Saturday, February 29, 2020

Prone Positioning for ARDS

I am a huge fan of proning patients who are in ARDS. At one point or another I'll cover the data behind proning like the PROSEVA trial (no time today or until at least June). There are a variety of ways to prone patients which reflect the disposable income of the facilities where you work and train. At the 3 institutions were I have worked and the others where I have done moonlighting shifts, we've all used some good ol' fashioned muscles and coordination.

The PDF quoted and linked here was published in December 2019 and is usually very key during flu season. I am not going to comment about the coronavirus but these patients are developing an ARDS-like syndrome where proning may work. I haven't seen any data, though. That being said, having the ability to prone patients and do it well could potentially save lives.

In the paper, they cover pretty much everything I would want them to in a document like this that's beneficial to all. They even discuss chest compressions and defibrillation in these patients, something we all fear.

The PDF is completely free and a direct link. I need to find out the citation for this bad boy. The authors did a great job and a big hat tip to them. There's a really nice safety checklist and nursing checklist included. 

How do you all prone at your institution?

Do you not prone at your shop because of fear of the tube coming out?


Have you ever had to perform CPR on a proned patient?




Link to FULL FREE GUIDELINES


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Friday, February 28, 2020

Norepinephrine versus Epinephrine for Cardiogenic Shock caused by a Myocardial Infarction

This is one sexy pilot study. The authors here decided to take a look at norepinephrine (NE) versus epinephrine in patients with cardiogenic shock s/p MI. They didn't use dopamine as they had noted an article that I have reference here where I discussed how dopamine actually increases mortality in cardiogenic shock compared to NE. 

The rationale why the authors went to NE was because data has shown that the myocardium may have a more favorable effect on myocardial O2 consumption. Epi was believed to cause more deleterious effects. Ultimately, though, none of this had been proven in a trial. Well, here is the trial. 
Over the course of 5 years they included 57 patients. See why I have such respect for these folks who do trials? I have no idea where I am going to be in 5 weeks, let alone 5 years. They measures a ton of parameters and did their statistical jumping jacks that I will not bore you with (but the article is entirely free for those curious minds out there). 

Ultimately, what we are about is how the patients did. With regards to their MAP, CI, and SVI, they were the same. As one would expect, the HR for the patients on epi was higher. Also expected, as epi hits more of the beta receptors, there was an increase in lactate in these patients (which doesn't mean they need more fluids).  

There was an early termination of the study, though, as 37% of the patients on epi went into refractory shock while just 7% of the patients on NE did the same (p=0.008). 
The authors acknowledge that it is a small trial but they were able to see a clear difference between the two groups. There are numerous other limitations to the study as well that they acknowledged.
When your patients are in cardiogenic shock, how do you all use your vasopressors/inotropes?

-EJ

Levy BC, Clere-Jehl R, Legras A, et al. Epinephrine versus norepinephrine in cardiogenic shock after acute myocardial infarction. J Am Coll Cardiol. 2018;72:173–82.

Link to Abstract

Link to FULL FREE Article



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Wednesday, February 26, 2020

Renal dose Dopamine, taking down a myth.

When one looks at the dates where the publications disproved "renal dose dopamine", you see three articles published in 2000, 2003, and 2004. It's 2020 and this has not yet been put to bed. Now, I’m all worked up about this because I’ve had clinicians tell me that it absolutely works. I saw it in residency, fellowship, and now in private practice. I’m sure some of you see it at your institutions, too.
There’s data that it improves urine output transiently but no data that it improves renal outcomes in critically ill patients. No changes in creatinine. No changes in renal replacement therapy rates. In fact, that whole discussion has been put to bed so much that there haven’t been any comments made on it over the last 15 years. No further trials attempting to prove it works. Is that why we’re still seeing it? Well, it’s time to bring the arguments against renal dose dopamine, or even using dopamine altogether back into the fray.
The data about it being beneficial was from the 60’s in animal and healthy human studies. The latest studies, however, say it doesn’t work and in fact may be harmful. I have attached some of my preliminary slides from my Vasopressors in 2020 lecture. These are some of my preliminary slides. More info will come from me directly as I present these but it should provide you with an idea of why we should rarely see dopamine in our ICU's anymore. 
Do you still all use dopamine? If so, what for?
I used to use it during codes as it was already packaged in the code carts. We have since gotten rid of these and my badass pharmacy colleagues prep me levophed drips within seconds. 

