Saturday, October 19, 2019

Thiamine and Renal Failure in Septic Shock Patients

Every possible option to decreased morbidity, mortality, and costs are worth looking at in my book. The study that I am reviewing at this moment was published in 2017. I am ashamed that I had not run into it until today. It's challenging to stay up to date in everything. I digress.

Some would quickly bash this study for it being small (n=70) and a post-hoc secondary analysis of a pilot study. I am not going to do that. Why not? Well first of all, I do not participate in research myself. Just reading and enjoying these studies. Also, thiamine has no side effects described in the literature. Third, it is an inexpensive medication. Fourth, if it does turn out to decrease the incidence of acute kidney injury and the need for renal replacement therapy, aren't you going to feel guilty for not adopting these strategies for your patients? I hate resorting to that but my responsibility is for patients. What happens if this data is wrong? Nothing. What happens if this data is right and no one does anything for several years? Many patients may suffer.


This article is completely free and I encourage you to download it and read it for yourself. Amongst the points illustrated by the authors, they mention that it's not only perfusion that injures the kidneys during sepsis. There are other factors listed in the article. The way that it is postulated that thiamine works for these patients is by assisting in the mitochondrial dysfunction. Data that I have found not listed in this article shows that thiamine deficiency could have an incidence between 20-70% of critically ill patients. 

What they found was 21% of the patients in the placebo arm of the trial went on to need dialysis. Just one patient, or 3% in the thiamine group went on to require this. The authors note that acidosis was the primary indication for dialysis in 66% of the patients who required it. I personally would like to dig deeper into these numbers as there is some data that thiamine administration helps decrease lactic acidosis. 

This data should make you wonder if the strategy that many clinicians take of providing more IV fluids to patients whose renal function deteriorates is the correct strategy. Are we going to look in the mirror in a decade and want to punch our past selves in the face?   

- EJ






Link to Abstract


Link to Full Article

ADDENDUM: The prospective RCT is going to be completed in July 2022. Here is the link to clinicaltrials.gov's study details here: LINK

Moskowitz A, Andersen LW, Cocchi MN, Karlsson M, Patel PV, Donnino MW. Thiamine as a renal protective agent in septic shock. A secondary analysis of a randomized, double-blind, placebo-controlled trial. Anns Am Thorac Soc. 2017;14(5):737–41.

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.

The primary source of compensation I receive for this page and Instagram work is via Amazon Affiliates. All this free education you receive is much out of the kindness of my heart but I also like to receive a check every month from Affiliate Marketing. No one likes to work for free. The best part is that it's of no cost to you. Here's how it works.

You click on the link for Will Owens' awesome ventilator book here: https://amzn.to/2myFxYm and whether or not you purchase the book I receive a small commission for whatever you buy on Amazon for the next 24 hours at no cost to you. For every copy of the Ventilator book people have bought off of my affiliate links, for example, I have earned $0.85. I know it's not big money but it helps motivate me to keep on plugging along doing this heavy lifting in Critical Care. Thank you for supporting my work!
- My Amazon Store

Thiamine, Ascorbic Acid and Corticosteroids: The Mechanisms by which they should help in Sepsis

Want some nerdy stuff? Well this is some nerdy stuff! I'm taking a nice deep look at this figure. I am not going to lie to you at this moment, October 19th, and tell you I know what all this means, because I don't. But people who are more intelligent that I am have suggested that these are the mechanisms by which thiamine, ascorbic acid, and corticosteroids should help in the treatment of septic patients. I have a lot to learn.

I hope I don't get dinged for copyright stuff but honestly if this offends you, let me know. I will take it down. I will likely go deeper into this article at a later time. Wanted to share this image with you right now, though.





Link to Abstract

Link to FREE FULL Article

Moskowitz, A.; Andersen, L.W.; Huang, D.T.; Berg, K.M.; Grossestreuer, A.V.; Marik, P.E.; Sherwin, R.L.; Hou, P.C.; Becker, L.B.; Cocchi, M.N.; et al. Ascorbic acid, corticosteroids, and thiamine in sepsis: A review of the biologic rationale and the present state of clinical evaluation. Crit. Care 2018, 22, 283.

