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
thinking critical care 
Great stuff – do you have any of the literature he cited – would love to dig in.
I touched on the venous side of the road in an old post – correlates with some of your discussion
https://pulmccm.org/intra-abdominal-pressure-renal-function/
Sorry
That link was not correct
https://pulmccm.org/critical-care-review/intra-abdominal-pressure-renal-function/
Fascinating and I will start trying it. Please write more. Would love if you could post some tracings of where and how you drop your doppler. Can you use it to differentiate acalculous cholecystitis from GB wall oedema secondary to right heart failure (or are they really the same thing?)
Hey, sorry I missed this! Not sure you could make a definite distinction echographically. My hunch is you’d need to look at infectious parameters… Certainly, evidence of congestion without other signs of infection could explain the (?incidental) GB appearance…
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.
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 pulsitility.
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. 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.
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.
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 was 0.75. He looked much better too. The second lactate was 1.3.
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.
Great case Korbin! Might have to turn it into a post!
Thanks for reading, much appreciated!
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 algorythm in order to identify the true portal pulsatility associated with right heart failure and fluid overload and a normal portal vein with pulsatility. (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.
André Denault
Yes, thank you Dr. Denault.
I absoulutely agree. To your point about young hyperdynamic patients, I found a study that showed portal vein pulsatility also to be a normal finding in thin patients as well.
The renal resistive index also has its limitations, as there are multiple factors that can cause an increased index.
I think, as you alluded to, the key here is really to look at the whole picture in your patient. Also, it’s important to know the limitations of each modality you are using. A normal E/e’ ratio may still result in wet lungs if the pulmonary vasculature is leaky, and also, we must remember that pressures do not necessarily give you an accurate idea of what the ventricular preload is, which is what we care about and why we would measure an E/e’ ratio in the first place!
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