Debaveye, Y., and Van den Berghe, G.: “Is There Still a Place for Dopamine in the Modern Intensive Care Unit?” Anesthesia and Analgesia. 98(2):461–468, February 2004.

Link to FREE PDF

Holmes, C., and Walley, K.: “Bad Medicine: Low-Dose Dopamine in the ICU,” Chest. 123(4):1266–1275, April 2003.

Link to CHEST Article

Bellomo R, Chapman M, Finfer S, et al. Low-dose dopamine in patients with early renal dysfunction: a placebo-controlled randomised trial: Australian and New Zealand Intensive Care Society (ANZICS) Clinical Trials Group. Lancet 2000; 356: 2139–2143

Link to NOT FREE Lancet Article

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Monday, February 24, 2020

Cardiac Arrest Survival Statistics

We’re getting better with our management of out of hospital cardiac arrest via quality bystander CPR. The majority of this credit should go to the organizations such as the AHA who puts together programs taught by firefighters, paramedics and EMT’s (forgive me if I screw up the semantics) to health care personnel and the lay public which empower those attendees to save lives with their training.

No matter how you look at it, the numbers are still pretty bad, but they’re getting better. 8.8% of cardiac arrest patients lived to be discharged from the hospital. Some nuisances behind those numbers include no quality of life being discussed, nor a breakdown of the etiology behind the arrests by subgroups. Nonetheless, the authors did a great job of compiling data from many different studies to give us an idea of what we can expect when our patients roll into our emergency departments and ICUs. 

Only 22% survive long enough to be admitted to the hospital.
In the last decade we’ve improved the survival to hospital discharge and 1 year survival. We should all pat ourselves on the back to some extent bc were the ones who do and will take care of these patients. I know that we sometimes prolong death, but we’ve all had some big wins that have given us purpose and made our hearts full with satisfaction for what we’re trained to do. A hat tip to the authors.

-EJ

Yan, S., Gan, Y., Jiang, N. et al. The global survival rate among adult out-of-hospital cardiac arrest patients who received cardiopulmonary resuscitation: a systematic review and meta-analysis. Crit Care 24, 61 (2020). https://doi.org/10.1186/s13054-020-2773-2

Link to FULL FREE Article

Link to Abstract

Yan, S., Gan, Y., Jiang, N. et al. The global survival rate among adult out-of-hospital cardiac arrest patients who received cardiopulmonary resuscitation: a systematic review and meta-analysis. Crit Care 24, 61 (2020). https://doi.org/10.1186/s13054-020-2773-2

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Sunday, February 23, 2020

Dopamine doesn’t belong in the ICU anymore

Link to FREE FULL ARTICLE and PDF

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Blood Pressure Measurements: Arterial Line vs Oscillometric Cuffs

We all do this every single day. We measure target many of our interventions in the critically ill patients to blood pressure. Whether it’s fluids, vasopressors, or blood pressure lowering agents, we obsess over these parameters. We feel warm and fuzzy if it’s okay. But are we using the right tool to find out these numbers?

I’ve always harped on arterial lines, although invasive, being the most reliable method of evaluating the blood pressure in our patients. If someone is critically ill on jet fuel, they’re getting an a-line. This is a fun study where they compared the oscillometric BP cuffs to a-lines in 736 patients.

When you look at the mean differences they obtained, the numbers weren’t too bad.
Systolic: 0.8mmHg
Diastolic: -2.9mmHg
Mean Arterial pressure: -1mmHg

This wouldn’t drive any of us crazy, right? We’d be cool with these differences if it avoids invasive (painful) interventions on our patients. But wait, there’s more. There was a large amount of variability which could lead to additional interventions.
Systolic: ± 15.7mmHg
Diastolic: ± 11mmHg
MAP: ± 10.2mmHg

The article goes as far as to say that BP cuffs would not pass the Association for the Advancement of Medical Instrumentation standards. There’s no data as to how this changes outcomes.

