!!). So for me, it changes nothing, because – if my institution hadn’t decreed (for no legitimate reason I can see) that I cannot use it in patients that I feel would benefit – I would still use it as an adjunct to septic shock management.
There are more studies around the corner, and hope they will come out before next may, so that Josh can give us an update for H&R2020 (#Hresus20)!
So for anyone not familiar with Lars (@LMSaxhaug on Medtwitter), if you are into applied resuscitation physiology, this is someone to follow. He seems to be Norway’s answer to Korbin Haycock (@khaycock2).
He is a POCUS researcher and currently a Cardiology/Internal Medicine Trainee, and I hope someone who will help take POCUS to another level. I’ve been meaning to chat with him for a while after some incredible threads on twitter really pushing the applied bedside physiology envelope.
So here is our first discussion, with a few more planned in the near future as we get down to the nitty gritty. But everything does need an intro.
So here is our discussion:
I think Lars makes some excellent points, particularly the need for global hemodynamic assessment, not having a narrow, almost single parameter threshold approach, as well as his point on adaptative tachycardia – though I am not in full agreement about the atrial fibrillation, but most definitely agree that most of the cases in the ICU are secondary, and deciding how much it is contributing to the hemodynamic compromise isn’t always clear.
Looking forward to further discussions, and I smell a panel discussion with Korbin and Jon-Emile on RVOT doppler!
So I recorded a chat with Domagoj (@domagojsono in the twitterverse), an anaasthetist-resuscitationist-intensivist from Freiburg a few months ago, but with H&R2019 and its aftermath, been slow in processing a lot of stuff I’ve got stocked… Apologies!
So in this one, DOmagoj and I discuss a bunch of resus topics, from eCPR to tissue oximetry. I’m really jealous of the fact that he does prehospital work with an ECMO van!!! …and with cool gear and of course, POCUS!
Here is the chat, hope it leads to thoughts, discussion and contribution!
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.