Fluid Resuscitation of Trauma Patients: 0.9%NaCl (saline) or Plasma-lyte?

I am not a trauma surgeon. I am not a trauma physician. I do not take care of trauma patients in my current practice. I did several rotations in the trauma intensive care unit during my fellowship training but by know means am I going to pretend to have the knowledge that my colleagues who do that every day have. The study I am going to be discussing today is a pilot study.

The authors were concerned about the metabolic acidosis that occurs from the elevated chloride concentrations in 0.9% NaCl which is 154mmol/L. Remember, reference values in the lab for chloride levels are between 98 and 109mmol/L. Also, there is data suggesting that an increase in chloride levels by just 5mmol/L could have deleterious effects on our patients. This hyperchloremic metabolic acidosis is not something new, we've known about its effects on the kidneys for decades now. I guess we've just been ignoring it.

I am a fan of whole blood to resuscitate trauma patients, but I my knowledge on the matter is weak. At the time being, patients receive a significant amount of crystalloids for resuscitation. The authors chose to use NS and plasma-lyte due to the fact that lactated ringers is contraindicated with blood products as it allows the blood to coagulate as it goes in due to the calciums effect on citrate.

Surgeons are trained, from my experience, to focus on base excess. When a patient you're taking care of them is sick, and you're giving them a call to give them the heads up of what's going on, one of the first questions you need to be prepared to answer is "what is the base deficit"? Plasma-lyte is a balanced salt solution that I have reviewed numerous times on instagram, my website, and youtube. Plenty of resources out there from me explaining this fluid. This focus on base excess is why they made this

They ended up with 46 patients enrolled in the study.

Plasma-lyte corrected the base deficit faster than 0.9% NaCl. Primary outcome achieved. Patients reached and remained in their normal acid-base physiology longer.

They also found that 0.9% NaCl leads to hyperchloremic metabolic acidosis, decreased serum bicarb levels, and worse base deficit.

Patients also had increased urine output with plasma-lyte compared to saline solution. There is some concern about whether gluconate causes some sort of increased urine production but this is not specified in this paper.

Some institutions worry about the added cost of plasma-lyte, which is approximately $1 on top of the cost of NS or LR depending on the institution and their contract. This study showed that providing plasma-lyte kept serum magnesium levels closer to normal (p=0.007). If you are a bean counter, you could potentially save some money by using plasma-lyte due to less cost of magnesium replacement. I may be stretching a bit but at least I am admitting that I'm stretching. The patients needed about 4gm of Mg in the NS group and no replacement in the PL group. I take back the part of me stretching. The authors state that the difference at their institution of cost between NS and PL is $0.76. 2gm of magnesium is $5.19. That means that PL may end up saving money and additional testing.

All in all, this is a pilot study. I have not personally seen the actual study. If you all have, feel free to correct me. This is not a full free article, unfortunately.

-EJ

Link to Abstract

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BiPAP should not be used in Immunocompromised patients

This was a post-hoc analysis of the FLORALI trial that I have reviewed before on this medium. In that study they compared patients who had hypoxemic respiratory failure by putting them on 1:1:1 on high flow nasal cannula (HFNC), standard oxygen therapy, and non-invasive ventilation (NIV aka BiPAP).

My interest was piqued in trying to find out what they defined as immunocompromised patients. They looked at patient with hematologic and solid malignancies, AIDS, drug induced, and steroid related. The etiology for the respiratory failure in these patients was mostly for pneumonia, whether opportunistic etiology or not.

To make it simple, they found that patients treated wit HFNC did better than patients who received NIV regarding rates of intubation as well as mortality.

Frat J-P, Ragot S, Girault C, et al. Effect of non-invasive oxygenation strategies in immunocompromised patients with severe acute respiratory failure: a post-hoc analysis of a randomised trial. Lancet Respir Med 2016;4:646–52.

Link to Abstract

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HYPERION: 33 vs 37 for targeted temperature management in cardiac arrest

I am going to be all over the place with this takedown. I’m a bit upset at what may happen as a result of this publication. I really wanted it to be a good study but it’s not. You’ll see why shortly. 

The good news is that there’s no difference in adverse effects to the patient by cooling them, just a lot of added cost. That’s my tidbit for those physicians who are going to take this data and run with it as if it’s gospel. 

My practice prior to this article was to do a normothermia protocol of 36 degrees after the NEJM trial from 2013. Is this one going to change my ways... from the outset it appeared as if it will, but, spoiler alert, it won’t. 

The objective of this study was to sort out whether we should cool our patients to 33 or normothermia of 37 in patients who suffer cardiac arrest with a non-shockable rhythm. 

