Fluid Stop Points! More POCUS goodness from Korbin Haycock. #FOAMed, #FOAMcc

I am really enjoying this exchange, and I think it is in the true spirit of #FOAMed to foster these discussions, as we have the opportunity to combine and fine tune our understanding of a topic from several really bright people’s view and experience. 

Korbin:

Jon-Emile, excellent points and insight. I should clarify a couple of my comments. To be specific, by “renal vein flow” I am referring to intra-renal venous flow. Apologies for my imprecision! Thanks for pointing that out.

Yes, a lot of these renal and portal Doppler patterns are surrogates of CVP. But I don’t think any of us would use CVP in isolation these days to make any decision what-so-ever on whether fluids were indicated in our patient.

Also, to clarify, I am not using intra-renal venous flow or renal resistive index as measures of non-fluid responsiveness. Rather, I use these measures as a stop point for attempting to solve the patient’s hemodynamic dysfunction with crystalloid regardless of whether or not my straight leg test tells me the patient is still fluid responsive.

And that is a key re-iteration to me. It is important to set these stop points and not only look at whether the cardiac output can be maximized. This has been tried. And failed. Let’s remember that sepsis is not inherently a disease of low flow. It isn’t cardiogenic or hypovolemic shock at the core.

My rationale for the strategy of using intra-renal Doppler, E/e’, and Lung US (now, I can include portal vein pulsatility) as a stop point for IVF administration is that I think the patient is best served to avoid iatrogenic edema of the upstream organs, primarily the lungs and the kidneys. These are the two organs (maybe you could put the endothelium in this category as well–glycocalyx being a whole other can of worms!) most easily damaged by the chase for optimizing every bit of fluid responsiveness. We have good evidence that getting wet lungs and swollen, congested kidneys is a bad thing, and we have these tools to hopefully warn us when we are pushing things too far.

Absolutely. And the whole glycocalyx is something to keep in mind, even if only to me mindful to disrupt it as little as possible.

Of course renal resistive index, intra-renal venous flow, portal vein pulsativity, and whatever else you like will have limitations and confounders. As long as you understand what can cause abnormalities with these tools, you can make an educated guess as to what’s going on. If our creatinine is off and our RRI is high, but intra-renal venous flow and portal vein flow is normal, perhaps the RRI is caused by something other than renal congestion, like ATN. If the portal vein is pulsatile, but the Doppler patterns of the hepatic vein, kidney and the heart look ok, maybe something else is wrong with the liver. But, if all our modalities are in agreement and pointing to congestion, we should perhaps believe that it’s congestion and stop the fluids. 

That is an awesome approach to integrating RRI. I’ve been toying with it for the last couple of days, and much thanks to Korbin, I think that the limitations of RRI can be overcome by using the rest of our clinical and POCUS data.

It isn’t a hard technique, though in some patients getting a good signal can be tricky.

I think that the kidney, being an encapsulated organ, and the fact that much of our crystalloid ends up as interstitial edema, the kidney will develop sub-optimal flow patterns before CVP would cause congestion. The same is true regarding the lung, except that it’s just related to increased pulmonary permeability due to inflammation. Regardless, the idea is to save organs, and the earlier you can detect the problem, the sonner you can stop battering the more delicate organs with fluid.

As I think we have all mentioned, you really have to look at the whole picture, and put it together to tell the story of what is wrong, so we can logically and thoughtfully treat our patients.

I really appreciate this discussion. Thanks!

 

 

Thanks to Andre, Jon and Korbin for making this very educative for all!

Cheers

 

Philippe

 

ps don’t miss the POCUS Workshops on venous assessment at  !!!

Portal Vein POCUS: A Reader’s Case and a Follow-Up to the Denault Discussion

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.

Kudos. 

 

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…

cheers

 

Philippe

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!

Don’t miss Andre running a POCUS workshop on PV/HV at  next april!

Philippe

 

A Discussion on Fluid Management Protocols with Rory Spiegel. #FOAMed, #FOAMcc, #POCUS

 

So Rory (@EMnerd) is in the process of working on a fluid resus protocol for Shock-Trauma, and asked me if we could have a chat about it, which I feel very honored for – and had a brief impostor syndrome crisis – but it’s always great to chat with people who are really bright, really physiological and after the same goal, to make patients better. Always a pleasure to chat with Rory, so here it is.

I really can’t wait to see their protocol, because I think this is a huge and complex endeavor, but has to be done.  I will try to put pen to paper (probably really pixels to a screen but that doesn’t sound as good) and put what I try to do for fluid resus on a diagram of sorts.

Love to hear comments and questions.

PS please skip the first 30 seconds which are a technical blank… Ièm not tech saavy so can’t trim it!

cheers!