This was a post hoc analysis (after the fact). This shouldn’t be too challenging to accomplish a prospective study looking at this in our critically ill patients. We have many patients who have a BP cuffs and an a-line in place. Why not just record cuff pressures every 15 minutes and obtain some data? Obviously it’s more complicated than that.

A hat tip to the authors.

T. Kaufmann, E.G.M. Cox, R. Wiersema, et al., Non-invasive oscillometric versus invasive arterial blood pressure measurements in critically ill patients: A post hoc analysis of a prospective observational study, Journal of Critical Care(2019)

Link to full article (not free)

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.

Saturday, February 22, 2020

Oscillometric devices vs Arterial lines. New data.

Why is it important to stay up to date? There’s a pendulum in medicine but there’s a time when the pendulum swing is going to bite you in the butt and you’re going to be wrong. Seems like I’m wrong.

I have an extremely popular post and YouTube video regarding how oscillometric devices are correct with regards to their MAP but not their SBP and DBP. I hadn’t found any studies to validate how the SBP and DBP applied. Now we have data. And I may have to eat my words. I’m cool with that, though. This study was published earlier today. I cannot get my hands on it to take it apart, but the data is compelling. They did some fancy statistics that I can’t admit to understand including Bland-Altman and error grid analyses. Although the averages seem to be close, the variations are as follows:
SAP 0.8 mmHg (±15.7 mmHg, −30.2 to 31.7 mmHg)
DAP −2.9 mmHg (±11.0 mmHg, −24.5 to 18.6 mmHg)
MAP −1.0 mmHg (±10.2 mmHg, −21.0 to 18.9 mmHg)

The interesting part is that the ICU is a world of details and although the differences were small. The variation between the two, radial arterial line and oscillometric cuff, was enough though to cause additional treatment changes in more than 20% of patients.

I despise reading abstracts and coming to conclusions but at this point I have no choice. Maybe tomorrow I’ll be able to take this apart entirely.

Link to abstract

EJ

Kaufmann T, Cox EGM, Wiersema R, et al. Non-invasive oscillometric versus invasive arterial blood pressure measurements in critically ill patients: A post hoc analysis of a prospective observational study [published online ahead of print, 2020 Feb 22]. J Crit Care. 2020;57:118–123. doi:10.1016/j.jcrc.2020.02.013

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Guidelines for Pain, Agitation/Sedation, Delirium in the ICU

I am currently working on a lecture where I discuss reducing the utilization of opioids in the ICU for our critically ill patients. The sources of pain are plentiful, unfortunately. Truth is, opioids are the best option for our patients at the time of this writing but we also need to work hard to try to minimize the exposure to this family of medications via alternatives. Which alternatives might you ask? In particular, I have taken deep dives into the utilization of ketamine, magnesium, gabapentin/pregabalin, NSAIDS, nefopam, acetaminophen, dexmedetomidine, as well as regional blocks performed by our anesthesia colleagues. 


The PADIS (pain, agitation/sedation, delirium, immobility, and sleep disruption) guidelines linked here, and are completely FREE to download, provide some direction as to how to better take care of our patients. When I write these lectures, and this may seem counterintuitive to some, I leave the guidelines for last and attempt to read everything under the sun on the topic so that it does not cloud my interpretation. I had read these guidelines in 2018 when they initially came out but now I have even more respect for the section on pain management bc the quality of the studies just aren't as good as we want them to be. Hence the "very low quality of evidence" tied to many of the recommendations made. I surprised that they even made a dosing recommendation for ketamine as the dosing behind most of the articles are pretty scattered.  
These guidelines are a monumental undertaking and I send a definite hat tip to the authors.

Devlin JW, Skrobik Y, Gélinas C, et al. Clinical practice guidelines for the prevention and management of pain, agitation/sedation, delirium, immobility, and sleep disruption in adult patients in the ICU. Crit Care Med 2018;46:e825–e873.

-EJ




Link to FULL FREE Article



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Saturday, February 15, 2020

Early Vasopressors in Septic Shock?

This is a question that is often asked. Do we give fluids until the patient no longer "responds to fluids" or start vasopressors early?

Here's my bias: I dislike arbitrarily pounding patients with fluids. It causes harm. We know this.