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.
The primary source of compensation I receive for this page and Instagram work is via Amazon Affiliates. All this free education you receive is much out of the kindness of my heart but I also like to receive a check every month from Affiliate Marketing. No one likes to work for free. The best part is that it's of no cost to you. Here's how it works.

You click on the link for Will Owens' awesome ventilator book here: https://amzn.to/2myFxYm and whether or not you purchase the book I receive a small commission for whatever you buy on Amazon for the next 24 hours at no cost to you. For every copy of the Ventilator book people have bought off of my affiliate links, for example, I have earned $0.85. I know it's not big money but it helps motivate me to keep on plugging along doing this heavy lifting in Critical Care. Thank you for supporting my work!
- My Amazon Store

Friday, October 18, 2019

Delirium in Mechanically Ventilated Patients: Let the Natural Light in!

I have great disdain for delirium. Natural light brings me great joy. Today, for example, the sun isn't shining bright. The day is cloudy and gloomy. I am, in turn, a little grouchy. Daylight savings is coming and I'm already upset about it. I can turn on the light but it won't be the same. This study was published today. How's that for so fresh and so clean?

Preventing and treating delirium is something we haven't quite figured out just yet. But studies like this one help us chip away at that giant piece of rock to eventually present a great sculpture. Bad analogy? Yep! In this study, the authors were curious to see whether patients having natural light would affect the incidence of delirium in patients who are on the ventilator (primary outcome). The secondary outcomes included the "duration of delirium, duration of coma, use of antipsychotics to treat agitation, the incidence of hallucinations, the incidence of self-extubation, duration of mechanical ventilation, ICU and hospital length of stay, ICU and hospital mortality."

This was a single centered trial with 195 patients. Out of their measured outcomes, they noted that the patients exposed to natural light had a reduced incidence of severe agitation (p=0.04). In addition, the patients exposed to natural light also had fewer hallucinations (p=0.04). Fortunately, this study is free and you can download it and read it yourself. I like natural light. It's free. It may not ameliorate delirium, but it is another tool in our tool belt to make these patients better.
-EJ






Link to Abstract


Link to full free PDF

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.

The primary source of compensation I receive for this page and Instagram work is via Amazon Affiliates. All this free education you receive is much out of the kindness of my heart but I also like to receive a check every month from Affiliate Marketing. No one likes to work for free. The best part is that it's of no cost to you. Here's how it works.

You click on the link for Will Owens' awesome ventilator book here: https://amzn.to/2myFxYm and whether or not you purchase the book I receive a small commission for whatever you buy on Amazon for the next 24 hours at no cost to you. For every copy of the Ventilator book people have bought off of my affiliate links, for example, I have earned $0.85. I know it's not big money but it helps motivate me to keep on plugging along doing this heavy lifting in Critical Care. Thank you for supporting my work!
- My Amazon Store

Thursday, October 17, 2019

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

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.

The primary source of compensation I receive for this page and Instagram work is via Amazon Affiliates. All this free education you receive is much out of the kindness of my heart but I also like to receive a check every month from Affiliate Marketing. No one likes to work for free. The best part is that it's of no cost to you. Here's how it works.

You click on the link for Will Owens' awesome ventilator book here: https://amzn.to/2myFxYm and whether or not you purchase the book I receive a small commission for whatever you buy on Amazon for the next 24 hours at no cost to you. For every copy of the Ventilator book people have bought off of my affiliate links, for example, I have earned $0.85. I know it's not big money but it helps motivate me to keep on plugging along doing this heavy lifting in Critical Care. Thank you for supporting my work!
- My Amazon Store



Saturday, October 5, 2019

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

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.

