73 yr old woman recovering from septic shock with abdominal distension and difficulty tolerating enteral feeds…
what do you see?
scroll below for the answer…..
Extensive third spacing from resuscitation has resulted in bowel edema and ascites. Another “benign” effect of massive crystalloid use… A bedside 22g US guided tap confirms benign transudate.
A 70 year old man with cough and fever…what do you see?
scroll down for an answer!
The ultrasound diagnosis is of a consolidation with a small pleural effusion. This can be referred to a “hepatization” as the appearance becomes quite similar to an unaerated organ. A sonographic air bronchogram is seen as well. Clinical correlation with the history and bloodwork strongly suggests a pneumonia.
For students or residents rotating though Santa Cabrini’s ICU, I will be attaching here a number of important articles – and adding to it frequently – which you should be familiar with and aware of. Please read them as we will undoubtedly be discussing these topics.
Fluid resuscitation in septic shock
Sepsis in European intensive care units_results of the SOAP study.
Congestive RF in CHF – Mullens
Thanks,
Philippe Rola
I’ll soon start putting up interesting bedside ultrasound loops and images (as soon as I can get this software figured out…), in the meantime, if anyone is interested, we have a casebook which can be found on the CCUS website (http://www.ccusinstitute.org or an e-version on iTunes (https://itunes.apple.com/us/app/50-case-studies-in-bedside/id599201706?mt=8).
thanks!
So here’s a common enough clinical scenario: An elderly patient with CHF presents in exacerbation, requiring significant oxygen and eventual NIPPV. He is admitted to a critical care bed. The next day, it’s noted that his creatinine has almost doubled. He remains on NIPPV. The intensivist is hesitant about how aggressively to pursue diuresis: he’s worried about worsening the “low-flow state” and the renal function.
I know I grew up hearing that as a resident, and never questioned it. On the surface, it makes plenty of sense. Someone with CHF has a “bad heart”, pre-renal failure is a definite entity, so why not?
So let’s examine those assumptions. First of all, not all patients who present with CHF actually have a bad ventricle, some may have valvular heart disease, hypertension with elevated filling pressures, etc… Secondly, few of our CHF patients are really in a severe “low-flow state”, since that would essentially be cardiogenic shock, a very different entity, even if along the same spectrum. More importantly, however, the renal autoregulation curve is actually broader that most of the rest of our tissues and organs. That makes it unlikely that, in someone normotensive (as most patients in CHF tend to be), worsening renal failure is attributable to a “low-flow state”. The ARF attributable to a low-flow state – which we see often enough – is the organ failure resulting from shock: shock liver, shock kidneys, etc…
So…what could it be? Let’s continue to apply basic physiological principles. What is the pathognomonic feature of CHF?
Congestion: pedal edema, ascites, effusions, anasarca, etc…
What if we had…congestive renal failure?
I have to credit a bright colleague of mine, Dr. Jason Fung (http://kidneylifescience.ca), for putting me on that track. As a bedside sonographer, what I could see in most of these patients is that their IVCs were still really full, and that most didn’t have other clinical signs of poor flow such as cool extremities and decreased mentation. And given that they were still in significant respiratory failure, I felt they needed diuresis. Also, the full IVCs suggest that these patients are on the flat part of the Starling curve (after all, that’s what the fluid retention causing CHF is trying to do!) and that they should not suffer a drastic drop in cardiac output with ongoing diuresis.
Well, Jason was the first to point out to me that the elevated IVC pressure (CVP) is directly downstream from the kidney! And directly by a couple of inches, the length of the renal veins! I have to say that was an embarrassing lightbulb moment, but a lightbulb moment nonetheless.
So let’s review renal blood supply and flow physiology. As is the case for any organ, the following applies:
Q = (P art – P ven) / R
where Q is renal blood flow (RBF), P art is MAP and P ven is CVP, and R is the renal vascular resistance.
Let’s keep that in mind.
Uniquely, the kidney has two set of arterioles which modulate the GFR and allow for the celebrated autoregulation curve. The resistance of each is controlled by the number of factors, hormones and drugs.