I don't know what people who aren't doing advanced hemodynamic monitoring of some sort mean when they say "they respond to fluids". "I gave a liter of fluids and the BP got better" for 30 minutes is not a determinant of fluid responsiveness. Remember, I've cited here before that critically ill patients extravasate 80% of that liter of fluids within one hour. What did you really do outside of feeling like you did something? The authors used PPV, SVV, echo with VTI combined with PLR, end-expiratory occlusion maneuvers, and capillary refill time. Did I mention that these authors are legends in the field? Well, they are.

In my opinion, providing pressors early provides a safety net of sorts to the organs to make sure they're being perfused. You've seen it often in your ED and ICU. Patient comes in sick. They're hypotensive, they get their 30cc/kg and their BP gets "better". The cuff cycles again 15 minutes later and their BP is now 60/30. How long did those organs go under-perfused? Minutes matter. We NEED to get better at this. After all, we are supposed to be the biggest badasses in medicine, yet we often shrug our shoulders and react when it's ugly instead of preemptively fixing the issues.

Turns out that very early vasopressors were beneficial to the patients. The definitions of the two groups are defined on my slides. The outcomes are also defined there for the sake of not taking up too much space.

This could be practice changing data. I personally start vasopressors really early in my practice. Some may say, let's wait for a prospective randomized clinical trial before putting this into practice. To those people I say, there's no harm in this. Also, you can't blind the physicians so when that study comes out positive some will say "oh but the physicians weren't blinded". Research. Sigh.

A hat tip to the authors. This article was published yesterday. How's that for cutting edge?

-EJ

Ospina-Tascón, G.A., Hernandez, G., Alvarez, I. et al. Effects of very early start of norepinephrine in patients with septic shock: a propensity score-based analysis. Crit Care 24, 52 (2020).



Link to Abstract

Link to FULL FREE PDF




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Friday, February 14, 2020

Weaning Order of Norepinephrine and Vasopressin in Septic Shock Patients

This is a post for all my Critical Care Nurses out there! Please tag and share with your friends and colleagues. When you have a patient in shock on norepinephrine and vasopressin and has turned the corner, which vasopressor do you turn off first: norepinephrine or vasopressin? From my hard digging through the internets I have only found three studies which touch on this topic. Also, this seems like a pretty simple RCT that I could actually do at my shop. Anyone interested in joining in on the fun to make it multi-centered? These slides to some extent will be featured in my Hawaii and Portland lectures later this year. Seems like I'll be heading to Brooklyn and Indian Wells, CA in 2021.

Here's what the data says. Spoiler alert: there's no 100% correct answer.

2010: Bauer, et al. did a retrospective study where the team found that patients did better if the NE was weaned first and the vasopressin was weaned second.

2017: Hammond, et al. also performed a retrospective study which found similar results: patients did better if they weaned off the NE first. So far so good for weaning off NE first.

2018: Jeon, et al. just had to throw a wrench into everything. This was a prospective randomized trial where the results were the exact opposite of the other two. Ugh. Those of you who have been hanging out with me long enough may recognize that I covered this study in March of 2019 when the page was just getting ramped up.

Well what's the right answer? I guess we just don't know. Dealers choice. The randomized trial should hold more of an answer due to it being higher on the scale of evidence. The studies are small, hence me considering on doing a trial on this since ultimately it's not going to cause any harm and I really don't have a bias. What do you think?

-EJ

Link to Article (not free)

Bauer S, Aloi J, Ahrens C, Yeh J, Culver D, Reddy A. Discontinuation of vasopressin before norepinephrine increases the incidence of hypotension in patients recovering from septic shock: a retrospective cohort study. J Crit Care. 2010;25(2):362.e7-362. e11.

Link to Article (not free)

Hammond DA, McCain K, Painter JT, Clem OA, Cullen J, Brotherton AL, Chopra D, Meena N. Discontinuation of vasopressin before norepinephrine in the recovery phase of septic shock. J Intensive Care Med. 2017:885066617714209

Link to Full FREE PDF

Jeon K, Song JU, Chung CR, Yang JH, Suh GY (2018) Incidence of hypotension according to the discontinuation order of vasopressors in the management of septic shock: a prospective randomized trial (DOVSS). Crit Care 22(1):131

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