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: 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: 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
So something has been trotting around my head for a few months, and it actually stems from a small and not-so-proud moment I experienced during a conversation with my wife, while she was still a resident.
She was telling me some of the stories of the day, and how one of her supervisors who had a mixed outpatient and ED practice, always pushed them to use PO fluids, get rid of IVs and get the patients home. I kind of scoffed, in a sadly typical acute care physician mode, saying how you had to be a bit more aggressive and give them IV fluids to revert their dehydration a bit faster.
Then I caught myself. Hmmm. What exactly am I saying this (con brio) on the basis of. Knowledge, or belief? I tried to find knowledge but came up woefully short. It seems I’m doing this out of habit, what I’ve seen/learned/believed in the two decades since someone handed me an MD degree. Damn.
So, I do believe in evolution. We have evolved platelets to stop bleeding, fibroblasts and osteoblasts that can fix bones, white cells that go mop up the messes, and all kinds of other good stuff. One thing we do NOT have is small openings in vascular structures that allow unprocessed, man-made fluids directly into the bloodstream. We make these. We insert tubing into normally sterile environment and infuse a vast number of medications directly into this fragile matrix of cells and organic colloid – with the best of intentions.
In our physiology, however, the ONLY way fluid ever enters the vascular spaces is by diffusion from the outside of the endothelial cell into the lumen, molecule by molecule and ion by ion.
So let me seemingly diverge for a bit…
Prior to the 1970’s, restricting oral intake was a “cornerstone” therapy of diarrheal illness, due to the pervasive belief that the GI tract needed time to heal and recover before resuming normal function. This was felt to be crucial. Hence, only IV therapy was used (in developed countries), and in the underdeveloped world, the death toll was appalling – especially among children. In the 40’s, Dr. Darrow of Yale started actually studying the GI tract fluid and electrolyte issue, and advocating oral rehydration with mixed fluids. He was able to bring infant mortality radically down in his practice, but it would take over twenty years before a groups started to formally look at this in the 60’s. Finally, in the late 70’s, the WHO pushed this out into the field, and the childhood worldwide mortality from acute diarrheal illness dropped by over 70%, from over 5 million deaths a year to a bit over 1 million – at that time.
Oral Rehydration Therapy (ORT) is now felt to be one of the most significant advances in modern medicine. Compared to that impact, all the critical care and cardiology trials are about as significant as a drop in a bucket. We’re not talking about composite end points and subgroup odds ratios of 0.85…
For a great review on this check out The History of Oral Rehydration Therapy by Joshua Nalibow Ruxin (google it). A great story of science and humanity, good and bad.
So, back to 2015 ED/ICU’s.
The question now becomes the following: why – in the presence of a functional gut – do I choose to entirely rely on non-physiological IV fluid resuscitation?
I can already hear the roars and the outrage and the cries of heresy. And heresy is certainly what this is (Heresy is any provocative belief or theory that is strongly at variance with established beliefs or customs – Wikipedia). But that doesn’t make it wrong.
So I would ask everyone – particularly the naysayers, to examine their knowledge and see if they actually have any at all that supports the strong conviction that IV fluids are the way to go in ALL cases (my N=1 principle precludes going for the one-size-fits-all therapeutic approach).
Now everyone agrees that, once patients are better, they should be on feeds with little maintenance fluids. I don’t think many will debate that. So that should be the basis to wonder whether, in the presence of a functional gut, a variable proportion of fluid resuscitation in acute illness should be enteral…
I’ll let everyone digest that.
Comments more than welcome.
More to come in Part 2.