The reason P ven is CVP is that the renal vein drains directly into the IVC, which drains in turn into the RA, the pressure is the same. Now some of you may have read my rants against CVP in some of my posts (see https://thinkingcriticalcare.com/2013/09/18/96/), but that is in reference to its use as a marker of preload and volume responsiveness. When the answer one is seeking is the downstream venous pressure, barring some pathological venous obstruction, CVP is it.
Hence, the higher the CVP, the lower the RBF.
This makes complete sense, but how often has anyone heard this mentioned in the management of renal dysfunction in CHF patients? As in the case for many things in medicine, we often forget (or are not taught to) link basic physiology (all that medical school stuff…) with clinical pathophysiology (…the “real” world).
Well, it turns out that fortunately, a bunch of smart people have been looking into this matter, and the best study in my opinion is by Mullens et al (JACC vol 53, n 7, 2009), which reveals a clear increase in prevalence of worsening renal failure with increasing CVP, but more interestingly, the lack of significant association between cardiac index and worsening renal failure, which is the “low-flow” traditional hypothesis. The most clinically important finding in this study, however, is their finding that failing to reduce the CVP to below 8 resulted in a 51% incidence of renal failure (vs 18% for those patients who were reduced to a CVP < 8mmhg).
An excellent review for this was recently published by Gnanaraj et al (Kidney International 83, 384-391, mar 2013), which reveals a fairly strong association between an elevated CVP and renal dysfunction.
So it seems fair to conclude that congestive renal failure is an under-recognized clinical entity that is commonly untreated (or even improperly treated) due to unfounded and unphysiological concerns.
Now something our group will be focusing on is a study on the use of IVC sonography in the assessment of CHF-associated renal failure. We believe that IVC ultrasound will provide a better, simpler and less invasive method to assess renal congestion.
The use of IVC ultrasound in CHF would not be new: Goonewardena et al (JACC Cardiovasc Imaging 2008; 1, 595-601, or imaging.onlinejacc.org/article.aspx?articleid=1109299) found that IVC size at discharge was the best predictor of readmission. In other words, if someone didn’t get your IVC down below 20 mm, you were much more likely to be readmitted.
As an ICU physician, I rarely discharge patients home. But I do make sure I get IVCs into a normal range (below 15mm generally) before my CHF patients leave my unit, and, especially recently, I do make sure to continue diuresis when faced with a distended IVC with little variation and worsening renal failure.
This is certainly a topic that merits further study, but I think there is enough good evidence and physiological rationale to hang up those old beliefs in a dark closet and start treating congestive renal failure.
Please let me know what you think, what your practice experience is, and if you have anything else to add!
thank you,
Philippe Rola
So here is the first in a series of mini-talks geared towards having us think about fluid resuscitation, which, for those in acute care of almost any type (ER, wards, ICU, anasthesia, surgery, etc…) is part of our daily routine. And that’s exactly what it shouldn’t be, routine. It should be carefully thought out and adapted to each individual clinical situation we’re facing.
So I’ve decided to approach this from a completely different angle, not looking at what we do, what’s available, and see what has been stacked up against what, etc, etc… Instead, I’ve decided to start the discussion from a completely theoretical standpoint and talking about something that doesn’t exist: The Ideal Resuscitation Fluid.
Please, let me know your thoughts!
Philippe
(sorry the last 40 seconds were cut – now the “full” 5 minutes are up! apologies, I am techno-challenged!)
Hi,
So here’s a short intro to what I’ll be calling the N=1 Podcasts. Why N=1? Because each patient we treat is just that, a single patient. Not a cumulated average result of a hundred or a thousand different people, and should be treated as such, meaning, know the good evidence that’s out there, be able to properly assess your patient and tailor your therapy appropriately.
Hope you like the concept, first real one should be up shortly!
Thanks
Philippe
I’m putting this question out there so that everyone can reach into their bag of tricks and tell me “this is how I know how much to give.” Because I really do want to know.
To the best of my knowledge, that answer does not exist.
Of course, someone can say “we have to give 2 liters of crystalloids!” loudly and clearly, raising a fistful of papers and guidelines where it is printed, black on white.
Now lets think about exactly what that question is really asking, which is: how much fluid can I safely give my patient to improve the hemodynamic status without a significant cost in terms of complications, both short and long-term?
What are the implications of this statement?
a. My patient must be volume responsive.
b. I must not cross the threshold of excessive fluid administration.
c. I must KNOW that fluid loading is the most appropriate therapy for my patient.