Within the methods, they excluded patients who were down for >10 minutes prior to chest compressions. This is hard to determine many times as families are never quite sure. I complement the 25 ICU’s who recruited 584 patients in this study. The fact that they allowed patients to be recruited for 300 minutes from their arrest time gives us insight that you don’t have to make the determination immediately on whether you have to cool the patient. Then again, such a high percentage did poorly that we don’t really know what’s the best time to get started. 

In how they rewarmed patients, it’s important to note from a practice standpoint that the sedation was tapered when the temp got above 36. That’s a nursing question I often hear. 

Within their outcomes, the primary was a favorable 90-day Cerebral Performance Scale where they wanted to see in particular if the patients had either a score of 1 or 2. A score of 1means Good cerebral performance or minor disability. A score of 2 means moderate disability. They called the patients or families on the telephone for follow up. People lie. I wish they would’ve had someone lay eyes on the patients. But people lie in both groups so this should be no big deal. should be. But it isn’t. You’ll see why. 

The secondary outcomes were all the typical ICU stuff: mortality, days on the vent, LOS in ICU and hospital, infections and adverse hematologic events. We know that cooling causes degrees of coagulopathy. 

With in the results, the authors assessed 2723 patients over the course of 4 years. That’s A LOT of cardiac arrests! Then again, 15 ICU’s. I imagine they’re all busy institutions. 

I was happy to see that an intravascular cooling catheter was only used in 14.8% of patients. I have always thought that they were a little too invasive for my tastes, especially if/when they start oozing. 

When looking at the actual outcomes, the best case scenarios still only had a 10.2% incidence of a CPC of 1 or 2. This is not a cure, team. Patients still do terribly. It’s helpful to let families know what to expect when a patient arrives in our ICUs in cardiac arrest. 

More than 80% of patients died in both groups. 81.3% vs. 83.2 in the 33 vs. 37 respectively. All of the secondary outcomes showed no difference. 

The supplementary text provides data as to how they handled withdrawal of care. Imaging was curiously nowhere to be seen anywhere in the paper. They do not mention abnormal CTs or any type of MRIs anywhere in this paper nor the supplementary text. I would be curious if they found anyone with loss of gray-white differentiation who did well. I wonder if they omitted that information so that they could collect a large enough sample size and families wouldn’t withdraw prior to completion of the study. Hmmmmm.  

I respect the heck out of the authors in the way they disclosed their limitations. They admitted that an outcome change in a single patient would make the primary outcome not significant. What am I supposed to do with that?!?! If one person lied about how well they were doing over the phone it would change the conclusions of the entire 4 years of work! This is why I don’t do research. 

The other caveat to the study is that they let the patients in the 37 degree group develop fevers. Correct me if I’m wrong but didn’t a subgroup analysis in the 33 vs 36 study from several years ago show that avoiding fever is the most important component in these patients? In my practice I discuss with the nurses that we need to be prepared for the fever and have meds on the medication list, not for if it will happen, but rather for when it will happen. Considering the study got started in 2014, this is something that hopefully they knew going into the study. 

I’m sticking with 36 in my practice. What do you all think? 

A hat tip to the authors. 

-EJ

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IV Vitamin C and ARDS: CITRIS-ALI

Here's my bias before I even read the article. I want to see a positive response in providing Vitamin C/ascorbic acid in patients who have Acute Respiratory Distress Syndrome. Why? Because I want me patients to do better with treatments that are inexpensive and easy to manufacture rather than the latest immunologic that ends in -mab and costs tens of thousands of dollars. If before you read this summary, you already think that Vitamin C is a bunch of bullpoop, you need some deep reflections in the mirror. You SHOULD want it to work. Now whether it does or doesn't is different and that's where the data comes in to play.

Ultimately, I'm sure I am going to write far more than what IG will allow me to write do you're more than likely going to have to go to my blog to read my thoughts.

The Study Drugs
Before we even get started, we need to look at the study drugs, or lack thereof. The cocktail that was used in the Marik trial that was monumental in finding a mortality benefit in sepsis included ascorbic acid at 1.5gm q6, thiamine 200mg, and steroids. There is a rationale as to why these three go together that Dr. Marik explains far better than I could ever explain. The three are necessary today. Heck, even Gianfranco Meduri has been using steroids for ARDS for years and it's not part of this study. Red flag number one. Not hating on the authors, I am just saying. Haven't finished reading on it yet. Reserve the right to change my mind. In fact, a quick search shows there's no mention of the word "thiamine" in the entire paper.

Outcomes
The primary outcome was modified sofa scores at 96 hours and biomarkers.
I am not going to go over the secondary outcomes but there are 46 of them. They're covering ALL the bases! Good job.

