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!



Twittercase: Fouled urine and #POCUS discussion. #FOAMed, #FOAMcc, #FOAMer

So I admitted a patient to the ICU yesterday from the ED.  He’s an 80-something gentleman from a nursing home with an indwelling catheter, and presented with stupor, hypotension, fever, leukocytosis and clearly infected urine.  His labwork showed a lactate of 5.3, a double-normal creatinine and, after 3 liters or so of crystalloid, he was started on norpeinephrine and hence came to the ICU. His extremities were fairly warm, and his cerebral saturation was 62%.

Before seeing the POCUS info, however, consider a clearly septic patient with AKI and elevated lactate. He did get 3 liters of fluids, but i’ve seen these patients get more fluids, whether for hemodynamics, lactate, AKI or any combination of the aforementioned.

Below is the clip, a quick POCUS sequence going from IVC (with hepatic vein flows), subxiphoid cardiac views, both lung views.

So here, we see a plethoric and fixed IVC (sorry I didn’t include the short axis but it was round and full, so in this case the LAX is reliable) with biphasic hepatic flow. Cardiac views show normal ratios and a poor LV function. Chest views show bilateral effusions and consolidations.

So what did I do?

  1. stopped fluids (I do not believe in routine maintenance fluids any more than in maintenance antibiotics or vasopressors).
  2. gave lasix (given that he is on the flat part of FS curve, I was unconcerned with some diuresis decreasing his preload, vasopressors and lactate notwithstanding, and with the goal to decongest his kidneys, likely suffering from congestive insult on top of the septic one).
  3. did not try to chase his lactate with increasing cardiac output (lactate being a great alarm bell and prognosticator, but little else, and because he was worm and with a decent cerebral saturation, I did not feel that there was a major cardiogenic component to his shock).

So what happened?

This morning, after a negative balance of 1,500 cc in 24 hours, his levophed dose has dropped by half, his lactate is normal and his creatinine is decreasing. A decade ago, I would have chased down the last ounce of volume responsiveness with fluids, aggressively trying to drive down the lactate and creatinine, and maybe, 24 hours later, he would have developed “ARDS” because he was “so sick.”  😉





Bedside Ultrasound Quiz Part 1: a 50 yr old man with dyspnea, acidosis, hepatitis and leg edema. #FOAMed, #FOAMer, #FOAMus

So last night, an interesting call from the ED about a 50 year old man who presented with a 3 week history of increasing dyspnea, leg edema, temp of 39,  a lactate of 3.9, an INR of 1.7, elevated LFTs and a WBC of 18, but a BP of 130/75.

Fortunately, I was dealing with a saavy ER doc with some POCUS capabilities, so he also told me he saw a pretty big IVC and he was a bit leery about giving fluids, though this looked like pretty severe sepsis with 3 or 4 affected organ systems…

So I asked him to hold fluids until I got there. Here is what POCUS found:

He revealed a past history of untreated hypertention, and a flu-like illness 3-4weeks ago.

What’s the diagnosis (-es) and management?

Answers & Clinical evolution in part 2 tomorrow!













Bedside Ultrasound Clip Quiz! A 72 year old man with fever, weight loss and tachycardia. #FOAMed, #FOAMcc, #FOAMer

So a 72 year old man is brought to the ER after collapsing at home. His family had noted weight loss in the last months, and recently some fever and general weakness.  His HR is 108, T 38.8, BP 80/40, GCS 14 – somnolent – he is in lactic acidosis (4.5) and renal failure (cr 180 – baseline 120), with some vague abdominal pain, a clear chest and warm extremities.

POCUS shows a normal IVC, normal RV/LV, A profile lungs, no ascites, and this on the left flank:


What is the main diagnosis?

Scroll below for the answer:










So the clip shows fairly severe hydronephrosis, the “bear paw” with very dilated calyces.  The patient was suffering from obstructed pyelonephritis due to massive retroperitoneal adenopathy later found to be lymphoma.  A couple of hours later he got a nephrostomy tube to take care of the septic source (double J could not pass) and his sepsis resolved within a few days, and he headed off to chemo for the NHL.

The advantage of POCUS here is. once again, the speed of diagnosis. He went straight from CT to the readied urologists and source control happened within a couple of hours. His relatively benign abdomen may not have prompted a rapid CT otherwise.

See here for more POCUS!