Philippe

 

A great comment by Dr. Korbin Haycock

One issue to consider is the degree of pulmonary vascular leakage. If, as in the case of sepsis, the pulmonary vasculature is more prone to the development of lung interstitial edema, lower LVEDP’s possibly will still result in as much lung wetness as higher LVEDP’s. Therefore, reliance of E/e’ ratios may not be the best measure of a fluid resuscitative endpoint in sepsis (and aren’t we really talking about sepsis resuscitation here?). I believe that it’s relatively clear that EVLW will adversely affect outcomes, but pushing for every bit of increased stroke volume/fluid responsiveness is less clear to be beneficial, even if it makes sense from a DO2/VO2 perspective (which may not be the real issue in sepsis anyway, as mitochondrial utilization of the DO2 provided may be the real problem, rather than DO2/VO2 balance). If the assumption is that the kidneys and lungs are the most delicate organs and most at risk to over aggressive fluid administration, and will impact mortality/LOS in the ICU, perhaps a combined strategy of attention to E/e’ ratios, development of B-lines, or the renal resistive index increasing would be a signal for a different strategy rather than fluids to increase venous return (i.e. switching from crystalloids to norepinephrine or vasopressin if the CO is elevated and will tolerate a minor ding from the increase in SVR). If any of those three variables indicate a problem, stop the fluids, switch to a vasopressor. If the issue is the CO rather than the SVR, use an inotrope instead. Of course RV/LV interactions as mentioned in the comments above must be considered. No point in giving fluids to an empty LV if the RV is failing–you’ll just congest the kidneys.

Tom Woodcock: The Revised Starling Principle and The Glycocalyx! #FOAMed, #FOAMcc

Screen Shot 2016-08-05 at 11.57.11 PM

So today, I had the chance of having a private tutorial with Dr. Thomas Woodcock (@thomaswoodcock) about the glycocalyx and the revised Starling principles.  For anyone interested in fluid resuscitation, this is an area you have to delve into. The basic principles we all learned (which are still being taught) are basically the physiological equivalent of the stick man we all started drawing as toddlers: overly simplified and far from an accurate representation of reality.

Now my first disclaimer is that I have been a colloid supporter for many years. My physiological logic for that had been to minimize the crystalloid spillover into inflamed/septic areas, particularly the lungs and abdomen, when those are the septic sources. However, I was likely misled by my education and lack of knowledge about the endothelium.

So I stumbled upon the whole glycocalyx thing a couple years ago, and this prompted me to try more enteral fluids – the only way fluids normally ever enter the vasculature – but little else. Aware that it’s there, but unsure what to do about it.

Now a year and a half ago, Andre Denault, my closest thing to a mentor, casually dropped the line to me about albumin not working. “Don’t use it. It doesn’t act the way we think it does.”  But it was a brief chat, and I didn’t get to pick his brain about it.  Just a few weeks ago, I discuss with Jon Emile (Kenny), and he’s coming to the same conclusion.  Damn. I’m finding it a bit harder to hang on to my albumin use, which is beginning to look a bit dogmatic and religious.

Here is Jon-Emile’s take on it – a must-read.

Here is Tom Woodcock’s site and article – another must-read.

And here is my discussion (in two parts) with Tom (to skip the silence, skip forward to about 30 seconds into each – sorry my editing skills are limited!)

 

Bottom line?

Probably stick to isotonic crystalloids, and some hypertonics.

 

Love to hear some thoughts!

Cheers

 

Philippe

 

 

CCUS Institute Bedside Ultrasound Mini-Fellowships. #POCUS #CME

The personalized CCUS Institute’s Mini-Fellowships (CME-eligible) are focused on bedside ultrasound and designed to take clinicians with some degree of proficiency in basic ultrasound to a whole other level. The opportunity to follow a seasoned clinical ER/ICU sonographer and see actual cases, learn the clinical integration of ultrasound data into decision-making is a unique one, outside of a handful of residency programs whose faculty includes experienced bedside sonographers. Basic how-to courses are great, and certainly the first step for those clinicians adding ultrasound to their armamentarium, but what we have seen, sadly, is after initial enthusiasm, many don’t really pick up the probe because the confidence to “make the call” simply isn’t there. Yet.

In a sense, it’s almost as if, as medical students, we’d read Bates, practiced physical exam on each (more or less normal ) other, and were then set out to make diagnoses and treat without having residents and attendings around to confirm our findings a few times, until we got the hang of it. Hmm. That would be rough.

Some physicians are fortunate enough to practice in a center where there are a few “veterans” of bedside ultrasound and can gain some acumen that way, but others may be the ones spearheading their institution into the 21st century, and it is from the comments of several of those, attending the CCUS Symposium (2008-2014 – perhaps a return in 2017) asking for the possibility of shadowing some of us, that the Mini-Fellowships came to be.

