Showing posts with label septic shock. Show all posts
Showing posts with label septic shock. Show all posts

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

Thursday, August 15, 2019

The gut microbiome alters immunophenotype and survival from sepsis



Link to Article

I've had very similar patients with very similar infections where one was out of the ICU in a short amount of time and the other died in flames. Many variables in play, of course, but you get my point. Could the gut microbiome hold a key regarding which patients do well and which patients don't? My ignorance on the matter is through the roof and my research made me stumble on this gem of a study. I am usually not a fan of mice studies but they have their place in medicine. Here, they showed how mice with almost genetically identical backgrounds who underwent cecal ligation and puncture to make them septic, and had completely different rates of death. One group obtained from a certain location had a mortality rate of 90% whereas the other group had a mortality rate of 53%. Then they had another group subset where they mixed females of the two groups (bc the males rip each other to shreds) for 3 weeks and then performed the same process. The group with the 90% mortality, after being cohoused, had the same mortality rate as that which had the 53% mortality. That’s absolutely fascinating! Now, the authors admit that there are other factors at play, but they did a ton of fancy genetic and bacterial testing to help explain the differences. I leave it up to them to better explain it. A definite 🎩 tip to them.

-EJ

Wednesday, August 14, 2019

Prediction of fluid responsiveness: an update



Link to Article

Link to PDF

If your way of determining whether a patient is fluid responsive or not is to see if the blood pressure went up after giving a bolus, you are doing it WRONG! You need to stop, take a deep breath, and reassess your way of thinking about fluid responsiveness. This (FREE!) article dives into why fluids should not be provided arbitrarily go make us feel good inside and make us feel like we at least "did something" in response to that low mean arterial pressure. No, I do not use SBP and DBP off of the BP cuff in my practice. More on that at another time. This article also goes briefly into why we should not be checking CVP (duh). Bottom line is that we can't accurately predict fluid responsiveness without an arterial line and some sort of device to predict stroke volume, stroke volume variation, cardiac index/output. You could have some really good echo nunchuck skills as well. This study also emphasizes why looking at IVC variations is not the best test. Ultimately, we all need to get better at this, myself included. I feel that this article is particularly important for nurses as you all are the ones who relay the BP concerns to the clinicians essentially ordering the fluids. These three authors are legends of critical care. A real treat that Annals of Intensive Care published this for free.
This article is going to be part of the bibliography for the talk I will be giving in Portland, OR in August of 2020.

-EJ

Friday, August 2, 2019

Optimal norepinephrine-equivalent dose to initiate epinephrine in patients with septic shock



Link to Abstract

I am quite confused by this article. I was hoping for some answers on how to manage norepinephrine and epinephrine in septic shock but instead I am left scratching my head wondering what in the world happened here. If you're on my page and following along in on this journey, then you know a thing or two about septic shock patients. This article was supposed to provide us with some data regarding when to start epinephrine on these patients once levophed was already running. Instead, you find a retrospective observational study with a statistically significant difference between the optimal dose group and the non-optimal dose group. Within the subgroup analysis, though, you can find that 83.3% of the optimal dose group was also on vasopressin while 62.3% of the non-optimal group was on vasopressin (p=0.001). Does this mean that there's a dose to start epinephrine when a patient is on norepinephrine, or does this mean that before starting epi, you should have vasopressin on board? 

-EJ

Purpose: The specific norepinephrine dose at which epinephrine should be added in septic shock is unclear. This study sought to determine the norepinephrine-equivalent dose at epinephrine initiation that correlated with hemodynamic stability.
Methods: Septic shock patients receiving both norepinephrine and epinephrine were included in this study. Classification and regression tree analysis was conducted to determine breakpoints in norepinephrine- equivalent dose predicting hemodynamic stability, with two cohorts identified. The primary outcome was hemo- dynamic stability, and secondary outcomes were shock-free survival, time to achieve hemodynamic stability, and change in SOFA score.
Results: Optimal dose group was identified as initiating epinephrine when norepinephrine-equivalent dose was between 37 and 133 μg/min. A total of 138 and 61 patients were classified in optimal and non-optimal dose groups, respectively. Baseline characteristics were similar between groups except vasopressin use was more fre- quent in the optimal dose group. More patients in optimal dose group versus non-optimal dose group achieved hemodynamic stability (40 [29%] vs. 9 [14.8%]), absolute risk difference 14.2% [95% CI 2.5–25.9%]; p = .03). On multivariable analysis, initiating epinephrine within the optimal norepinephrine-equivalent dose range was independently associated with higher odds of hemodynamic response (OR 3.06 [95% CI 1.2–7.6]; p = .02). No dif- ferences were observed in other secondary outcomes.

Conclusions: Initiation of epinephrine when patients were receiving norepinephrine-equivalent doses of 37–133 μg/min was associated with a higher rate of hemodynamic stability.

Monday, July 29, 2019

Ascorbic Acid, Thiamine, and Steroids in Septic Shock: Propensity Matched Analysis


Link to Article


Another day, another Vitamin C article. This one came out just two weeks ago, it’s not free, and the results are a bit strange. There are larger trials in the works. If I were part of the group of these authors, I’d be itchy to get my data out ASAP as well. Just 31 patients in each arm of this trial. Heck, even I could replicate this trial in my 20 bed MSICU if I wanted to over 1.5 years. The problem is that my bias admittedly is for the cocktail to work. I am wide openly admitting that, everyone. I have a bias. I want it to work bc I want my patients to live.  
There are numerous parts of this study that seem strange to me. 
1. the ICU mortality of the control arm is 42%. This number should not be quite as high based on the latest data. That could lead the p-value of 0.004 to be perhaps a bit too small. But considering that they used the same strategies to manage septic shock these pts in both arms, it’s still valid for that institution. 
2. The duration of the vasopressors were longer in the experimental arm. This makes NO sense as Vitamin C is a co-factor in the endogenous creation of catecholamines. Heck, even the authors admitted this was strange. 
3. There was no significant difference in hospital mortality. They probably needed a high n to get this to show a difference. The hospital medicine and palliative teams must be great at getting code status’ changed so that people don’t bounce back to the unit. 
4. Pts did not get off of the ventilator faster. Word on the street is that there’s preliminary data suggesting that it helps this process that just isn’t out yet. Stay tuned. 
Lastly, everyone is worried about renal failure. No difference in AKI here, folks. In fact, I am yet to see one report in any of these trials talking about renal calculi secondary to vitamin C in sepsis. 

What are your thoughts on the matter? Is your shop using this yet? Are you a believer or a skeptic?