The primary source of compensation I receive for this page and Instagram work is via Amazon Affiliates. All this free education you receive is much out of the kindness of my heart but I also like to receive a check every month from Affiliate Marketing. No one likes to work for free. The best part is that it's of no cost to you. Here's how it works.
You click on the link for Will Owens' awesome ventilator book here: https://amzn.to/2myFxYm and whether or not you purchase the book I receive a small commission for whatever you buy on Amazon for the next 24 hours at no cost to you. For every copy of the Ventilator book people have bought off of my affiliate links, for example, I have earned $0.85. I know it's not big money but it helps motivate me to keep on plugging along doing this heavy lifting in Critical Care. Thank you for supporting my work!
- My Amazon Store

Thursday, October 3, 2019

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

Tuesday, October 1, 2019

ARDS and Vitamin C/Ascorbic Acid: 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

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.

The primary source of compensation I receive for this page and Instagram work is via Amazon Affiliates. All this free education you receive is much out of the kindness of my heart but I also like to receive a check every month from Affiliate Marketing. No one likes to work for free. The best part is that it's of no cost to you. Here's how it works.

You click on the link for Will Owens' awesome ventilator book here: https://amzn.to/2myFxYm and whether or not you purchase the book I receive a small commission for whatever you buy on Amazon for the next 24 hours at no cost to you. For every copy of the Ventilator book people have bought off of my affiliate links, for example, I have earned $0.85. I know it's not big money but it helps motivate me to keep on plugging along doing this heavy lifting in Critical Care. Thank you for supporting my work!
- My Amazon Store

Monday, September 30, 2019

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.

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.

The primary source of compensation I receive for this page and Instagram work is via Amazon Affiliates. All this free education you receive is much out of the kindness of my heart but I also like to receive a check every month from Affiliate Marketing. No one likes to work for free. The best part is that it's of no cost to you. Here's how it works. 

You click on the link for Will Owens' awesome ventilator book here: https://amzn.to/2myFxYm and whether or not you purchase the book I receive a small commission for whatever you buy on Amazon for the next 24 hours at no cost to you. For every copy of the Ventilator book people have bought off of my affiliate links, for example, I have earned $0.85. I know it's not big money but it helps motivate me to keep on plugging along doing this heavy lifting in Critical Care. Thank you for supporting my work! 
- My Amazon Store

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.

The primary source of compensation I receive for this page and Instagram work is via Amazon Affiliates. All this free education you receive is much out of the kindness of my heart but I also like to receive a check every month from Affiliate Marketing. No one likes to work for free. The best part is that it's of no cost to you. Here's how it works. 

You click on the link for Will Owens' awesome ventilator book here: https://amzn.to/2myFxYm and whether or not you purchase the book I receive a small commission for whatever you buy on Amazon for the next 24 hours at no cost to you. For every copy of the Ventilator book people have bought off of my affiliate links, for example, I have earned $0.85. I know it's not big money but it helps motivate me to keep on plugging along doing this heavy lifting in Critical Care. Thank you for supporting my work! 

My Amazon Store

Saturday, September 28, 2019

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

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.

The primary source of compensation I receive for this page and Instagram work is via Amazon Affiliates. All this free education you receive is much out of the kindness of my heart but I also like to receive a check every month from Affiliate Marketing. No one likes to work for free. The best part is that it's of no cost to you. Here's how it works. 

You click on the link for Will Owens' awesome ventilator book here: https://amzn.to/2myFxYm and whether or not you purchase the book I receive a small commission for whatever you buy on Amazon for the next 24 hours at no cost to you. For every copy of the Ventilator book people have bought off of my affiliate links, for example, I have earned $0.85. I know it's not big money but it helps motivate me to keep on plugging along doing this heavy lifting in Critical Care. Thank you for supporting my work! 

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Thursday, September 26, 2019

High Flow Nasal Cannula: Does it Ventilate COPD Patients?

I've reviewed numerous mechanisms of action and functions of High Flow Nasal Cannula 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

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.

The primary source of compensation I receive for this page and Instagram work is via Amazon Affiliates. All this free education you receive is much out of the kindness of my heart but I also like to receive a check every month from Affiliate Marketing. No one likes to work for free. The best part is that it's of no cost to you. Here's how it works. 