Musings with Jon-Emile & Philippe – Fluid Resuscitation: Physiology and Philosophy! #FOAMed, #FOAMcc, #FOAMer

So here, Jon-Emile and I explore a topic I’ve posted about before ( so I can see if a master physiologist agrees with my rationale (…not just my rationale but supported by a ton of literature many choose to overlook!).

Please visit for Jon’s awesome physiology tutorials!

Love to hear listeners’ thoughts!




The Great Septic Debate (Part 2): Resolution? #FOAMed, #FOAMcc

So, echoing my thoughts form the end of the debate, Steven adds:

Well, I didn’t expect to see my name in a headline, but I suppose it’s a hazard one should expect when they go spreading their arguments across the interwebs!

In truth, I don’t think that Dr. Lynn and I really think that much differently on these issues. We both desire for the science of sepsis to continue developing and to be better than it is. I, personally, would love to be a part of the clinical trials that use genome-based data to determine which treatment arm a patient belongs in. We both deplore any “old guard” attempting to prevent the onward march of discoveries that make our knowledge and abilities more complete. I am actually sorry that some young scientists feel intimidated and that there is anything less than civility and scientific curiosity in our community. Period.

Likewise, I would be shocked if Dr. Lynn did not at least use the observation of infection, SIRS, and organ dysfunction as physical markers of sepsis and warning signs that intervention is necessary. It will be true for a very long time that it is going to be an interaction between two human beings that initiates the diagnosis and treatment of sepsis. A physician will recognize a patient in distress by some means and start the process. For now, these findings are the best we have, and they should prompt us to intervene before the completely diagnostic test results are available. Even when we have the tricorder, something is going to trigger the doc to pull it out of a pocket and use it.

OK, so I have to admit that Dr. Lynn stung me a little with his characterization of TNF-alpha as a “biomarker”. I would rather say that TNF is one of the heavy hitters in the proteomics of sepsis, and I’ll bet that I can get him to concede that point! It stimulates receptors and causes other actions to take place, it’s synthesis and release are regulated and dysregulated; it’s more than just a marker! And I ABSOLUTELY agree that the failure of TNF-directed therapies stems from the fact that they were given both to patients who could benefit from them and patients who, with better characterization, we would have known had no chance of benefitting. The same goes for high dose corticosteroids, anti-endotoxin antibodies, IL-1 directed therapies, and coagulation based therapies. In fact, that’s what I’ve been teaching my trainees for years – if you can call bemoaning the fact that we can’t yet recognize and separate responders from non-responders teaching. We have a desperate need for understanding better, and the science MUST be encouraged. Again, period. Or full stop, for those of you who have that bent! That is, I think, Dr. Lynn’s argument in a nutshell.

I REALLY appreciate the interchange. It is healthy and necessary. The two of us are aiming at the same thing – fewer people dying from sepsis. I haven’t met Dr. Lynn (though I hope to), but I suspect that he spends more hours in his day formulating and doing the new science, while I spend more hours in my day pushing people who think that it isn’t sepsis until it’s shock and multiple organ failure to do something about it before it gets that far. Those are both important parts of the war, but in the end, it is the same war. And we are allies in it.

Steven Q Simpson

And, soon after, Lawrence reaches for that handshake:

I agree completely with Dr. Simpson. We all teach that a good history, physical, basic lab, and a high degree of vigilance for subtle signs of sepsis are pivotal. This includes the use of awareness campaigns which simplify sepsis to something easily understood and screening protocols to assure vigilance. These are great advances.

I also share Dr. Simpson’s concern about empowerment of naysayers who may use the promulgation of the imperfections of sepsis science as a reason not to move forward with early action based detection protocols.

Relevant TNF-alpga, I have to agree that it likely has a fundamental role in some phenotypes of sepsis including the sepsis-like syndrome generated in Ebola patients.

So Dr. Simpson and I probably agree on most sepsis related issues.

To explain a little further, many years ago our research team applied for an NIH grant to define the dynamic relational patterns of all the lab and vitals over time in infected patients. The reviewers did not seem to comprehend why we wanted to do that since a standard for a single unified phenotype of sepsis was already widely accepted. Yet had they realized the need for these types of complete data sets, the entire time time series matrix of vitals, lab, biomarkers, and treatment for each case would have been acquired in PROcess , ARISE, and Promise. This would have occurred if the entire field of scientists had not convinced themselves they already knew that “sepsis/septic shock ” comprised a unified phenotype, “an entity” “a single condition” “a thing or object” definable by a few static thresholds.