They enrolled 167 patients. This is remarkable that they were able to enroll this many patients in these 7 centers from 9/14 until 11/17.

Results
Let's talk results. That's why you're here. Are you going to start giving vitamin C to your patients with ARDS, yes or no?

Primary outcome: mSOFA and biomarkers: NO DIFFERENCE.
Secondary outcomes: 43 of 46 had NO DIFFERENCE.

But here is the kicker. The three secondary outcomes that had a difference are pretty important.
1. All-cause mortality (p=0.03). 46.3% in the placebo group vs. 29.8% in the Vitamin C group
2. ICU-free days (p=0.03). Patients were transferred out of the ICU faster in the Vitamin C group
3. Hospital-free days (p=0.04) 22.6 in the vitamin C group vs 15.5 in the placebo

Think of all the money that could be saved by this inexpensive vitamin in shortening time in the hospital. $6 a dose, if I'm not mistaken.

No difference in the biomarkers? Well, this may be my off-kilter idea but maybe we are looking or do not full understand our biomarkers.

There were NO adverse effects that occurred during the trial! I've had many people talk about kidney stones, renal dysfunction, terrible side effects of vitamin C. Well, there were none.

Now, there are many limitations in this study. The authors admit to that full and well. Physicians like myself who are on the pro-vitamin C side will interpret the data the way I just did. Those who are contrarians on the matter will be able to look at the numbers and interpret it differently. They will point out all the flaws in the study and throw the findings of the endpoints in the trash. I may be completely off base with my interpretation of these results, but I want to do EVERYTHING that's reasonable to take care of my patients. And if that means spending $24 a day on Vitamin C, I will do it.

If you were the patients on the ventilator with ARDS, would you want the doctor treating you to give you vitamin C?

-EJ




Link to Abstract

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Cordis vs MAC Introducer: What is the difference between the two?

This is a topic better handled by Surgeons than myself but I haven't seen anyone do it. Here I go! @buckparker, you're invited to chime in at this party, bud. @physiciandoodles inspired me to create this post.

Quick! This patient needs to be resuscitated with blood STAT! Call for the massive transfusion protocol and grab me a Cordis STAT! Do you know what this means? Do you know what it means if they asked for an introducer? For many years I was confused myself. I mean, aren't they both just large bore central lines for the purpose of infusion blood quickly or floating a central line? Well yes, they are. But depending on what institution you work at, you may get a funny look on your face if you ask for it by the non-standard name. Non-standard for that institution, of course. I will make this clear, though, as I posted this earlier in the life of my instagram page. You can get A LOT done in a massive bleed with two solid 16 gauge peripheral IVs. Many times you do not need to puny central line. But there are times when patients mean business and they needs all and a catheter of this type is necessary. Okay, let's get started.

First of all, the MAC introducer. This is a proprietary product from Arrow/Teleflex. MAC is a trademarked name that stands for multi-lumen catheter. You may say to yourself, well Eddy, a triple lumen catheter should be a MAC line too! You're not wrong, but we can't make this already challenging job easier on ourselves, right? MAC introducers can come with anywhere from one to three lumens. You could float a swan through many of them, but not all. It is essentially like a "Cordis" but it could have another line. The MAC also has the dilator in the catheter as my colleague Zahid, @zvhvd, pointed out.




A "Cordis" is also an introducer, but the word Cordis is the brand name of the product. A Cordis is the same introducer, but only has one side port. You can also float a swan through this puppy. 

There are other manufacturers who make similar products that I am not going to cover here for the sake of time. Your friendly neighborhood ICU should have one of these introducers in stock. Familiarize yourself with where it is because the day you need it, the patient NEEDS it.

- EJ

Photo credits for Arrow/Teleflex Products

Photo credits for Cordis Products

Copyright gods: If the photos posted upset you, let me know and I will take them off. Just trying to teach here.

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Vasopressin: Titratable Doses? Monotherapy in Septic shock?

This is what I love about the community in social media. We all just push each other to be better. Rishi posted today about titratable Vasopressin and, me being the data junky that I am wanting to know every study I could possibly know under the sun, had two studies in my back pocket ready to share with everyone. I was planning on sharing this study with you all further down the road but, Rishi indirectly pushed me so here I am sharing this article with you all rather than going out for a run. No, there's no one study where they just looked at titrating vasopressin. What this study does show us, though, is that the authors used vasopressin as a titratable medication as well as a mono therapy medication (that means not just adding it to norephinephrine when it reaches X dose. Studies like this indirectly guide us to what can and can't be done moving forward in medicine. If you get into trouble with a patient, one can justify it by saying "the VANISH study showed that it's safe to use it in this manner". I'm always worried about the lawyers, I'm not going to lie.