You click on the link for Will Owens' awesome ventilator book here: https://amzn.to/2myFxYm and whether or not you purchase the book I receive a small commission for whatever you buy on Amazon for the next 24 hours at no cost to you. For every copy of the Ventilator book people have bought off of my affiliate links, for example, I have earned $0.85. I know it's not big money but it helps motivate me to keep on plugging along doing this heavy lifting in Critical Care. Thank you for supporting my work! 

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Wednesday, September 25, 2019

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.

The primary source of compensation I receive for this page and Instagram work is via Amazon Affiliates. All this free education you receive is much out of the kindness of my heart but I also like to receive a check every month from Affiliate Marketing. No one likes to work for free. The best part is that it's of no cost to you. Here's how it works. 

You click on the link for Will Owens' awesome ventilator book here: https://amzn.to/2myFxYm and whether or not you purchase the book I receive a small commission for whatever you buy on Amazon for the next 24 hours at no cost to you. For every copy of the Ventilator book people have bought off of my affiliate links, for example, I have earned $0.85. I know it's not big money but it helps motivate me to keep on plugging along doing this heavy lifting in Critical Care. Thank you for supporting my work! 
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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.

The primary source of compensation I receive for this page and Instagram work is via Amazon Affiliates. All this free education you receive is much out of the kindness of my heart but I also like to receive a check every month from Affiliate Marketing. No one likes to work for free. The best part is that it's of no cost to you. Here's how it works. 

You click on the link for Will Owens' awesome ventilator book here: https://amzn.to/2myFxYm and whether or not you purchase the book I receive a small commission for whatever you buy on Amazon for the next 24 hours at no cost to you. For every copy of the Ventilator book people have bought off of my affiliate links, for example, I have earned $0.85. I know it's not big money but it helps motivate me to keep on plugging along doing this heavy lifting in Critical Care. Thank you for supporting my work! 

My Amazon Store

Tuesday, September 24, 2019

High Flow Nasal Cannula in Acute Decompensated Heart Failure data leaves much to be desired.

Fortunately in the critical ill population, we do not necessarily have to abide by the saying that "if all you have is a hammer, everything looks like a nail". What I'm referring to is regarding utilizing high-flow nasal cannula in acute heart failure exacerbations. I already dissected how HFNC generated a "PEEP" equivalent airway pressure and the data behind that statement. The amount of PEEP varies and it drops by a statistically significant difference if the patient has their mouth open. If a patient presents to the emergency department, or someone gets overzealous with maintenance fluids, with an acute heart failure exacerbation, there is data that I will be reviewing here where HFNC is an option. But let's be honest with ourselves, though, non-invasive ventilation (colloquially known as BiPAP, although CPAP has data for working as well) is the better option because it provides positive airway pressure more reliably that HFNC. Sometimes these patients just need the ventilator as well. All three studies are FREE that I am going to be reviewing here and I recommend you read them for yourself rather than trusting my takedown of them. That's your disclaimer.

The first study published in 2011 out of Spain was a look at just 5 patients. I know, don't fall off of your seat. I can't criticize because I don't do any research outside of read other peoples research. One needs to remember that in 2011 the HFNC systems were not readily available for historical context. These 5 patients were treated in the emergency department with NIV and then I guess they were diuresed aggressively there. Why do I guess? Well the study does not report the BNP nor the achieved diuresis in these 5 patients. Big weakness in the study. They looked at a multitude of parameters that would be standard for a study of this nature, i.e. to see if HFNC is better than the other oxygen devices, but there are big problems. You see, the authors looked at the parameters before HFNC and then 24 hours AFTER HFNC. What they don't say is how much the patients were diuresed in the interim. Of course the PaO2 is going to improve. Of course the dyspnea is going to improve. Of course the respiratory rate is going to improve! Anyway, this is a study worth sticking in our back pockets to know it happened and move forward.