Now when you start looking at those questions and really wondering whether you have a definite answer for all of them, if becomes quite difficult. It is much easier to say “well, such-and-such study says people do better if I give them x amount.” This is probably true, that most people do better with a certain amount of fluid. But not everyone, because there are a lot of variables within those three questions.
Lets go through these questions:
My patient must be volume responsive – this is worth an entire podcast/lecture/article and there are a number of technologies and techniques out there which have both physiological and practical merit. I’ll get into that soon, but the short answer is that a passive leg raise (PLR) coupled with good cardiac output monitoring would be the “gold medal,” bedside ultrasound of the IVC’s global dynamics would be the “silver medal” and most of the rest would be “bronze medal” material at best. I won’t even mention the traditional physical exam or history or labs, not only do they not make it onto the podium, they didn’t make it into the stadium. I have to thank Scott Weingart (www.emcrit.org) for the sports analogy which I think is really excellent, since making the podium is actually pretty good and the difference between the three medalists may not always be that great.
I must not cross the threshold of excessive fluid administration – this one is dicey, because that’s where you have to factor in the patient’s oncotic pressure, hydrostatic pressure, both of which can be somewhat estimated, but mostly the degree of leak or “capillaritis”, both systemic and local, and that, at initial presentation, is impossible. The best you can do is a very broad classification from not too leaky to really, really leaky. And that’s not science. Now my good and highly esteemed friend Daniel Lichtenstein (the true founder of bedside ultrasound) published the FALLS Protocol, which basically says you can fill someone up until the appearance of B lines (during resuscitation) by lung ultrasound is certainly right that you should stop at this point, but I would contend you probably need to stop a bit before the edema is actually happening, especially since, in all likelihood and especially with crystalloids, the extravasation will continue for a while. The SOAP and VASST studies clearly showed an association between positive fluid balance and mortality, all other factors adjusted. Hence, this question is almost impossible to answer with knowledge. An educated guess is the best we can hope for.
I must KNOW that fluid loading is the most appropriate therapy for my patient – now this is almost philosophical and anxiety-arousing, because it forces us to challenge the fundamentals of our therapy. In certain cases, it is quite clear. If someone has been hemorrhaging or overdiuresed into shock, it is fair to say that you know they need fluids. However, if we are dealing with a vasodilatory circulatory failure, why do we feel compelled to treat it with a therapy best reserved for hypovolemic circulatory failure… Hmmm. Food for thought. Perhaps we can start by looking back and seeing what the basis is for our almost unshakeable beliefs that fluids are benign and that vasoactive medications are evil… But that is for the near future.
Please, let me know what you think. I hope someone disagrees strongly.
Philippe Rola
I was recently scanning the literature in preparation for our symposium, and came across what should have been a 2003 instead of a 2013 publication in the March issue of the CCM Journal, entitled “Point-of-Care Ultrasound to estimate Central Venous Pressure: A Comparison of Three Techniques.”
I have to admit this is a pet peeve of mine, from the standpoint of a clinical physiologist, which is, as far as I’m concerned, what any physician looking after critically ill patients should be, at least some of the time.
So our real question is: is my patient fluid-responsive? And perhaps a corollary question would be: is he fluid tolerant?
As a longtime bedside sonographer, physiology, experience and slowly growing evidence all support my using IVC sonography as a tool to assess volume responsiveness. It isn’t perfect, and personally, I find the common M-mode, two-point measurement to be inadequate compared to a global assessment of the IVC, but it certainly is far closer to “the truth” we seek than CVP.
This then begs the question: why on earth would we be seeking to correlate one type of data to another which is clearly more removed from “the truth” we seek?
The use of CVP is largely cultural and deeply ingrained. There are some limited ways and pathologies in which it can be useful, but not as a measure of preload. My friend Paul Marik published a piece that was both enlightening and entertaining in Chest a couple of years ago which I would have thought would have been the final nail in the coffin for the use of CVP as a preload tool, but it endures…even in the latest surviving sepsis guidelines…
A testament to religion over science.
Philippe Rola
note that this was first posted in my buddy Matt’s awesome website pulmccmcentral (http://pulmccm.org/2013/critical-care-review/why-do-we-bother-to-check-cvp/) please check it out!