Mini-Fellowship Structure

Montreal Mini-Fellowship: Participants shadow one of our instructors (ICU attending) during the regular working days and discuss the cases and ultrasound-relevant aspect of each case (more often than not the case in entirety), and are able to practice their ultrasound skills. The duration is flexible although we generally suggest a minimum of two or three days. Each day would usually be about 6-8 hours, some may be more.

Toronto Mini-Fellowship: Participants get a dedicated and highly experienced preceptor (Dr. Edgar Hockmann) who is not on clinical service but with access to the ICU patients, and will provide a structured and dynamic session adapted to the participant’s needs and abilities.

The case exposure will be mainly ICU as well as ER and ward patients. The focus will be on acute care issues. After two days, participants who had a basic ability in ultrasound should be fairly comfortable with assessing volume status, cardiac function, perform lung ultrasound, be able to identify and assess intrathoracic and intr-abdominal fluid collections, assess the kidneys, bladder and gall bladder, measure optic nerve sheath, assess carotid flow and some may have exposure to trans-cranial doppler. The focus may be shifted depending on a participant’s interest.

This takes place in Montreal, Quebec or Toronto, Ontario, Canada.

Participants will have the opportunity to work with handhelds, midrange and high-end ultrasound devices.

Space is limited as we can generally only accommodate 1-3 participants per month.

 

CME

So, great news, finally went thru the CME process and lo and behold, the Mini-Fellowships qualify for 25 Section 2 credits (regardless of the length) and 3 hours of Section 3 credits (per day of fellowship). For you americans:

Through an agreement between the Royal College of Physicians and Surgeons of Canada and the American Medical Association, physicians may convert Royal College MOC credits to AMA PRA Category 1 Credits™. 

Bonus!

Upcoming participants will also receive a copy of the forthcoming handbook:

covercover-back

Requirements 

Please have basic experience in bedside ultrasound. We don’t want to teach you about depth and gain. We’re happy to fine tune your views but not to introduce you to the main cardiac views. It would just be wasting your clinical time. We’re here to show you how to assess pathology and integrate your findings into clinical decision-making. Take the basic group course to learn the views, or be self-taught from youtube/iphone and practicing on your patients. You don’t have to be great, but to get the most out of this experience it shouldn’t be your first time holding a probe.

Registration

email me at philipperola@gmail.com or reach out on twitter @ThinkingCC

Tuition

Montreal Mini-Fellowships: 550$ CAN / 450$ USD per day for 1 physician, 450$ CAN / 375$ USD per person per day for 2, and 375$ CAN / 325$ USD per person per day for 3 physicians (maximum)

Toronto Mini-Fellowships: 800$ per half day (4h).

100% refundable until you start. Even if you don’t show up. Really. We’re not in it for the business. We get to go home earlier if you don’t come.

Testimonials:

« I have had the chance to participate in a shadowing experience with Dr Rola at the Scarborough General Hospital ICU during two days in 2013. As a general internist and assistant program director, this experience really opened my eyes regarding the use of bedside ultrasound in general internal medicine and for IM residents. I think I would have benefited more of this experience if I had done more training previously, and I encourage future participants to do so. However, I came back from this experience with a very clear idea of the benefit of CUSE for my patients and for our residency training program. I really saw how ultrasound was used ‘in action’, in a much more realistic way than what is usually shown in CPD meetings. I also saw its limitations and the skills I needed to develop to generate good images (not something you can learn over the weekend!). Since then, I participated in formal trainings and licensing activities (more than 250 supervised US on acute care patients) and now practice bedside ultrasound autonomously. We now offer a bedside ultrasound training for our residents with the help of the emergency medicine department and an ultrasound-guided procedural simulation lab. Nothing in CPD has improved my practice and benefited the health of my patients as much as bedside ultrasound training. »

Alexandre Lafleur, MD, MSc (Ed.), FRCPC
Spécialiste en médecine interne
CHU de Québec – CHUL
alexandre.lafleur.1@ulaval.ca

“Thank you very much for the exposure and teaching offered via the CCUS “Mini-Fellowship.”  These few days allowed me to enormously improve my mastery of bedside ultrasound in clinical decision-making in critical care. I recommend the experience to clinicians already having experience in bedside ultrasound, but who feel they could benefit from the expertise of an instructor to attain a level beyond basic courses and available textbooks.”

Mathieu Brunet, MD, GP/ER/ICU, Magdalen Islands, Quebec, Canada

“The CCUS Mini Fellowship In House training is very essential in to experience the echo skills that we get from the courses,being supervised in ICU will offer the chance to be corrected and get real live practice/exposure by being at the bedside and learn what is priority in echo for the best of patient care. The in-house experience is very helpful, practical, I recommend this training to any physician involved in ER, ICU, CCU, Anesthesia and rapid response team.”