The second study by Roca also out of Spain in 2013 wanted to assess if HFNC helped with the hemodynamic parameters. They hypothesized that HFNC in patients with heart failure could be associated with a decrease in preload without changing the cardiac output. To look at this, patients got sequential echo's to assess cardiac function. Pretty good setup if you ask me. The 10 patients enrolled in this study were all stable. Therefore the data needs to be extrapolated to the sick patients. They did a baseline TTE on these patients, then hooked them up to the HFNC system at 20L, checked an echo, then at 40L of flow, and checked an echo. They did all sort of echocardiographic wizardry to obtain their results. They found that HFNC may be associated with a decrease in preload justified by the lack of IVC collapse on inspiration without any changes to cardiac function. IVC measurements are their own can of worms when used for resuscitation but this is very standardized and methodical. The most interesting finding that I enjoyed was the decrease in respiratory rate noted by these patients. At baseline, their RR was 23 breaths per minute. At 20L this fell to 17 bpm. At 40L this fell to 13 bpm. Cool stuff! Note that the patients were receiving just flow in this study as the FiO2 was set to 21% (room air). The authors chose to not use patients in acute decompensated heart failure for this study as there would have been too much variability in the subjects themselves along with their responses to the treatments interfering with to the measures. Obviously if they dump out a liter due to furosemide their hemodynamic parameters are going to change and it'll mask out the effect of the HFNC or provide confounders.

The third and last study I'm going to share with you all today comes from our colleagues in South Korea who performed a retrospective cohort analysis where patients were divided into a HFNC group or an intubation group after oxygenation with a facemask at a flow rate of 10L/min or more. These authors jumped on the opportunity to look at this data as they hadn't seen any published data about using HFNC in patients with acute heart failure exacerbations. They looked at approximately 5 years of data to place 73 patients in the intubation group and 76 patients in the HFNC group. Since this was a retrospective study, the decision as to what arm the patients fell in was at the discretion of the physician at bedside. The authors are just looking back in time at why they decided to do it and how the patients did. It seems as if they ignored the NIV data. I could be wrong. The baseline characteristics of the two arms were similar with nothing too eye catching. These patients were looked at for 6 hours. There were no statistically significant changes in the physiologic responses between the two groups. There was also no difference in the clinical outcomes between the two groups. This oddly, in my opinion, includes vasopressor/ionotrope use. I mention this because patients who are intubated typically have sedation. Also, the medications utilized for intubation could have an effect on hemodynamic parameters that are not noted here. It's just something that, from a personal experience standpoint, has me a bit curious. The p-value for that is 0.051. If the sample size would've been larger, I'm sure that would've been a notable difference. The authors noted all these limitations to their study and agree that what we really need is a prospective, multicentered, randomized, controlled trial. I agree

To conclude, I think the best we have right now in the absence of concrete data is clinical judgment, my favorite. One could try to place the patient on HFNC to either keep them away from the ventilator or even keep them from being annoyed by the CPAP/BiPAP mask which is typically uncomfortable, limits the ability to eat, speak, and other fun activities. If it fails, it fails. Your RT may be a little annoyed at you and may say "I told you so", but ultimately we have to do what's best for the patient. Thoughts? Please read these articles for yourself. A hat tip to all the authors. 

- EJ





Link to Abstract

Link to Full FREE PDF



Link to Abstract

Link to not free PDF




Link to Abstract

Link to Full FREE PDF
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.

The primary source of compensation I receive for this page and Instagram work is via Amazon Affiliates. All this free education you receive is much out of the kindness of my heart but I also like to receive a check every month from Affiliate Marketing. No one likes to work for free. The best part is that it's of no cost to you. Here's how it works. 

You click on the link for Will Owens' awesome ventilator book here: https://amzn.to/2myFxYm and whether or not you purchase the book I receive a small commission for whatever you buy on Amazon for the next 24 hours at no cost to you. For every copy of the Ventilator book people have bought off of my affiliate links, for example, I have earned $0.85. I know it's not big money but it helps motivate me to keep on plugging along doing this heavy lifting in Critical Care. Thank you for supporting my work! 