First of all, I would like to commend those involved in the Surviving Sepsis Campaign’s Guidelines. It is a tremendous endeavour that, without a doubt, has heightened awareness and their growing implementation has and will save many lives.
I would, however, also like to point out that guidelines are exactly what the term implies, and not necessarily a gold standard to aspire to and adhere to in religious fashion. The reason this is so is the inherent variability in human physiology and pathology. If, out of 100 patients a treatment would help 10 but harm 1, the numbers and studies would clearly support its broad use. We’d win more than we’d lose. However, as physicians, we treat the one patient in front of us, not the hundred, so I find it difficult to believe that such blind application of a recipe would be the most Hippocratic practice to apply.
We know that our patients are widely different, and around the corner is point of care immunology that will tell us, in all likelihood, that even patients we think are similar on the surface will have widely different immune profiles and will respond to treatment differently.
There are a few recommendations which, to me, make little physiological sense, particularly in certain circumstances:
I don’t think it necessary to belabour the point about CVP. As a static measure, CVP has clearly been disproven to have any relevance in predicting volume responsiveness. Its persistence is a testament to cultural faith rather than science.
I would find it unethical to blindly bolus large amount of crystalloids (which we all know end up 70-80% extravascular) in a patient when it takes about 10 seconds to rule out a pre-existing, septic cardiomyopathy or a volume-intolerant state. Even more so when dealing with pathologies where third-spacing is a concern (pulmonary and intra-abdominal pathologies) since those leaky capillaries is where most of that fluid resuscitation will end up. Yes, I am implying that a worsening chest x-ray is not always and only due to worsening disease… Physiologically, perhaps non synthetic colloids or hypertonics may be a better option…
I would find it equally unethical to blindly put a patient on dobutamine who may have hyperdynamic ventricles and possibly still a volume-responsive state. Again, determining this takes seconds.
Yes, clearly I admit to a bedside ultrasound bias. It allows us to look inside our patients. Isn’t that what we’re always trying to do?
I can already hear voices and keyboards claiming the “lack of evidence,” and they would partly be right. That evidence is slowly but surely growing.
Unfortunately, point of care ultrasound has come of age in the era of evidence based medicine, and, as such, is required to “pass” that scrutiny whereas most of what is currently being done was “grandfathered in” and given a bye. I would be interested in seeing the compelling evidence for the use of a stethoscope.
The evolution of evidence based medicine is an interesting scientific, commercial and social development. From the positive study publishing bias to the general lack of epidemiological knowledge of our community, and without mentioning the darker side of research and publishing, it is unfortunate that almost every statement by a physician, to be taken seriously, must be backed by a hand raising a publication. And how many of those do we see torn down a month, a year or five later, thoroughly disproven? The pendulum of evidence-based medicine has perhaps swung too far…
Note that I’m not trying to discredit the countless number of truly well-designed and well-executed studies that contribute immensely to medicine – which would otherwise be reduced to little more than expert opinion – just that careful analysis of both the evidence and the case at hand is primordial.
I think that as physicians, it is our duty to look very closely at the individual patient, the care of whom we are privileged to have as a responsibility, and individualize our treatment plan to his specific problem given his specific physiology, and not blindly implement a recipe, even if it would happen to be the right one 9 out of 10 times.
Philippe Rola
please note that this was first posted on september 5th, 2013 on my buddy Matt’s website, pulmccm.org (http://pulmccm.org/2013/uncategorized/surviving-sepsis-guidelines-useful-patients-deserve-individualized-care/)
Go visit, its great, and you can see some fun follow up comments, too!
Glenn says:
it’s a sensitive decease in a sensitive time. Time is of the essence in treating septic shock and severe sepsis. If you wait for primary MD to individualized the care for these patients,it’s probably too late.EGDT save lives.
Thanks for commenting Glenn, and I can’t agree more. EGDT does save lives when compared to the usual care of 2001 (see my latest post on the ProCESS trial as that may no longer be the case in some institutions), but the mistake is strict adherence when you do have the capabilities to detect conditions where a protocol “violation” would be beneficial to the individual patient in front of you. Again, I’m not knocking EGDT, it was a great step, but in a set of stairs we have to keep climbing.
Philippe
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