Joe Choufani, MD, Internal Medicine/Cardiology, St-Lawrence Health Association, NY

“Thanks for everything. I really appreciate you sharing your vast fund of knowledge with me.”

Sean Sue, MD, ER, Philadelphia

CME

So, great news, finally went thru the CME process and lo and behold, the Mini-Fellowships qualify for 25 Section 2 credits (regardless of the length) and 3 hours of Section 3 credits (per day of fellowship). For you americans:

Through an agreement between the Royal College of Physicians and Surgeons of Canada and the American Medical Association, physicians may convert Royal College MOC credits to AMA PRA Category 1 Credits™., #CME

Enteral Fluid Resuscitation (EFR): Third-world medicine in the modern ED/ICU? (ORT part 2) – #FOAMed, #FOAMcc, #FOAMer

Screen Shot 2015-02-10 at 7.15.16 PM Enteral Fluid Resuscitation in the ER/ICU? For those who did’t come across it, part 1 of this series can be found here: http://wp.me/p1avUV-e8 So back to bringing the basics back to our ultra-tech world… Can I actually use this field technique in my bright and shiny ICU? Can I use oral hydration as a cutting edge therapy in my life-and-death patients? Sounds strange. Sounds like I should be using a precise device which lets me know exactly how much fluid has gone into my vascular space, because that’s where I want it to go, and I want to control exactly the composition of my serum electrolytes, etc, etc.  We like to control. But do we really? We actually have absolutely no idea how much of a fluid bolus remains intravascularly, in any one patient.  It will depend on his/her pre-existing venous filling, his serum protein levels, the integrity of the glycocalyx, and probably a few more things we don’t even know yet.  And as I rapidly distend atria, I release ANP which damages my glycocalyx further. Hmmm… As I mentioned in the last post, the only way fluid enters our vascular space is via the endothelial cells at the level of the GI tract for the most part. All “venous access” is iatrogenic. I do believe that the endothelial cells, by and large, will do a better job – in concert with the kidneys and rest of the blood cells – of controlling the plasma than we will, if given the chance. What logically follows is that, in the presence of a functional gut, I can consider using Enteral Fluid Resuscitation – that is, giving fluid for hemodynamic purposes, not just “maintenance,” by an enteral tube of some sort. So what could I give?   What’s in it? The current reduced osmolarity WHO/UNICEF formula contains approximately the following: Screen Shot 2015-02-10 at 7.24.28 PM So, lets take a closer look at the players: 75 mmol/l of sodium, 75 mmol/l glucose, some potassium and the rest basically to balance the electroneutrality. The whole thing hinges on the glucose-sodium cotransporter, which drags sodium and water in along with the “desired” glucose.  Optimal water absorption takes place with Na between 40-90 mmol/l, glucose 110-140 mmol/l, and an osmolality around 290.  A higher Na may cause some hypernatremia, and a higher osmolality may result in water loss. Here is our friend the enterocyte illustrating just how this kind of solution will allow sodium absorption: Screen Shot 2015-02-10 at 7.31.54 PM   Do-it-Yourself Enteral Fluid Resuscitation Solution: So I’ve got a neat DIY option if I don’t want to break out the powder and start mixing in the middle of my unit: 0.45% or 1/2 NS plus 30 ml of of D50 would give us Na 77, Cl 77 and glucose 74, with an osmolality of 228. Pretty close. That’s what I’ve been using. How much? Well, I like the slow and gradual. Some of the rehydration data out there supports some pretty huge amount of fluids, but this has been done mostly in healthy but dehydrated athletes – not the case for most of our patients. I’ve been going with 250ml every 1-2h, as – for now – an adjunct to IV fluid therapy. This is conservative and completely arbitrary, but essentially a glass every hour or two certainly doesn’t seem excessively taxing. Who can I give this to? You do need a functional gut, so for now, my criteria are (1) essentially normal abdominal exam, (2) obviously no recent bowel surgery, (3) a patent and functional gut as far as I know, (4) no ultrasound evidence of ileus or gastric distension. But how can I be sure it’s going in the right place?  I can’t. Just like I can’t be sure my IV fluids are staying in the right place. But I do check – IVC ultrasound (gross but better than skin turgor!), urine output, HR, BP, etc. None of those are perfect as they are all multifactorial, but that is the nature of the game. The other thing I check is gastric distension by bedside ultrasound every couple of hours – obviously, if I’m just getting a fluid filled stomach, there’s no point, and eventually harm may ensue. When should I stop? Whenever you clinically decide you don’t need/want any further fluid resuscitation. As far as I am concerned, might as well stop the IV infusions first and have the enteral going after – in the end, you are hoping your patient will go back to drinking and not require a PICC line for discharge, aren’t you?  So you stop when the patient does it on his or her own. I’d really like to know if anyone out there is doing something like this. It would be great to compare notes and evolution. Drop a line!   cheers, Philippe