The goodies in this article and what I want you to focus on today is not necessarily the conclusions of the article nor all the subgroup analysis, but rather I want you to look at the methods on how they performed the study.

Patients were able to receive titratable doses of vasopressin up to 0.06U/min. That means that they were able to exceed the 0.04U/min you and I use every day.

They also titrated to a MAP of 65 or 75. Note that they did not use a systolic blood pressure. I have covered why you shouldn't do that unless you have an arterial line on youtube and here in the past.

The MAP of 75 is also important because there's data that higher MAP's in patients with chronic hypertension is better for them. I see shops where the MAP goal is 60 and that's just plain stupid and only acceptable on a case by case scenario.

Patients in this study received vasopressin as monotherapy for septic shock and it did not cause issues.

There is much to be said about the methodology of this trial which I am not going to get into today. I'll be here forever. Instead, you can hear me take it apart live in Hawaii in May 2020.

A hat tip to the authors.

- EJ





Link to Abstract

Link to FREE PDF

Gordon AC, Mason AJ, Thirunavukkarasu N, et al. Effect of early vasopressin vs norepinephrine on kidney failure in patients with septic shock. JAMA 2016; 316: 509.

Although great care has been taken to ensure that the information in this post is accurate, eddyjoemd, LLC shall not be held responsible or in any way liable for the continued accuracy of the information, or for any errors, omissions or inaccuracies, or for any consequences arising therefrom.

Diabetic Ketoacidosis: PlasmaLyte vs. 0.9% Sodium Chloride for Resuscitation

Can we start looking at our diabetic ketoacidosis protocols and changing them? This study from 2012 is admittedly small, retrospective, and leaves a lot to be desired. But their findings are significant in my opinion. Usually studies need large sample sizes to prove their endpoints. Here, the endpoints were proved (within their methodology) with this small sample size. The article is not free and I bet that more people would benefit from the knowledge one could gain from it if it wasn't hidden behind the paywall. Grrrrrrr. Here are the benefits of using plasmalyte over saline.
1. the mean arterial pressure was improved in the PL group p less than 0.05
2. there was improved urine output in the PL group in the first 4-6 hours p less than 0.05
3. the patients who received NS had higher potassium levels than the PL group between the 6-12 hour mark. Remember, PL has 5meq/L of K while NS has ZERO. Can we drop this hyperkalemia with LR and PL nonsense already?
They disclose the COST of plasma-lyte in Australia to be $1.94/L vs. $1.17/L of NS. It's not $30 a liter like I've heard in the past. This was in 2012.
Okay, this is a short one. I need to go. My wife wants us to enjoy our Saturday and for me to not be such a nerd reading articles.
BYE!
- EJ



Link to Abstract

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HFNC: Does it Ventilate COPD Patients?

I've reviewed numerous mechanisms of action and functions of High Flow Nasal Cannula (HFNC) but I haven't touch on whether or not it works to help ventilate patients. I have discussed in the mechanisms of action that it does wash out the CO2 from the dead space in the nasopharynx, oropharynx, etc, but does that show a numerical decrease in the PCO2? The studies I had reviewed prior to this one weren't promising. 

One of the indirect ways that HFNC can bring down CO2 is by bringing down the patients respiratory rate. There's plenty of data to support the decrease in the respiratory rate. Since the person isn't breathing as hard nor as fast, less CO2 is produced. Less CO2 is produced means the patients needs to be ventilated less. Things get better. Prior to this study, though, the data just wasn't there to show that this actually happened in a statistically significant way. I've said this before and I'll say this again, I will not recommend HFNC to a patient with a COPD patient sucking wind in the ED with an exacerbation that has a gas that looks like 7.06/96/66. That patient either needs some non-invasive ventilation with a very close eye or the endotracheal tube.

In this study they placed COPD patients, not in exacerbation, on HFNC and measured a number of parameters but you and I are here for the CO2. Patients had their PCO2 measured at baseline, on 20L HFNC, and at 30L HFNC. At 20L the PCO2 was at approximately 91 (plus or minus 6.7)% of their baseline and at 30L their PCO2 was at approximately 87.4 (plus or minus 6.2) % of their baseline. That data was statistically significant.

This may be completely out of bounds but if we can (although I probably shouldn't) extrapolate that to a patient with a PCO2 of 60, 20L should bring them down to approximately 54.6 and 30L down to 52.4. Something is better than nothing and if you can hold the patient over while they get their steroids and nebulizations, it may be worth a try in the real world.

