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.
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…
In Greek mythology, Prometheus (/prəˈmiːθiːəs/; Greek: Προμηθεύς, pronounced [promɛːtʰeús], meaning “forethought”) is a Titan, culture hero, and trickster figure who is credited with the creation of man from clay, and who defies the gods by stealing fire and giving it to humanity, an act that enabled progress and civilization. Prometheus is known for his intelligence and as a champion of mankind.
So, fresh from reading Jon’s post, I felt I had to add a bit of nuance in my previous post to what I feared some might extract as a take-home message, even if in fact, we are not that differing in opinion at all – which Jon expressed here:
i agree with ultrasound for finding the uncommon causes of shock. these examples seems to permeate twitter and make ultrasound very appealing. because ultrasound is non-invasive, it makes the risk-to-benefit ratio very low for these uncommon but highly-lethal and treatable causes.
but that needs to be compared to the risk-to-benefit ratio of ultrasound for the more common causes of shock – like ‘non-cardiogenic, septic’ etiologies as seen in SHOC-ED. here, “static’ ultrasound [as per the RUSH and ACES protocols] – per SHOC-ED – appears to be neither helpful nor harmful. your read of the discussion is perfect, but i was depressed because it read as if the authors only realized this ex post facto – study of previous monitoring utensils [e.g. PAC] should have pre-warned the authors …
i will take some mild issue with markers of volume responsiveness and tolerance. you are correct on both fronts – but what the data for the IVC reveals – perhaps paradoxically – is that true fluid responders can have a very wide-range of IVC sizes from small to large and unvarying … this was born out in most of the spontaneously breathing IVC papers [airpetian and more recent corl paper] the sensitivity was rather poor.
the same *could* be true for the opposite side of the coin. a large great vein may not mean a volume intolerant patient. i tried to exemplify how that could be so in the illustrative case in my post. an elderly man, with probable pulmonary hypertension and chronic TR who probably “lives” at high right-sided pressures. nevertheless, he likely has recurrent C. diff and is presenting 1. hypovolemic and 2. fluid responsive despite his high right-sided pressures. portal vein pulsatility *could* be quite high in this patient – but he still needed some volume.
the obvious underlying issue here – which I know you are well attuned to – is that a Bayesian approach is imperative. when you PoCUS your patients, you are inherently taking this into consideration – i know that you are a sophisticated sonographer. my hidden thesis of the post is that if ultrasound findings are followed in a clinical vacuum and followed without really understanding the physiology [which can explain clinico-sonographic dissociation – like the patient in my fictitious case]… disappointment awaits.