So this is why we say the young should call for reform ASAP of sepsis science (not sepsis awareness) and at the upcoming SCCM. Imagine a mult-center trial where these complete time matrices are generated and we define the phenotypes. We can define the phenotypic subtypes and then examine treatments in relation to these.

One might think of sepsis syndrome as analogous to the syndrome of CHF where there is systolic failure, diastolic failure, hypertensive failure, and valvular failure defined phenotypes of CHF.

Perhaps we might have sepsis with capillary membrane failure phenotype and/or, vascular muscle failure phenotype, coagulation control failure , neutrophilic control failure, TNF-alpha mediated immune control failure.

These are simply general gross simplistic considerations, Discussion points.

However the final conclusion of my original post is that, beginning at this SCCM, we must stop trying to explain away the anomalies caused by the past sepsis dogma and accept that these anomalies ARE counter instances. We must accept that we cannot rely on research which uses billing codes as data or by using retrospective controls at the same time the denominator balloons as a function of awareness.

Then we can finally assure that we do not fool ourselves because the world depends only on us. There is no back up. We must accept that we need a new surge of sepsis research ASAP, and… a new direction.

This, along with the effort and dedication of Dr. Simpson team, the Sepsis Alliance, and the SSC (now gathering the entire time series matrix of all the diagnostic and treatment data and not just thresholds) will produce an exciting future. If this happens, it would be great to be a young sepsis scientist in 2015.

So yes Dr. Simpson and I actually agree. We are simply fighting the war on sepsis from different fronts.

Most Respectfully
Lawrence Lynn

Thanks again Steven and Lawrence for what I think was both a really informative AND formative discussion.


Limited EGDT in Zambia Study: Salt Water Drowning Syndrome… #FOAMed, #FOAMcc

So in this month’s issue of Critical Care Medicine, an interesting article was published, where investigators took a (necessarily) simplified version of EGDT to Zambia and applied it to septic patients. It turned out they had to stop it early due to an excessive number of cases of respiratory failure in the treatment group.  The difference was – you guessed it – they got “aggressive” volume resuscitation – up to 4l in the first 6 hours – guided by JVP assessment, and blood and dopamine if needed.


The amounts received by 6, 24 and 72h were 2.9, 3.9 and 5.6 l for the treatment group vs 1.6, 3.0 and 4.3 l.

Now lets keep in mind that the patients, for the most part, did not have access to critical care, so the limited resources for ventilatory support made stopping the trial a bit early the only reasonable thing to do. Mortality in the treatment group was 64% and control 60%. High numbers, but this is explained in part by the prevalence of HIV (80%) and TB (37% of the HIV positive patients), so this data can’t necessarily be extrapolated to all populations, but to me, this is physiological support for the concept that aggressive fluid resuscitation – as I have stated in prior posts/podcasts – is most dangerous in those patients where the septic source – presumably “leaky” is ill-equipped to handle extra-physiological fluid.  In these patients, as Myburgh states in a sepsis talk, “noradrenaline is the fluid of choice,” and although perhaps a bit tongue in cheek, this certainly speaks to my beliefs of resuscitating to euvolemia rather than to the lack of volume responsiveness (

Additionally, these patients were not hypotensive, and lactate was not available – local limitations of medical system. Hence the definition of severe sepsis triggering aggressive fluid resuscitation was based  on SIRS type criteria, rather than some form of volume assessment.


Bottom line?

Be cautious in aggressive fluid administration in pulmonary sepsis. What, I really dislike when people say “be careful” or “be cautious,” because let’s face it, that doesn’t really mean anything, does it?  It doesn’t tell you what to actually do… We are frontline clinicians, so I’ll say to limit fluid resuscitation in pulmonary sepsis.  2 litres up front?  Probably ok so long as I have a varying, mid-size IVC (maybe 10-15mm – arbitrary and chronic pulmonary disease and hypertension have to be factored in) and a decent heart, but I don’t want to get to the point of no longer being fluid-responsive. Rather, go to pressors a bit earlier, perhaps, and no need for ongoing “maintenance” fluids at 100-150 cc’s an hour – remember that 80% of this wonderful therapy ends up where we don’t want it to.





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