- EJ



Bräunlich J, Köhler M, Wirtz H. Nasal highflow improves ventilation in patients with COPD. International Journal of Chronic Obstructive Pulmonary Disease. 2016;1077-1085.

Link to Abstract

Link to Full Free Article

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Hyperchloremia: We've known it is harmful to the kidneys since 2012

It has been 7 years since this study came out, and many since. Here we are still using saline like it's benign. Part of the problem is that clinicians get set in their ways and just don't read. Sorry if that offends anyone, but it's true. Some say, "this has always worked and I haven't seen a problem with it" so they keep doing what they're doing. Our job is to cause no harm. I'm trying my best to minimize that but after all, we are all human. Being lazy is no excuse, though.

This article from 2012 shows a study that was performed on 12 healthy volunteers. It was a randomized, double blind, cross over study. I bet they were either college students or medical students; the mean age was 22. This was not disclosed in the article, of course. The participants received either 2L of 0.9% NaCl or plasma-lyte over an hour on separate occasions 7 to 10 days apart. If you still don't know what Plasma-lyte is, you must be new here. They did some bloodwork as well as MRI's. They must have had some good funding here.

Amongst the results, they found a significant difference in the serum chloride, as expected (p < 0.0001) and a much lower strong ion difference (p = 0.025) in the saline group. All the other electrolytes were unremarkable. From the MRI results, they found lower mean renal artery flow velocity (p = 0.045) and lower renal cortical tissue perfusion (p = 0.008) in the saline group. This proves that hyperchloremic metabolic acidosis is not benign.

A hat tip to the authors.

-EJ




Link to the article: 

Chowdhury AH, Cox EF, Francis ST, et al. A Randomized, controlled, double-blind crossover study on the effects of 2-L infusions of 0.9% saline and plasma-lyte 148 on renal blood flow velocity and renal cortical tissue perfusion in healthy volunteers. Ann Surg 2012; 256: 18–24.

Although great care has been taken to ensure that the information in this post is accurate, eddyjoemd, LLC shall not be held responsible or in any way liable for the continued accuracy of the information, or for any errors, omissions or inaccuracies, or for any consequences arising therefrom.

Diabetic Ketoacidosis: Using Balanced Salt Solutions instead of 0.9% Sodium Chloride

We all know the order sets for DKA, a bunch of 0.9% NaCl first boluses then drip, insulin drip, replace electrolytes, glucose gets to a certain number, change the fluids to 0.9% NaCl that contains dextrose, wait for the anion gap to close, give long acting insulin, wait a bit, turn off the drip, discharge planning. It's simple stuff, really. I may have oversimplified it but you know exactly what the protocol is at your facility. Truth is, though, is that the best for these sick patients? Would they do better with lactated ringers or plasma-lyte?

This study from 2011 states that there are 100,000 hospitalizations for DKA annually in the US. They knew from prior literature that using a bunch of saline solution causes a hyperchloremic metabolic acidosis. They wanted to see if it would happen in this patient population. They conducted a randomized double blind study providing these patients with either 0.9% NaCl solution or Plasma-lyte. For those of you who do not know what plasma-lyte is, go check out my YouTube videos (/shameless plug). They used their typical DKA protocol for their institution which is described in the article.

The study took 24 months and they ended up with 23 patients in the "normal saline" group and 22 patients in the plasma-lyte group. It was entertaining to see that at baseline, before a drop of fluid was even given, the serum chloride of the saline group was less than the PL group: 94 vs 98 (p=0.027). When the study was said and done, however, the chloride level was 111 in the NS group and 105 in the PL group (p < 0.001). I don't know if you've had time to look at the older things I've written/posted but there's a particular study that comes to mind where the authors found that an increase in serum chloride by 5 increases your chances of developing acute kidney injury. There was also a significant difference in the serum bicarb level where the NS group has a bicarb increase of 7 whereas the PL group had an increase of 9 (p=0.023). The authors did not follow renal function in these patients from what I am able to see. The authors admitted that they didn't know what the clinical significance of all this is. I believe we have data now with more recent studies to show us what the clinical significance actually is.

- EJ



Link to Abstract

Mahler SA, Conrad SA, Wang H, et al. Resuscitation with balanced electrolyte solution prevents hyperchloremic metabolic acidosis in patients with diabetic ketoacidosis. Am J Emerg Med 2011; 29: 670–674.

Although great care has been taken to ensure that the information in this post is accurate, eddyjoemd, LLC shall not be held responsible or in any way liable for the continued accuracy of the information, or for any errors, omissions or inaccuracies, or for any consequences arising therefrom.