My Amazon Store

Monday, September 23, 2019

Ketamine for Rapid and Delayed Sequence Intubation

Alternatives to Rapid Sequence Intubation: Contemporary Airway Management with Ketamine
What are your experiences with ketamine for intubations?

I am really glad that I stumbled onto this article that was shared by @the_resuscitationist and @medicotactico.

When you're dealing with airways and medications that have can concerning adverse effects, you really shouldn't trust me on anything and should read the article yourself. Link in bio. This one is also completely free! Also, everything I typed for this post didn't fit in the space allowed by IG, so if you want to finish reading all my thoughts, you have no choice but to head over to my website. It is what it is and this article got me fired up!

For my physicians/NP/CRNA/PA colleagues who manage airways: How do you utilize ketamine for these situations?

For my ICU and ED nurses who push this medication: what have been your experiences with it?

The first thing the authors state is something those of us in the ICU or ED’s already know, establishing an airway is the riskiest commonly performed procedure in acute care. I do not proceed with pushing meds unless I have all my ducks in a row and I have plan A, B, and C easily accessible.

Here’s what happens with ketamine versus other agents that are commonly used: the patient becomes dissociated, they get that glassy look in their eyes, basically disconnected, but the brain stem reflexes stay intact... well... most of the time. You need to be prepared for it to hit the fan at any time. The patient should continue to breath spontaneously. The patients hemodynamics should also be augmented. Again, the key word is “should”. I’ve seen patients become apneic as well as hypotensive but more on that later. I’m just glad I’m not the only one who has seen these effects which are described in the literature. Nurses, don’t push ketamine like a bolus. Push it over 30-60 seconds. I know there’s a ton of adrenaline rushing in those rooms and you're used to pushing meds.

Here’s a strategy I learned from this article. Go ahead and push the ketamine when the patient is agitated and thrashing to allow for preoxygenation. The patient should chill out and when they cease thrashing, one can move forward with a preoxygenation strategy. They even explained certain cases where patients were provided with ketamine for this reason and then didn’t even need intubation.

What’s the dose? 1-2mg/kg of IDEAL body weight.

One of the things that I have noticed clinically when administering ketamine to establish and airway is the clenched jaw. Here, the authors recommend using midazolam, propofol, or even a sub-induction dose of etomidate. Just be aware that these agents bring their own baggage to the party.

Here's what the authors say about the hypotension related to ketamine. First, you need to know whether you think the patient is catecholamine depleted. In other words, they are in shock and they are running out of steam. Those patients should be resuscitated to the best of your ability and you may have to cut the dose in half. Again, read the article for yourself.

Lastly, the authors discuss using ketamine for sedation but it should be kept at dissociative doses or else your patient is going to have some no-so-good experiences. You may need to add some propofol at that point.

For respect of the authors, I will stop there. Read it for yourself. Again, it's free! Thank youuuuu!

- EJ





Link to Article

Link to FREE PDF

Merelman, A., Perlmutter, M., & Strayer, R. (2019). Alternatives to Rapid Sequence Intubation: Contemporary Airway Management with Ketamine. Western Journal of Emergency Medicine, 20(3), 466–471.

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.

The primary source of compensation I receive for this page and Instagram work is via Amazon Affiliates. All this free education you receive is much out of the kindness of my heart but I also like to receive a check every month from Affiliate Marketing. No one likes to work for free. The best part is that it's of no cost to you. Here's how it works. 

You click on the link for Will Owens' awesome ventilator book here: https://amzn.to/2myFxYm and whether or not you purchase the book I receive a small commission for whatever you buy on Amazon for the next 24 hours at no cost to you. For every copy of the Ventilator book people have bought off of my affiliate links, for example, I have earned $0.85. I know it's not big money but it helps motivate me to keep on plugging along doing this heavy lifting in Critical Care. Thank you for supporting my work! 
My Amazon Store